UWorld Medicine

Tx for binge-eating disorder

CBT, behavioral weight loss therapy, SSRI, Lisdexamfetamine, topiramate.

Tx for Bulimia nervosa

CBT, nutritional rehab, and SSRI (fluoxetine) <-- combo of these is 1st line tx

Clinical findings present in all congenital infections (so aren't distinguishing features)

IUGR, HSM, jaundice, blueberry muffin spos

s/sx Angelman syndrome

developmental delay, jerky gait, happy demeanor, hand FLAPPING, seizures. Disease of genetic imprinting from deletion of maternal copy of 15q11-13 (so they just have Dad's.. so think Daddy's little angel)

Plummer-vinson syndrome can have:

esophageal webs, dysphagia, iron deficiency anemia, glossitis.

How do condylomata lata present?

"got a lata problems if you have syphilis" (secondary syphilis) Plaque-like reddish-brown velvety lesions at intertriginous areas

What's the week cut off for distinguishing chronic HTN (before pregnancy) to gestational HTN?

20 weeks.

What's the percentage considered high grade for carotid stenosis?

70-99%

What's an abnormal Anke-Brachial Index?

<.90 is Abnormal (considered dx of occlusive PDA) 0.91- 1.30 is normal >1.30 means there is calcified and uncompressible vessels and you need more vascular studies.

What is fetal HR that is considered fetal tachycardia?

>160.

Chronic cough from post-nasal drip can last up to how many weeks?

>8 weeks; postnasal drip can be associated with allergic rhinitis. Cough d/t mechanical stimulation of the afferent limb of the cough reflex in the upper airway.

Ulnar nerve entrapment, where does it happen?

@ the elbow: at the medial epicondyle groove.

What kind of hormone change does small cell carcinoma of the lung usually cause? (paraneoplastic syndrome)

ACTH production and SIADH.

What is elevated in mixed germ cell tumor?

AFP is elevated and usually beta-hCG. is also elevated.

Pt passes out during exertion/exercise. What is the cause of the syncope?

AS, HCM, or anomalous coronary arteries

What is acetazolamide? MOA? what condition is it in used it? and how does it work?

AcetaZOLAmide is carbonic anhydrase inhibitor that treats pseudotumor cerebri by decreasing CSP production inorder to treat the increased ICP in that condition.

What do you expect to be excreted in the urine with someone with DM nephropathy?

Albumin (Albuminuria)

autoimmune disorder with circumscribed patches of hair loss. Hair shafts show narrowing close to the surface and may be broken off.

Alopecia areata

Zinc deficiency presentation:

Alopecia, pustular skin rash (perioral region & extremities), hypogonadism, impaired wound healing, impaired taste, immune dysfunction

How do pts with selective IgA deficiency typically present?

Asymptomatic but may have recurrent respiratory infection.

What's the mutation in Hairy cell leukemia?

BRAF mutation

Untreated hyperthyroid bone disease. What are they at greatest risk of developing?

Bone loss. Too much thyroid hormone --> osteoclast activity

MCA stroke

Classic stroke, aphasia, contralateral hemiparesis

Burning rubber or plastic can result in what kind of poisoning

Cyanide poisoning/inhalation

Immunosuppressant with SE of gum hypertrophy?

Cyclosporine.

What's the mutation in Marfan's?

Fibrillin 1 gene mutation

When you suspect MS, what do you want to do next?

Get an MRI!! T2-weighted imaging will show multifocal, ovoid, subcortical white matter lesions located in periventricular, juxtacortical, infratentorial, and spinal cord areas.

Woman on long term OCP what kind of solid liver mass might you find on their liver that cold hemorrhage or turn malignant?

Hepatic adenoma

Pt has eye pain and vesicular eruption involving cornea or iris. What are you thinking?

Herpes zoster ophthalmicus

What is it when pt has small and large bowel distention and hypoactive bowel sounds and no air fluid levels on imaging?

Ileus (usually associated with medial condition, or post-op)

Bitter almond breath is characteristic of :

Inhaled cyanide.

Ischemic cardiomyopathy leads to what kind of HF?

Ischemic cardiomyopathy is LV systolic dysfunction d/t CAD or prior MI. So you would see decreased LVEF. HFrEF (decreased LV EF)

Pt presents with gradual proximal muscle weakness without prominent pain, muscle spasm, or trismus (so main symptom is weakness). What is mechanism of polymyositis?

It's an inflammatory myopathy mediated by cytotoxic T-lymphocytes

Mutation in Polycythemia vera?

Jak2

Vitamin A helps protect against M&M with what infection?

Measles!

Iron deficiency presentation

Microcytic anemia

You get bit by low-risk wild animal (squirrel, chipmunk, mouse/rat, and rabbit), what do you do?

No PEP required for bites by low risk animals

What is triple therapy for H.pylori infection?

PPI, amoxi, clarithromycin

Pt with very high PTH level and high Ca and low Phosphorus comes in. He comes in for follow up of his mild HTN. His neck has no masses on physical exam. 24 hr urine calcium excretes 325mg, DXA with normal bone mineral density. Renal U/S shows small <5mm stones in both kidneys. What do you do next?

Parathryoidectomy. -Recommended in symptomatic hypercalcemia (fatigue, complication), complications (oestoporosis, nephrocalcinosis, nephrolithiasis, impaired renal function) or at sign. risk for complications (ex: serum calcium >1 mg/dL above normal or urinary calcium excretion >400/day), or it's a young pt <50yo likely to have complications during their lifetime. should be offered surgery. -Why is CT scan not the correct answer? First, don't pick and extended CT scan that is looking everywhere, since you aren't suspecting malignancy here. This is simply a parathyroid adenoma (most common)or hyperplasmia. If you were to do CT it would be to look for pheo since parathyroid tumors can be part of MEN2A, but you would only imagine to evaluate MEN2A if there is evidence of ***multi-glandular hyperparathryoidism or additional endocrine tumors***

Abdominal pain, dark urine that is due to hemoglobinuria what could this be?

Paroxysmal nocturnal hemoglobinuria. (also look for hemolysis, cytopenias and hyper coagulable state)

Side effect profile: Aripriprazole

Partial DA agonist; approved for adjunct tx in MDD

Young female athlete with chronic overuse of the knee. Pain over anterior knee that is reproduced by extending the knee while compressing the patella (patellofemoral compression test). May have swelling of anterior knee. What does this pt have?

Patellofemoral pain syndrome (PFPS)

Common SE of dihydropyridine CCB amlodipine?

Peripheral edema.

Crampy lower abdomen and back pain during menses, normal exam. (usually young pt; teenager in the stem)

Primary dysmenorrhea

What conditions do you expect a ***urine*** test for reducing substances to be positive?

Pts with glucosuria and galactosuria.

What is a CV side effect of macrolides (ex: azithromycin)

QT prolongation

Someone has hx of prostate cancer and now has bony mets after androgen ablation (orchiectomy). What's the next step?

Radiation therapy.

Symptoms of Vitamin K toxicity

Rare to see this.

Where is the obstruction usually in Hirsprung's?

Rectosigmoid Failure of neural crest cell migration; aganglionic section.

What if a patient has relapse of MM? What drug can you use?

Relapse of MM: use Daratumumab (anti-CD38 drug) how DARe M-M come Back..tx w/ DARatuMuMab..

What kind of study allows for calculation of the relative risk? how come?

Retrospective cohort studies allow for calculation of relative risk, because the RF exposure is determined before the outcome is known.

Pt with suicide attempt now presents with bradycardia, AV block, hypotension, diffuse wheezing. He is also lethargic and has cool/clammy extremities. Hx of HTN And CAD (no psych hx or psych meds). What do you think they took? Why do you think that?

Sounds like either a BB, CCB, digoxin, or cholinergic agent. But the wheezing is specific for BB overdose. Wheezing bc of the brochospasm that happens with Beta-2 blockade.

What is the most common cause of bacterial meningitis? what kind of organism is it?

Strep pneumo Gram positive cocci (in chains)

Why is there a single S2 sound for transposition of the great vessels?

The pulmonary components of S2 is not heard bc it's behind the aorta; in TGV, the aorta is anterior and so you hear it more. CXR shows narrow mediastinum "Egg on a string appearance" This infant will have cyanosis right away.

What do pro- and retro- spective cohort studies have in common?

They are both taking RFs and looking at ***disease incidence***.

What is IV Alteplase?

Thrombolytic agent: improves neuro outcomes in pts with acute ischemic stroke if given within 4.5 hrs of symptom onset. (do it only after noncontrast heat CT shows it's not hemorrhagic stroke)

What are the preventive (ppx) migraine meds?

Topiramate - think about if I had a migraine, I'd be a Tapir that has to nap and go to sleep in a dark room... but instead i could take Topiramate! Divalproex sodium (sodium valproate) TCAs (amytriptyline) Bete blockers (propranolol) - think about Mariel taking a beta blocker for her migraines

Again, what are the preventive/prophylactic meds for Migraine HAs?

Topiramate, Beta-blockers (ex: propanolol), TCAs (ex: amytriptyline), or Divalproex sodium.

What do two-sample t-test and two-sample z-test compare?

Two means

What do you treat atypical pneumonia, like Mycoplasma pneumonia with?

Tx with azithromycin

When do you see Struvite stones?

UTI with Proteus (urease producing bacteria)

What is Selegiline?

a monoamine oxidase inhibitor.

When would you think more gastric cancer? symptom presentation-wise?

abdominal pain with GI ulcers and bleeding, but you would have associated weight loss, early satiety, and dysphagia.

BL loss of central vision in older patient (>50 yo) What's the dx? why does it happen?

age-related macular degeneration d/t degeneration and atrophy of central retina (macula), retinal pigment epithelium, Bruch's membrane, and choriocapillaries.

Pt with DVT, livedo reticularis, hx of recurrent miscarriages, what are you thinking she also has? on labs?

antiphosopholipid syndrome (she's prone to clots), r/t Lupus anti-coagulant and SLE... so think she's also got prolonged PTT on labs

When do you give sodium thiosulfate?

as antidote for cyanide poisoning. Setting of fires or occupational exposure (mining, pesticides). Pts with cyanide poisoning have markedly elevated lactate levels (>10 mEq/L), when normal is 0.5-2.2 mEq/L

Vitiligo, caused by

destruction of melanocyte (auto-immune conditions) Tx: Limited dx: topical steroids Extensive/unresponsive dz: oral steroids, topical calcineurin inhibitiors, PUVA.

How does HPV infection as a cause of oropharyngeal cancer presents?

dysphagia, bleeding, mass on exam.

What muscles are affected in myasthenia gravis? What is the tx? Are there abnormal muscle enzymes (ex: creatine kinase) in MG?

facial and distal limb muscles and sometimes proximal muscles. Weakness worsens with activity in MG. treat with pyridostigmine (cholinesterase inhibitor) No, muscle enzymes are generally normal in MG.

What does Lyme disease show on CSF?

lymphocytic pleocytosis. Borrelia are double-membrane spirochetes

MVP sound

mid-systolic click & late systolic murmur heard best over cardiac apex

What does a p-value reflect?

random variability.

What is the Hawthorne effect?

study subjects know they are being watched . Solve with placebo control and blinding both investigators and participants

Unilateral, often progressing to BL eye involvement. Eye stuck shut in morning. Watery, scant, stringy mucus discharge. Discharge doesn't reappear after wiping (like with bacterial conjunctivitis). Burning, sandy, gritty feeling with prodrome (eye sx preceded by typical nasopharyngeal symptoms). Common in late summer/fall and can occur in clusters or small epidemics. Lasts longer (several days) than allergic conjunctivitis. Conjunctivae has diffuse injection, follicular "bumpy."

"Pink eye": Viral conjunctivitis.

Best non-pharmacologic ways to impact BP?

#1) Lose weight #2) DASH diet (which is a diet to stop HTN, "Dietary Approaches to Stop Hypertension": high fruits/vege/legumes/low fat dairy products/low saturated and total fat) #3) Exercise: 30 min/day 5-6x/week Note: cessation of cigarette smoking helps lower overall risk of cardiovascular disease but doesn't directly lower BP.

Symptoms of B2 (riboflavin) deficiency

(Oral symptoms) -Angular cheilosis (think 2 corners of mouth, B2 deficiency) -Stomatitis -Glossitis Seborrheic dermatitis (scaly scalp)

Tell me about Maternal Thyroid testing in the 1st Tri of Pregnancy For Total T4 Free T4 TSH

(Think of this time as a increased metabolic state... so need more thyroid hormone... so that's what happens) Total T4: Increased Free T4: Unchanged or mildly increased: - beta-hCG stimulates thyroid hormone production in 1st Tri - Estrogen stimulates TBG; thyroid increases hormone production to maintain steady free T4 level TSH: decreased - Increased beta-hCG and thyroid hormone suppresses TSH secretion.

What the the most important ***pathogenic factor*** for the development of a Zenker diverticulum? Where do ZDs occur?

***Motor dysfunction*** - Upper esophageal sphincter dysfunction and esophageal dysmotility are believed to cause ZD. ZD develop immediately above the upper esophageal sphincter with posterior herniation between the fibers of the cricopharyngeal muscle.

Young female patient and her hair is falling out and she has a receding hair line. She has extensive facial and back acne. Abdomen is obese. What test do you want to do? What do you think she has? How to dx? How do you tx her?

***Oral glucose tolerance test.*** You think she has PCOS and these pts are at increased risk for metabolic syndromes like DM, which is why you want to do the OGTT (gold standard test for dx T2DM) Think she has PCOS since she has irregular periods, is obese, and has male pattern baldness and acne, indicating androgen excess. Dx: can be made clinically, but can also get u/s to show polycystic ovaries. Tx: first line is weight loss, can use OCPs for menstrual irregularities and clomiphene citrate for ovulation induction.

In addition to POOP or "severe distress due to pain" (Stephanie, don't ignore the pt's complaint of pain", and a cardiac Mi hx that could suggest cardiac embolic events (a. fib, valvular disease, cardiovascular aneurysm), what else supports the dx of acute mesenteric ischemia (gut MI)?

***Rapid onset severe PERIUMBILICAL PAIN: think acute mesenteric ischemia. ***Pain out of proportion to exam findings: "severe distress d/t pain" Hematochezia (late complications) RFs: acute on chronic atherosclerosis, embolic source (thrombus, vegetations), hyper-coagulable d/o. Labs show: leukocytosis, elevated amylase (not super duper elevated like pancreatitis but elevated) and phosphate levels, metabolic acidosis (will see either elevated lactate or decreased bicarb suggesting metabolic acidosis) Dx: CT angio (preferred) or MR angio. Can do mesenteric angiography if dx is unclear.

Asian pt has bloating, flatulence, abdominal cramps, and exploosive watery diarrhea after eating diary. Her abdomen is distended and she has borborygmi (stomach is rumbling). What do you expect to find on testing?

- Positive Hydrogen breath test - Nothing really with her urine - Everything else will be stool related: pH of stool will be low (acidic, bc of fermentation), expect increased stool osmotic gap (>50 bc of the the non-metabolized lactose is this in there, causing the osmotic diarrhea), and positive stool test for reducing substances -Do not see steatorrhea bc that has to do with fat malabsorption whereas lactose intolerance is a problem with carbohydrate malabsorption

What are two commonly used drug classes that are also commonly associated with drug-induced pancreatitis (note: there are many more, just name 2)?

-ACE-inhibitors -Thiazide diuretics

What SEs can you see with TCAs (ex: amitriptyline)?

-Orthostatic -Anticholinergic (dilated pupils, flushed skin, hyperthermia, decreased bowel sounds... Blind as a bat, Red as a beet, Hot as a hare, dry as a bone) -Anti-histamininic -Cardiac SEs

What's on your ddx when you hear the pt describe seeing: flashes of light and floaters

-Retinal detachment (also has curtain) -CRAO (also has curtain) -CMV retinitis (can lead to complications of blindness and retinal detachment)

Pt is on Pit (oxytocin) and you are giving her a whole bunch to induce labor. What complication are they at risk for?

-Tachysystole: All agents used for labor induction (including oxytocin) can cause uterine tachysystole: abnormally frequent contractions; >5 contractions in 10 minute averaged over 30 min period. FHR tracing abnormalities are more common with tachysystole d/t insufficient uterine relaxation between contraction that can cause placental spiral artery constriction, decreased placental blood flow and fetal hypoxia. So tachysystole is associated with increased risk for -section, low umbilical cord PH and NICU admission. Also increase the risk of: -Tetanic (intense, prolonged) contractions, particularly in high doses. -Hypotension:: can occur with rapid infusion of high dose oxytocin (more relevant in immediate postpartum time during which boluses of oxy are given to prevent and treat pp hemorrhage.. just be aware that a SE of oxy is also hypotension) -Hyponatremia: since oxytocin is similar in structure to vasopression (ADH... remember both oxytocin and ADH are the two hormones released from the posterior pituitary...so reasons to say they are similar structurally), so high doses of oxy can lead to water retention and hyponatremia.

When do you see uric acid stones

-When urine is acidic. (Think Uric.. Uri-ne is Acid-ic) -When there is increased cell turnover, thereby resulting in hyperuricemia and hyperuricosuria. -Dehydration

General rule for side effect profile for atypical antipsychotics -pines vs -dones

-pines (olanzapine, quetiapine, asenapine, clozapine): increased risk for weight gain, metabolic syndrome, DM -dones (risperidone, lurasidone, ziprasidone, iloperidone): increased risk for movement disorders (Risperidone.. is whisphering and moving around in the move theater), cardiac conduction problems (Z and QT prolongation)

Tetanus exposure. How do you decide whether to give Tdap vaccine and tetanus immunoglobulin?

1) Ask has pt had 3 lifetime doses to determine if you'll be giving tetanus immunoglobulin (TIG) Answer is Yes- then don't give TIG 2) Ask when the last time they had a tetanus vaccine was. -clean wound, give tetanus vaccine if no booster in the last 10 years -dirty wound, give tetanus vaccine if no booster in last 5 years 1) Ask if pt has had 3 lifetime doses to determine if you'll be giving TIG Answer is No- then give tetanus vaccine -clean wound, don't give TIG -dirty wound, also give TIG Note: current recommendation for kids is to get a 3 dose series at age 2, 4, and 6 months of age. Then another dose at 15-18 months and another one at 4-6 years (so a total of 5 shots). Then as adults, they should get a single dose of Tdap followed by revaccination (booster) of tetanus and diphtheria every 10 years.

What are some treatments in addition to fiver, antispasmodic agents (hyoscyamine, dicyclomine), and TCAS or SSRIs that you could give to pts with ***constipation-predominant*** IBS?

1) Fiber 2) PEG (polyethylene glycol) - nonabsorbed bowel lubricant 3) Lubiprostone: chloride channel activator: use if PEG doesn't work. (Think.. "lub" up the bowels to treat the constipation) 4) Linaclotide (guanylate cyclase agonist: use if PEG doesn't work.

HIGH YIELD: Side effects of cyclosporine (immunosuppressant that inhibits the transcription of interleukin-2 and several other cytokines, mainly the T-helper lymphocytes)

1) Nephrotoxicity: most common & serious SE. Reversible acute azotemia or irreversible progressive renal disese. Hyperuricemia (increased BUN), accelerated gout, hyper-K, hypo-phosphatemia, hypo-Mg are all part of the renal-induced dysfunction. Rarely, hemolytic uremic syndrome (HUS) may be seen. 2) HTN: d/t renal vasoconstriction & Na retention. (Us CCB to tx) 3) Neurotoxicity: HA, visual changes, seizures, mild tremor, akinetic mutism (often reversible) 4) Glucose intolerance: fairly common. Pt who are also taking prednisone steroids may have hyperglycemia 5) Infections: seen in 40% of pts 6) Malignancy: increased risk of SCC of skin and lymphoproliferative disease 7) Gingival hypertrophy (gums hypertrophy!) 8) GI symptoms: anorexia, N/V/D. (common but mild) TL:DR; Cyclosporine SEs: ***gum hypertrophy, hirsutism***, ***renal toxicity***, ***neurotoxicity***, normal GI intolerances of N/V/D, worsened primary care stuff like HTN, glucose intolerance, infection and watching for malignancy. Memory tool: think about someone cycling on or spreading spores on your gums... cyclosporine.. so that irritates the gums and causes gum hypertroph.

What do you expect to see in all the different tests you can do for lactose intolerance?

1) Positive hydrogen breath test (surprisingly) 2) Positive stool test for reducing substance 3) Low stool pH (acidic bc of fermentation products) 4) Increased stool osmotic gap (osmotic gap is high bc of the unmetabolized lactose and organic acids; it's >50 in all forms of osmotic diarrhea) -There should not be any steatorrhea bc that is usually a product of fat malabsorption, not carbohydrate malabsorption

There are 4 primary manifestation of rosacea. What are they?

1) erythematotelangiectatic rosacea: redness and facial flushing, telangiectasias, rough/scaling/burning discomfort 2) papulopustular rosacea: small papules andpustules resembling acne 3) Phymatous rosacea: chronic, irregular thickening of skin, usually involving nose 4) Ocular rosacea: involvement of cornea, conjunctiva, and lids with burning or "foreign body sensation," blepharitis (eyelid inflammation), keratitis (inflammation of cornea), conjunctivitis, corneal ulcers, or recurrent chalazia (cyst on eyelid d/t block oil gland)

What are some treatments in addition to fiver, antispasmodic agents (hyoscyamine, dicyclomine), and TCAS or SSRIs that you could give to pts with ***diarrhea-predominant*** IBS?

1) riFAXiMIN: non-absorbable abx with modest effect in diarrhea predominant IBS (Memory tool... this almost looks like the antispasmodic ending -mine, expect it's a little different -min... can still use it on Adriano and his IBS... Memory tool.. he's far away so has to fax his "mine" statement.. but only "-min" makes it... but his message is not received.. to think ... non-absorbable abx with modest effect in diarrhea predominant IBS.) 2) Alosetron: serotonin inhibitor (needs special permission to use) Memory tool: Al sitting on the toilet.. bc he has IBS diarrhea.. so give him AloSetron... S in the middle.. think serotonin inhibitor 3) Eluxadoline: mu opioid receptor agonist (relieves pain, slows bowels since it's an opioid receptor agonist)

When is Chorionic villus sampling done? What does it get? How is it physically done?

10-13 weeks Place catheter into intrauterine cavity (either trans-abdominally or trans-vaginally) and aspirate chorionic villi from the placenta. This allows you to get fetal karyotype (to do genetic tests)

How do you abort an acute attack of cluster headache? (symptoms of headache behind one eye that is excruciating, sharp and steady, lasts 15-90 min, can wake you up from sleep, and has associated sweating, facial flushing, nasal congestion, lacrimation and pupillary changes)

100% oxygen inhaled. or SubQ sumatriptan.

When is Amniocentesis done? What does it get? How is it physically done?

11-14 weeks Stick needle through the abdomen into the amniotic sac and get amniotic fluid. Allows you to get fetal karyotype.

How do you stage a pressure ulcer? (1-4 and unstageable)

1: intact skin, non-blanchable with local redness 2: shallow ulcer, or possible intact/ruptured bliter 3: full-thickness loss, see subQ fat 4: full-thickness loss, see anything underlying like muscle, bone, tendon unstageable: full-thickness loss, eschar (anything past stage 3 has full-thickness loss)

AV Block

1st Degree: PR prolongation 2nd Degree: - Mobitz Type I (Wenckebach): Increasing PR interval and then a dropped QRS - Mobitz Type II (Non-Wenckebach): Constant PR interval, and then a dropped QRS 3rd Degree: PR and QRS are not synced at all

How does IV mannitol work to treat acute glaucoma?

1st line tx for acute glaucoma. osmotic diuretic that works immediately to decrease intraocular pressure.

Tx for essential tremor (gets worse with action, usually on hands and BL, often has family hx)

1st line: Beta blocker (ex: propranolol) Could also use anticonvulsants (ex: primidone) or small amounts of alcohol will make it better, or benzo (ex: clonazepam but this is not usually the choice)

What is the treatment for reactive arthritis?

1st line: NSAIDS!!! (not Abx. Since this is a type of seronegative spondyloarthropathy; treat with NSAIDS!!!!!)

How do you tx PCOS? First line, for menstrual regulation, or ovulation induction?

1st line: weight loss For menstrual regulation: OCPs For ovulation induction: Clomiphene citrate

What are the treatment options for PCOS

1st line: weight loss OCPs for menstrual regulation Clomiphene citrate for ovulation induction

Pt who comes in for sudden onset severe pain in right leg that started 5 hours ago. Leg feels numb. Hx of anterior wall MI 2 months ago that was not re-vascularized bc he present too late. Apical impulse displaced to the left. 3/6 holosystolic murmur at apex radiates to axilla. Right leg cold to touch. Palpable femoral pulse but not popliteal, posterior tibial, or dorsalis pedis pulses on right. Pulses on left are fine. EKG with normal sinus rhythm, deep Q waves in leads I, aVL, and V2-V5 with 4mm ST segment elevation, unchanged from what he had 2 months ago. What is the likely dx?

2 months ago... he had an big MI..and now he's throwing arterial clots (absent pulses, acute limb ischemia) So think about LV aneurysm (happens 5days-3months s/p MI) Ventricular aneurysm is a late complication (up to 3 months later) of acute STEMI. A mural thrombus is present in up to 50% of pts with LV aneursym and can lead to systemic embolization. Note: hallmark of ventricular aneurysm on EKG is persistent ST segment elevation after recent MI along with deep Q waves in the same leads. (so the description where his EKG was the same as before when he has his STEMI.. that's a BIG FAT CLUE to dx of LV aneursym, think about that if the pt then also starts throwing arterial clots; systemic embolization of the thrombus can lead to acute arterial occlusion and can cause stroke, mesenteric ischemia, and acute upper and lower extremity ischemia.

When are you thinking about DTs?

2-4 days after last drink (48-96hrs) Confusion, agitation, fever, tachycardia, hypertension, diaphoresis, hallucinations (autonomic excitation, agitation, tremor, altered sensorium)

Chronic HTN vs gestational, whats the week cutoff?

20weeks gestation. If they have HTN before that, then it's chronic HTN If they get HTN after 20 weeks, it's gestational HTN Pre-eclampsia: add on proteinuria or end organ damage Eclampsia: add on seizures Chronic HTN with superimposed pre-eclampsia: worsening HTN to already existing HTN (that was there prior to 20 weeks), new or worsening proteinuria, or end organ damage

Increased BNP, what clinical sign best correlates with this?

3rd heart sound. S3 is a low frequency diastolic sound produced by the passive ventricular filling during early diastole. It's best heard over the cardiac apex in the left lateral decubitus position. An abnormal S3 (louder and higher pitch, S3 gallop) is commonly heard in pts with CHF d/t LV systolic dysfunction, and it correlates with elevated LA &/or ventricular filling pressure and serum BNP levels.

If asked about which clinical sx best correlates with the lab finding of elevated serum BNP, what is the answer?

3rd heart sound.. -commonly heard in pts with CHF d/t LV systolic dysfunction (up to 99% specificity) and correlates with elevated LA &/or LV filling pressures and serum BNP levels. Note: don't pick extremity edema... think about how that can have a lot of other causes and not just heart etiology. When you think of elevated BNP, think of 3rd heard sound. When you think of 3rd heard sound, think of elevated BNP

Where is Bartholian gland cyst located?

4 and 8 o'clock at the posterior introitus and dairn through ducts into the vestibule. They provide lube to the vestibule and are not usually palpable unless the duct is blocked which results in fluid buildup and cyst formation. Usually seen in women <30yo. See mobile, soft, non-tender, well-circumscribed mass behind the labium majus with vaginal extension. Larger cysts may cause discomfort during sex, walking, sitting, or exercise. Symptomatic cysts --> do I&D and may use Word catheter.

IF someone has a anterior mediastinal mass, what is on your differential?

4T's: thymoma, teratoma (must include other germ cell tumors), thyroid neoplasm, terrible lymphoma. Note: Most pts with non-seminomatous germ cell tumors (yolk sac, choriocarcinoma, embryonal carcinoma) have elevated AFP, with a good number also having elevated beta-HCG

rapid onset red macules, vesicles, bullae with necrosis and sloughing of epidermis and mucosal involvement after either medication or other triggers (Mycoplasma pneumoniae, vaccination, graft-vs-host disease), what do you call it if it cover <10% BSA, and then >30% BSA. What are drugs that can cause SJS?

<10% BSA: Stevens-Johnson Syndrome (SJS) >30% BSA: Toxic epidermal necrolysis (TEN) Drug triggers: Allopurinol, Antibiotics (Sulfonamides), Anticonvulsants (Carbamazepine, lamotrigine, phenytoin), NSAIDs (piroxicam), Sulfasalazine

Who just gets albuterol if they have asthma?

<2days/week- daytime sx <2x/month- nighttime awakenings just albuterol (SABA)

What is the cut off measurement for when you can do methotrexate therapy in an ectopic pregnancy?

<3.5 cm (More risk of failure with methotrexate if the pt has an ectopic >3.5 cm)

What is the GA that you give mag. sulfate for neuroprotection (to decreased risk of neuro complications like CP) of the fetus?

<32 weeks gestation (if you are expecting imminent delivery and fetus is <32 weeks, mag them.... Memory tool: Think Mg++ is the abbreviation for magnesium.... so think there are 2 cations. there.. so have that remind you of thirty-TWO week GA (<32 GA) as the cut off for when you give mag for neuroprotection)

BPP scores. what do the following scores mean? <4 6 8-10

<4: indication for delivery to prevent IUFD 6: equivocal 8-10: Normal

Kidney stone less than what size will you just increased fluids intake to >2L/day and have them pass spontaneously with conservative management?

<5mm

Placenta previa is when the placenta covers the os. If the placenta is more than this distance from the os, then you can do vaginal delivery.

>2cm from the cervical os.

Define each of the categories when determine how to read a TB skin test?

>5 mm induration: for high risk pts like HIV+, recent contact with know TB case, nodular/fibrotic changes on CXR consistent with previously healed TB, organ transplant recipient/otherwise immunosuppressed >10mm induration: for mod risk pts like recent immigrants (<5 years) from TB endemic place, IVDUs, work or live in high risk place (hospital, nursing home, prison, homeless shelter), Microbio lab staff, Higher risk for TB reactivation (ex: DM, prolonged steroid therapy, leukemia, ESRD, chronic malabsorption syndromes), kids <4yo or those exposed to adults in high risk categories. >15mm induration: all of the above plus healthy individuals.

Leukocyte >50,000 what are you thinking. How about >100,000?

>50,000: Leukemoid reaction. -d/t severe infection -LAP (Leukocytes Alkaline Phosphatase) score is high -More mature neutrophil precursors seen (Metamyelocytes (Bands) > myelocytes or promyelocytes) >100,000: CML (BCR-ABL fusion) -LAP score is low -Less mature PMNs (metamyelocytes < myeloctyes) -Absolute basophilia seen

What is the most common supraventricular arrhythmia in hyperthyroidism? (occurs in 5-15% of pts)

A. Fib with RVR. Thyroid hormones cause an increase in beta-adrenergic receptor expression, which leads to an increase in sympathetic activity

Pt with hyperthyroid sxs can also include what 2 things you always miss?

A.fib. Proximal muscle weakness Proximal muscle weakness: is consistent with myopathy. Chronic hyperthyroid myopathy presents with proximal muscle weakness weeks to months after onset of hyperthryoidism. Objective findings may include muscle atrophy. Tx of the hyperthyroidism is usually going to improve the myopathy

Teenager who has muscle weakness, myotonia, cataracts, cardiac conduction abnormalities, but the big thing is that they have the myotonia, which is delayed muscle relaxation, usually affects facial muscles, intrinsic hand muscles, and ankle dorsiflexors. What is the genetic pattern and what is this disorder called?

AD expansion of CTG trinucleotide repeat in DMPK gnee on chromosome 19q 13.3 This is called Myotonic Muscular dystrophy.

What is alcoholic hallucinosis and when are you thinking about it?

AH is visual, auditory or tactile hallucinations. Pt has intact orientation. VSS. (so not autonomic instability like in DTs) So they just have hallucinations only without VS changes or changed orientation. Timeline: same as seizures, in first 1-2 days (12-48 hours)

Pt has imagining that shows cortical and subcortical atrophy and secondary ventricular enlargement, what do you think they have?

AIDS dementia complex.

What is the med Riluzole used to treat? Are there abnormal muscle enzymes (ex: creatine kinase) in this condition?)

ALS (Amyotrophic lateral sclerosis): the progressive neurodegenerative disorder that causes asymmetric upper (spastic weakness, hyper-reflexia) and lower (muscle atrophy, fasciculations) motor neuron features. No, muscle enzymes are generally normal in ALS

What is the tetrad of neuroleptic malignant syndrome?

AMS (confusion), rigidity (generalized muscle rigidity), fever (>40C or 104F), autonomic instability (anormal vital signs, sweating) NMS happens when you take antipsychotics (it's a life-threatening drug reaction to DA antagonists) -Tx: STOP THE ANTIPSYCHOTICS!! or restart dopamine agents, supportive care (hydration, cooling), ICU, Dantrolene or bromocriptine if refractory.

How dow cyanide toxicity present?

AMS, lactic acidosis, SEIZURE, COMA!!. So if pt has hx of nitroprusside INFUSION (which breaks down into NO and cyanide ions), and then they are altered, have lactic acidosis, are SEIZING and in a coma, then think about cyanide poisoning.

young 33 yo male with mild exertional SOB and "pounding" heart over last 5 months. He's aware of his hearbeat when lying on his left side. BP 150/45. What is likely responsible?

AR. Has wide pulse pressure, "water hammer"/Corrigan pulse (rapid, abrupt upstroke followed by rapid collapse of the peripheral pulse), and LV enlargement. When you lie on the left side, that brings the enlarged LV closer to the chest wall and causing a pounding sensation and increased awareness of heart beat. Causes: Aortic root dilation (Marfan, syphilis), Postinflammatory (rheumatic heart disease, endocarditis), congenital bicuspid aortic valve.

What is a complication of massive transfusion that I should know about when they show you a CXR with BL alveolar infiltrates after a pt got 5L bolus IVFs but has no s/sx of overload (no JVD, S3, or cardiomegaly on CXR)?

ARDS: respiratory distress, diffuse crackles on lung exam, severe hypoxemia, BL alveolar infiltrates on CXR, all of which are not completely explained by volume overload. Note: ARDS risk factors include infection, trauma, and other causes including massive transfusion.

How can you tell if something is statistically significant?

AS long as the p value is < 5% aka if p < 0.05 (bc you move the decimal point over 2x to get percentage) As long as p < 0.05, then it's statistically significant. In the example: p = 0.001 is statistically signifiant bc it's less than 0.05.

IVDU gets peri-valvular abscess, how does that usually manifest?

AV block in pt with endocarditis, you should really think about peri-valvular abscess. (Note: Tricuspid valve endocarditis doesn't usually cause cardiac conduction abnormalities... but peri-valvular abscess will) since the abscess can affect the adjacent cardiac conduction tissues.

25 yo pt has episodes of palpitations but he can stop them by immersing his face in cold water. This maneuver stops the palpitations by directly altering what?

AV nodal conductivity. Abrupt onset regular tachycardia that resolves with cold-water immersion is consistent with paroxysmal supraventricular tachycardia (PSVT) -Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common form of PSVT and frequently develops in young patients with structurally normal heart. palpitations are the most common presentation but some have dizziness, SOB, or CP -AVNRT is d/t 2 conduction pathways (slow and fast) in the AV node. (so the palpitations happen bc of a re-entry mechanism) ***Vagal maneuvers: carotid sinus massage, cold-water immersion/diving reflex, Valsalva maneuver, eyeball pressure all increased parasympathetic tone in the heart and result in temporary slowing of conduction in the AV node and increase in the AV node refractory period, leading to termination of the AVNRT. (Note: these have to do with the AV node; not the SA node... SA node is up top in the atrial while AV node is down in the ventricles; the SA node is not part of the reentrant pathway)

Pt is on glucocorticoids, now they have hip pain and reduced ROM and joint instability in one hip. What's going on?

AVN (osteonecrosis of the femoral head) - common complication of glucocorticoid use. Characterized by progressive hip pain in the groin, thigh, or buttock that worsens with activity and relieved with rest. Progression of disease --> reduced ROM (usually abduction and internal rotation), rest pain, and joint instability. First few months, X-ray is often normal, and MRI is more sensitive test.

What are some specific dx test for chronic pancreatitis

Abdominal X-ray: 50-60% sensitive for calcifications of the pancreas, but it's very specific for chronic pancreatitis when you do see those calcifications. Abdominal CT: 80-90% sensitive for pancreatic calcifications Secretin stimulating testing: Most accurate dx test. Place NG tube, an unaffected pancreas will release large volume of bicarbonate-rich fluids after IV injection of secretin.

Migraine headaches. There are abortive and preventative medications. What are they? When do you consider giving prophylactic migraine meds?

Abortive: sumatriptans, NSAIDs, Acetaminophen, Antiemetics (metoclopramide, prochlorperazine), Ergots (dihyroergotamine) Preventive: Topiramate, Divalproex sodium, TCAs, Beta-blockers (propranolol) Prophylactic migraine medications: think about these when pts have frequent (>4/month) and long-lasting (>12 hours) episodes, the sx are disabling and prevent regular activities despite abortive tx, abortive tx doesn't work, or they are over-using NSAIDs as abortive tx and are now having rebound HAs

How do you define a variable decel. with fetal heart monitoring (VEAL CHOP)? What do you do if you see variable decels?

Abrupt fetal heart rate decreased to the nadir followed by quick return to baseline (looks like a V). Drop from baseline to nadir occurs in less than 30 second, so it really is quick. The duration of the entire decel is 15 seconds to 2 minutes; Variable decels are not always associated with contractions, which is another clue. Since variable decels are r/t cord compression, so first thing to try is just reposition mom and see if that helps reduce the cord compression and improve blood flow to the placenta. (for intermittent variable decels). If these efforts fail, then do amnioinfusion as 2nd line tx. Bc the cord could be being pressed on (compressed) from decreased amniotic fluid after ROM, putting saline back in the amniotic sac may decreased cord compression and eliminate variable decels. Note: Recurrent variable decels is another story; those occur with >50% of contrations and need treatment since fetal acidosis can develop with increasing frequency and severity of decels.

Polysomnography shows generalized spike-wave activity of 3 Hz, what is the dx?

Absence seizures. (begins in childhood, around age 4-10)

What's needed for CLL (chronic lymphocytic leukemia)

Absolute lymphocytosis (>100,00) -CLL is clonal proliferation of normal, mature appearing B lymphocytes that function abnormally. You see markedly elevated WBC ct. Most common sx is fatigue. WBC ct is usually at least >20,000 with 80-95% lymphocytosis!!!!! Half of pt are hypogammaglobulinemia. Anemia and thrombocytopenia can occur from marrow infiltration or autoimmune warm IgG antibodies. The body doesnt' make antibodies when the body needs them to fight and infection, but instead attacks normal RBC and plts... *SMUDGE cell** LA and HSM are common.

Delta wave and you think WPW (wolff-parkinson-white syndrome) and ventricular preexcitation, what is this due to?

Accessory conduction pathway that directly connects the atria and ventricle, bypassing the AV node. EKG shows characteristics shortened PR interval (<0.12 seconds), widened QRS complex, and "slurred" upstroke of QRS complex ("delta wave")

Cervicofacial disesae (nonpainful, chronic, mandibular mass). Anaerobic, acid-fast negative (unlike Nocardia which is partially acid-fast) . Gram-positive, filamentous rod.

Actinomyces (Sketchy: the Israeli soldier. So it's a Gram-positive filamentous rod; it's more the mass on his face)

Graft vs. Host disease. Hx of BMT and 2 weeks later, there's maculopapular pruritic rash mostly on face, hands, and feet. Also has diarrhea positive for occult blood. LFTs are abnormal. What's the pathophys?

Activation of donor T lymphocytes (Bc it's Graft Vs. Host) Remember EH, the doctor checked her hands and feet and alway asked about diarrhea. Note: B cells are not involved (B cells are more immunoglobulins I think) Note; It's not the hosts T lymphocytes bc that would be rejection of the graft that would results in depression of myelopoiesis and failure to generate blood cells would be severe neutropenia for several consecutive days and increased risk of infection.

Pulmonary artery cath shows low cardiac index and elevated pulmonary capillary wedge pressure, what's the dx?

Acute MI (heart is not functioning as it should as a pump)

Older 63yo Asian woman with severe right sided HA for last 2 hours around her right eye. She has vomited. See halos and lights and never had a HA like this before. Takes tolterodine for urinary incontinence. PhyEx: nonreactive dilated right pupil and red right eye. Excessive lacrimation. Visual acuity is decreased. ESR: 35 (elevated): Dx?

Acute angle closure glaucoma. D/t sudden narrowing or closure of anterior chamber angle. Lens is located more forward and rests against the iris. This partially covers the anterior chamber angle and prevents normal flow of aqueous humor (through the pupil and into the anterior chamber) so intra-ocular pressure increases. Sudden angle closure typically occurs as a response to pupillary dilation from meds (ex: anticholinergics like tolterodine, sympathomimetics, and decongestants) or other stimuli (dim light). Acute ACG is more common in women (esp >40yo), Asian and Inuit populations and individuals with farsightedness. Pts typically develop rapid onset of severe eye pain and may see halos around lights. Affected eye will be injected and pupil will be dilated and poorly responsive to light. Pts develop tearing and HA with N/V and intra-ocular pressure increases. Untreated ABC leads to severe and permanent vision loss within 2-5 hours of sx onset. (think about Alex & Emily's mom being at risk for this bc she's >40yo, Asian, and is farsighted. hopefully she doesn't' have to take any of those meds)

Pt with RLQ abdominal pain for several hours, tender with guarding. Lying supine with hips flexed and pain is worse when hips are extended. WBC 14,000 and UA with 10-20 leuks/hpf and 1+ blood. Cause?

Acute appendicitis: obstruction of the appendix lumen. So the hip extension is the PSOAS SIGN!!! (pain with right hip extension; don't miss that clue) Other exam signs: -McBurney's point tenderness -Psoas sign: pain with right hip extension -Obturator sign: pain with right hip internal rotation -Rovsing sign: RLQ pain with LLQ palpation Clinical signs: N/V/anorexia, initial diffuse abdominal pain (visceral pain) that later localizes to RLQ (somatic pain) and mild leukocytosis. Dx: clinical dx. can also do u/s or CT scan Tx: surgical appedectomy

How do you tell acute cellular rejection (first 90 days) from bacterial infection (usually in 1st month) in a pt with recent liver transplant?

Acute cellular rejection: fever, RUQ pain, elevated LFTs. Bacterial infection: also has significant leuks and hemodynamic instability that makes bacterial infection more likely if those are present (aka suggest sepsis) Infections after liver transplant: <1 month: bacterial causes from operative complications (hepatic abscess, biliary leak, wound infection) or hospitalization (IV catheter, external drain) 1-6 months: opportunistic pathogens (CVM, aspergillus, Mycobacterium tuberculosis) bc of high dose immunosuppression > 6 months: Immunosuppressant sat maintenance level. At risk for getting typical Community-acquired pathogens (at higher rate than general population)

Fever, jaundice, RUQ abdominal pain (Charcot traid) is consistent with what dx? Can also have pentad by adding confusion & hypotension (Reynolds pentad). Ultrasound or CT will show what?

Acute cholangitis: common bile duct dilation on imagining. If not treated promptly, can lead to septic shock. Labs: elevated WBCs, neutrophilia, elevated AP, GGT, and direct bili. Biliary stasis predisposes to AC and the most common causes are d/t bile duct obstruction from gallstones, CA, or stenosis. In setting of stasis, the bile-blood barrier can be disrupted and allow bacteria and toxins to go into the blood stream. Tx: supportive care, broad spectrum Abx and biliary driange by ERCP with sphincterotomy. Can also do biliary decompression with percutaneous transhepatic cholangiography and open surgical decompression.

S/sx Listeria

Acute fever, confusion, HA, eck stiffness, CSF with ***PMN pleocytosis*** --> think bacterial meningitis. Listeria is foodborne illness (raw meats/veges/unpasteurized milk probducts, prepackaged meats). Think about this in babies <2 yo and elderly >50, pregnant or otherwise immunocompromised person. -Blood culture with Gram-positive Bacilli -Presentation: can present shortly as bacterial meningitis after gastroenteritis (within hrs- days of exposure) or can have prolonged incubation period (up to months following exposure)

Pt presents with ascending weakness and minor sensory symptoms (acral/peripheral body part paresthesias) and areflexia, this all happened after an infection. What is the mechanism of Guillain-Barre syndrome?

Acute immune-mediated, demyelinating polyneuropathy, usually postinfectious.

Leading cause of urinary incontinence in elderly patients?

Acute infections, especially UTIs. So get a UA with culture to r/o UTI in a elderly patient with new urinary incontinence. Especially if pt also has acute delirium.

Abdominal pain, dark red/brown urine, pigmented urine d/t prophyrins (and not hemoglobinuria). what would that be?

Acute intermittent porphyria.

Pt with patchy sensorimotor neuropathy and autonomic dysfunction. Caused by partial deficiency of porphobilinogen deaminase (enzyme involved in heme synthesis)

Acute intermittent porphyria.

What's the problem when you have hx of medication use, rash, eosinophilia, increased serum creatine. UA shows abundant WBCs, many are eosinophils. No gross hematuria.

Acute interstitial nephritis (AIN: med use and eosinophils is the clue)

Pt has CABG and now POD3 he has dyspnea and worsening retrosternal pain despite continuous use of morphine. He has widened mediastinum, a.fib with RR, and cloudy fluid in the sternal wound that is draining. Wha't going on?

Acute mediastinitis: possible complication of cardiac surgery that is usually d/t intra-op wound contamination. Usually presents post op within 14 days with fever, tachycardia, chest pain, leukocytosis, and sternal wound drainage or purulent discharge. CXR will show WIDENING MEDIASTINUM in non-post op mediastinitis but can also be seen in post-op mediastinitis after cardiac surgery. Dx: usually made clinically and confirmed during surgery when pus is noted in mediastinum. Tx: post-op mediastinitis requires drainage, surgical debridement with immediate closure, and prolonged Abx therapy. (Mortality rate of 10-50% even with appropriate tx... need to go in and drain it, you can't just give abx alone)

S/sx lithium toxicity

Acute toxicity: GI: N/V/D, late neuro sequelae Chronic toxicity (neurologic): confusion, agitation, ataxia, tremors/fasciculations Management: Hemodialysis for severe cases.

What's the problem when you have ischemic or nephrotoxic insult (AKI), Cr elevates, UA shows granular casts, hematuria, and renal tubular epithelial cells?

Acute tubular necrosis (ATN) -Think about this after AKI and you see renal tubular epithelial cells (Note: ATN typically does NOT cause isolated hematuria as seen in the sickle cell trait pt)

What kind of hearing loss do you expect with ototoxic medications?

Acute, subacute, or slowly progressive BL tinnitus and SN hearing loss as a result of damage to cochlear hair cells &/or CN8. ex: aminoglycosides, loop diuretics.

What do you treat acute prostatitis with? what about chronic?

Acute: TMP-SMX or flouroquinolones Chronic: fluoroquinolones (think of nice fresh smelling flowers... fluoroquinolones for your prostate) Usually d/t E.coli. Note: you would have gotten a mid-stream urine sample to help direct the abx therapy. but empiric antibiotic therapy with TMP-SMX or fluoroquinolone should be started while awaiting culture results; tx should be continued for 4-6 weeks in most cases.

When pt is dying of cancer and has really bad cancer pain and is having pain between morphine doses and is waking up at night from the pain, you already increased in frequency of her short acting morphine, what do you do about her pain - next steps?

Add sustained related (long acting opioid) morphine. Note: Don't pick increase the short acting morphine frequency because that is unlikely to provide adequate pain coverage and would needlessly burden the patient and won't provide adequate overnight pain relief.

Nasal polyps can cause chronic congestion and may be associated with recurrent upper respiratory infections, but they are associated with kids with CF and can be seen on exam. So if they describe a kid with chronic upper respiratory infections but they say that his nasal turbinates are not enlarged or red on exa, but that his tonsils are enlarged and has mucopurulent post-nasal drip. And antihistamines and intranasal steroids don't help and he still "can't breathe through his nose," what are you thinking is the dx?

Adenoid hypertrophy <-- can't see these on physical exam. (vs you would be able to see nasal polyps on physical exam so the answer is not nasal polyps, but instead big adenoids)

Persistent nasal obstruction in a kid, what are you concerned about?

Adenoid hypertrophy. may present as chronic congestion refractory to medical management. Affected kids are predisposed to recurrent otitis and sinusitis. These kids have nasal congestion that doesn't respond to medicines. Hx may have chronic upper airway obstruction (recurrent sinus/ear infections, mouth breathing, sleep disturbances/snoring d/t apnea) The adenoids are not easily accessible and not visualized during physical exam. The dx is suggested if there is mucopurulent nasal discharge, postnasal drip, elongated/flat facial features (d/t changes in structure of palate, jaw, teeth).

68yo Pt has long smoking hx, 15 lb weight loss over the last year, CXR shows hyperinflation of lungs and small cardiac silhouette, no mention of mass. She uses 2L/min of oxygen at home. Poor exercise capacity bc SOB and poor appetite. Pulse ox at 92%. Thin, mildly cachectic. Coarse breath sounds. Thin extremities with decreased muscle mass and trace edema.Most likely cause of pt's weight loss?

Advanced COPD. IF it sounds like COPD, it is COPD. Don't jump to conclusion about lung cancer. COPD has a smoking hx too and there is no mention of mass on the CXR so don't assume it's cancer. This pt's weight loss is r/t pulmonary cachexia: loss of lean muscle mass associated with COPD. BMI < 20 or weight loss >5% is often used to suggest this pulmonary cachexia. Occurs in 20-40% of pts with COPD and leads to impaired balance, increased susceptibility to lung infections and increased mortality. This is severe/advanced COPD disease. D/t increased work of breathing that uses more calories, systemic inflammation that leads to decreased appetite and catalyzing skeletal muscle breakdown, skeletal muscle hypoxia and glucocorticoid use can also contribute

Little girl with precocious puberty (breast and pubic hear; Tanner stage 3 at 6yo). She has advanced bone age of 8yo. Basal LH level is high. So what is the next stage in evaluation?

Advanced bone age, with high basal LH (means it's a central pituitary lesions making the endogenous hormone that is causing the precocious puberty). If the basal LH was low, you would do a GnRH stimulation test and if LH as high, you would still conclude it's a central lesion. However, if the LH is Low, then you conclude it's a peripheral lesion - making the endogenous hormone, either adrenals (get adrenal CT scan) or gonads (get pelvic ultrasound)

What is HIV associated dementia?

Affects deep gray matter structures and causes subacute cognitive, behavior, and motor deficits. Imagining shows cerebral atrophy with ventricular enlargement.

What is presbycusis? What kind of hearing loss do you expect with this?

Age-related hearing loss: progressive BL symmetric & predominately high-frequency SN hearing loss that occurs over many years with subjective tinnitus, advanced age, and absence of other neurologic signs. Due to degenerative changes of the inner ear or cochlear portion of CN8. Pts with prebycusis often describe hearing well in one-on-one conversations in a quiet room. They have difficulty hearing social conversation, especially when there is competing background noise.

What is the feared side effect of the antithyroid drugs (PTU and MMI)?

Agranulocytosis. (Can happen with both antithyroid drugs) Caused by immune destruction of granulocytes and most cases occur within 90 days (3 months) of treatment. Routine monitoring of granulocyte count is not cost effect and so not done. Current recommendation say taht if the pt complains of fever and sore throat, the STOP the antithyroid drug and measure the WBCs. If WBC ct is less than 1,000/cubic mm then need to discontinue the drug permanently. IF the WBC ct is >1,500/cubic mm, then the antithryoid drug toxicity is unlikely the cuase of the sore throat and fever.

Pt with slurred speech, unsteady gait, incoordination, disinhibited behavior, drowsiness. What drug(s) did they likely take?

Alcohol or benzos

What are some triggers for gout?

Alcohol use, surgery/trauma (so if stem has pt who gets painful single joint a few days after surgery, think about gout triggered by that surgery/trauma), dehydration, certain meds like diuretics or baby ASA. Diet triggers: high protein foods (meat, seafood), high fat foods, fructose/sweetened beverages, heavy ETOH use. Underlying medical conditions (HTN, obesity, CKD, organ transplant) are also at increased risk usually presents rapidly acute (usualy 1st metatarsophalangeal joint but can be at knee and ankle). Usually develop overnight or early in the morning, with max intensity within 12-24 hrs.

PT with hx of asthma or COPD, they have cough and lobar infiltrate and bronchiectasis... also see labs with high eosinophils. What are you thinking?

Allergic bronchopulmonary asperigillosis (ABPA) Think about ABPA with poorly controlled asthma with recurrent exacerbations; severe disease can have recurrent infiltrates, fever, cough productive of brown sputum, and hemoptysis. Central bronchiectasis is present, but ABPA is dx with skin testing and Aspergillus-specific IgE levels. Presentation: recurrent respiratory exacerbations, uncontrolled asthma sx, and eosinophilia is consistent with ABPA infection. Tx: oral corticosteroids for several months in combo with antifungal agent itraconazole. Hx: asthma or CF CXR: recurrent fleeting infiltrates, bronchiectasis on CT Dx: Eosinophilia, positive skin test for Aspergillus, positive Aspergillus-specific IgG, elevated Aspergillus-specific and total IgE.

How do you choose between allergic conjunctivitis and atopic keratoconjunctivitis?

Allergic is just some guy with red watery, itchy eye with some distorted vision from the excess tearing without blurred vision. On exam: there's BL injection with "granular" appearance of the conjunctiva. May have "gritty" sensation. Mild eyelid swelling and clear discharge. Lung: few scattered wheezes. Vs. Atopic: more severe form of ocular allergy. You have itching, tearing, THICK mucus discharge, photophobia, blurred vision. Atopic is more severe with prolonged course, potential vision impairment d/t corneal involvement and thickening of eyelids and surrounding skin.

What are the gout meds that you used to manage gout chronically (but should not be started until the gout is quiescent as they can trigger an attack if started acutely)?

Allopurinol & febuxostat: reduce serum uric acid levels by inhibiting uric acid produciton Probenecid: removes renal excretion of uric acid and used as 2nd line if allopurinol and febuxostat are ineffective.

What is an inherited condition that leads to emphysema and liver damage?

Alpha-1 antitrypsin deficiency

Early onset- basilar predominant emphysema with SOB and chronic sputum production?

Alpha-1 antitrypsin deficiency.

What should you know about digoxin and amiodarone?

Amiodarone can increase the serum levels of digoxin and cause toxicity in pts with stable digoxin regiment. Acute digoxin toxicity: (memory tool... something digging at your stomach - anorexia, N/V/abdominal pain; digging at your muscle - fatigue, weakness; digging at your eyes - color vision changes; and your head - confusion; digging at your HEART!! - life threatening arrhythmias)

What cardiac medication requires that you do PFTs?

Amiodarone. Class III anti-arrhythmic med that manages ventricular arrhythmias in pts with CAD and ischemic cardiomyopathy. But it is a "dirty drug" and can have pulmonary toxicity and total camulative dose so should be monitored with baseline CXR and PFTs.

How do you treat cryptococcal meningitis that presents with fever, malaise, HA?

Amphotericin B & flucytosine!

Pt with infectious endocarditis and cultures come back and show either penicillin resistant enterococcus or HACEK organism, what do you treat them with?

Ampicillin-sulfabactam

Pt with hx of RA now has nephrotic syndrome (generalized edema, 4+ proteinuria), liver palpated 5cm below costal margin, BL kidney enlargement. You do renal biopsy. What do you expect to find on path?

Amyloidosis: amyloid deposits that stain with Congo red and are apple-green birefringent under polarized light. These amyloid deposits are seen in the glomerular BM, blood vessels, and interstitium of the kidneys and can be seen on electron microscopy as randomly arranged thin fibrils. -Deposits may have light chain (AL amyloidosis) or abnormal proteins (AA amyloidosis) -NOTE!!: RA is the most common cause of AA amyloidosis in the USA.

What does an ANOVA test compare?

Analysis of variance compares means of 3+ variables

Men: Uneven hair thinning at the frontotemporal hairline and vertex (top-back of your head) Women: thinning at vertex (top-back of your head) and sides with preservation of hairline. What is this?

Androgenetic alopecia

What does a Sertoli-Leydig cell tumor secrete?

Androgens --> defeminization & masculinization. Women of childbearing age may have flattening of breasts and scanty, irregular menstruation, ultimately leading to amenorrhea. Can develop hirsutism, coarsening of facial features, voice deepening, and clitoral enlargement

Pt with mechanical prosthetic valve can cause mechanical trauma and destruction of circulating RBCs that give pts mild, asymptomic anemia. Or they can have significant dysfunction that causes marked anemia. Typically accompanied by para-valvular regurgitation, which is evidenced by Holosystolic murmur at cardiac apex (for prosthetic mitral valve). What do you expect to see on labs?

Anemia. Low Hct/Hgb Elevated LDH Elevated indirect bili Decreased haptogobin May see low pts bc of mechanical destruction of those as well. Peripheral smear: may show red cell fragments and schistocytes.

Sudden onset blurred vision, severe eye pain, N/V with exam showing red eye with hazy cornea and fix, dilated pupil. Think about

Angle closure glaucoma

What is the gene defect usually in hereditary spherocytosis? what's the usual inheritance pattern? Classic triad presentation? what lab findings do you see in HS?

Ankyrin gene 75% cases are AD but can be AR due to spontaneous mutation. Presentation: hemolytic anemia, jaundice, splenomegaly (bc spleen eating up all the hemolyzed RBCs) Labs: see hemolytic anemia. increased MCHC and RDW. See spherocytes on peripheral smear. Coombs test is negative bc this is not an autoimmune hemolytic disease. (MCHC - mean cell hgb concentration - is high bc of the membrane loss and RBC dehydration. See high RBC distribution width bc of various forms (reticulocytes, spherocytes, normal RBCs)

What is confounding? How is it solved in case-control studies?

Another variable other than the one you are studying that also has an effect on the outcome. Solve by matching variables that can be confounders (ex: age, race, SES)

Pt with diabetic neuropathy. He has 20 years of DM. On physical exam: decreased proprioception and vibration sense in the feet. Ankle jerk reflexes are absent, finger-to-nose and heel-to-shin tests are normal. Pt sways and tends to fall when his eyes are closed. BL hammer toe deformities are present in the feet. What is predominantly responsible for his neurologic symptoms?

Anoxopathy of the LARGE nerve fibers. Positive sx (pain, paresthesias, allodynia - pain response from stimuli that doesn't normally elicit pain): from small fiber injury Negative sx (numbness, loss of proprioception and vibration sense, diminished ankle reflexes): from LARGE fiber invovmenet TL:DR: -Positive sx = small fiber injury (think about.. little things make make or break your down, can make you positive (positive sx) or they can hurt you (pain, tingling); small fibers = positive sx like pain paresthesia allodynia) -Negative sx = larger fiber injury (think about when you don't have something large that you want, you get all negative; large fibers = negative sx lke missing sensation and missing ankle reflexes)

You have an HIV+ pt with low CD4 count and now they have intermittent bloody diarrhea, abdominal pain and unintentional weight loss. What do you think the cause is? Picking between crytosporidium, CMV, and Mycobacterium avium complex. How do you decide?

Answer: CMV bc that causes bloody diarrhea. Crytosporidium has sever WATERY diarrhea. MAC has watery diarrhea with high fever (>102.2F) Whereas CMV has frequent, small volume diarrhea, HEMATOCHEZIA (Bloody!!), and abdominal pain.

You put a pt under general anesthesia and now their BP and HR is wildly high (BP 250 systolic), what happened? Options: Pheo or Thyroid storm

Answer: Pheo. Just giving anesthesia can cause pheo's catecholamine surge

29yo pt with hx of Hasimoto's thyroiditis and taking levothyroxine. She is now presenting with N/V, severe generalized abdominal pain, and hypotension. Her BP 70/50, HR 110, and RR 24. PhyEx shows dry and pigmented mucous membranes. Skin creases also show increased pigmentation. Labs: Na 130 (low), K 6.1 (high), Bicarb 18 (low), BUN 33 (high), Cr 1.3 (high), BG 56 (low), Hgb 10.8 (low), normal plts and leuks. 70% PMNs, 10% eosinophils (high), 20% lymphocytes. Random serum cortisol 3.2 (low bc normal is 5-25), ACTH level is 142 (normal is 9-52). What is the pathophysiologic mechanism of this pt's disorder? What does she have to begin with?

Answer: autoimmune So she definitely has primary adrenal insufficiency (Addison's disease) since she's presenting with hypotension, pigmentation (and high ACTH), hyponatremia, hyperkalemia, eosinophilia, markedly elevated ACTH levels, and low cortisol levels despite hypotension and stress). Most common cause of primary adrenal insufficiency in developed countries is: autoimmune adrenalitis. (responsible for more than 80% of pts with primary adrenal cortical insufficiency) Note: ~50% of pts with autoimmune primary adrenal insufficiency (Addison's disease) have autoimmune diseases involving other endocrine glands (ex: thyroid, parathyroid, and ovaries). Other non-endocrine autoimmune conditions like pernicious anemia and vitiligo are also common.

what eye issue is associated with ankylosing spondylitis (locker back and buttock pain, worse in the mosting, relieved with warm water and OTC pain meds (relieved with exercise but not rest), morning stiffness, limited ROM with lumbar spine and x-ray that shows bamboo spine)?

Anterior Uveitis Other findings: Arthritis (sacroiliitis) Reduced chest expansion & spine mobility Enthesitis (tenderness at tendon insertion sites) Dactylitis (swelling of fingers/toes) Uveitis!! Complications: Osteoporosis/vertebral fractures Aortic regurg. (d/t scarring of valve cups) Cauda equina Labs: Elevated ESR, CRP, HLA-B27 associatoin Imaging: X-ray of sacroiliac joints, MRI of sacroiliac joints.

Young female athlete (playing soccer, tennis, or basketball) tries to get around another player (rapid deceleration or direction change; or pivoting on lower extremity with foot planted), and hen she feels a "popping" sensation and she has immediate pain and rapid swelling. The knee is swollen and tender, she hesitates to bear weight on it. Aspiration of the knee yields ***gross blood joint fluid***. What is the most likely injury?

Anterior cruciate ligament (ACL) injury ACL tears occur with high contact sport (blows to knee) or with significant twisting force. Pt experience a "popping" sensation during the injury with RAPID ONSET of severe pain and HEMARTHROSIS (significant effusion/hemarthrosis) and the feeling of joint instability when bearing weight on that knee. So if the vignette describes sports injury with big swollen knee and there is gross blood when they aspiration the joint, then it's an ACL tear. (MCL and meniscal tears aren't usually associated with significant hemarthrosis unless there is a concurrent ACL tear)

Other than antipsychotics, what other drugs are you concerned that there may be EPS symptoms (akathisia, dystonia, cogwheeling, parkinsonism)?

Anti-emetics: prochlorperazine, promethazine, metoclopramide -these are also DA antagonists (just like antipsychotics) Note: metoclopramide is the gut motility agent you can use for diabetic gastroparesis.. i guess it helps your nausea bc it gets the food going through your GI tract so it doesn't back up... so know this is DA agonist.. so can cause EPS symptoms.. Memory tool: these antiemetics that can cause EPS symptoms all have letters like "prochlorp-, pro-, -clop-" so think of those as the ones that make you have EPS symptoms. TL;DR: Antiemetics (Prochlorperazine, promethazine, and metoclopramide) with DA antagonists properties can cause EPS symptoms of dystonia, cogwheeling, parkinsonism.

Pt with allergic reaction, when should you just treat with anti-histamine and when should you give IM Epi?

Anti-histamine in pt with mild drug-induced hypersensitivy reaction (type 1). Urticaria & pruritus without systemic symptoms are usually treated with antihistamines and tx of the offending drug is discontinued. -This pt with multiple urticaria and mild excoriations of upper and lower extremities, and tonsils with mild erythematous without exudate or swelling. Give antihistamines only. Epinephrine and corticosteroids are reserved for more severe reactions with systemic symptoms (ex: anaphylaxis). (Respiratory symptoms (dyspnea, wheezes, stridor), abdominal symptoms (diarrhea, cramping), or vital sign instability)

What's the most specific antibody in scleroderma (but not present in a lot of them, only 20-30% of pts have this but it's the mots specific)

Anti-topoisomerase SCL-70 is most specific for scleroderma.

Half of pts with CREST syndrome (limited scleroderma) have this antibody.

Anticentromere.

TCAs are antidepressant but they also have what other property?

Anticholinergic properties. So be careful using them in an older patient who may have BPH, you could cause urinary retention by reducing detrusor contraction and preventing urethral sphincter relaxation.

Somatic symptom disorder (worried about HAs despite appropriate medical evaluation and reassurance) that doesn't respond to general measures (seeing same doctor reguarly, avoiding unnecessary tests and specialist referrals, exploring psychosocial stressors, promoting stress reduction and healhty behaviors - sleep hygiene, relax techniques, exercise, diet, return to productive activities) can be treated with what medication?

Antidepressants (SSRIs are 1st line) and also do CBT. (SSRI preferred but TCAs can also be used)

When do you give N-acetylcysteine?

Antidote for acetaminophen OD

Localized, shallow, painful ulcer with a gray base. What are you thinking?

Aphthous stomatitis

Sample from lip. presents with recurrent, self-limiting ulcerations of oral cavity that do not affect surfaces covered by keratinized stratified squamous epithelium. Histo shows ***shallow, fibrin-coated ulcerations with underlying mononuclear infiltrates.*** What does this describe?

Aphthous ulcers (cancer sores)

Pt with pancytopenia following drug intake, exposure to toxins, or viral infection, what should you suspect? Presents with infection, petechiae, low hgb. BM biopsy shows "marked hypocellular marrow with decreased megakaryocytes and precursors of the erythryoid and myeloid cell lines" <-- aka invades BM and causes decreased production or hypoplasia

Aplastic anemia.

Pt with infectious endocarditis and cultures come back and show it's due to penicillin-susceptible Viridans streptococci. hat do you treat them with?

Aqueous Penicillin G (note: this med has no staph coverage, but you're using it bc you know it's d/t strep Viridans)

If pt with infective endocarditis is found to have penicillin-susceptible Viridans streptoccci as the causative organism, what is the drug of choice then?

Aqueous penicillin G for native IE d/t penicillin-susceptible strep Viridans (note: Penicillin G has no staph coverage, so it's not empiric tx bc usually IE is d/t staph aureus, it's only when you know it's bc of strep Virdans that you would choose this Abx regimen)

Which SGA are least likely to cause weight gain and DMs?

Aripiprazole and ziprasidone. (Think A&Z are least likely to cause metobolic issues)

Post-menopausal woman gets ER+ breast cancer, what do you use to treat her? what are you worried about as a side effect and so what do you check before starting this treatment?

Aromatase inhibitors (ex: anastrozole, letrozole). these meds can increase risk of osteoporosis. So get baseline bone density scan before starting aromatase inihibitors

Garlic Breath

Arsenic poisoning (ex: well water contamination)

What's the mechanism that causes pulmonary HTN in pts with systemic sclerosis (CREST syndrome, Scleroderma)?

Arterial intimal hyperplasia (Hyperplasia of the intimal smooth muscle layer --> leads to increased pulmonary vascular resistance; which is called "Pulmonary Arterial Hypertension") Will see normal FEV1 and FEV1/FVC ratios on PFTs.

SCD and osteonecrosis. what are the 2 main blood supply sources of the femoral head?

Ascending arteries & Foveal artery (within the ligamentum teres) Note: the foveal artery is patent early in life, but may become obliterated in older patients. SCD pts get osteonecrosis d/t disruption of the microcirculation int he bone by sickling as well as increased introasseaous pressure d/t bone marrow hyperplasia. Since kids have a patent foveal artery, the femoral head gets blood supply through that 2nd channel as well early in life, so aseptic necrosis of the femoral head is uncommon in kids but the risk rises in older pts.

32 yo young pt comes in with CHF symptoms but she was otherwise normal before. She doesn't drink alcohol. What do you want to ask aboit in the history? How strange... she was okay and now she's in heart failure?

Ask about recent cold, hx of recent URI can cause sudden onset cardiac failure in otherwise healthy patient with dilated cardiomyopathy (also dilated cardiomyopathy like the ETOH induced version). Viral/idiopathy myocarditis is most commonly seen after Coxsackievirus B infection (in 3.5-5% of infected pts). Parvovirus B19, HHV6, adenovirus, and enterovirus can also do it. Make dx with echo, shows dilated ventricles with diffuse hypokinesia resulting in low ejection fraction (systolic dysfunction). Tx largely supportive, involving management of CHF symptoms.

Someone who is in CHF, heart is give, EF 25%, but they have clean coronaries. Why would they have this HF? What is likely to reserve this pt's heart function

Ask in their history of there is heavy alcohol use with other signs of heavy alcohol use, like macrocytic anemia, thrombocytopenia, ad AST:ALT ratio >2:1. If so, complete abstinence from alcohol can reverse (improve or normalize) the LV function over time. (Alcoholic cardiomyopathy is a dx of exclusion in pts with dilated cardiomyopathy and hx of alcohol abuse)

IF pregnant pt is depressed... then you want to

Ask them about suicidal ideations (but if it just says MONITOR them for SI, then that's not the correct answer bc you don't want to just monitor them, you want to intervene and treat them with an SSRI) So recommend Sertraline as SSRI and discuss risk/benefits. You want to intervene if you think pt is depressed. (Note: SSRI are not associated with congential malformations - with the exception of paroxetine which has been associated with a slightly increased risk of cardiac malformations in some studies.. Memory tool: think of little parots with heart defects)

Pulmonary disease (upper lobe cavitary disease) in immunocompromised patient. Microscopy shows acid-fast negative, hyphae.

Aspergillus (Sketchy is the farmer running from the crop plane)

Med given to reduce risk of early recurrence of ischemic stroke. Should be given within 24 hrs to all pts presenting with ischemic stroke.

Aspirin. Aspirin + dipyridamole OR clopidogrel is recommended for pts who have recurrent stroke on ASA therapy.

Why is ceftriaxone contraindicated in neonates?

Associated with cholestasis and leads babies to be at high risk of developing cholestasis, it also results in higher levels of Bili (which we don't want in newborns)

When do you offer external cephalic version?

At term (>37 weeks) bc before that, the babies is just moving around in there.

Basilar or vertebral strokes

Ataxia, vertigo (supply ears), also supply brain stem Vertebral: face and cerebellar (double vision, dysphagia, dysarthria)

What is the most common cause of primary adrenal insufficiency?

Autoimmune adrenalitis: involves both humoral and cell-mediated immune destruction of the adrenal cortex. Note: half of pts with autoimmune adrenalitis have other autoimmune disorders; this may flare up in the postpartum time. So look for stem that mentions a postpartum patient but she didn't have massive blood loss so you're not thinking Sheehan syndrome with pituitary infarct and secondary adrenal insufficiency, but instead the postpartum time is actually supporting the dx of primary adrenal insufficiency with this autoimmune etiology.

What's Lichen planus?

Autoimmune condition with glassy, bright red erosions and ulcerations of the vulvovaginal area

What are you expecting to see if you are thinking positive direct Coombs test?

Autoimmune hemolytic disease. -Either warm agglutinin (AIHA) or cold agglutinin (AIHA) Warm agglutinin: -Hx of drug exposure: ex: Penicillin, or hx of viral infections, or hx of autoimmmune condition like SLE, immunodeficiency state, or lymphoproliferative dz (ex: CLL) -Now they're hemolyzing (worsening fatigue and exertional dyspnea, Hct is low with normal MCV, reticulocytes are high, they have large spleen and mild scleral icterus) -Can have asx to life-threatening anemia. -Direct Coombs Positive: anti-IgG, anti-C3 or both (memory tool: think Anti-IgG... think G for hx of penicillin, like penicillin G causing this) -Tx: steroids, splenectomy if there is refractory disesae Cold agglutinin: -Hx of infection with Mycoplasma pneumonia, or infectious Mono, or lymphoproliferative diseases -Now they have anemia, livedo reticularis and acral cyanosis (of hands and feet) with cold exposure that goes away with warming. -Direct Coombs positive with anti-C3 or anti-IgM (memory tool, think about this as the cold one with M diseases like Mycoplasma or Mono..), not usually IgG. -Tx: avoid cold temperatures, treat with Rituximab +/0 fludarabine -Complications: ischemia & peripheral gangrene. Lymphoproliferative d/o.

What's the most effective therapy for MM in pts under age 70?

Autologous bone marrow transplant with stem cell support. This would be used after induction chemotherapy with lenaLidomide and steroids (dexamethasone glucocorticoid)..

Pt with thyrotoxicosis (palpitations, tachycardia, weight loww) and elevated thyroid hormones and low TSH. RAIU shows high uptake in a nodular pattern. So now you are thinking this is either toxic adenoma (unicentric uptake) or mutinodular goiter (patchy distribution) So what is the process responsible for this pattern of elevated thyroid hormone?

Autonomous thyroid hormone production -from hyperplastic thyroid follicular cells.

Pt with acute glaucoma. Hx of DM and HTN, then sudden unilateral eye pain when fixing a light bulb. Pain is not relieved by medications. Associated with headache and then loss of vision. Pt is in intense pain, has nausea, eye is red with conjunctival flushing. Pupil is mid-dilation and non-reactive to light. Eye feels hard on palpation. This is a medical emergency. What drug should you AVOID in these patients? What meds do you treat acute glaucoma with?

Avoid Atropine. Mydriatic agents like atropine can precipitate glaucoma because they dilate the pupil, they can also worsen he glaucoma. Do treat with the following meds to reduce the increased intraocular pressure: - mannitol (1st line tx given IV, osmotic diuretic that works immediately), - acetazolamide (carbonic anhydrase inhibitor that rapidly reduces further production of aqueous humor, thus decreasing intraocular pressure), - timolol (beta-blocker, given topically, decreases production of aqueous humor to decrease intraocular pressure), - pilocarpine (opens canal of Schlemm and allows drainage of aqueous humor, rapidly reducing intraocular pressure, given topically)

ASA-exacerbated respiratory disease (AERD): non-IgE mediated reaction that results in ASA-induced PG/LT misbalance. Seen in pts with hx of asthma or chronic rhinosinusitis with nasal polyposis. Characterized by bronchospasm and nasal congestion after ASA ingestion. Also called a "pseudoallergic drug reaction" How do you manage it ?

Avoid NSAIDs, desensitize if NSAIDs are required. And Use LT receptor antagonist (montelukast) instead.

Pt has subtotal gastrectomy. What are you concerned about in his future?

B12 deficiency.

If it says pearly and ulcer, go with pearly and pick what kind of cancer?

BCC. -Features of BCC: Persistent open sore that bleeds/oozes/crusts, reddish patch or irritated area, PEARLY/translucent NODULE Elevated/ROLLED BORDERS with CENTRAL ULCERATION, pale-scar-like areas with poorly defined border. BCC only rarely spreads to distant body parts. Treat by preventing invasion to nearby tissues and structures. Use MOHs surgery to treat. (Note: SCC usually from a precursor lesion like AK or 3rd degree burn and has overlying hyperkeratosis; think of SCC as more keratin, extra dry skin)

When do you irradiate RBCs before transfusions?

BMT recipients, acquired/congenital cellular immunodeficiency, blood components donated by 1st or 2nd degree relatives.

What does neutrophilic pleocytosis on CSF indicate

Bacterial meningitis

Fever, chills, septic shock and DIC within minutes-hours of transfusion?

Bacterial sepsis

How to dx Zenker diverticulum?

Barium esophagram (preferred), esophageal manometry (don't stick anything hard in there like endoscope bc could perforate it)

Histo showing invasive clusters of spindle cells surrounded by palisaded basal cells. "spindle cells & palisading," what do you think of?

Basal Cell Carcinoma (BCC)

Hx of lesion in sun exposed area. Histo with invasive clusters of spindle cells surrounded by palisaded basal cells. What does that describe?

Basal cell carcinoma (BCC)

What kind of infarct is it if pt has motor functioning impairment (hemiparesis, dysarthria-clumsy hand syndrome)?

Basis pontis (basilar pons) infarction.. Memory tool: you have such a clumsy hand that you can't grab the ponpons. ... so dysarthria-clumsy hand syndrome is basilar pons infarct

Why do we treat asx bacteriuria in pregnancy?

Bc of the increased risk for pyelonephritis during pregnancy. All pts should be screened for asx bacteriuria during 1st prenatal visited and treated. Pregnancy has increased P hormone that causes smooth muscle relaxation and ureteral dilation. These changes mean ASB during pregnancy is more likely to result in pyelonephritis. ASB is also associated with increased risk of preterm labor and low birth weight. So all women should be screened in the 1st prenatal visit. Most common organism: E.coli Others: Klebsiella, Enterobacter, GBS 1st line tx: cephalexin, amoxi-clavulanate- nitrofurantoin, fosfomycin Need to do test of cure (repeat urine culture) after abx treatment is completed.

Symptoms of B1 (thiamine) deficiency

Beriberi Wernicke's encephalopathy

How to tx open angle glaucoma?

Beta blocker like Timolol eye drops as initial management. Laser trabeculoplasty as adjunctive measure. If continous increase in intraocular pressure, surgicaltrabeculectomy is done.

How does topical Timolol work to treat acute glaucoma?

Beta blocker, decreases production of aqueous humor, decreasing intraocular pressure

What do you use to treat a. fib with RVR in hyperthryoidism?

Beta-blockers (ex: propranolol, atenolol) as initial therapy to control HR and hyperadrenergic sxs. Propranolol also decreases conversion of T4 to T3 in peripheral tissues. The beta-blocker should be initiated as soon as hyperthyroidism is diagnosed and should be continued until the hyperthyroidism is adequately treated with thionamides, radioiodine, &/or surgery.

What does systematic error represent?

Bias.

3 week old boy with 1 week hx jaundice. Stool is always been "kind of pale colored." (BIG CLUE, DON'T IGNORE). Breast fed and feeds well. Mom's O+ blood. Exam shows jaundice and hepatomegaly. Labs: Hgb 15, Tbili 10.3, Dbili 8.1 (so majority D bili aka conjugated bili). Coombs negative. Most likely dx?

Biliary atresia. Initially well appearing kid followed by jaundiced, acholic (pale) stools or dark urine, hepatomegaly, and conjugated hyperbili (>2 mg/dL), and mild elevated transaminases. (No functional biliary system so can't get bile to stool which is why pt has pale stool) -1st step in eval: abdominal u/s will show absent/abnormal gallbladder. Failure of liver to excrete tracer into small bowel on scintigraphy is highly suggestive of biliary atresia and dx GOLD STANDARD is CHOLANGIOGRAM in the OR. Once biliary atresia is confirmed, a Kasai procedure (hepatoportoenterostomy) should be done. Virtually all pts will require liver transplant, but Kasai procedure allows time for growth and reduces M&M of hepatic transplant

S/p cholecystectomy and now pt has lower grade fever, RUQ tenderness, N/V and pt has imaging done. What do you think it is if pt has biliary dilation? What do you think it is if they do NOT have biliary dilation?

Biliary dilation: retained gallstone No biliary dilation: biliary leakage <-- one of the most common complications s/p cholecystectomy. Associated leukocytosis and obstructive-appearing liver enzymes (elevated bili, AP) are often present. Note: the bili is usually only mildly elevated as the peritoneum is able to reabsorb much of the leak; at times, esp with large leaks, there can be bilious ascites. Most cases of biliary leak occur 2-10 days after procedure. ON imaging, most pts have relatively normal-appearing biliary duct or only mild dilation (which can be from the post-op state alone).

Lap chole pt has persistent abdominal pain, N/V, fever, and increased leuks, bili and AP also elevated, 4 days after having the operation. RUQ u/s shows normal sized biliary ducts. What's the likely cause of these symptoms?

Biliary leakage Note: most cases present 2-10 days after the procedure. On imagining you see relatively normal appearing biliary ducts or mild dilation (which can be from the post-op state alone) STEPHANIE ALL THE SIGNS ARE POINTING TOWARD SURGICAL COMPLICATION OF BILE LEAK AND INFECTION. There is no evidence of a retained gallstone. Don't ignore the clues the question is giving you. If it was a retained gallstone, you would see significant biliary dilation on imaging.

24 yo pt with fibroadenoma (palpable breast mass). You want to know what is the best method to CONFIRM the dx?

Biopsy is the only way to CONFIRM the dx (Note: although imaging tests with ultrasound &/or mammogram are the appropriate next steps in management, only biopsy will confirm the dx. Needle aspiration is done for small cystic or solid lesions, while core biopsy is preferred for larger solid masses.

56yo guy with oral ulcer on his tongue that he noticed a month ago and causes him pain and burning with eating. 25year smoking hx and 1-2 cans beer most nights. Sexually active with male & female partners. Ulcer with raised margins on tongue. Hard 1cm cervical node present. what should you do next?

Biopsy the lesion. -nonhealing ulcer with indurated edge and hard, immobile lymph node is suspicious for malignancy, esp with tobacco use. ***Tobacco use is the single greatest RF for head and neck cancers, increasing cancer rate by 5-25x.. ETOH use also promotes oncogenesis and some viral infections (HPV, EBV) also do it. Most cancers of head and neck are squamous epithelial. -Most manifest in oral cavity as hyperplastic white (leukoplakia) and dysplastic red (erythroplakia) pre-CA plaques. If you suspect oral CA, biopsy the lesion. If CA is indeed present, CT scan of head and neck with contrast can help determine tissue invasion and staging.

Pt presents with skull getting bigger and hat not fitting (thickened cortices and mixed lytic and osteoblastic lesions), nuclear bone scan shows increased uptake in skull and tibia. elevated AP, elevated bone turnover. How do you tx Paget's disease of the bone - drug class and example?

Bisphosphonate (ex: alendronate, zoledronic acid) to inhibit osteoclasts and suppres bone turnover.

Pt with breast cancer met to the bones, and she has bone pain and her Ca is slightly high at 11.4. What do you give her?

Bisphosphonate therapy. Mild hypercalcemia (<12) doesn't require urgent therapy but hypercalcemia of malignancy may worsen over time and bisphosphonates can inhibit the osteoclastic activity, stabilizing the destructive bone tumors and reduce the risk of skeletal related events like pathologic fractures or malignant hypercalcemia.

Pt with direct blunt abdominal trauma to his lower abdomen and pelvis. Diffuse abdominal pain and dull pain in left shoulder. Left shoulder looks fine. Diffuse abdominal pain with guarding. What do you expect to see on CT abdomen?

Bladder DOME rupture. The bladder dome (top of the bladder) is right adjacent to the peritoneal space. So if that ruptures, then you can have bladder contents leak into the peritoneum, which causes peritonitis, which causes the abdominal pain, guarding, and phrenic nerve irritation that causes referred pain to the ipsilateral shoulder (Kehr sign) since the innervation of the shoulder comes from the C3-C5 spinal nerve rooms ("3,4,&5 keeps the diaphragm alive"), these roots are also the origin of the phrenic nerve that innervates the diaphragm.

35yo male from Wisconsin who works outdoors wood cutting & construction. Fever, night sweats, productive cough, unintentional 17lb weight loss over 3 months. Multiple ***skin lesions that are well-circumscribed, verrucous, and crusted***. CXR with left upper lobe consolidation and 2 **lytic lesions in anterior ribs***. Cause of current symptoms?

Blastomycosis. -Geography, skin involvement, lytic bone lesions Fungal infection that occurs most often near the Great Lakes, Mississippi river, & Ohio River basin (Wisconsin has highest infection rate). Pulmonary and CXR findings resemble TB and histoplasmosis but systemic blastomycosis may cause characteristic ulcerated skin lesions and lytic bone lesions.

What chemotherapy drug cause pulmonary fibrosis and so you should do PFTs to get a baseline and also test at regular intervals?

Bleomycin --> pulmonary fibrosis.

obese young female has HA with N/V. She takes OCPs, funduscopy shows papilledema. what complication can occur with this otherwise benign disorder?

Blindness. She has pseudotumor cerebri (benign intracranial HTN) in young obese female with HA with normal neuroimaging and elevated CSF pressure. See papilledema and visual field defects and sometimes 6th nerve palsy. Provoking agents may be glucocorticoids, Vit A or OCPs. Tx with weight reduction and acetazolamide if weight reduction fails.

STEMI in II, III, aVF and also in I and aVL CP, sweating, JVD, positive Kussmaul's sign (increased JVD with inspiration), **clear lung fields***, ***Hypotension (80/50)***. What's causing the hypotension?

Blood backing up. bc right heart isn't working... and II, III, and aVF is inferior STEMI with right ventricular MI, usually supplied by right coronary artery, so hypotension is d/t right ventricular infarct. -RV failure --> decreased preload and resultant hypotension. So also treat these pts (without pulmonary congestion) with boluses of IV Fluids (isotonic saline) to improve RV preload and facilitate LV filling. Note: don't give nitroglycerin therapy bc hypotension can be acutely worse follow nitro therapy. Avoid giving preload reducing medications like nitrates since these pts are preload dependent and should get IV fluids instead.

How does Giardia present?

Blunting of microvilli --> watery, foul-smelling diarrhea. Infection typically acquired from contaminated water. Incubation pt 7-14 days.

Most accurate test for multiple myeloma? (Don't get tricked!)

Bone Marrow Biopsy Since Multiple myeloma is defined by >10% of plasma cells on bone marrow biopsy and no other condition is associated with this finding, bone marrow biopsy is the most accurate diagnosis. Don't pick SPEP. Although Monoclonal immunoglobulins, which create an "M" spike on SPEP is found with MM, that "M" spike can also be see in MGUS (monoclonal gammopathy of unknown significance), which occurs commonly in elderly patients and MGUS is not MM. MGUS also doesn't require you to do anything, bc only 1% transform into myeloma. So MGUS requires no treatment. So getting a SPEP doesn't tell you if it's MGUS or MM, you still need to get a bone marrow biopsy to evaluate for myeloma. - Also, the first initial test you would do with MM is x-ray of the affected bone to look for lytic lesions.

Major mycophenolate toxicity

Bone marrow suppression. (inhibits inosine monophosphate dehydrogenase, which is the rate limiting enzyme in de novo purine synthesis) Memory tool: M for Mycophenolate and bone Marrow suppressin.

What kind of symptoms are seen in conus medullaris syndrome?

Both UMN and LMN symptoms as the conus is part of the spinal cord (vc cauda equina lesions is just LMN sx since the conus is part of the peripheral nervous system)

What's the difference between Gilbert's and Crigler-Najjar syndrome?

Both are indirect hyperbili bc of inherited deficiency of UDP-glucuronyl transferase --> un-conjugated (aka indirect) hyperbili. Gilbert: mild form, they have some of the enzyme. jaundice during times of stress. CN: more severe form, they don't have any of the enzyme. Present early in life and require liver transplant.

Order of puberty development. What comes first, next, and last?

Breast (thelarche): usually 1st sx of puberty in girl (age 8-12) Pubic hair (pubarche) follows (but can also occur 1st) Menses (menarche) is last and is around Tanner stage 4 (about 2-2.5 years after breast buds develop). Average age is 12.5y but not considered abnormal till <1 if development of secondary sex characteristics has been normal. -The 6 months before menarche, girls get a grwoth spurt. Example: pt at age 14 with normal breast and pubic hair development with 3cm growth (from 5ft to 5ft1in... that's a lot for 3 months) in past 3 months, likely undergoing her puberty growth spurt and about to have menarche in the next 6 months. So she's doing fine. Reassure the mom and reevaluate if menarche doesn't occur by age 15.

How long do you have to have symptoms to be schizophrenic vs schizophreniform vs brief psychotic d/o?

Brief psychotic d/o: >1 day & < 1 month. (full return to function) Schizophreniform: >1 mo & <6 mo Schizophrenia: > 6 months (requires functional decline)

Pt with lots of stressors and she has psychotic features (hearing voices). Several days alter, she is discharged from the psych ward and at 2 week follow up, she's normal again, what is the dx?

Brief psychotic disorder. Brief psychotic d/o: >1 day, < 1 month (return to full function) Schizophreniform: > 1 month, < 6 months (Functional decline not required) Schizophrenia: > 6 months (Requires functional decline)

28 yo pt has chronic cough. A year ago he had a severe episode of pneumonia that required 4 days in the ICU. Since then, he's had intermittent episodes of cough productive of THICK, YELLOW sputum occasionally streaked with blood. He's SOB and fatigued. He's lost 13 lbs this year. He takes albuterol for wheezing and SOB. No other past medical hx. Crackles over lower lung fields with scattered wheezes. What does he have?

Bronchiectasis: permanent destruction and dilation of the airways. s/sx: cough with daily mucopurulent sputum production. Rhinosinusitis, SOB, hemoptyosis***, crackles, wheezing ***Persistent cough with mucopurulent sputum that may be streaked with blood*** Pathophys: infectious insult with impaired clearance Etiology: Airway obstruction (cancer), rheumatic disease (RA, Sjogren), toxic inhalation, chronic/prior infection (aspergillosis, mycobacteria), immunodeficiency (hypogammaglobulinemia), congenital (CF, alpha-1 antitrypsin deficiency) Eval: HRCT (high res. CT) of chest for initial dx. -immunoglobulin quantificaiton -CF testing, sputum culture -PFTs. CXR: bronchial dilation and irregular peripheral opacities, suggesting dx but need High resolution CT to make the official definitive dx. Note: recurrent cycles of infection, inflammation and tissue damage to the lungs can cause bronchiectasis. that ultimately leads to bronchial dilation and airway DESTRUCTION. To develop bronchiectasis, you need a infectious insult combined with impaired bacterial clearance. A single severe episode (often necrotizing) pneumonia (ex: involving ICU level care) can contribute to development of bronchiectasis through massive tissue damage and permanent structural lung changes that lead to impaired bacterial clearance.

What does bullae rupture mean? what does it cause?

Bullae is another word for bleb. Rupture of lung bullae or blebs lead to secondary spontaneous pneumothorax and present with dyspnea, and subcutaneous emphysema.

Symptoms of B5 (pantothenic acid) deficiency

Burning feet syndrome (Mnemonic: think about burning your 5 digits on your feet with a frying pan... pantothenic)

Hospitalized pt who got broad spectrum abx with new onset perfuse watery diarrhea, fever, elevated white count, recent Abx use, and mild abdominal tenderness, think what? Dx? Tx?

C. diff. Dx: stool PCR (GET STOOL TOXIN TESTING!) Tx: with Oral metronidazole or vancomycin (Note: if pt has all of these things.. don't get distracted by the fact that they had surgery and get a CT scan of the abdomen... no, it's just simple C.diff bc the patient is int he hospital and got broad spectrum antibiotics)

Preconception counseling in pt with African descent. Concerned for thalassemia anemia. What is your first step?

CBC along with hemoglobin electrophoresis if pt is of African descent.

Tx for anorexia nervosa?

CBT, Nutritional rehab ***Olanzapine (SGA) if no response to CBT and nutritional rehab

What's the genetic abnormality in Fragile X?

CGG trinucleotide repeat on X chromosome (Memory tool: "see (C), he's a G"... CGG repeat) s/sx: intellectual disability, long/narrow face, large/protruding ears, macrocephaly, macro-orchidism

HIV+ pt. Something is wrong with his retina. But he feels no pain (PAINLESS). Funduscopy shows FLUFFY or granular retinal lesions near the retinal vessels with associated HEMORRHAGES. What organism is causing this retinitis?

CMV

What is the most common congenital infection transmitted transplacentally worldwide? (affects about 1% of all live births) 1 day old girl with petechaie, jaundice, 10th percentile on weight and length charts, HC is <3 percentile. HSM. Mom has hx of fever and sore throat in 2nd Trimester. Her RPR is nonreactive. No rubella antibody.

CMV - most commonly occurs during primary infection of the mom who might have nonspecific febrile illness (or be asx). Think about CMV (since it's the most common congenital infection) when there is infant growth restriction, HSM, jaundice, and petechaie (which are all kind of non-specific symptoms bc those are findings in all congenital infections) Most specific CMV findings: periventricular calcifications & small head. May have sensorineural hearing loss later on that develops.

HIV+ pt comes in complaining of floaters and blurred vision in his right eye. Denies ocular pain. He is noncompliant with anti-viral medications. CD4 is now <100. Now you see on fundoscopic exam: yellow-white exudates immediately adjacent to the fovea and retinal vessels. Several white patches are present on the oropharygneal mucosa. What is the dx?

CMV retinitis has the classic presentation of "yellow-white fluffy hemorrhagic lesions along the vasculature" (NO OCULAR PAIN with CMV retinitis) This is a full thickness inflammation that moves centripetally along the vasculature, causing edema and scarring. Pts experience blurred vision, floaters, and photopsia (sensation of flashing lights). Lesions near the fovea and optic nerve may cause blindness, and scarring greatly increases the risk of retinal detachment. Dx: with fundoscopic exam Tx: oral antivirals (valganciclovir). If lesion is near the fovea or optic nerve, intravitreal injections are added. Note: all pts should start anti-retroviral therapy (2 weeks after starting CMV tx) to prevent recurrence and progression.

What's the difference between fundoscopic exam for CMV retinitis and toxoplasmosis chorioretinitis? what about pt symptom presentation?

CMV retinitis: No ocular pain. yellow-white fluffy hemorrhages ALONG the vasculature Toxoplasmosis chorioretinitis: PAIN PAIN PAIN!! with lesions NOT along the vasculature; lesion is in non-vascular distribution.

What are some infectious causes of primary adrenal insufficiency (note: they are not the most common cause of Addison's disease in developed countries bc autoimmune adrenlitis is the most common cause)

CMV, fungal infections, TB

HIV pt has large linear ulcers in the esophagus, they have focal substernal burning pain with odynophagia, large linear ulcers (generally shallow and in distal esophagus) on endoscopy and presence of intra-nuclear and intracytoplasmic inclusion on biopsy. What are you thinking is the organism? what is the tx?

CMV, treat with ganciclovir.

1 day old has petechiae, jaundice. Mom had limited prenatal care but had week of fever and sore throat during pregnancy. Nonreactive RPR, absent rubella antibody. Baby is 10%tile weight and length and HC is <3%tile. Kiddo has diffuse petechial rash, jaundice to face and trunk, HSM. Cause?

CMV: most common congenital infection -Supported by findings of periventricular calcifications and microcephaly. Can also present as asymptomatic. both symptomatic and asx infants can later develop neurodevelopmental abnormalities, such as sensorineural hearing loss. Since the mom's serology confirms she did not have syphilis or rubella, don't pick those.

What happens if you drink isopropryl alcohol?

CNS depression, ***Disconjugate gaze***, absent ciliary reflex -High osmolar gap, NO increased AG or metabolic acidosis (that's what Uworld says.. but I thought this was part of MUDPILES... double check)

What can cause SIADH? What's the tx?

CNS disturbances: stroke, hemorrhage, trauma Meds: SSRIs, NSAIDs, carbamazepine (to trigeminal neuralgia, or for seizures) Lung disease (pneumonia can cause SIADH!!) Ectopic ADH secretion (small cell lung cancer can cause SIADH) Pain, nausea even can cause SIADH!! Tx: restrict fluids and give salt tablets (since they are hyponatremic) -Give hypertonic saline (3% saline) for severe hyponatremia.

What's something that can happen with longstanding/chronic COPD?

COPD with Cor Pulmonale. Cor Pulmonale is the impaired function of the RV caused by pulmonary HTN that occurs d/t underlying lung disese (COPD, ILD), pulmonary vasculature (idiopathic pulmonary artery HTN), or Obstructive sleep apnea. -So think about a pt with long smoking hx, COPD barrel chest, and now has lots of swelling pitting edema, a big liver edge and when you push on the abdomen, the JVD distention is seen. Presents with: exertional symptoms (DOE, angina, syncope), anorexia, abdominal pain (d/t hepatic congetion), peripheral edema. PhyEx: shows loud P2 (pulmonic component of 2nd heart sound) and RV 3rd heart sound, TR murmur (holosystolic at LLSB, augments with inspiration), elevated JVP with hepatojugular reflex, hepatomegaly with pulsatile liver, and can also see ascites or pleural effusion. Dx of Cor pumonale based on clinical features and Echo (RVH, TR with RA enlargement; so the pulmonary HTN causes blood to build up in the right heart and messes up everything in the right heart) -If you need definitive dx, can do right heart cath to get elevated pulmonary artery systolic pressure (>25 mmHg is pulmonary HTN) Note: There is no mention of liver disease or cirrhosis so don't pick increased portal venous resistance (portal HNT) bc that is seen with liver cirrhosis or extrahepatic portal vein thrombosis and isn't any of the other stigmata of chronic liver disease mentioned: like the palmar erythema, spider angiomata, caput medusae, gynecomastica. Or complications of ascites, SBP, or variceal bleeding. -Know that the heaptojugular reflex is related to Cor Pulmonale and RV failure, and NOT NOT NOT NOT NOT NOT liver cirrhosis. Makes sense it has to do with HF because it has to do with JVP and blood backing up, which can include in the liver, but has nothing to do with cirrhosis.

Pt complains of sudden painless monoocular vision loss for several hours. Has "shade dropping over my eye." Hx of similar episodes in the past that resolved spontaneously. Hx of HTN and hyperlipidemia.

CRAO!!!! (Don't pick venous when you think it's CRAO because CRAO stands for Central Retinal ARTERY Occlusion) -Pick "Arterial embolic occlusion" On Fundoscopic exam, expect to see pale optic nerve, maybe a white thrombus in the retinal artery, cherry red macula and retinal whitening. Should work the patient with CRAO up for ultrasound imagining of the next to look at the carotids to evaluate for stenosis. Treat with atherosclerotic treatment (aspirin, statin) and if it's cardioemobolic (ex: a.fib), then use long-term anticoagulation (ex: warfarin).

What are features of systemic sclerosis?

CREST syndrome with vascular dysfunction. -Calcinosis cutis -Raynaud's -Esophageal dysmostility with reflux (ex: GERD) -Sclerodactylyl -Telangiectasias Vascular dysfunction is a prominent component of the disease in African American patients. Raynaud's can proceed other disease manifestations by several years. Note: pulmonary arterial hypertension (PAH) is common with the limited cutaneous subtype of SS (aka CREST syndrome) -PAH happens bc of intimal hyperplasia of the pulmonary arteries and typically present with progressive dsypnea. -May also experience exertional syncope or pre-syncope (ex: lightheadedness) d/t RV failure and inadequate venous return to the left atrium. Physical exam: should have ***RV HEAVE*** or parasternal heave, which is an impulse palpated immediately left of the sternum that suggest RV enlargement. (RV gets big bc of pulmonary HTN and that will cause a RV Heave). A loud pulmonary component of the 2nd heart sound a sxs of RHF (ex: peripheral edema, hepatomegaly) may also be present

What is osteogenesis imperfecta associated with? What's the inheritance pattern? What is the gene mutation? What are the associated findings/symptoms?

CT d/o (AD inheritance; mutation of COL1A1) Al l types have osteopenia. Associated with blue sclerae, hearing loss, recurrent fractures, opalescent teeth. They have normal intelligence. Depends on severity, but can have recurrent fractures, easy bruisability, hypotonia, and hearing loss. Many pts with OI have dentinogenesis imperfecta ("opalescent teeth" with blue-gray to yellow-brown discoloration caused by discolored dentin shining through the translucent and weak enamel. Both primary and permanent teeth are affected) -OI pts have normal intelligence. (Think about Connie (dentists) treating people with OI and their opalescent teeth)

When do you do a CT scan of the abdomen/pelvic in a pt with uncomplicated pyelonephritis (Fever, CVA tenderness, leukocytosis with bands, UA positive nitrites, many WBCs and >100 bacteria/hpf)?

CT scan if there is no clinical improvement in the first 72 hours -Tx: empiric oral abx against gram negative organism (ex: fluoroquinolone). Save imaging for when pts has persistent clinical symptoms despite 2-3 days (48-72 hrs) of therapy, history of nephrolithiasis, complicated pyelo, or unusual urinary findings (ex: gross hematuria, suspicions for urinary obstruction)

Pt with aortic dissection (Type A) can extend into the pericardial space, causing hemopericardium and rapidly leading to cardiac tamponade and cardiogenic shock. What is the initial dx study you should do for HDS pts?

CTA: study of choice for HDS pts with no evidence of renal dysfunction. Will show intimal flap separating true and false lumens. Note: MRA is most time consuming and required administration of gadolinium contrast, which should be avoided in pts with mod-severe kidney disease d/t risk of nephrogenic systemic fibrosis. Note: TEE is preferred if pt is hemodynamically instabile or has renal insufficiency (since the other modalities use contrast)

Pt has bitemporal hemianopsia and has DI. CT Head shows CALCIFIED (white) mass in the suprasellar space. What is this?

Calcified is Craniopharyngiomia. -Low grade malignancy from remnants of Rathke pouch -Optic chiasm compression --> vision sxs -Pituitary stalk compression --> endocrinopathies (GH deficiency, DI) Note: Pituitary adenomas can also present as bitemporal hemianopsia but are not calcified and would have manifestation s of hormone secretion like prolactinoma with galactorrhea and amenorrhea. Note: Rathke clef cysts are also derived from Rathke pouch remnants. If they are big, they can present similarly to craniopharyngiomas. But they occur in the SELLAR region and are not calcified.

What condition can you see autoimmune hemolytic anemia (and would therefore have a positive Coombs test)?

Can be seen in systemic lupus erythematosus (SLE)

PT with Lupus you start them on hydroxychloroquine (safe, well tolerated med; it's a DMARD) What's the exam you want to do on these pts periodically what you're afraid may occur as a SE of this otherwise safe DMARD?

Can have RETINAL toxicity on rare occasions. Can also have IRREVERSIBLE vision loss: most common after 5-7 years of tx. So pts on hydroxychloroquine should have a baseline ophthalmologic exam with annual reassessment beginning after 5 years. IF you are caring for a pt with lupus and they are on hydroxychloroquine, you need to check their their vision- eye exam as baseline before you start the med and also reassess every year starting after 5 years on the med bc the retinopathy tends to have after 5-7 years of taking hydroxychlOrOquine... have those O's remind you to check their eyes. "HI, i'm here to check your O.Os." (Hi-droxychlOrOquine)

What is ocular rosacea?

Can involve the cornea, conjunctiva, and lids and cause burning or foreign body sensations, blepharitis, keratitis, conjunctivitis, corneal ulcers, and recurrent chalazia. Sxs may not be concurrent with skin findings. Note that it can lead to vision loss. Mild sxs treated with lid scrubs, topical antibiotics (metronidazole, erythromycin), and ocular lubricants. More severe cases require systemic abx and topical immunosuppressive agents (glucocorticoids, cyclosporine) 63yo mane eye discomfort. Sensation of "dirt in my eyes" with redness and tearing for the last 3 weeks. Attempted tx with saline irrigation and oral antihistamines but had to d/c due to urinary hesitancy and nocturia. Exam shows increased vascularity and mild redness of conjunctivia. Red and scattered pustules involving cheek and nose. Dx: ocular rosacea

What if someone with H.pylori infection is resistant to triple therapy?

Can use metronidazole or tetracycline as alternative antibiotics, and adding bismuth (#83 on the elemental chart) may aid in resolution of treatment resistant ulcers.

Be careful with giving supplemental oxygen to advanced COPDers bc it can do what?

Can worsen hypercapnia bc of a combo of increased dead space perfusion causing V/Q mismatch, decreased affinity of oxy-Hgb for CO2 and reduced alveolar ventilation. Hypercapnia also causes reflex cerebral vasodilation and may induce SEIZURES. So be careful with using oxygen, goal of oxyhemoglobin sat is 90-93% in these pts or PaO2 60-70 mmHg. Pts who have sign. acidosis or have severely reduced LOC need mechanical ventilation

What kind of infection can cause penile balantitis (inflammation of the glans), phimosis (narrowed foreskin that cannot be retracted), esp. in diabetic pts. Usually painful or itchy red rash with foul-smelling thick discharge.

Candida infections. Note: phimosis is foreskin that cannot be retracted. vs paraphimosis is emergency where a retracted foreskin cannot be placed back (donut sign)

What are CYP450 INDUCERS. Would decreased the effect of Warfarin?

Carbamazepine, phenytoin, Ginseng, ST John's wort OCP Phenobarbital Rifampin. Note: theses would decrease bleeding risk and increase thrombosis risk. Leafy green vegetables would incrase Vitamin K and decrease the anticoag effect of warfarin. and decrease bleeding risk and increase thrombosis risk

Why is re-feeding syndrome so dangerous?

Carbohydrate intake stimulates INSULIN!!! and that promotes the cells to take up K, phosphorus, and Mg. This can deplete the serum of those electrolytes and cause arrhythmias and cardiopulmonary failure. Phosphorus is used to make ATP. Deficiencies in K and Mg are what can cause the heart arrythmias.

flushing of face, diarrhea, bronchospasm, what kind of tumor is in the small intestines?

Carcinoid syndrome (carcinoid tumor is in small intestine 70-80% of the time and doesn't usually involve the pancrease)

Pulsus paradoxus: systemic arterial pressure that falls >10 mmHg during inspiration (exaggerated drop in blood pressure); When do you see it?

Cardiac tamponade (bc of increased pressure within the pericardial sac). *** KNOW THAT PULSUS PARADOXUS CAN ALSO BE CAUSED BY OTHER CONDITIONS WITHOUT PERICARDIAL EFFUSION: such as: -severe asthma -COPD (Normally there is small 2-5mmHg drop below atmospheric pressure for the intra-thoracic pressure with inspiration. In severe asthma or COPD, the drop in intra-thoracic pressure is greatly exaggerated (up to 40mmHg). This negative pressure causes pooling of blood in the pulmonary vasculature, decreasing LV preload. Marked expansion of the lungs in asthma and COPD can also impinge upon outward expansion of the heart. This leads to excessive drop in BP that is detected as pulsus paradoxus*** TL:DR: Pulsus paradoxus: seen in cardaic tamponade, severe ASTHMA! & severe COPD!!

2 day old baby. didnt' pass his hearing screen, had IUGR, mom had international travel and fever in 1st trimester with 5-7 days of joint pain after the illness. Kiddo is <5th percentile on growth charts, there's a loud murmur over the left 2nd ICS. what other findings do you suspect?

Cataracts He has congenital rubella syndrome: sensorineural hearing loss, cataracts, PDA, purpuric blueberry muffin rash. & mom has hx of 1st trimester febrile illness with arthritis.

Clinical findings for congenital infection with Rubella

Cataracts, heart defects (ex: PDA)

What is amaurosis fugax?

Caused by atheroemboli from the carotid arteries and causes TEMPORARY vision loss as opposed to the persistent vision loss.

What is Behcet syndrome? how does it manifest?

Causes gential aphthous ulcers that are recurrent and painful. Most occur on the scrotum and heal spontaneously in 1-3 weeks.

IF a pt only has glucocorticoid deficiency but no problems with aldosterone production, what are you thinking they have?

Central Adrenal insufficiency (since Aldo production is regulated by RAAS).

Elderly pt presents with sudden loss of vision in eye, occurs on waking this morning. Hx of HTN and smoking. Funduscopic exam shows: -swelling of optic disk, retinal hemorrhages, dilated and tortuous veins, and cotton wool spots. Likely Dx?

Central Retinal Vein Occlusion (VEIN!! Read carefully) Funduscopic findings: -Venous dilation & TORTUOSITY d/t venous occlusion -Scattered & diffuse hemorrhages d/t backup of blood & increased resistance, leading to ischemic damage -"Blood & thunder" appearance d/t diffuse hemorrhages -Cotton wool spots -Disk swelling Clinical presentation: acute, unilateral, painless loss of vision suggests CRVO.

Sudden loss of vision in one eye. Hx HTN. fundoscopic exam shows swelling of optic disk, scattered and diffuse retinal hemorrhages, dilated and tortuous veins, and "cotton wool spots"

Central retinal vein occlusion (CRVO)

Pt with long history of heavy alcohol use (>10 years). He has progressive difficulty walking and frequently falls over the past year. Difficulty with balance when walking up and down the stairs and has to brace himself against a wall even when walking on a flat surface. Proprioception and vibration sense are normal. He has a wide-based gait and can't tandem walk. Heel-shin test is abnormal but finger-nose test is normal. What is causing his ambulatory dysfunction? what cells specifically are degenerated? Tx?

Cerebellar degeneration d/t ETOH neurotoxicity -see this in heavy ETOH use >10 years. -d/t degeneration of Purkinje cells (cerebellar vermis) as these neurons are largely responsible for truncal coordination so pts get wide-based gait and postural instability but upper extremity limb coordination and cognitive function are preserved. Tx: stop drinking ETOH and supplement nutrition to prevent disease progression (however they will not improve). Use assistive walking devices like waters and canes.

What kind of herniation is it if the cerebellum is pushed through the foramen magnum

Cerebellar tonsillar herniation. Manifests as: neck tilt, flaccid paralysis, coma, BP instability, resp. arrest.

HA, hearing loss, vertigo, tinnitus, balance problems. What kind of mass suspected?

Cerebellopontine angle (CPA) tumors (ex: acoustic neuromas, meningiomas)

41yo pt with "lower uterine segment mass" that extends laterally with "BL hydronephrosis" in pt with LBP and HIV. What are you thinking about?

Cervical cancer. Early cervical CA symptoms: irregular vaginal bleeding and postcoital spotting d/t bleeding from cervical lesion itself. AS tumor extends laterally through the parametrium and pelvis (LBP), cervical cancer can lead to obstruction of the surrounding blood vessels and lymphatics (lymphedema) and ureters (hydronephrosis). IV pyelogram or CT scan is used to evaluate for hydronephrosis. Cervical cancer is an AIDS-defining illness. Immunosuppressed pts have persistent HPV infection --> neoplasia or malignancy. So pap screening is more frequent in the years immediately following dx.

Complications of cervical conization as intervention for CIN 2 & CIN 3.

Cervical stenosis, preterm birth, preterm PROM, 2nd Tri pregnancy loss.

Neisseria gonorrhoeae infection in a woman, what do you expect the sxs to be for cervicitis, PID, and gonococcal pharyngitis? Dx?

Cervicitis: mucopurulent discharge, irregular bleeding PID: fever, lower abdominal pain Gonococcal pharyngitis: (Get it from oral sex) typically asymptomatic but can present with pharyngeal edema and non-tender cervical LA Dx: confirmed by NAAT for gonorrhea.

Lid discomfort. Chronic, granulomatous inflammation of the meibomian gland. Appears as hard, painless lid nodule.

Chalazion

What is this a description of? Multiple*** and deep ulcers Base may have gray-yellow exudate*** Organisms often clump in long parallel strands ("school of fish") Initial lesion IS painful

Chancroid (Haemophilus ducreyi)

Painful genital papule that turns into pustule and erodes into an ulcer. Rare in USA, think about this in pts with high risk sexual practices

Chancroid d/t Haemophilus ducreyi

What causes septal widening and hemosiderin-loaded macrophages?

Characteristics of pulmonary edema d/t left sided heart failure, which can cause secondary pulmonary HTN. Would expect pleural effusion and pulmonary edema (ex: Kerly B lines, BL infiltrates) on CXR>

Young female pt in her 30s with hx of chemo and trying to have a kid but now you find that she has vaginal dryness. What do you expect for FSH, LH, Prolactin, TSH?

Chemo kills your ovaries. So you're not pushing out Estrogen and so your FSH and LH will be high. Prolactin and TSH not affected so should be normal. This is aka hypogonadotropic hypogonadism in women <40yo "primary ovarian failure" d/t absence of developing follicles. Chemo targets rapidly dividing cells, including the granulosa and theca cells of the ovaries. Chemo pts have shortened reproductive capacity even if menses returns. Ovarian failure --> decreased Estrogen and so negative feedback increases FSH And LH. Tx with hormone replacement provide relief of menopausal sxs and bone loss protection but doesn't affect fertility. Cryoperservation may be a thought.

2x2 table, what kid of statistical test do you use to assess the association of the exposure to the outcome?

Chi-square test. Whenever you see 2x2 table, think chi-square test. Mnemonic: "i want to sit at a table and drink chai with my nuclear family (2 parents and 2 kids; 2x2 table) = Chi-square test. Think of ANOVA as more letters, so comparing means f 3+ variables. Note: 2 sample z-test and 2 sample t-test are used to compared two means, not proportions.

35yo healthy female goes to Caribbean islands and came back recently. She has had 3 days of fever and malaise. Marekd pain in hands and wrist joints. Temp 103F. Monogamous relationship. Macular skin rash on body and mild cervical LA. No oral ulcers. Swelling and tenderness of BL hands, wrist, and ankle joints. Labs: Plt 120,000 (low), Leuks 2,900 (low). Likely dx?

Chikungunya fever. From vector: Aedes mosquito (same as dengue fever) Incubation: 3-7 days Presentation: High fevers, severe polyarthralgias (virtually always present), HA, myalgia, conjunctivitis, maculopapular rash, leukopenia (decreased WBCs), thrombocytopenia (decreased plts), elevated liver enzymes. Dx: confirm with serologic testing. Management: supportive care (resolves in 7-10 days), Development of chronic arthralgias, may require methotrexate, in approximately 30%.

Pt had cardiac cath and stent placed about 5 days ago for CP. Now he has N/abdominal pain, painless purple mottling of both feet, Luek with 12% eosinophils, incrased BUN, Cr, 1+ protein on UA and WBC and RBC on UA, and low complement. What's going on?

Cholesterol emboli Think about systemic atheroembolism from disruption of the stherosclerotic plaque. Think about this in pt with constellation of acute/subacute renal failure, typical skin manifestations (Livedo reticularis), GI symptoms (N/abdominal pain) after recent vascular procedure... LAbs show ***eosinophilia, eosinophiluria,*** and ***hypo-complementemia*** in recent atheroembolism. If dx unclear, biopsy skin or kidneys for confirmation.

Pt has cardiac cath done and now they have livedo reticularis, and increased Cr. What's going on?

Cholesterol emoblism (artheroembolism) caused by recent cardiac cath. You disrupted the plaque and the debris showered into the circulation, which can occlude arterioles and cause tissue/organ ischemia. -Can go to brain (cerebral infarct), intestinal ischemia, GI bleeding, pancreatitis, AKI, skin manifestations "blue toe syndrome" (cyanotic toes with intact pulses), livedo reticularis, gangrene, ulcers. Retina may show Hollenhorst plaque, bright, yellow, refractile plaques in retinal artery that indicate proximal source like the internal carotid artery (since that feeds into the retinal artery) Tx: supportive tx. Can reinforce indication for statin tx in these pts.

What is a finding that separates gout (monosodium urate crystals) from pseudogout, making pseudogout with CPPD (calcium pyrophosphate arthritis)more likely?

Chondrocalcinosis (calcification of articular cartilage), seen on X-ray Pseudogout (CPPD) will have rhomboid shaped, positive birefringence and CHONDROCALCINOSIS on imaging.

What should you think about that is associated with pseduo-gout (rhomboid crystal)?

Chondrocalcinosis on imaging (meniscal calcification) Pseudogout (acute calcium pyrophosphate dihydrate (CPPD) crystal arthritis). Release of CPPD crystals from sites of chondrocalcinosis (calcification of articular cartilage into the joint space). Often occurs in the setting of recent surgery or medical illness. Knee is commonly affected. Identifying chondrocalcinosis on x-ray of joint with acute arthritis est. the dx of probable CPPD crystal arthritis. Synovial fluid analysis shows inflammatory effusion (15-30k), rhomboid-shaped, positively birefringent crystal. Tx: Intra-articular glucocorticoids. NSAIDs, Colchine.

53yo man with 2 episodes of hemoptysis over the past week. He has a 2 year hx of morning cough producing about 1 tablesppon of white sputum. Last week, he started coughing up small amounts of blood, happened 2x. 30 year smoking hx. Likely cause?

Chronic bronchitis His longstanding smoking and chronic productive cough with recent hemoptysis is consistent with chronic bronchitis. (Definition: chronic productive cough >3 months in 2 successive years. Leading cause is cigarette smoking) Note: he'll need chest imaging to r/o malignancy. Note: it's not bronchiectasis bc there's not mention of recurrent respiratory tract infections and the hx doesn't point towards COPIOUS mucopurulent sputum, both of those thigns would be more consistent with bronchiectasis.

67yo woman with progressive fatigue & anorexia for 6 months. Last 8lbs and has early satiety. Slightly thin but well nourished. Spleen tip is palpable with deep exhalation. Hgb 8.6 (low), Leuks 42k (high). FISH shows abnormal chromosome 22. What does she have? What's an important target for treating this pt's disease?

Chronic myeloid leukemia (CML) - clonal myeloproliferative d/o driven by abnormal fusion of BCR-ABL gene d/t translocation between chromosome 9 & 22. This gene causes Leukemogenesis (so really high leukocyte count in the 42,000 range) d/t ***constitutively active tyrosine kinase.*** -Peripheral blood smear shows dramatic leukocytosis (often >100,000) with absolute basophilia and shift towards very early PMN precursors (promyelocytes, myelocytes) 1st line tx: for CML pts is a tyrosine kinase inhibitors like ***imatinib***

When would you expect to see pancreatic calcification?s

Chronic pancreatitis d/t chronic ETOH use can present with abdominal pain radiating to the back, N/V, and imaging shows pancreatic calcifications.

Pt has had TB in the past and treated, now they present with fatigue, productive cough with blood-tinged sputum, weight loss last few months and right sided rhonchi and crackles, and what looks like cavitary lesion on chest CT scan. What is most likely dx?

Chronic pulmonary aspergillosis. -bc RF for this is lung disease/damage from prior TB bc that allows a cavity for the fungus ball to live in. Pt will have serology + for Aspergillus IgG. -Think about this if >3 months of weight loss (>90%), cough, hemoptysis, fagitue, and cavitary lesion that may have a fungus ball in it. -Tx: resect the Aspergilloma if possible and use Azole meds since it's fungus. Embolization if there is sever hemoptyosis.

MAC (mycobacterium avium complex) presents with GI and pulmonary infections. How do you treat it?

Clarithromycin & ethambutol

What are signs of typical angina. what about atypical? or nonanginal?

Classic angina: 3/3 sxs: -Typical location (substernal), quality and duration of CP -Provoked by exercise/emotional stress -Relieved by rest/nitro Atypical: just 2/3 sxs Non-anginal: <2/3 sxs

If you're deciding between arrhythmia and seizure, and they say the pt suddenly passed out and had several muscle jerks while unconscious but then point to recent hx of MI and frequent ectopic beats, and a apical holosystolic heart murmur radiating to the axilla, that means they are pointing you toward arrhythmia. But what about the muscle jerks?

Clonic jerks can occur during ANY syncopal episode that is prolonged and associated with cerebral hypoxia, regardless of etiology. The pt's hx of structural heart disease (prior MI, MR murmur) along with frequent ectopic beats likely is arrhythmia as cause of syncope. Pt with arrhythmias usually have underlying cardiac d/os (CAD, cardiomyopathy, valvular heart disease) and may not have any prodromal sx prior to the syncope. If they were trying to point you to seizure, you would have presence of a trigger stimuli (lack of sleep, emotional stress, loud music, flashing lights), presence of prodromal aura, head deviation or unusual body posturing, tongue laceration, or prolonged post-ictal phase with confusion and disorientation.

If you have high BP in your upper extremities but low BP in your lower extremites, what are you thinking?

Coarctation of the aorta (congenital narrowing of the aortic arch, usually just distal to the origin of the left subclavian artery)

What are the sxs of lithium toxicity?

Coarse tremors, ataxia, AMS, N/V, hypotension.

Pt with increased HR and BP, diaphoresis, and dilated pupils. They are euphoric and have self-confidence, increased arousal and improved performance on tasks of alertness and vigilance. What drug did they likely date?

Cocaine.

Fungal infection of the lungs that causes fever, cough, and night sweats. May involve skin, meninges and skeleton, but is endemic in the Southwest USA.

Coccidioidomycosis

What is considered a stronger study between cohort studies, case control, or cross-sectional studies? why?

Cohort studies are stronger than case-control or cross-sectional studies bc of their greater ability to prove causation.

How does viral gastroenteritis usually present?

Combination of vomiting and diarrhea (small intestine mucosal inflammation --> watery diarrhea bc disruption of water reabsorption)

Best initial treatment for multiple myeloma?

Combo of dexamethasone (glucocorticoid) with lenalidomide (chemo), bortezomib (chemo), or both. Dexamethasone + LenaLIDomide, bortezomib.

What's the progression of treating acne?

Comedonal: Tx: Topical retinoids, salicylic/azelaic/glycolic acid. Inflammatory: Mild: Topical Retinoids + Benzol peroxide Mod: Topical Abx (erythromycin, clindamycin) Sever: Oral Abx Nodular (cystic): Mod: Topical retinoids + benzoyl peroxide + topical Abx Severe: + Oral Abx Unresponsive sever: Oral isotretinoin

What is transient synovitis?

Common self-limiting hip disorder that often follows a viral infection ("reactive synovial inflammation from viral infection). Fever and concerning lab findings are uncommon (so pt with transient synovitis would not have fever or leukocytosis)

Pt with gout, what do you treat them with?

Commonly use NSAIDS like indomethacin

What are you comparing when you are doing a case control study? what's the time frame?

Compare RF frequency (taking diseased cases and non-diseased control cases) Time frame: Present --> past

What are you comparing when you are doing a retrospective cohort study? what's the time frame?

Compare disease incidence (reviewing past records, taking + and - RFs) Time frame: present --> past

What are you comparing when you are doing a prospective cohort study? what's the time frame?

Compare disease incidence (taking + and - RFs) Time frame: present --> future

What are you comparing when you are doing a cross sectional study? what's the time frame?

Compare disease prevalence (taking + and - RFs) Timeframe: present

What are you comparing when you are doing a clinical trial? what's the time frame?

Compare outcomes of interest (for control and treatment groups) Time frame: present --> future

Pregnant pt with SLE, what is the the greatest risk of the disease to the fetus?

Complete AV block. ***KNOW THIS!*** SLE in mom, think complete AV block in baby.

Causes of Cauda equina syndrome?

Compression of spinal nerve roots from metastatic cancer, disc herniation or rupture, spinal stenosis, tumors, infection, hemorrhage, iatrogenic injury. Spinal cord ends at L1-L2 in adults and the lumbosacral nerve roots below that level form the cauda equina, which floats int he CSF. The cauda equina provides sensory innervation to the saddle area, motor innervation to the sphincters (anal and urethral) and parasympathetic innervation to the bladder and lower bowel. Cauda equina lesion causes LMN signs (flaccid paralysis, hypotonia, hyporeflexia, muscle atrophy and fasciculations) as the nerve roots are part of the peripheral nervous system. JUST KNOW THAT CAUDA EQUINA SYNDROME IS COMPRESSION OF THE SPINAL NERVE ROOTS

pt with 3 day hx of fever, chills, sore throat and difficulty swallowing. Now has fever, muffled voice, tender and enlarged cervical lymph nodes on one side, uvula is deviated. What are you concerned for?

Concerned about peritonsillar abscess. The "hot potato voice" and uvula deviation suggest complication of tonsillitis. Pts with peritonsillar abscess have prominent unilateral lymphadenopathy. This can be fatal if there is airway obstruction or spread of infection to parapharyngeal space, which amy lead to involvement of carotid sheath. initial tx is aspiration of the abscess and starting IV abx. Surgery may be needed if purulent material cannot be removed with aspiration alone.

Poor dentition --> aspiration pneumonia with foul smelling sputum. What kind of organisms are you concerned about and what do you treat them with?

Concerned for oral anaerobic organisms. Treat with clindamycin ("Clean out that dirty mouth!") that has anaerobic coverage. -Could also use metronidazole + amoxicillin (don't use metronidazole monotherapy bc high rates of failure), Amoxicillin-clavulanate, or a carbapenem.

What is a reason why it might be hard to correct a pt with chronic alocholism's potassium to get it to the normal range after being low?

Concurrent low magnesium. Remember Tyler saying correct their Mg first and then it will be easier to correct their K.

Pt with 2 sexual partners in the last year, one is know to have been treated for syphilis. She also had an abnormal pap last year with ASCUS. Now she has multiple, small, papular growths on the vestibule of the vulva and over the labia majora. Some are fragile and bleed on manipulation. Dx?

Condylomata acuminata (HPV 6 & 11 infection) -So i guess they do bleed -Multiple pink or skin colored lesions. can be smooth, fllat papules or exophytic/cauliflower-like growths. Tx: Chemical: Podophyllin resin, Trichloroacetic acid. Immunologic: Imiquimod Surgical: Cryotherapy, laser therapy, excision (for larger lesions)

Pt has hx of high risk behaviors, elevated LFTs, hepatomegaly and positive HCV antibody. What do you want to do next?

Confirm dx with ***Hep C virus RNA PCR testing*** The virus may spontaneously clear in about 1/2 of affected patients, the dx of chronic infection is a 2-step process that requires both a positive serologic test for HCV antibody *what you have) and then a confirmation with a molecular test for the presence of circulating HCV RNA (what you will get next). After you confirm HCV with dual testing, the pt should be evaluated to identify the HCV genotype and extent of liver fibrosis. Finally, they should be considered for treatment with direct acting antiviral agents (ex: ledipasvir-sofosbuvir)

First step in the evaluation of Cushing syndrome is to do what?

Confirm that there is indeed hypercortisolism. You can do that with one of 3 tests: -Late-night salivary cortisol assay -24-hour urine free cortisol measurement -overnight low-dose dexamethasone test If you confirm hypercortisolism, then ACTH levels are measured to see if it's an ACTH dependent or independent cause

What can hyperglycemia in 1st Trimester cause in the fetus?

Congenital heart disease Neural tube defects Small left colon syndrome Spontaneous abortion

Pt with family hx of sudden death, increased QT interval, syncope triggered by exercise/startle/sleeping. what does this likely have?

Congenital long QT syndrome.

Why would a Turner syndrome baby girl have edema when she is born?

Congenital lymphedema d/t abnormal development of lymph network. (that's why they have webbed neck, carpal and pedal edema) Accumulation of protein-rich interstitial fluid in the hands/feet/neck (webbed neck). Severe obstruction of lymphatic vessels can result in the cystic hygroma of the neck and fetal hydrops. lymphedema is generally nonpitting (as opposed to pitting edema in Liver failure or CHF or nephrotic syndrome)

What is the kind of hyperbili that is ALWAYS pathologic?

Conjugated hyperbili is always pathologic. (see conjugated hyperbili in acute cholecystitis, see it in biliary atresia)

What are physical exam signs that point to Marijuana use?

Conjunctival ingestion. Increased appetite (munchies) Tachycardia, tachypnea, HTN (all these VS are increased), dry mouth. Slow reaction time (slurred speech, impaired coordination, attention, concentration, short term memory) Impaired cognition, judgment and coordination (affects ability to operative automobiles and increases the risk of motor vehicle collisions)

Pt has CHF (exertional dyspnea, paroxysmal noctural dyspnea, pulmonary and peripheral edema, hx of MI), what are you likely to see associated with this pt?

Constriction of efferent (exit) renal arterioles. In CHF, there is activation of the RAAS and production of Ang II causes ***preferential vasoconstriction of efferent renal arterioles,*** which increases intraglomerular pressure in attempt to maintain adequate GFR.

41 yo woman with TB is started on RIPE therapy. One month later at her follow up, her sx have improved and she feels much better. Her AST is 75 and ALT is 97. What do you do with her treatments?

Continue the current tx. Note: INH is associated with sever INH hepatitis and a much milder hepatotoxicity. If s/sx of INH hepatitis (looks like viral hepatitis sxs), then you should discontinue the INH medication. However, about 10-20% of pts taking INH will have mild, subclinical hepatic injury wiht only minor elevations of serum aminotransferases (typically <100) Prognosis is excellent and this is usually a self-limited issues and INH should be continued with close follow up. This pt is relatively young and asx so she can keep taking the INH as long as her liver function tests are regularly monitored and remain only mildly elevated.

What kind of sound would you hear with AV fistula?

Continuos bruit

Pt getting breast cancer tx and advised not to get pregnant during it. Family hx of BRCA2. what method of birth control is recommended?

Copper IUD. Avoid hormone methods in pts with breast CA. Estrogen & progesterone may have proliferative effects on breast tissue. Concerning for hormonal receptor positive Br cancer, and BRCA2 carriers tend to have Estrogen receptor positive breast cancer. Copper IUD is safe long term and hormone free. 99% effective in preventing pregnancy bc copper causes a cytotoxic inflammatory response. Good for 10 years.

What does AIDS dementia complex imaging look like?

Cortical and subcortical atrophy and secondary ventricular enlargement.

If someone has status epilepticus (seizing >5 minutes), then they are at increased risk for

Cortical laminar NECROSIS (no oxygen > ischemia > necrosis)

What to think when you see livedo reticularis?

Could be normal finding in women during cold weight Could be sx of vasculitic (polyarteritis nodosa, SLE) or vasoocclusive (cholesterol embolization, antiphosphlipid syndrome, cryoglobulinemia) disorder. Note: if pt has LR and acute leg swelling (thinking DVT) and hx of recurrent miscarriages, think about antiphospholipid (APL) syndrome, which is associated with arterial occlusive complications (stroke, retinal artery occlusion). ATL is also associated with thrombosis, prolonged PTT (think SLE.. prolonged PTT).. d/t binding of phospholipid reagents in the assay by the antiphospholipid antibodies (Lupus anticoagulant) -mixing of the pt's plasma with LA with normal plasma will NOT correct the partial thromboplastin time in contrast with pts with clotting factor deficiencies where the addition of normal plasma will supply the necessary factors to normalize the assay.

If pt has syncope that is brought on by strong emotions and preceded by lightheadedness, weakness, blurred vision and lasts a few minutes and has rapid recovery of consciousness, EKG and orthostatic BPs are obtained and are normal. So she passes out bc of vasovagal syncope, what is the next step in management?

Counterpressure maneuver education. -Leg crossing with tensing of muscles, handgrip & tensing of arm muscles with clenched fists during the prodromal phase can improve venous return and cardiac output, sometimes aborting syncopal episodes. (Note: sometimes high risk settings like with airline pilots or commercial drivers, they require temporary activity restriction until these counter-pressure maneuvers are proven to be effective) (Reassure pts of benign natures of vasovagal syncope. Avoid triggers (stress, prolonged standing) and use physical counter-pressure maneuvers during prodromal phase to abort or delay an episode of syncope)

Pt has 10 days of fatigue and lots of watery diarrhea. He just got back 9 days ago from a trip from Eastern Europe where he was hiking and swimming in local lakes/streams. Has increased bowel sounds. Stool is negative for leuks and fecal occult blood. What organism is likely responsible?

Cryptosporidium parvum Note: bacterial and viral pathogens are most common cause of traveler's diarrhea. This pt without fecal leuks or occult blood is more likely to have a parastic infection since traveler's diarrhea tends to have dysentery (bloody, mucoid diarrhea). Also, parasitic organisms like cryptospordium parvum, cyclospora, and giardia are responsible for most cases of ***prolonged,*** profuse, watery diarrhea. C. parvum is an intracellular protozoan transmitted via the ingestion of contaminated water (drinking, swimming).

Pt presents with yeast infection (itchy rash under the breasts with high BMI) What will the lesion likely show?

Culture with budding yeast Dx is mainly based on clinical features, but could get KOH prep or fungal culture of skin scraping and would show "pseudophyphae with budding yeast forms (blastoconidia). Tx: topical anti-fungals (nystatin, micon-azole) with good skin hygiene and measures to keep the affected area dry. Intertrigo is an inflammatory condition involving occluded skin surfaces: axillae, groin, inframammary folds, abdominal folds. Most commonly d/t Candida species. Note: don't pink "segmented hyphae on KOH prep" bc that is tinea cruris, which is caused by a dermatophyte.

Pt with hx of daily ETOH use, renal insufficiency, last drink 4 days ago. Presents with severe HTN and associated acute end-organ complications (renal failure, sx of CHF), indicating he had HTN emergency. He is treated with nitroprusside (vessel vasodilator that works quickly and his symptoms get better. The next morning, the nurse finds him confused, agitated, and he has a generalized tonic-clonic seizure. BP still really high 176/95 (decreased from before) and HR 102 (decreased from before). What's happened?

Cyanide toxicity When you give someone nitroprusside, look for cyanide toxicity as SE. Metabolism of nitroprusside releases NO and cyanide ions. NO induces arteriolar and venous vasodilation. However, if you give pts prolonged infusions or higher doses of nitroprusside, or you give to a pt with renal insufficiency, they can have cyanide toxicity. CNS --> AMS, lactic acidosis, seizures, coma. Initial improvement of HTN followed by acute neuro change. This is likely due to cyanide toxicity following prolonged nitroprusside infuession in the setting of renal insufficiency. Note: this presentation may look like ETOH withdrawal, but ETOH withdrawal usually peaks during the 2nd day following cessation (and this pt is already at day 4), and seizures are most likely at 12-48 hours.

Know the SE of nitroprusside, med that is used in severe HTN when pt is in Hypertensive emergency with end organ failure. This drug is an IV vasodilator that has quick onset and offset and used for rapid BP control. but you want to be careful bc of SE of:

Cyanide toxicity. don't want to infuse nitroprusside. Bc metabolism of this drug releases nitric oxide and cyanide ions. NO induces arteriolar and venous vasodilation (which is what you want during hypertensive crisis). but then you have to deal with the possibility of cyanide toxicity: can occur in pts receiving prolonged infusions or higher doses of nitroprusside and is most common in pts with renal insufficiency.

Pt with chronic sinopulmonary infections, nasal POLYPS!!, bronchiectasis, digital clubbing. Pancreatic insufficiency, infertility d/t absent deferens (azoospermia), and failure to thrive (low percentiles on the growth chart). What do they have?

Cystic fibrosis

Positive psychotic symptoms, related with these kinds of receptors

DA receptors (that's why antipsychotics are DA antagonists... since when you've got positive psychotic symptome, it's a DA receptor thing)

AG metabolic acidosis with abdominal complaints, hyperglycemia, and positive serum ketones, think about

DKA

Side effect profile: Olanzapine?

DM, weight gain Memory tool: think of a big 'O' -for a big fat O guy... DM and weight gain with Olazapine

Treatments for RA. Options?

DMARD: -Non-biologics: Methotrexate (preferred initial tx***): Methotrexate, hydroxyclOrOquine (careful need eye exams), sulfasalzine, lefluomide, azathiprine (heme and GI toxicities) -Biologics: etanercept, infliximab, adalimumab, tocilizumab, rituximab. NSAIDS & COX inhibitors (ex: celecoxib) as adjunctive tx for symptom relief (don't reduce disease progression) Glucocorticoids (steroids) can also relieve sx and short term radiographic progression but not effecting in preventing eventual joint destruction and can result in generalized bone loss (osteoporosis)

What would you see on dx workup in Duchenne Muscular dystrophy? what about in Beckers?

DMD: absent dystrophin seen on muscle biopsy (so seen earlier around age 2-3) Becker: reduced dystrophin on muscle biopsy (so milder weakness that presents later in childhood) note: Genetics is X-linked recessive deletion on dystrophin gene on chromosome Xp21

Weight considerations for oral DM agents.

DPP4 : weight neutral GLP-1 (incretins): decrease weight

Pt has pain and swelling over inner aspect of her right eye for the past two days. Exam of eye reveals tenderness, edema and redness over medial canthus. Slight pressure over the area causes expression of purulent material. Visual acuity is normal. What's the most likely dx?

Dacryocystitis: infection of the lacrimal sac.. think about the place that allows you to cry is infected "da-cry-o-cystitis" Usually occurs in infants and adults >40yo. Acute dacryocystitis has sudden pain and redness in medial canthal region. Purulent discharge can be noted from the punctum. Usual organisms: staph aureus, and beta-hemolytic strep. Usually response to systemic abx therapy

How would you treat someone who presents ill with tetanus?

Debride infected wound, start Abx, give human tetanus immunoglobulin (to bind residual circulating toxin) and give tetanus toxoid.

What is happening to cause botulism symptoms?

Decreased Ach release from the pre-synaptic terminals of motor neurons --> acute onset BL cranial neuropathies and symmetric descending flaccid paralysis. Prodrome of GI symptoms (N/V/D) comes before the muscle weakness

Turner's patient, look out for what developing in the future?

Decreased bone mineral density. Since they have ovarian dysgenesis that leads to "streak ovaries" and premature ovarian failure, they are estrogen deficiency and that leads to minimal or no thelarche (breast development). Estrogen also normally **inhibits** osteoclast-mediated bone resorption, leading to increased bone mineral density. So lack of estrogen in TS mean increased bone resoprtion, which causes decreased bone mineral density and increased risk of osteoporosis. Estrogen replacement therapy is therefore given to girls with Turner's syndrome to promote sexual maturation and reduce risk of osteoporosis TL;DR: Turners has streak ovaries so no estrogen and estrogen affects bone mineral density. So no estrogen means decreased bone mineral density (bc there is no estrogen to inhibit the osteoclasts so bone gets resorbed --> decrease bone mineral density)

Normal changes in aging heart

Decreased resting and maximal CO, decreased max HR, increased contraction and relaxation time of heart muscle, increased myocardial stiffness during diastole, decreased myocyte number, and pigmented accumulation in myocardial cells.

What changes can you see in healthy pregnant patient when compared to non-pregnant state?

Decreased serum Cr. (so a normal Cr is actually an elevated Cr in a pregnant patient bc their serum Cr should actually be lower) Normal adaptations of pregnancy: - increase GFR, renal blood flow, renal BM permeability --> decreased serum BUN and Cr, increased urinary protein excretion. -Increased hypercoagulable state (to minimize bleeding during delivery) -Changes in plasma volume -- mild dilutional anemia. Note: d/t the increased renal function during pregnancy, pt on meds that are renally excreted (ex: gabapentin) need close monitoring and dose adjustmnet Note: Serum Cr of 1.2 would be upper limit of NL in non-pregnant woman but is considered renal insufficiency in a pregnant woman.

Stress incontinence: what is the etiology? Aka what's another way to describe it?

Decreased urethral sphincter tone and urethral hypermobility.

How does a nitroglycerin rapidly relieve chest pain?

Decreases LV wall stress (note: although nitrates may have coronary vasodilation, the benefit of that is uncertain. so DO NOT pick that as the answer) We do know that: Nitrates relax vascular smooth muscles, causing systemic venodilation and increased peripheral venous capacitance. They decreas cardiac preload resulting in decreased in LV end-diastolic and end-systolic volume. This in turn leads to decrased LV systolic wall stress (which reflects afterload - and a decreased in myocardial oxygen demand, resulting in relief of anginal symptoms. This is a much bigger effect so pick this, "decreased LV wall stress" is what relieves the symptoms bc we decreased preload and decreased the stress on the LV.

What is the cut off GA to give betamethasone?

Definitely want to give to fetuses < 34 week GA. (can also +/- give it to fetuses <37 weeks GA)

What is happening in achalasia?

Degeneration of neurons within the myenteric plexus. Pt has gradual onset solid and liquid dysphagia d/t uncoordinated peristalsis and failed relaxation of LES. Esophageal manometry will show high LES resting pressure.

Pt has trigeminal neuralgia. What causes it?

Demyelination of the nerve nuclei. -the demyelination leads to improper signaling of the nerve and paroxysms of severe pain. Note: remember it's demyelination because multiple sclerosis, the autoimmune demyelinating CNS disorder, is one of the few conditions where TN presents bilaterally. (Remember the UWorld question where the woman has TN but 2 weeks ago, she had right hand numbness that lasted 2 weeks and resolved spontaneously, alluding to her 1st symptom of MS and now she has TN, which is d/t demyelination)

Pt with unintentional weight loss and occassional diarrhea over past few months shows up with rash on her buttock for 10 days that is intensely itchy and burns. (intensely pruritic erythematous papules, vesicles, and bullae that occur symmetrically in grouped clusters on extensor surfaces of elbows, knees, back and buttock). lotions don't help. What does she have? Tx?

Dermatitis herpetiformis, a reaction to dietary gluten associated with celiac disease. Initial tx: Dapsone (anti-inflammatory and immunomodulatory properties; provides rapid relief of symptoms). (Picture Kim's suitemate Nikki saying "give me some dap" (She probably took dapsone when she was first diagnosed with celiac disease in college) Long term: gluten-free diet.

Pt with proximal symmetric muscle weakness in upper and lower extremities. You see a heliotrope rash (eruption on face accompanied by periorbital edema), shawl sign (rash on chest/lateral neck) and Gottron's papules ("vialaceous" slightly scaly papules overlying joints; these are pathognomonic for this condition) on hands rash on face, difficulty rising from seated position or climbing stairs. Erythematous rash on upper chest and "violaceous" periorbital edema. What do they have? What do you have to screen for in the future? What do you expect on labs?

Dermatomyositis Screen for INTERNAL malignancy in the future. (ovarian, lung, pancreatic, stomach, colorectal, non-Hodgkin lymphoma). Do regular age-appropriate cancer screenings in these patients (super important) Labs: increased Cr phosphokinase (CPK) usually 10x upper limit of normal. Autoantiboides like Anti-Jo-1 (antisynthetase antibody) and anti-Mi-2 (anti-helicase)

Kid with Primary noctural enuresis: (wetting bed at night, age >5yo), You've tried all the lifestyle modifications (minimized fluid intake before bed, avoid surgary/caffeinated drinks, void before bedtime, rewards system) and even the bedwetting alarm. What do you do?

Desmopressin!!!!! ("Press in" to the parents to try the lifestyle modifications first.. but if you already "pressed in" for them to try that.. then you can use Desmo-"pressin") Note: you would add oxybutynin (anti-chol) if the kid also had daytime incontinence. Note: TCAs are not used first bc they have more serious SEs (increased suicidality, cardiotoxicity). So reserved for pts who don't respond to desmopressin.

43 yo G3P3 lady has strong desires to urinate that occur all of a suddent and he can't "hold in" her urine before getting to the toilet. What is the cause of this incontinence? what can she do?

Destrusor contractions/overactivity -1st line tx: bladder training (resist urge to void for longer durations to increase bladder capacity) and kegels. -2nd line tx (if behavioral therapy is not successful): can use antimuscarinics: oxybutynin, tolterodine to inhibit involuntary detrusor contractions Note: REMEMBER that antimuscarinics like oxybutynin mainly act on the destructor muscles to relax it (sphincter relaxation is just a small second effect, the main effect is on the detrusor muscle)

Urge incontinence: what's the etiology aka another way to describe it?

Detrustor hyperactivity

What is otosclerosis? What kind of hearing loss do you expect with this?

Development of sclerotic changes within the ossicles of the middle ear, resulting in progressive conductive hearing loss with a normal otoscopic exam.

What are 2 conditions that present with low CD4+ lymphocyte counts? One is an infection, and one presents shortly after birth.

DiGeroge syndrome (manifests shortly after birth) & HIV infection; since CD4 counts are low, these pts are susceptible to opportunistic infections

What is the leading cause of ESRD in the USA?

Diabetic nephropathy! (Everyone has the 'betus') Characterized by: Increased extracellular matrix, BM thickening, mesangial expansion, and fibrosis 1) 1st year with DM: glomerular hyperperfusion and renal hypertrophy with increase in GFR 2) 1st 5 years of DM: glomerular BM thickens, glomerular hypertrophy, mesangial volume expansion with GFR returning to normal 3) Within 5-10 years of DM: Microalbuminuria, later progresses to overt nephropathy

4mo old male infant with progressive lethargy, poor feeding, fatigue, increasing pallor for past 4 weeks. He has webbed neck, cleft lip, shielded chest (think shield = diamond), triphalangeal thumbs, pale mucous membrane and conjunctivae. Mild tachycardia, systolic ejection murmur over LUSB. Hb 8 (low). WBC and plts normal. MCV 104 (high). What do you think he has?

Diamond-Blackfan anemia

What do you do for a pt with OA medicine-wise?

Diclofenac <--know this is just an NSAID Note: initial management should be non-med with exercise, weight loss, activity modification. NSAIDs (ex: diclofenac) are drug of choice for pain relief but do not alter the progression of the disease. Note: pts who fail conservative measures can be considered for intra-articular glucocorticoids injections. However, oral glucocorticoids like prednisone don't have a role in OA like they do in RA. and other inflammatory arthropathies.

What are some things people with calcium kidney stones can do to prevent recurrence of kidney stones?

Dietary changes: increase fluid and citrate intake. Reduce Na, protein, and oxalate intake. Keep calcium intake normal. Meds: Use ***thiazide*** diuretics, alkalinize the urine (K citrate, bicarb salt), or allopurinol (for hyperuricosuria-related stones) Note: Thiazide diuretics causes mild volume depletion, which leads to compensatory rise in reabsorption of Na and water with resulting increased passive reabsorption of calcium. Thiazides are also thought to modulate calcium channels on the tubular membrane. Lowering urinary concentrations of calcium reduces its precipitation as insoluble calcium salts.

Clinical findings for congenital infection with Toxoplasmosis

Diffuse intracerebral calcifications, severe chorioretinitis

What might you see in the nail of someone who has a lung cancer?

Digital clubbing ("drumstick" appearance", flattening of nail folds, and shininess of nails and distal finger) -associated with malignancy or chronic hypoxic pulmonary disease (ex: CF, bronchiectasis)

What is the tx for digoxin toxicity?

Digoxin-specific antibody (Fab) is the antidote for digoxin toxicity

Pt with lower extremity swelling for past 2 years and hx of several episodes of cellulitis involving the left leg. Now she present with firm edema of the left lower extremity. No warmth or erythema. Examiner cannot lift the skin from the dorsum of the toes on the left foot, but is able to do so with toes on the right foot. What's the most likely cause of these symptoms?

Disruption of lymphatics. This pt has lymphedema. Likely due to chronic inflammation (recurrent cellulitis), other causes can be obstruction (malignancy), lymph node dissection, congenital (ex: turner syndrome), or parasitic infection (filariasis). Presentation: swelling, pain, heaviness. Early: soft skin, pitting edema Late: firm thickened skin, non-pitting edema Stemmer's sign: inability to lift skin on dorsum of 2nd toe is highly specific for lymphedema. Dx: based on clinical presentation, but duplex ultrasound imaging may be useful in some cases. Tx: weight loss, limb elevation and compression, physiotherapy (ex: lymph drainage by massage).

Pt has HELLP syndrome Presents with pre-eclampsia, N/V, RUQ abdominal pain. -Has Hemolysis (MAHA) Elevated Liver enzymes, Low Platelet count -You are planning to delivery and give Mag for seizure ppx, and antiHTN drugs. What is causing the RUQ abdominal pain?

Distention of the liver capsule. Serious liver problems: centrilobular necrosis, hematoma formation, thrombi in portal capillary system. These all cause swelling with distention of the hepatic capsule (Glisson's capsule) which is causing the RUQ or epigastric pain. Note: AP is normally elevated in pregnancy.

Meds to treat alcoholics? (3)

Disulfiram (acetaldehyde dehydrogenase inhibitor... acetaldehyde builds up and you feel crappy_ Naltrexone (opioid receptor antagonist) Acamprosate

Pt has hx of lower abdominal pain and fullness for 1 week and burning on urination and pneumaturia for 1 day. Exam shows tender mass in left lower quadrant of abdomen. Which is the most likely cause of these symptoms?

Diverticulitis!! Know that fistula formation (bowel with bladder --> air in urine... pneumaturia) is a complication of diverticulitis. Note: Diverticular disease accounts for about 79% of cases (almost 80%, so on the test choose diverticulitis). Colon cancer accounts for about 15% and Crohns disease only about 5% of cases. SO IF YOU THINK PNEUMATURIA, THINK DIVERTICULAR DISEASE AKA DIVERTICULITIS!!!

Gross lower GI bleeding (large volume bright red blood) that is painless, associated with lightheadedness and hemodynamic instability in adults

Diverticulosis. is most common cause.

What do you want to make sure you do to exclude gastric cancer in patients with gastric ulcers?

Do an endoscopy to go in there and look and get a biopsy to make sure there is no associated gastric cancer (since gastric cancer is present in 4% of patients with gastric ulcers)

42 yo with abdominal discomfort. He has hepatomegaly and liver u/s shows 10-cm smooth, round cyst with daughter cysts inside. What is the associated exposure here?

Dogs Echinococcus granulosus: from dog tapewarm with sheep as intermediate host. Humans are incidental host when they ingest the eggs. Initially ax for years. Liver cyst is most common (mass effect: RUQ pain, N/V, hepatomegaly. Rupture: fever, eosinophilia). Lung cyst: cough, chest pain, hemoptysis. Dx: Imaging: large, smooth hydatid cyst with internal septations. Labs: IgG E. granulosus serology Tx: Abendazole. Percutaneous therapy (>5 cm or septations), surgery (if rupture)

When correcting severe hyponatremia with hypertonic (3%) saline, what is the rate you want to go at so you can avoid pons dying (osmotic demyelination syndrome, which is a fatal complications with dysarthria, quadriparesis, and coma)?

Don't correct more than 8 mEq/L over the first 24 hours.

Major Azathioprine toxicities?

Dose-related diarrhea, leukopenia, hepatotoxicity (liver toxicity) Purine analog that is converted to 6-MP. Acts by inhibiting purine synthesis.. so think about inhibiting gut cell turnover and WBC production... so dose related diarrhea and low WBC ct.

Down Syndrome, what do you find with MSAFP, estriol, beta-HCG and inhibin A?

Downs baby says "Hi!" So bet-HCG and Inhibit A are elevated while MSAFP and estriol are decreased

Abx to treat community acquired pneumonia (CAP) if macrolide resistance is suspected

Doxycycline If macrolide resistance is suspected, use doxycycline

What do you treat Ehrlichiosis (tickborne illness from southwest USA, like in Arkansas)

Doxycycline (think about how it would be really far to DRIVE down to southeastern and south central USA... so think of drinking and the car's wheel and then think of DOXYCYCLINE) Presents with: acute febrile illness with malaise and AMS. Not associated with rash. has confusion, AMS, clonus, neck stiffness. Labs show: low WBC, low plots, elevated LFTs and LDH (so it seems they're hemolyzing and the liver is affected) Dx: clinical. Definitive dx can be made by seeing the "intracytoplasmic morulae in the monocytes (WBCS) and through PCR testing"

Other than autoimmune hemolytic anemia, what is another reason for a positive Coombs test?

Drug-induced immune hemolytic anemia can be a rare complication of ibuprofen and would cause a positive Coombs test (bc it's ab immune mediated hemolytic anemia)

You need to increase levothyroxine dose when pt becomes pregnant. Why?

During pregnancy, Estrogen induces an increase in serum Thyroxine-binding globulin levels, requiring an increase in the amount of thyroid hormone needed to saturate the binding sites. Thyroxine production also increased d/t stimulatory effects of hCG on TSH receptors (hCG and TSH have similar alpha subunits) These changes --> increase in total thyroid hormone level with minimal increase in free hormone level and decrease in TSH. Note: hCG stimulates thyroid hormone production in 1st trimester, and those suppress TSH secretion. So when pregnancy is detected, hypothyroid pts should have their levothyroxine increased by about 30% when pregnancy is detected.

How do you dx vasovagal syncope?

Dx clinically. Can also do upright tilt-table test in uncertain cases.

Tense bullae on flexural surfaces, axilla, groin. Subepidermal cleavage with IgG deposits at BASEMENT MEMBRANE. What is the dx? What does the autoantibody target?

Dx: Bullous pemphigoid Autoantibody targets: Hemidesmosomes at the Basement Membrane.

Pt has progressive proximal muscle weakness and diminished/absent reflexes, but oddly they improve following isometric muscle contractions (called "post-exercise facilitation). What is the dx? What do you have to rule out?

Dx: Lambert-Eaton syndrome Need to rule out small cell lung cancer; so get a CT Chest. (Note: yes, this is an autoimmune condition caused by antibodies against ***presynaptic*** voltage-gated calcium channels.. but want to rule out the cancer first)

Kid with pertussis, How do you dx and what are the txs?

Dx: Pertussis culture or PCR, Lymphocyte-predominant leukocytosis Tx: Macrolides (ex: azithromycin, clarithromycin)

42 yo pt has 2 syncopal episodes the last 3 days. She was well until about a month ago and then she started having increased fatigue and feeling weak. For the past 2 weeks, she's had anorexia, nausea, abdominal pain. BP is low (86/52), pulse 90, RR 18. Abdomen if mildly tender. You see hyperpigmenation in the palmar creases. What other findings do you expect. What's her dx?

Dx: chronic primary adrenal insufficiency (usually autoimmune and can initially present as these non-specific symptoms) -Can also be d/t infections, hemorrhagic infarction, or metastatic disesae. Presentation: nonspecific fatigue, weak, anorexia, weight loss, GI sx, salt cravings, ***postural hypotension***, ***hyperpigmentation or vitiligo***, ***hyponatremia***, ***hyperkalemia***, may lead to acute adrenal crisis (abdominal pain, shock, fever, AMS) Dx: get ACTH, serum cortisol, and high dose (250 ug) ACTH stimulation test. Note: Primary adrenal insufficiency (usually autoimmune adrenalitis) also known as Addison disease can have these nonspecific sxs initially. Aldo deficiency causes volume depletion (hypotension, postural dizziness, syncope). Skin can have patchy hyperpigmentation (d/t co-secretion of melanocyte-stimulating hormone with ACTH) and vitiligo (d/t autoimmune destruction of melanocytes) - so you can have hyperpigmentation or de-pigmentation. . ***Hyponatremia is the most common electrolyte abnormalitis bc loss of mineralocorticoid secretion (aldo) leads to urinary loss of sodium, volume depletion and compensatory increase in release of ADH (to try to make up for that loss of volume since you don't have aldo. Cortisol deficiency also triggers increased secretion of CRH (corticotropin-releasing hormone), which directly stimulates ADH release. So the result is you get retention of free water and a dilutional hyponatremia. For K+, aldo deficiency also causes hyperkalemia in the majority of pts, sometimes accompanied by mild hyperchloremic acidosis.***

What's a super common presentation of endometriosis that pts report?

Dysmenorrhea and noncyclic pain that can be worsened by exercise. If they report a pt with pain worse by exercise and then you find a adnexal mass or fullness confirmed on u/s and a finding of a homogenous cystic ovarian mass, then that's a chocolate cyst (endometrioma) - which can be the only clinical manifestation of endometriosis. Note: Infertility is a common consequence of endometriosis, esp. with the presence of endometrioma. Surgical resection of endometriomas usually improves fertility.

What are the 3D's for endometriosis presentation? So what do you tx them with? (don't think too hard about this one)

Dysmenorrhea, Deep Dyspareunia, Dyschezia (pain with defecation) Tx: OCPs (don't think too much about whether OCPs will help her pain if she's having sex... just remember that Dyspareunia is a sx of endometriosis and you tx endometriosis with OCPs and NSAIDs. OCPs reduce pain by ovulation suppression, which may result in atrophy of endometrial tissue).

Most common site of ULNAR nerve entrapement is the?

ELBOW!!! (Do NOT choose wrist for ulnar nerve entrapment, at the medial epicondylar groove is most common)

What is a psych condition that Lorazepam is used to treat?

EPS side effects of antipsychotics -Lorazepam is used to treat akathisia. (think about someone flailing their arms about and the benzo calming their arms down)

What is a psych condition that Diphenhydramine is used to treat?

EPS side effects of antipsychotics. -used to treat acute dystonic reations

Predictors of poor prognosis in schizophrenia.

Early onset (ex: age 16), no clear precipitant, prodromal phase (ex: idiosyncratic thinking and perceptual disturbances, deterioration in academic or occupational functioning, increasing social isolation), and gradual onset of psychosis. Negative symptoms: flat affect, loss of motivation, anhedonia. Family hx Male gender

Pt with difficulty walking, weakness and occasional pain in thigh muscles, stumbles and falls several times this past week. She takes HCTZ and metoprolol. Hyporeflexia and decreased strength in all muscles. EKG with flat and broad T waves, occasional premature ventricular contraction. Likely cause of current complaints?

Electrolyte disturbances Hypo-kalemia can cause weakness, fatigue, muscle cramps. When it's severe (<2.5): paralysis, hyporeflexia, tetany, rhabdo, and arrhythmias can happen. EKG shows U waves, flat and broad T waves and premature ventricular beats. (can also get a.fib, torsades, and v.fib) Note: She takes K-wasting diuretics, which is the likely cause of her low K. Other causes: diarrhea, vomiting, anorexia, hyper-aldo.

Mom in 1st trimester of pregnancy is vomiting too much (hyperemesis gravidarum) and has weight loss of >5% pre-pregnancy weight. What are you concerned about monitoring with this patient?

Electrolytes (worried about her vomiting too much and getting hypokalemia; and also hypochloremic metabolic acidosis) & ***Ketonuria.*** Check for ketones in Ashley Goh/Freeman's urine when she was pregnant and losing weight. Tx: severe HG with dehydration, ketonuria, and electrolyte abnormalites is indication admission to hospital for IV antiemetics, rehydration and electrolyte repletion

What do you see on electron microscopy for MCD? on biopsy?

Electron microscopy: diffuse effacement of foot processes of podocytes (renal epithelial cells) Kidney biopsy: light microscopy findings would be normal.

What has the greatest sensitivity for dx-ing HF?

Elevated BNP levels. hormone from ventricular myocytes in pts with CHF in reponse to high ventricular filling pressures. An elevated plasma BNP has HIGH SENSITIVITY (>90%) for dx of CHF. Elevated levels of circulating BNP correlate with the severit of LV dysfunction and are useful in differentiating CHF from other cause of dyspnea. In most pts with SOB d/t CHF, their BNP levels were >400. Whereas a level <100 has high negative predictive value for cHF as a cause of SOB. Levels <100 are considered low and should prompt the search for a noncardiac cause of SOB.

What do you expect in the CSF of pts with bacterial meningitis? (same for fungal and TB meningitis)

Elevated protein (bc the bacteria is in there) Low glucose (bc bacteria is eating up the glucose) Elevated WBC counts (bc body is trying to fight bacteria) RBC should be normal (or if it's increased may just mean trauma to capillary or vein during the LP)

What does elevation of the head of the bed have to do with pressure ulcers?

Elevation of the head of the bed >30 degrees can cause the pt (who is neurocognitively impaired and bed-ridden) to slide in the bed, causing skin friction and increasing the risk of pressure ulcers

Who do you do ECT in?

Emergency conditions: Pts who aren't eating/drinking, have imminent suicide risk, pregnancy Pts who are treatment resistant or have psychotic features. Note: careful, think about safety if pt has had recent MI or severe CV disease, space occupying brain lesion, recent stroke or unstable aneurysm.

How do yo distinguish COPD's chronici bronchitis and emphysema via DCLO?

Emphysema has low DLCO (can't diffuse bc the aveoli are all destroyed) -Note: emphysema has decreased vascular markings and hyperinflated lungs. Chronic bronchitis has normal DLCO (bc alvoelar and capillary structures are intact) -Note: chronic bronchitis has prominent bronchovascular markings and mildly flattened diaphragm -Pts with prominent chronic bronchitis may demonstrate more pronounced hypoxemia than patients with emphysema. Note: Asthma can have normal or increased DLCO. Note: DLCO measures gas exchange between the alveoli and pulmonary capillary blood.

When do you see panacinar and when do you see centriacinar alveolar destruction?

Emphysema is destruction of the alveoli. - Smoking --> centriacinar (Memory tool: think about smoke hitting the central parts and destroying the central parts.. = centriacinar) - Alpha-1-antitrypsin deficiency --> panacinar (Memory tool : think about genetic problem just affecting everywhere, so panacinar)

Chlamydia and gonorrhea treatment in women.

Empiric tx: both Azitromycin & Ceftriaxone Confirmed Chlamydia with NAAT: Azithromycin Confirmed Gonorrhea with NAAT: Ceftriaxone & Azithromycin (bc of abx resistance) Memory tool: always need at least one "C" between the dx and treatments.

Features of rabies?

Encephalitis: hydro-phobia (water fear), aerophobia (fear of air), pharyngeal spasm, spastic paralysis, agitation -Feeling of water or air triggers involuntary pharyngeal muscle spasms. Many pts are disoriented and agitated with fluctuating mental status. Incubaton pd is 1-3 months and almost all pts die within weeks of developing symptoms. Paralytic: ascending flaccid paralysis. Tx: Post-exposure ppx: rabies immune globulin and rabies vaccine immediately after exposure to high risk wild animal (bat, raccoon, skunk, foxes; dogs (in developing worlds)) -Make sure to clean wound thoroughly with soap and water and get urgent post-exp ppx (rabies immune globulin and rabies vaccine), which can prevent life-threatening encephalitic or paralytic rabies disease.

Organisms that cause travelers' diarrhea and are typically associated with dysentery (blood, mucoid diarrhea)

Entamoeba histolytica, Shigella

AA male pt presents to ER with fever, jaundice, abdominal pain and dark urine. HR 100. Peripheral smear shows BITE CELLs and rbc inclusions after crystal violet staining. What condition does he have?

Enzyme deficiency. G6PD deficiency. He is presenting with acute hemolytic crisis with bite cells & Heinz bodies, consistent with G6PD deficiency. He is missing the enzyme that creates NADPH, the cofactor needed to created glutathione and prevent oxidation of hemoglobin. Without that enzyme, Hgb becomes oxidized and denatures into Heinz bodies. The denatured Hgb disrupts RBC membranes and causes hemolysis. This reaction usually occurs in response to oxidant drugs (ex: anti-malarials, sulfas) ad infections. Fava beans can precipitate hemolysis. X lined recessive, common in AA men.

Gradual onset pain, dysuria (urinary frequency, urgency, urethral discharge). Induration, swelling and tender epididymis. Pyuria and bacteriuria. Symptoms relieved by scrotal elevation What's going on?

Epididymitis

What should you suspect (not just metastasis, but a specific problem that metastasis can cause) in pt with hx of malignancy who develops back pain with motor and sensory abnormalities (ex: bowel/bladder dysfunction are late neuro findings), or says pain is WORSE at night when in the recumbent position? What should you do without delay (next best step). even before an MRI?

Epidural spinal cord compression MUST be suspected in any pt with hx of malignancy and new motor and sensory abnormalities. (Note: infection (epidural abscess) and spinal injury (MVC) can also cause spinal cord compression) IV Glucocorticoids should be given without delay. MRI is then indicated. -Glucocorticoids decrease vasogenic edema (caused by obstructed epidural venous plexus), help alleviate pain, and may restore neuro function. Once imagining confirms ESCC, neurosurgical consultation is usually required. Note: Pain is worse in the recumbent position bc that causes distention of the epidural venous plexus when lying down

What's the difference in presentation for epidural hematoma and subdural hematoma.

Epidural: has brief period of unconsciousness followed by lucid interval. It's usually injury to sphenoid bone that results in lacreation of the middle meningela artery, so the hematoma RAPIDLY expands and there is a quick deterioration of consciousness and sxs of elevated ICP (N/V, HA). If you don't treat it you can get uncal herniation and that has a dilated pupil on ipsilateral side of lesion (d/t oculomotor nerve compression) along with ipsilateral hemiparesis (d/t contralateral crus cerebri compression). emergent craniotomy should be done in pts with FND to prevent brain herniation. (Uncal herniation has ipsilateral CN3 palsy and hemiparesis) Subdural: occurs because of tearing of bridging veins so you have much more of a SLOW bleed after traumatic head injury. Symptoms of HA and confusion occur gradually over 1-2 days.

Infection of episcleral tissues between the conjunctiva and sclera. Pt complains of acute onset of mild-mod discomfort, photophobia, and watery discharge. Exam shows diffuse or localized bulbar conjunctival injection.

Episcleritis.

Botulism. Treatment?

Equine serume heptavalent botulinum antitoxin (equine antitoxin therapy) apparently we get our antitoxin for botulism from horses (equine). Note: in addition to honey for babies, and improperly canned foods, can also get botulism from aged seafood (ex: cured fish)

What is a cholesteatoma? What kind of hearing loss do you expect with this?

Erosive and expansive growth consisting keratinizing squamous epithelium, which can cause destruction of the bones of the middle ear (ossicles) and SN structures of the ear. Conductive &/or Sensorineural hearing loss associated with intermittent ear discharge, tinnitus, and balance problems. Otoscopic exam shows a discrete white plaque on the TM w/ or w/o perforation or retraction

Early lyme disease symptoms? Treatment?

Erythema migrans (the bulls eye rash) and nonspecific symptoms (fatigue, HA, myalgias, arthralgias) Timeline: days-1 month Tx: oral doxycycline

superficial skin infection that also affects intertriginal areas. Has well demarcated , thin, red-brown plaques with wrinkling and fine scale. Has coral-red appearance under Wood's lamp

Erythrasma. caused by Corynebacterium munitissimum (Memory tool: think of the guy who manages the HHA clinic.. "Erasmo" .. think of his having this Erythrasma infection.. with well demarcated plaques in intertriginal areas... and if we shine a Wood's lamp (clinic is nestled in the woods..) you'll see a coral-red appearance. Is he a "corny guy or quiet/mute"? Corynbacterium munitissimum as the cause.

Pt has who is an alcoholic has been vomiting for a few hours and now has sudden-onset retrosternal and upper abdominal pain. You feel crepitus in the suprasternal notch. What's going on?

Esophageal perforation. (likely d/t Boerhaave syndrome, happens especially when pt is resisting the vomiting reflex) You are feeling pneumomediastinum, the suprasternal crepitus (subQ emphysema). The pt's sudden restrosternal pain is contamination of the mediastinum with gastric contents. You may also see odynophagia, dyspnea, and sepsis (fever, hypotension, tachypnea) Dx: confirm with CXR, contrast esophagram (leaks at perf site), or chest CT. Tx; surgical emergency, so need to immediately consult surgery. Make pt NPO, give IV PPI, broad spectrum Abx, and nutrition, do surgical drainage and debridement of infected or necrotic areas.

What does a granulosa tumor of the ovary secrete?

Estrogen So see precocious puberty (2ndary sex characteristics in girl <8yo) in kid & bleeding/endometrial hyperplasia in menopausal woman.

60 year lady with persistent feeling of having always to go to the bathroom. For 3 years, she has involuntary urine loss multiples times a day and urgency to void during the night that often awakens her to find her underwear wet. She also has vaginal itching, drying, menopause 8 years ago, hx total hysterectomy with BL salpingo-oophrectomy, hx of recurrent UTIs during the past year. Exam with smooth vaginal epithelium with patchy erythema, vulvar skin with reduced elasticity with labia minora retraction. Likely cause?

Estrogen deficiency. She has vulvovaginal dryness, urinary incontinence recurrent UTIs. All those point to estrogen deficiency. The bladder trigone, urethra, pelvic floor muscles and endopelvic fascia all have E receptors and are maintained by adequate E levels. Low E (this pt had her ovaries removed) result sin atrophy of superficial and intermediate layers of the vagina and urethral mucosal epithelium. Decreased urethral closure pressure and loss of urethral compliance contribute to urgency, frequency, UTIs and continence (stress and urge)!! THERE ARE ESTROGEN RECEPTORS ON YOUR BLADDERAND URETHRA!!! I DID NOT KNOT THAT. Mod-severe cases with prodominant urinary sxs, treat with low-dose vaginal E therapy.

Older pt has a fall and daughter found him on the floor. We're not sure of the etiology of his fall so what do you want to do first? X ray shows he has a hip fracture.

Evaluate both his fitness for surgery as well as etiology of the fall with EKG, cardiac markers and CXR.

What do you worry about as a SE for SSRIs in elderly pts?

Even something like sertraline you can be worried about SIADH in an older pt. So if the question has an older pt who just started on SSRI and now has hypotonic (serum osmolality < 275) hyponatremia, then you're thinking SIADH

What is selection bias?

Ex: using less ill pts for a drug end of the trial and sicker pts for the placebo side. Makes the drug look more successful than it actually is.

What is Meniere disease? What kind of hearing loss do you expect with this?

Excessive accumulation of endolymph in the membranous labyrinth. Characterized as recurrent episodes of vertigo, unilateral aural fullness, tinnitus, and SN hearing loss.

What's the most appropriate next step in dx for BCC? (67yo landscaper with lesion on his chest; 8mm lesion with ulcerated base and shiny, slightly raised borders). Most appropriate next step in dx?

Excisional biopsy with narrow margins (Note: not punch biopsy) AKA Mohs micrographic surgery: removal of skin cancer under dissecting microscope with immediate frozen section is precise, so allows you to remove skin cancer with minimal loss of normal tissue. No need to remove a wide margin with Mohs surgery so you can do "excisional biopsy with narrow margin"

Main excitatory hormone? Main inhibitory hormone?

Excitatory: Glutamate (Memory tool: excited about your mate so you're glued to your mate.. glutamate is main excitatory hormone) Inhibitory: GABA (Gamma-aminobutyric acid)

If you have a pt with epigstric burning that doesn't get relieved by antacids for several months now and it's brought on by heavy lifting at work and takes about 10-15 minutes to go away. He has hx of SLE, HTN, but EKG is normal. What do you do next?

Exercise EKG. Stress test this patient to risk stratify them.

What can you advise for a pt with OA in addition to weight loss, regular moderate activity, and simple analgesics?

Exercise to strengthen their quad muscles can reduce the abnormal loading on the joint and protect the articular cartilage from further stress. Initial management of OA: weight loss, regular mod. activity, simple analgesics (ex: acetaminophen), PT and home exercise program to strengthen the quad muscle and protect the articular cartilage from further stress. Quad muscle strength declines with age, and the pain and stiffness of OA may induce pts to reduce activity, leading to disuse atrophy of the quads. This causes abnormal loading of the articular cartilage and accelerates the degeneration of the joint. Note: randomized trials have shown arthroscopic lavage and debridement in OA is ineffective so don't pick arthroscopic lavage. Pick exercise!!!! for OA.

What do you expect to see on the bone marrow biopsy with Multiple Myeloma (abnormal monoclonal production of IgG or IgA by a certain type of cell)

Expect to see the abnormal plasma cells take over the bone marrow and don't see the variety of cells you would normally see in the bone marrow. (The abnormal plasma cells are what are making the monoclonal IgG and IgA. Those clog up the kidneys and lead to kidney failure. Making all of those also mean lots of nuclear material turnover to make them so that results in hyperuricemia. So you see increased BUN and Cr and renal failure. You also see infection because you're making all these abnormal immunoglobulins and not making actual functional immunoglobulins that are able to fight infection)

If pt has a threatened abortion (bleeding with closed cervical os, and fetus with normal HR on u/s), what do you do?

Expectant management; reassurance and repeat U/S DO NO hospitalize her for bed rest and obs, there is no evidence to suggest that helps, in fact bed rest may be bad because it's associated with increased risk of venous thromboembolism. Threatened abortions frequency have uncomplicated pregnancy with normal outcomes.

Pt is 11 week pregnant and she has no medical problems, but has family hx of mom and maternal aunt having hypothyroidism. Her thryoid function 6 months ago was normal. Now she has the following findings 6 Months ago: TSH 2.5 Free T4: 1.1. Now: TSH 0.2 Free T4: 1.7 (normal for 1st Tri: 0.9- 2.0) Most likely responsible for the temporal change in pt's thryoid lab findings with pregnancy?

Explanation: she has elevated levels of hCG. Thyroid hormone production increases during pregnancy to cope with metabolic demands. This is done by 2 mechanisms: -Estrogen stimulates synthesis/increase in thyroxine-binding globulin (TBG), and decreases TBG clearance, leading to increased total bound (but not free) thyroid hormone levels. Pts with normal thyroid reserve will increase thyroid hormone production to maintain free hormone levels. -hCG (hormone that increases with pregnancy; this hormone also shares a COMMON ALPHA SUBUNIT with TSH and a very similar beta subunit) directly stimulates TSH receptors, this results in increased hormone production with feedback suppression on pituitary TSH release (causes increased production of thyroid hormones) IN pts with normal thyroid function, the net effect resembles subclinical hyperthyroidism with increased total T3 and T4, normal (or mildly increased) free T4, and suppressed TSH, although pt remains clinically euthyroid. (So in pregnancy, think about it as looking like subclinical hyperthyroidism) Note: high levels of hCG during pregnancy can also lead to hyperemesis gravidarum and is associated with a transient hyperthyroid phase. (So pregnancy is subclinical hyperthyroidism... and when you throw up alot it also is associated with transient hyperthryoid phase... just remember that pregnancy is a state where you have more metabolic processes going on so your body is like HEY! I need more thyroid hormone, so your body goes into this hyperthyroid mode) Note: TBG (thyroxine-binding globulin levels) are generally increased during pregnancy d/t Estrogen.

What's the distribution on skin for contact dermatitis?

Exposed areas to the allergen. Tx: topical corticosteroids (ex: hydrocortisone)

How does scabies present? how do you tx?

Extremely itchy, burros and small red papules seen. Rash located in the webs of hands/feet, flexor wists, extensor elbows, axilla, umbilicus, genitalia (where the scabies babies can hide) Spread by direct person to person contact. (It's a mit infestation with "sarcoptes scabiei") Tx: Topical 5% permethrin (Gross, don't "permit" that to happen.. permethrin) - or - Oral ivermectin.

AR d/o with pancytopenia, macrocytosis. Dx around age 8. Many deformaties: cafe-au-lait spots, microcephaly (small head), microphthalmia (small eyes), short stature, horseshoe kidneys, absent thumbs (no thumbs! :( ) What do they have?

Fanconi's anemia

Target BG for determining gestational DM

Fasting < 95 1hr PP: <140 2hr PP <120 Tx: dietary modifications as first line, then Insulin or metformin as 2nd line.

What are signs of digoxin toxicity?

Fatigue, anorexia, nausea, blurred vision, disturbed color perception, cardiac arrhythmias. CV: life-threatening arrhythmia GI: anorexia, N/V/abdominal pain Neuro: Fatigue, confusion, weakness, ***color vision alterations***

How do you know someone has OA?

Features: >50yo, pain worse with activity and relieved by rest, crepitus, ***Joint space narrowing*** on x-ray. Risk of OA is increased in pts with prior joint injury or abnormal joint alignment.

Pt gets vascular access (cardiac cath) and then has mild discomfort at the access site after the procedure. There is increased swelling, pulsatile mass and you hear a systolic bruit. What is happening?

Femoral artery psuedoaneurysm -bulging, pulsatile mass -systolic bruit

What can maternal hyperglycemia cause in the fetus in the 2nd and 3rd trimesters?

Fetal hyperglycemia, hyperinsulinemia Increased metabolic demand --> fetal hypoxemia --> increased EPO --> polycythemia Organomegaly Neonatal hypoglycemia Macrosoma --> shoulder dystocia --> brachial plexopathy, clavicle fracture, perinatal asphyxia.

What is thyroid storm?

Fever as high as 104-105F, tachycardia, HTN, CHF cardiac arrhythmias (ex: a.fib), agitation, delirium, seizure, coma, goiter, ***LID LAG*** (if you see this buzzword, think about thyroid storm), tremor, warm/moist skin, N/V/D, jaundice. Caused by thyroid or non-thyroid surgery, acute illness (ex: trauma, infection), childbirth, acute iodine load (ex: iodine contrast) Tx: -beta-blockers (propranolol) to decrease adrenergic manifestations. -PTU followed by iodine solution (SSKI) to decrease hormone synthesis and release -Glucocorticoids (ex: hydrocortisone) to decrease peripheral T4 to T3 conversion and improve vasomotor stability. -Identify trigger and treat, supportive care.

How does cerebral malaria present? (Think about Katie Fridel)

Fever, AMS, delirium, seizure.

What's the presentation for Suppurative (infectious) thyroiditis?

Fever, erythema, severe pain at thyroid gland, with asymmetric goiter d/t abscess formation. Usually in kids and adults who are immunocompromised. (suppurative means pus forming.. so think infection) In kids or immunosuppressed, asymmetric goiter bc abscess, fever, hurts

What are the features of TRALI (Transfusion-related acute lung injury)?

Fever, hypotension, non-cardiogenic pulmonary edema within 6 hours of getting blood product. There is normal LV function with TRALI So you typically have normal so Pulmonary Arterial Cath (PAC) shows normal or high cardiac index and low/normal PCWP

IBS treatments

Fiber in diet Antispasmodic agents (Hyoscyamine, Dicyclomine) TCAs or SSRIs Memory tools: -"Eat your fiber Adriano" -Adriano is spastic and says "Mine!" .. so give him antispasmodic agents - hyoscyaMINE, dicycloMINE. -Put him on TCA or SSRI.

What is the mutation in Congenital Contractural Archynodactylyl?

Fibrillin 2 gene mutation

Young female pt with HTN and she has bruit under her right ear. What are you thinking as cause?

Fibromuscular dysplasia (systemic noninflammatory disease that affects renal and internal carotid arteries --> arterial stenosis, aneurysm or dissection) -90% women -Internal carotid artery stenosis!!!! (recurrent HA, pulsatile tinnitus, TIA< stroke) <-- subauricular systolic bruit -Renal artery stenosis: 2ndary HTN, flank pain. <-- abdominal bruit Dx: imaging preferred. (ex: duplex UA, CTA, MRA) over catheter based arteriography Tx: Anti-HTN meds (ACE/ARBs as 1st line), percutaneous transluminal angioplasty, and surgery if that's not successful.

19yo female with recurrent HAs. She has these HAs for years, but it has recently gotten worse. They last several hours and remit spontaneously or after taking OTC acetaminophen. No N/V/abdominal pain, sweating or fever. 6 months ago, she was told she has high BP. Today it's 175/100 in Right arm and 170/102 in left arm. Systolic bruit!!!! is heard under the right ear. Most likely cause of her HTN?

Fibromuscular dysplasia: systemic non-inflammatory disease that typically affects the renal and internal carotid arteries and leads to arterial stenosis, aneurysm, or dissection. Less commonly affects vertebral, iliac, or mesenteric arteries. Most common presentation is recurrent HAs caused by carotid artery stenosis or aneurysm. May also see pulsatile tinnitus, neck pain, flank pain or sx of TIA (focal weakness, vision loss). HTN occurs bc of renal artery stenosis leading to secondary hyperaldosteronism. Abdominal bruit may be presentn. ***In young pts, SUBAURICULAR SYSTOLIC BRUIT is highly suggestive of FMD as carotid atherosclerosis should NOT be present. Even in older pts, these bruits suggest FMD as the subauricular location indicates involvement of the internal carotid artery, which in contrast with the carotid bulb, is not commonly affected by atherosclerosis.** -90% women (in adults) -Internal Carotid Artery Stenosis!! (Recurrent HAs, pulsatile tinnitus, transient ischemic attack, stroke) -Renal artery stenosis (secondary HTN, flank pain) -PhyEx: subauricular systolic bruit, abdominal bruit -Dx: imagining preferred (ex: duplex US, CTA, MRA), Catheter based arteriography -Tx: Antihypertensives (ACE inhibitors or ARBs as 1st line), Percutaneous transluminal angioplasty (PTA), surgery (if PTA unsuccessful) Note: Pheo doesn't make sense since she is negative for all of those symptoms. Renal artery atherosclerosis doesn't explain the carotid bruit. So in this stem... look for an answer that fits for carotid bruit.

AntiHTN meds in pregnancy

First line (safe): -Methyldopa -Labetalol (beta blocker) -Hydralazine -Nifedipine (CCB) 2nd line -Thiazide diuretics (not preferred; in general volume depletion should be avoided in pregnancy) -Clonidine CONTRAINDICATED IN PREGNANCY -ACE inhibitors (worried about fetal kidneys) -ARBs (same, worried about fetal kidneys) -Aldo blockers (ex: spironolactone, eplerone) -Direct renin inhibitors (ex: Aliskiren) -Furosemide (remember Sketchy with mom at side of roller coaster with spider (Teratogen) on her pregnant belly shirt)

What do you use to treat condylomata acuminata (genital warts) in pregnancy? (they tend to increase in size and vascularity in pregnancy bc of the natural immunosuppressive state and hormone alterations)

First line: topical trichloroacetic acid as 1st line tx. Note: Safe to use in pregnancy: liquid nitrogen, laser ablation, electrocautery Not safe in pregnancy: imiquimod, podophyllin resin bc they can be teratogenic. Note: :( Perinatal transmission may rarely result in juvenile onset respiratory papillomatosis, which benign warty tumors form on the larynx or vocal cords, resulting in stridor and chronic hoarseness/cough. C-section is recommended when large condylomata block the introitus or multiple perineal lesions pose a bleeding risk with vaginal birth.

If you suspect lupus, what do you get first?

First, get the more sensitive test: ANA. If the ANA is positive, then get the more specific anti-ds-DNA to confirm the dx.

What's the ASD murmur?

Fixed split S2 (May also have mid-systolic ejection murmur (flow increase across pulmonary valve) and a mid-diastolic rumble (flow increase across tricuspid valve)

How does atopic dermatitis present in terms of distribution over the skin? How do you tx it?

Flexor surfaces: neck, popliteal fossa, antecubital fossa, volar wrist (side it flexes towards), dorsal ankle (side it flexes towards) for atopic dermatitis (eczema) Tx: topical corticosteroids (ex: hydrocortisone)

Be careful when you use Flumazenil, why?

Flumazenil is a benzo reversal agent (benzo antagonist) and it's only used when the overdose for benzos is acute. AND you are CERTAIN CERTAIN CERTAIN that there is no chronic dependence on benzos. This is because use of Flumazenil on a benzo-dependent patient can cause seizures. Since it's an antagonist, it causes acute withdrawal, which can manifest as tremors or SEIZURES, similar to DTs from alcohol withdrawal

What Abx treatments most commonly associated with C.diff infection after use? (Name 4)

Fluoroquinolones, penicillins, cephalosporins, and clindamycins

Common benign nonvascular liver lesions that typically presents as solitary hepatic mass with selective arterial enhancement and central stellate scar on CT or MRI? How do you manage it?

Focal nodular hyperplasia (FNH): most common benign nonvascular liver lesion. Normally asx and most cases are found incidentally. Most are small (<5cm), solitary and d/t hyperplastic response to hyperperfusion d/t inappropriately large artery found at the center of the lesion. CT/MRI shows hypo- or iso-dense lesion with "arterial enhancement" and "a central stellate scar" More common in women and may be estrogen sensitive so pts on OCPs tend to have larger, more vascular lesions. FNH is generally stable and does not normally have complications. Manage conservatively: some docs will tell the women to d/c OCP and do serial exams for pts with masses >8cm. (Note: symptomatic, large (>8cm) FNH may be surgically resected but otherwise is not indicated since FNH does not undergo malignant transformation or have high likelihood of complication (ex: hemorrhage)

Pt is an IV Drug users. You see cavitary lesions in the lung periphery***(big clue). What is the likely organism?

For IVDUs, think about staph aureus for IE and then that can have vegetations that embolize to the lungs and cause characteristics nodular infiltrate with cavitations (so staph aureus is the IVDU organism)

What is salvage therapy? what is an example?

Form of treatment for a disease when a standard treatment fails. Ex: man with prostate cancer gets radial prostatectomy with good margins and PSA is undetectable but then at follow up he has PSA of 9, and now he's getting salvage therapy with radiation therapy because the standard treatment of prostectomy failed. This particular salvage radiation therapy can provide long-term disease control for localized recurrent disease.

Pt with sever pain from anterior abdomen into scrotum and penis, skin edema, crepitus, blisters/bullae, need urgent surgical evaluation. what do they have?

Fournier gangrene... that was the really bad necrosis in the groin I saw during my surgery rotation.

Sudden diffuse abdominal pain and abdomen is rigid with sx of peritonitis (later becomes distended). What will you see on imaging?

Free air under the diaphragm! This is duodenal perforation.

How does N. fowleri present?

Fresh water amoeba --> acute meningoencephalitis: fever, HA, vomiting, AMS, seizures and mortality rate of 99%.

What is Functional hypothalamic amenorrhea? vs. Primary ovarian insufficiency?

Functional hypothalamic amenorrhea: -d/t excessive physical training, very low calorie diet/starvation, weight loss, chronic illness, stress/depression, anorexia nervosa. -All the hormones are decreased from the top of the chain: Hypothalamus makes less GnRH --> pituitary makes less LH and FSH --> Ovaries make less Estrogen. This kind of amenorrhea is d/t disruption of HPO Axis. Note: in addition to amenorrhea, pts also have conditions 2/2 hypo-E including infertility, vaginal dryness, and stress fractures. Tx: behavioral to increase caloric intake but should also include estrogen repletion for those unable or unwilling to tx the underlying etiology (not wanting to modify exercise patterns, unable to decrease stress levels) Primary ovarian insufficiency: pts with this will have amenorrhea and vasomotor symptoms (hot flashes/flushes, night sweats), and high serum FSH levels. (remember that increased FSH is diagnostic of menopause; remember that if the ovaries are failing or insufficient, then that's menopause)

What kinda of organism is cryptococcal meningitis caused by?

Fungus! So you would see slightly elevated proteins and low glucose levels. Can be detected by India Ink preparations.

Pt with inferior MI (Lead, II, III, avF) is given nitroglycerin.... not great bc it's possibly right heart MI which if you give nitro, can plummet their BP bc they are preload dependent. So 3 minutes later his BP is 75/50, JVP is <3 cm H20 above the sternal angle at 30-45 degrees, and he's cold and diaphoretic. What do you do for him now?

GIVE HIM FLUIDS!!! He's preload dependent so he needs fluids. Answer = normal saline bolus. Hypotension and JVP <3 in pt with suspected RVMI strongly suggests cardiogenic shock d/t inadequate RV preload. So give fluids to increase preload (can only give isotonic fluids if you're bolusing the pt) (Note: also be careful with giving beta-blockers (metop) if the pt is bradycardic or in cardiogenic shock)

What is the mutation that causes MEN2A & MEN2B?

Gain of function mutation with RET proto-oncogene on chromosome 10

CMV encephalitis presents with confusion and FNDs with evidence of multifocal micronodules or ventricular enhancement How do you treat CMV?

Ganciclovir

Tylenol OD, pt is not showing sx yet, what do you do?

Gastric decontamination with activated charcoal if pt presents within the first 4 hours of ingesting >7.5g acetaminophen and get serum acetaminophen levels. Then you want to give N-acetylcysteine (NAC)

When you have a pt with gastrinoma (presents with diarrhea, large/recurrent/multiple ulcers pas the duodenum that recur even after eradication of H.pylori) .... and they also have Hypercalcemia... what's going on there?

Gastrinoma is in the MEN1 syndrome (Pituitary, Parathyroid, Pancreatic... the pancreatic should also include gastrinomas). So if the pt has MEN1 they could also have a parathryoid issue with too much PTH that is causing increased Ca levels.

What is this a description of? Multiple, small grouped ulcers Shallow with red base Multi-nucleated giant cells and intra-nuclear inclusions (Cowdry type A) Initial lesion IS painful

Genital herpes (HSV 1 & HSV 2)

Penetrating trauma; falling with object in your mouth (Ex: toothbrush, pencil) or neck manipulation (Ex: yoga, sports). Then has gradual onset hemiplagia, aphasia, neck pain, "thunderclap" headache. What dx test do you get? What is the suspected dx?

Get CT or MR angiography. Suspect: Traumatic carotid injury (internal carotid artery dissection) Injury to posterior pharynx can injury internal carotid artery that is just lateral and behind the tonsillar pillars. Carotid artery dissection is rare but potentially severe complication of penetrating trauma, seemingly minor oropharyngeal trauma (fall with object in mouth) or neck strain/manipulation (yoga, sports). Intimal injury to the internal carotid artery can result in dissection or thrombus formation, which occurs over hours to days and can extend into the middle and anterior cerebral arteries. Pts may have neck pain, "thunderclap" HA, and sx of ischemic stroke (hemiparesis, facial droop, aphasia). Dx of carotid artery dissection is confirmed with CT or MR angiography.

Pt presents with tender, boggy prostate, fever, chills, perineal pain, has urge to pee and dysuria. Dipstick shows positive leuk esterase. What is next step? What do you NOT do? How do you treat them?

Get a culture of urine sample collected mid-stream. Do NOT urethral cath this patient bc pt with acute bacterial prostatitis may have inflammation involving the urethra and if they develop urinary retention may actually need suprapubic cathertization of the bladder. Tx: (usually E.coli is organism) - Acute: TMP-SMX or fluoroquinolones -Chronic: Fluoroquinolones

46yo pre-menopausal woman with an adnexal mass that is felt on pelvic exam. What's the next step?

Get a pelvic U/S to confirm the adnexal mass is ovarian. After that, you could consider a CA-125 based on the u/s findings and pt's medical hx. However, the CA-125 has low specificity in pre-menopausal woemn as it can be elevated for other benign reasons (ex: endometriosis, fibroids, lupus) and ovarian cancer is less common before menopause. OVARIAN CANCER IS LESS COMMON BEFORE MENOPAUSE. CA-125 is mainly useful in POSTmenopausal women and is NOT recommended for the initial evaluation of an adnexal mass in pre-menopausal patients. Note: she's not old enough.. she's still pre-menopausal so she has different reasons why her CA-125 could be elevated. So don't get a CA-125. plus you'd want to confirm the adnexal mass is adnexal, so get a pelvis U/S. Also, ultrasound can help you tell the difference between say an ovarian vs a fallopian mass, it has high specificity for detection of malignant sonographic features (ex: thick septations, solid components). It's not invasive, well tolerated, is readily available, and is cost effective).

What do you do if someone's penis breaks during sex (aka penile fracture)?

Get a retrograde urethrogram: want to see if the blood extravasated out. They ruptured their corpus cavernosum since they tore the tunica albuginea which surrounds it. You want to see if there was urethral injury, which is a common complication of penile fracture, so that's why you want to do the retrograde urethrogram. Indications are if there are signs of urethral injury: blood at the meatus, hematuria, dysuria, urinary retention (trying but not being able to pee) Note: don't chose Color Doppler u/s, you don't do that for a flaccid penis (bc in PF, there is usually detumescence), you would door color doppler u/s sometimes when you're evaluating testicular torsion.

Pt has a breast mass, dx with invasive ductal carcinoma. It's HER2+ and she's started on trastuzumab, what do you need to check before starting this drug?

Get an Echocardiogram Trastuzumab is a monoclonal antibody often used with adjuvant chemotherapy in pts with HER2+ breast cancer. A know side effect is cardiotoxicity and can lead to decline in LVEF and overt HF. The extent of cardiotoxicity are amplified when trastuzumab is used in combo with chemotherapy meds that are also cardiotoxic (like doxorubicin) Need to also reassess with echo at regular intervals during therapy. Med should be discontinued in pts who develop symptomatic HF or significant decline in EF (ex: >16% points from baseline). Note: this cardiotoxicity is usually reversible and patient do better when you stop the drug. Mnemonic: think... woman finds out she has Br cancer, and it's a "tra-gedy" (give trastuzumab) because then her heart breaks (cardiotoxic).

Pregnant pt at 19week GA comes in with N/V, RLQ pain that has gotten worse over last 12 hours. Temp: 100.4. Mod. abdominal tenderness to palpation in RLQ with guarding. Leuk 16,000. Next step?

Get an abdominal u/s Likely appendicitis but leuks can be elevated in normal pregnancy or in appendicitis. so get an ultrasound and use graded compression technique. Noncompression and dilation of the appendix are dx of appendicitis. USeful in pregnancy bc no ionizing radiation (If u/s is non-dx, may get an MRI to assess further)

Elderly pt on a bunch of cardiac meds has several beats of V. Tach. What is the next step in managing this pt?

Get her electrolytes. After you stabilize the pt, the 1st thing is to look at cause of V.tach. Electrolyte imbalance d/t diuretics is most likely cause. Furosemide (loop diuretic) commonly causes hypo-K and hypo-mag. If uncorrected, both hypo-K and hypo-mag can lead to V.tach. Also, Hypo-K potentiates SEs of digoxin, which includes arrhythmias like V.tach. So you should get serum 'lytes and serum digoxin levels as the most reasonable first steps.

Pt with BB overdose presents with bradycardia, AV block, hypotension, and diffuse wheezing. He is also lethargic with cool/clammy extremities. You secure the airway, give IV fluids (isotonic) and atropine to deal with the hypotension and bradycardia. But his bradycardia and hypotension don't improve. In addition to ensuring adequate oxygenation, what's the most appropriate next step? Why do you do that?

Give Glucagon! Refractory or profound hypotension with BB overdose, the next step is to give IV glucagon. This is bc glucagon increase intracellular levels of cyclic AMP and have been effective in treating both beta blocker (BB) and calcium channel blocker (CCB) toxicity. Should also give other things simultaneously or in succession: IV calcium, vasopressors (EPI/NE), high dose insulin/glucose, IV lipid emulsion therapy.

Pt with pre-eclampsia with severe features, but she's also bradycardic (HR <60). What medication do you give her to control her BP quickly? what med do you want to avoid bc she is already bradycardic?

Give IV Hydralazine - works quickly Avoid IV labetalol (since it's an alpha and BETA-blocker that could slow her HR even more and result in dizziness and lightheadness, which you don't want)

Pt has bulimia nervosa. What med is most effective?

Give SSIR (fluoxetine) combined with CBT and nutritional rehab Memory tool: think of these people as just being anxious about weight gain.. and so they throw up.. so think of treating bulimia with SSRIs

Pt who takes warfarin, she took OTC cold medications (which have acetaminophen in them that can potentiate anticoagulant effects of warfarin and decongestants that may elevated BP even more), has stroke symptoms and increased ICP symptoms (N/V/HA/AMS), spot that lights up on head CT, and INR of 5.2 (really high aka supratherapeutic since goal is between 2-3, meaning high bleeding potential), what's the next best step to take?

Give them ***Prothrombin complex concentrate*** (PCC; this contains Vitamin-K dependent clotting factors II, VII, IX, and X and offers rapid (min) and short-term (hrs) reversal of warfarin. Also give IV Vitamin K.(although it takes 12-24 hours to take effect bc promotes clotting factor synthesis in the liver). Fresh Frozen Plasma (FFP) can also be considered if PCC is not available (but this takes longer to prepare and give and requires more volume infusion compared to PCC) They have a serious intracerebral bleed due to excess anticoagulation with warfarin. So they need to have immediate reversal of their anticoagulation. Use IV Vitamin K and prothrombin complex concentrate. These reduce the risk of death and permanent disability.

Pt drinks ethylene glycol (anti-freeze) and you find they have AG metabolic acidosis and CVA tenderness and urine is red with calcium oxalate crystals. What do you do next?

Give them Fomepizole (so they can piss... pizzle it out) -Note: could also give them ethanol to inhibit the alcohol dehydrogenase, sodium bicarb to alleviate the acidosis, and hemodialysis in cases of severe acidosis or end organ damage. Note: you give fomepizole bc it's a competitive inhibitor of alcohol dehydrogenase. You give ethanol bc it prevent further breakdown of ethylene glycol into its toxic metabolites and so is an integral part of tx.

You gave a pt 0.45% NS (hypotonic fluid) and now they are hyponatremic and have headache and lethargy (hyponatremic encephalopathy), what do you do next?

Give them hypertonic (3%) saline. This is an emergency, give them hypertonic (3%) saline with close monitoring of electrolytes.

22yo returned from Mexico about 2 weeks ago. 1 week later, developed abdominal pain, N/V/D. Those sxs resolved spontaneously. He has hx of IVDU but completed a drug rehab program recently. Presents with 4 days of fever, double vision, painful swelling around the eyes, significant muscle pain in neck and jaw muscles. He has 101F, vital signs otherwise normal. Has subungal splinter hemorrhages, periorbital edema, chemosis (swelling/edema of conjuctivia). Lungs are clear. No cardiac murmurs. Abdomen soft nontender, no organomegaly. Leuks: 10,500 (within normal but on the high side), PMN 56%, Eosinophils 21% (pretty high), lymphocytes 23%, CK is 220. Most likely dx?

Given recent travel and symptoms that are more GI symptoms and then muscle/eye symptoms (different form the IE symptoms), think about something that would cause you GI upset (something you ate) and then go to your muscles/eyes. Also the labs show eosinophilia (>20% is hallmark of Trichinellosis), which is a parasitic finding.. so think about parasitic worms. So undercooked pork with worms in it: Trichinellosis. Undercooked pork has parasitic roundworm in it. More endemic in Mexico, China, Thailand, central Europe, Argentina. When you first eat it, your gastric acid releases the encysted larvae, which invade your small intestine and develop into worms (intestinal stage; asx or have abdominal pain/N/V/D). Female worms can release new larvae (up to 4 weeks later) that migrate and encyst into striated muscle (muscle stage; local/systemic findings due to larval migration- fever, subungal splinter hemorrhages, conjunctivitis, retinal hemorrhage, periorbital edema, chemosis (swelling/edema of conjunctiva), also pain, tenderness, swelling, weakness of neck/arms/shoulders). Eosinophilia (>20%) is the hallmark of the dz. Can also see elevated CK and leuks. Diagnosis is suspected clinically w/ triad of PERIORBITAL EDEMA, MYOSIS, EOSINOPHILIA. Severe dz can involve heart, lungs, CNS.

progressively worsening HA, visual abnormalities, focal motor weakness, cognitive deficits. What kind of mass suspected?

Glioblastoma multiforme

What is the earliest renal abnormality in a pt with DM?

Glomerular hyperfiltration. -that is the major pathophys mechanism of glomerular damage in DM pts. Create intraglomerular HTN leading to progressive glomerular damage and renal function loss. -THE EFFECTIVENESS OF ACE INHIBITORS (WHICH YOU WANT TO GIVE TO DIABETICS!!) IS RELATED TO THEIR ABILITY TO REDUCE INTRAGLOMERULAR HTN AND THEREBY DECREASE GLOMERULAR DAMAGE!!!! Note: Then the first change that can be quantitated is thickening of glomerular BM. That is followed by mesangial expansion. Nodular sclerosis is superimposed later and is specific for diabetic nephrOpathy.

If you're distinguishing between symptomatic gonococcal pharyngitis and EBV infectious mononucleosis, what is the difference between the physical exam findings for the pharyngitis and the cervical lymphadenopathy of the two infections?

Gonococcal: may have pharyngeal edema (or asx) will be non-tender cervical LA. EBV infectious mononucleosis: may present with exudative pharyngitis and ***tender*** cervical LA (and also will have fatigue, rash, and splenomegaly)

What presents with tophi?

Gout, only gout. Tophi are extra-articular collections of urate crystals in pts with chronic gout. You would see needle-shaped, negatively birefringent crystals. Note: pseudogout does NOT present as tophi.

What kind of organism is Vibrio vulnificus?

Gram negative bacteria Foodborne illness from shellfish 2 Most common manifestations: Wound infection and septicemia (septic shock, bullous skin lesions, DIC)

What kind of organism is Campylobacter?

Gram negative bacteria. System sx: fever, myalgia, dizziness, Enteritis: abdominal pain, diarrhea, bloody stools Late complications: reactive arthritis, Guillain-Barre syndrome

What kind of organisms does amp-gent cover?

Gram-negative aerobes. Not good for anaerobic coverage.

What kind of organism is Legionella?

Gram-negative bacteria Found in contaminated water supplies Infection: high fever, lethargy, HA, stupor, GI (V/D/abdominal pain), slow onset of CAP (cough, dyspnea, lobar infiltrate).

What is this a description of? Extensive progressive ulcerative lesions without LA. Base may have granulation-like tissue Deeply staining gram negative intracytoplasmic cysts (Donovan bodies) Initial lesion Not painful

Granuloma inguinale (donovanosis) (Klebsiella granulomatis)

7yo girl with precocious puberty (breast development, grown 3 inches in 3 months, pubic hair). She's 70%tile in weight and 98%tile in height. She has a pelvic mass and white odorless vaginal discharge. What is the likely dx?

Granulosa cell tumor. Will have increased estrogen and presents at precocious puberty in a kid. Postmenopausal woman may have bleeding or endometrial hyperplasia.

Where does the rash of scarlet fever (d/t strep pyogenes) usually begin?

Groin armpits and is red, blanching, and papular.

SEs of cyclosporine immunosuppressant you should definitely know about.

Gum hypertrophy Hirsutism Nephrotoxic (hyperuricemia, accelerated gout, hyper-K, hypo-phosph, hypo-mag) Neurotoxicity HTN Glucose intolerance (hyperglycemia) Increased risk for SCC of skin GI symptoms

What is the most likely involved pathogenesis in a patient with persistent upper abdominal epigastric pain that reveals 4cm mass at the stomach along the greater curvature that is biopsied and showed to be consistent with low-grade lymphoma arising from mucosa-associated lymphoid tissue (MALT)

H. pylori infection. H. pylori infection is found in 90% of pts with MALT tumors. It plays a role in pathogenesis of extranodal marginal zone B cell lymphomas (MALT) of the stomach.

What is Chlorpheniramine?

H1 antihistaminic receptor blocker: reduces action of histamine on H1 receptors, decreasing the allergic response. Also has anti-inflammatory effects by blocking histamine release from mast cells and limits secretory response to inflammatory cytokines.

How do pts with cavernous sinus thrombosis present?

HA, fever, proptosis (protrusion of eyes), and ipsilateral deficits in CNs III, IV, VI, and V (opthalmic and maxillary branches)

What's a treatment for Calcium stones?

HCTZ: decreases urinary Ca excretion and used in managment of recurrent hypercalciuric renal stones.

Diastolic dysfunction (HF). What do you see in the EF? what kind of cardiomyopathy?

HFpEF (can't fill is the problem so EF is preserved) Concentric/hypertrophied

Systolic dysfunction (HF). What do you see in the EF? what kind of cardiomyopathy?

HFrEF (reduced EF) Dilated cardiomyopathy (usually d/t to prior MI; "ischemic cardiomyopathy")

Pt with HIV now has s/sx of pneumonia. What organism is the likely organism?

HIV pts are at increased risk for CAP (esp if CD4 ct <200). Strep pneumo causes the majority of cases of CAP so still pick CAP weven with HIV pt. "Rusty sputum" is classic of pneumococcal pneumonia but is not always seen. Recommended that you give Strep pneumo vaccine as ppx.

Cotton-wool retinal lesions that are rarely hemorrhagic and tend to resolve weeks-months.

HIV retinopathy

HIV pt with CD4 ct <200 and longstanding HIV Disease. Subacute onset of increasing apathy and imparied attention, subcortical (ex: basal ganglia, nigrostriatal) dysfunction occurs early with symptoms such as slowed movements and difficulty with smooth limb movements. Followed by signifiant cortical neuronal loss and memory decline. Adherence to antiretroviral therapy decreases the chance of developing this, and resuming tx may improve sxs. "slowed down over past 6 months, uninterested in what others are saying, increasingly forgetful. poor adherence to HIV meds. CD4 ct was 220 6 months ago, makes jerking movements with legs as he walks towards exam table"

HIV-associated dementia.

HPV, what HPV viral types cause cervical cancer?

HPV 16 & 18. Tobacco use is another major RF. Other RFs: -early onset sexual activity -multiple sexual partners -immunosuppression (HIV infection, chronic glucocorticoid use)

Most common cause of corneal blindness in the USA?

HSV infection. (herpes simplex virus)

What's a SE of EPO that you have to watch for by monitoring pt's BP?

HTN

70yo guy has worsening fatigue. He doesn't go to the doctor. His labs show 10.5 Hb (low), and BUN 50 (high) and Cr 3.0 (high). U/s shows BL small kidneys and no evidence of hydronephrosis. Kidney biopsy shows "intimal thickening and luminal narrowing of renal arterioles with evidence of sclerosis." What is the most likely cause of his findings?

HTN!!! This is likely benign nephrosclerosis 2/2 HTN. HTN is 2nd leading cause of ESRD in the USA. HTN <-- --> Nepphropathy. Renal vasculature is exquisitively sensitive to damages incurred during systemic HTN. Arteriosclerotic lesions of afferent and efferent renal arterioles and glomerular capillary tufts are the most common renal vascular lesions seen. As HTN progresses, there is progressive decrease in renal blood flow and GFR. Nephrosclerosis is characterized by "hypertrophy and intimal medial fibrosis of renal arterioles" Glomerulosclerosis is characterized by "progressive loss of glomerular capillary surface area with glomerular and peritubular fibrosis." Microscopic hematuria and proteinuria occur d/t these glomerular lesions. The kidneys generally decrease in size (so they are small for that reasons)

Neuroleptic malignant syndrome (NMS), when does it happen? what are the symptoms?

Happens after starting an antipsychotic. (sx start within 2 weeks of starting the antipsychotic; mortality rate is 10-20%) Sxs: (Tetrad): Fever (>104F) Confusion (AMS) Muscle Rigidity (generalized)*** Autonomic instability (abnormal VS, sweating) Note: the rigidity and hyperthermia may cause muscle necrosis, creating elevated in creatine kinase. Leukocytosis and electrolyte abnormalities are also common Tx: Stop the antipsychotics and restart DA agents (since antipsychotics are anti-DA), supportive care (hydration, cooling bc of the fever), ICU, give dantrolene or bromocriptine if refractory

When you see TPO antibodies, what should you think of?

Hashimoto thyroiditis (which is chronic lymphocytic thyroiditis) - which presents as hypothyroidism.

Pt with systemic sclerosis can also have kidney problems. If you see marked HTN And AKI, then think about scleroderma renal crisis (SRC), which can occur in 20% of pt. Usually occurs in the first 5 years of dx. Increased vascular permeability, activation of coag cascade and increased renin secretion. Pts have sudden onset renal failure, malignant HTN (blurry vision, HA, nausea) and UA has mild proteinuria. Peripheral smear will show what?

Have MAHA (similar to HUS/TTP) or DIC with fragmented RBCs (Schistocytes) and thrombocytopenia. Peripheral smear with Schistocytes (for Systemic Scleroderma with Scleroderma Renal Crisis). ALL THE S's ... SSc has Schistocytes if there is SRC.

Pt has a panic attack (30 minutes chest pain while sitting in class. He has SOB, tingling around his mouth and is lightheaded, he's stress about not doing well with his classes). Phyexam is normal. What do you do to manage him?

Have him breath into a paper bag (remember when I did that when I was having a panic attack when my cousins were going to leave from visiting when we were in disney land together, my parents had me breath into a paper bag)

If you're concern about a pt having hypoglycemia and you've ruled out exogenous insulin use and sulfonylurea use. Then you're thinking it may be a beta cell tumor or a non-beta cell tumor. How do you distinguish the two?

Have them fast supervised and then draw labs. Beta cell tumor (insulinoma) will show elevated c-peptide levels and serum insulin and pro-insulin level >5 and they will still be hypoglycemic. (you know it's a tumor bc you watched them fast and normally in hypoglycemia, pts stop secreting insulin) Also with beta-cell tumor, you will see negative IGF-II (insulin-like growth factor) with Non-beta cell tumors, you will see serum IGF II measured since the non-beta cell tumors make insulin-life growth factor.

What is a hct that you're like, wow, that's too high? What can cause it?

Hct <65% in term babies Etiology: delayed cord clamping, in-utero hypoxia (mom's HTN or smoking), poor placental gas exchange (mom's DM).

COPD pt comes in with worsening pedal edema, abdominal distention, fatigue for several weeks. He has distended neck veins, loud 2nd heart sound, BL LE edema, and moderate ascites. You give him furosemide, on the first day he has high urine output but then his renal function worsens and he has decreased urine output. What's going on?

He has COPD and pulmonary HTN (ex: loud pulmonary component of the 2nd heart sound... A2P2... so loud 2nd heart sound is the pulmonary component), indicated decompensated right-sided HTN (from the pulmonary HTN backing up into the right heart) You initially improved his cardiac function and his urine output was high the first day after you gave him furosemide bc you decreased the RV end-diastolic volume (preload), but you have to know that RV dysfunction pts are pre-load dependent and so they are super super super sensitive to excessive volume loss. HE still has edema, but now he also has AK d/t IV volume depletion (pre-renal AKI) as seen by the flat neck veins on repeat exam.

27yo man comes in. He's a computer programmer and has a sedentary life. He has an unremitting nose bleed. He had a similar episode a year ago. PhyExam shows several ruby-colored papules on his lips that blanch partially with pressure. His fingers are clubbed. Labs show Hct of 60% (high). WBC and platelets are normal. Why does he have an increased hematocrit?

He has Osler-Weber-Rendu syndrome (aka hereditary telangiectasia): we know this bc of his recurrent nose bleeds and telangiectasis on his lips. These patients also have widespread AV malformations. The AVM can happen in the lungs, which causes blood to shunt directly from the right to the left of the heart without getting properly oxygenated, this leads to chronic hypoxia and shows up as digital clubbing and reactive polycythemia (aka his elevated hematocrit). So the reason he has an elevated hematocrit is because of AV shunting from his AVM that are due to his osler-weber-rendu syndrome. Note: this is NOT polycythemia vera (the myeloproliferative disorder that typically causes increased production of all 3 blood cell lines and splenomegaly. Lean away from polycythemia vera because 1) not all 3 cell lines are elevated. 2) telangectasias and digital clubbing are not part of PV 3) median age for PV is around 60yo and this guy is in his 20s.

HIV+ pts with CD4 count 46. Has temp 100.1F and trouble with arm/face over the last week, with 1-2 min episodes of jerking and twitching. Daily HAs for several weeks and associated nausea. Mild blunting of left nasolabial fold. Left arm 4/5 strength, 3+ DTR. MRI shows ***several*** ring-enhancing lesions at grey-white matter junction and basal ganglia. Next step in management?

He has SEVERAL ring enhancing lesions in his brain and CD4 count is <100, HA/confusion/fever/FNDs, so he has toxoplasmosis. Need to treat with sulfadiazine & pyrimethamine ***plus leucovorin to prevent hematologic side effects***. (should be prophylax-ing with TMP-SMX when CD4 count is less than 100, also make sure he's taking his antiretroviral medications) You would also find he is positive for toxoplasma gondii IgG.

Pt has hx of business trip where he recently flew to China. he's at home and he falls down from a brief syncopal episode (wife does not witness that, she just hears a loud thud), he wakes up immediately after but is SOB. Hx of HTN and smokes ppd. Temp 100.4F, HR 124, RR 22.BP 85/65 (note BP IS LOW in large one of these..) Spo2 89%. BL lower edema, more on the left side. His BMI is 32. Sinus tachy with T wave inversion leads V1-V3. CXR with right basilar atelectasis. What is cause of his syncope?

He has a PE. About 10-15% of pts with PE present with SYNCOPE!!!! (KNOW THIS). Most PE pts present with acute onset SOB, CP, tachycardia. Low grade fever and sx of DVT (unilateral LE edema) may be present, and large PEs have HYPOTENSION!! (yes this does happen in large PEs, know that) and hypoxemia. Massive PEs can have sudden occlusion of >50% of the pulmonary arterial circulation and cause rapid increase in pulmonary vascular resistance and RV pressure load. This results in RV dysfunction and sudden loss of CO. Pt can present with sudden cardiac death, syncope or presyncope. Acute PE can also cause pts to present with sudden cardiac death, syncope, or presyncope. Acute PE can also cause syncope d/t cardiac arrhythmia induced by RV strain and ischemia, or d/t vasovagal response to PE. Obesity, smoking, recent long-distance travel all increase risk for PE. ECG shows sinus tachycardia and may show evidence of Right heart strain (ex: T wave inversion in leads V1-V3)

t with longstanding diabetes (like 20 years of it) and now has symptoms of abdominal fullness, N/V, boating, constipation, early satiety. There is a "splash" heard over the stomach on auscultation when moving the patient. What's going on? what do you do next in management of this patient?

He has diabetic gastroparesis, which is basically neuropathy of the stomach, it doesn't feel the stretching that is usually the stimulation for it to move. So he has gastric dysmotility which is why he is having his symptoms, the food isn't moving along in his GI tract. No need to do tests since it's pretty obvious what he has, so the next step is just to treat by increasing his GI motility; which you can do with drugs: erythromycin and metoclopramide. Note: Metoclopramide is a gut motility stimulator, used to tx GERD and to treat diabetic gastroparesis. (Memory tool.. looks like metro-ride... motility agent... it moves things... metro-ride...metoclopramide) Erythromycin is an antibiotic but it's also a gut motility stimulator. (memory tool: think about the fact that erythromycin is a macrolide.. and in sketchy it's depicted by the crows. so think of them being mobile and being able to go everywhere...s o they are used to treat a wide variety of things... infections.. topical erythromycin to treat new born baby conjunctivitis from neisseria gonorrhea, used in atypical pneumonias... and now here.. they can also fly over here an treat a patient with diabetic gastroparesis... since it's also a gut motility agent). s

31 yo white male with joint pain. He has knee pain, right heel, and low back pain. Recently tx for urethral discharge. He's afebrile. VSS. Right knee is swollen, tender and warm to touch. Tenderness over Achilles. See mouth ulcers. Synovial fluid of right knee shows WBC 10K, PMN leuks but gram stain negative. What meds should you start with this pt?

He has reactive arthritis. -Type of seronegative spondyloarthropathy. Classic reactive arthritis consists of triad of NONgonococcal urethritis, asymmetric oligoarthritis, and conjunctivitis ("can't see, can't pee, can't climb a tree"). The arthritis often involves the knee and SI spine, which explains the back pain. -In addition to the Classic triad: mucocutaneous lesions (oral ulcers) and enthesitis (Achilles tendon pain) are common findings in reactive arthritis. -Bc not all sx are always present, there should be high suspicion for reactive arthritis in the cases of any asymmetric oligoarthritis associated with urethritis, conjunctivitis, or mouth ulcers. Synovial fluid analysis is usually sterile. NSAIDS are the 1st line tx during acute phase of this condition. You treat reactive arthritis with: NSAIDS!! (not antibiotics; you would choose antibiotics if this pt has gonococcal septic arthritis, which is difficult to dx from reactive arthritis, but would likely have a fever)

54 yo man found unresponsive at home. Hx of HTN but he's not compliant with his meds and smokes cigs and crack cocaine. BP 176/98. Unresponsive to sternal rub. Right pupil widely dilated and unresponsive to light. Intermittent extended posturing of left arm and leg. DTR 4+ in left extremities. Babinski present on left side. Which of the following is most likely cause of pt's symptoms?

He's extensor posturing after having a really high BP and also doing cocaine... so likely hypertensive hemorrhage, which can also lead to uncal herniation bc of mass effect pushing temporal lobe (uncus) laterally and downward against the tentorium cerebelli. This will then compress CN3 and result in dilated, nonreactive ipsilateral pupil. Further displacement causes midbrain compression with contralateral extensor posturing, coma, and respiratory compromise HTN hemorrhages most commonly occur in the basal ganglia (~50% occur in the basal ganglia) and may results in uncal hernation. Sx include a dilated, nonreactive IPSILATERAL pupil, contralateral EXTENSOR posturing, coma, and respiratory compromise.

17yo AA teen has episode of gross hematuria that resolves by itself. VSS. No abnormalities on PhyExam. Lab: Cr 0.9 (normal). Dipstick UA shows: Mod blood, many RBC/hpf, but otherwise negative. Urine microscopic exam: numerous INTACT RBCs No other findings. (so basically he's fine except there's blood in the urine; intact RBC blood) What is the likely cause of this pt's hematuria?

He's got SICKEL CELL TRAIT!!! THEY CANT CONCENTRATE URINE (ISOSTHENURIA) AND MIGHT HAVE PAINLESS HEMATURIA AS THE ONLY SYMPTOM!! HOW DID I MISS THAT!! Answer: Renal Papillary ischemia/Necrosis Gross hematuria and UA with normal appearing RBCs suggest extra-glomerular etiology. Painless hematuria likely d/t renal papillary ischemia/necrosis. The relativley low local partial pressure of oxygen in the vasa rectae predisposes the affected RBCs to sickling. Papillary necrosis can occur with massive hematuria bc the episodes are usually mild & resolve spontaneously. UA shows normal appearing RBCs. Other renal complications: can't concentrate urine (vasa rectae damage with inability to maintain concentrated medullary gradient) and distla renal tubular acidosis (tubular damage with impaired H+ secretion) (not acute cystitis - which is an UTI of the bladder: which would show up with dysuria, urinary frequency, UA with many WBC and bacteria with positive nitrites and leuks)

Alcoholic with ascites now has AMS, ataxia, or ***asterixis*** (flapping tremor of outstretched, dorsiflexed hands). What do you do to treat them?

He's got hepatic encephalopathy and the ammonia is building up causing neurotoxicity from the impaired liver function. So give Lactulose to decrease the blood ammonia. -lactulose or lactitol are non-absorbable disaccharides that are preferred for lowering serum ammonia. Colonic bacteria metabolize the lactulose to short chain fatty acids (lactic acid, acetic acid). This acidifies the colon to stimulate conversion of the absorbable ammonia to non-absorbable ammonia (an ammonia trap) --> BMs that facilitate fecal nitrogen excretion. Titrate the med to make 2-3 semi-formed stools daily.

Pt with STEMI but they also mention he has BL basilar crackles that extend halfway up the lung fields and that sublingual nitro isn't working. They started oxygen, aspirin, clopidogrel and atorvastatin. What should you add to that (they dont give you cath lab as a choice, although you would do that for definitive management of the STEMi) ?

He's having flash pulmonary edema r/t the MI. So we need to treat the pulmonary edema and we do that with furosemide loop diuretic! to relieve the pulmonary edema by decreasing cardiac preload. It also causes venodilation that further decreases preload.

43 yo woman comes in with abdominal pain and dark urine. She has RUQ tenderness but no guarding or rebound. Labs show anemia (8.9), low plots (134,000), sxs of hemolysis (Tbili 6.3, LDH 740, Haptoglobin 30 (normal is 50-150 so this is low). MRI abdomen shows hepatic vein thrombosis!! What is the dx?

Hemolysis + Cytopenias + thrombosis = Paroxysmal nocturnal hemoglobinuria. Workup: Get CBC, LDH, haptoglobin, Indirect hyperbili: these will all show hemolysis. UA: will show hemoglobinuria Flow cytometry will who absent CD55 and CD59 (which are needed to inhibit the MAC attack, which is why there is hemolysis in the first place)

What are some important causes to associate with membranous glomerulonephritis?

Hep B & C (think about my and May's dads being "members" of our families... membranous glomerulonephritis) Syphilis Gold Penicillamine SLE RA.

Tx for DVTs that is safe in pregnancy?

Heparin (unfractionated or LMWH) -Heparin is safe in pregancy. -Warfarin is not safe in pregnancy. Warfarin wages war on the baby = teratogenic. Note: DVT during pregnancy, then tx is continued for at least 3 months. Before stopping the tx, repeat duplex u/s shoudl be done to assess if the thrombus is stll there and if you need to extend tx.

Pregnant woman with sickle cell trait gets DVT, what do you treat her with?

Heparin is safe in pregnancy: Unfractionated heparin or LMWH. IF there are no bleeding concerns, tx of choice in DVT for pregnant women is unfractionated heparin or LMWH. Daily LMWH injections are used for long term therapy. Tx of DVT during pregnancy is continued for at least 3 months (through remainder of pregnancy and 1st few weeks postpartum). Before stopping tx, repeat duplex u/s to assess if thrombus remains as this would extend tx length. Teratogen: warfarin is a teratogen so DO NOT DO NOT DO NOT give warfarin in pregnancy (warfarin wages war on the baby) Note: this pt has multiple RFs for DVT including hypercoagulable state of pregnancy - elevated endogenous hormones and increased stasis of blood in lower extremities from pressure on the IVC, and also sickle cell trait (has 2-4 fold increased incidence of DVT)

What is safe for pregnant women with DVT?

Heparin! Un-fractionated or LMWH are both okay. Treat with heparin as long as they don't have bleeding concerns.

If you can push on the belly (the liver) and the JVD goes up, what is that called and what condition does that point to?

Hepatojugular reflex -Seen in Cor Pulmonale (chronic lung disease --> pulmonary HTN --> right heart - specifically right ventricle- failure) Signs of RV failure: -elevated JVP -RV 3rd heart sound -TR (bc its in the right heart) -Hepatomegaly with pulsatile liver -Lowe extremity edema, ascites, or pleural effusion Echo: s/sx of increased right heart pressure RH cath: pulmonary systolic pressure >25 mmHg

23 yo male from Scotland has fever, severe abdominal pain, fatigue, N/V and can't eat. Has hx of anemia and "cola-colored urine". HR 102, RR 16. RUQ tenderness worse with deep inspiration. Splenomegaly and jaundice are present. Leuk 13k, hgb 10 (low), MCV 88 (normal), MCHC 46% (high), Retic 12% (high), TBili 2.3 (high), Dbili (0.5) - so it's mostly indirect bili so it's Gilbert's or a hemolytic anemia and this is way more than Gilbert's at this point so leaning towards hemolytic anemia. LFTS normal, LDH 1000 (high), Coombs test negative. Likely cause of his anemia?

Hereditary spherocytosis: an inherited deficiency of ankyrin and spectrin (proteins for scaffolding RBCs). The sphere-shape is not flexible so its gets trapped in fenestrations of the spleen's red pulp. Presentation/Labs: expect increased MCHC, hemolytic anemia, jaundice and splenomegaly in pt of N. European descent. Short life span of spherocytes and chronic hemolysis --> high hgb turnover and excess bili that overwhelm conjugation and elimination from the body (so mostly indirect bili). Hyperbili --> jaundice, dark urine, and pigmented gallstones (calcium bilirubinate). Can have classic acute cholecystitis signs d/t the gallstones. In addition to cholecystectomy, pt will need folate supplemenation as chronic hemolysis consumes folate. May need splenectomy to minimize the hemolysis.

What kind of injury causes a positive straight leg test? What are associated symptoms of this problem?

Herniated disk: acute pain that radiates to the thighs and typically below the knee. Straight-leg raise test is positive in herniated disk.

32yo man. pain, watering and redness in left eye for 2 days. similar symptoms a few months ago. See vesicles and dendritic ulcers in the cornea, what does he have?

Herpes in the eye! Herpes simplex keratitis. Can cause corneal blindness. Mostly occurs in adults. Usually the recurrences are precipitated by excessive sun exposure, outdoor occupation, fever, or immunodeficiency. Corneal vesicles and dendritic ulcers (most common presentation) are characteristic. Diagnosed clinically but epithelial scrapings will show multi-nucleated giant cells. Tx with antiviral therapy (oral or topical)

Presentation is recurrent labial or peri-oral ulcerating lesions that usually resolve within 2 weeks. Tzanck prep of vesicular fluid shows giant cells. What does this describe?

Herpes simplex virus (HSV)

HIV+ pt presents with deterioration of his vision over the past week. He initially experiences eye pain and mild conjunctivitis, followed by rapid progressive visual loss. Exam of his eyes shows marked ***keratitis.*** Funduscopy shows widespread, pale, peripheral retinal lesions and central ***necrosis of the retina.*** What organism likely caused this?

Herpes simplex virus (HSV) or Varicella-zoster (VZV) In HIV pts, both HSV and VZV can cause severe, acute retinal necrosis associated with PAIN, KERATITIS, uveitis, and funduscopic findings of peripheral pale lesions and central retinal necrosis.

Nerve inflammation from viral reactivation, what do you think of?

Herpes zoster (shingles) -would expect neuritis followed by dermatomal vesicular rash.

What do you expect to see on peripheral smear with a pt with thalassemia minor?

Heterozygous pt for B-thalassemia, so they are typically asymptomatic and peripheral smear shows microcytic TARGET cells.

Pt with Klinefelter syndrome (XXY), what would you expect to see with their FSH and LH levels?

High FSH & LH levels in Klinefelter syndrome (XXY). this is a problem with primary hypogonadism (testicular fibrosis).. so i guess that's why the FSH and LH are high, trying to make the hormones by increasing FSH And LH. Also see azoospermia, gynecomastia, decreased intelligence, increased axial skeletal growth, and the high FSH and LH.

Know what med can induce psychosis.

High dose glucocorticoids (used for allergies, asthma, inflammatory or autoimmune conditions) Glucocorticoids can cause psychosis or mood disorders (manic/depressive sxs)

Bronchiectasis: how do you confirm the dx?

High resolution CT scan of chest (needed for initial dx)

Side effect profile: Clozapine

High risk for agranulocytosis; need to monitor CBC on regular basis, never us as 1st line tx

What are the side effects you see with HCTZ/chlorthalidone use?

High: glucose, LDL, TG, uric acid, calcium Low: K, Na, Magnesium.

Pt has hx of thyroid cancer that was treated by removing the thyroid 10 years ago.and he's been treated with calcium carbonate and calcitriol. But now he has serum hypo-Ca and high phosphorus levels, difficulty walking, involuntary movements, HA, blurry vision, resting hand tremor and increased muscle tone in and lower extremities. His funduscopic exam shows fullness of the optic cups. CT Head w/o contrast shows extensive calcifications in basal ganglia BL. What's going on?

His thyroid resection caused the parathyroids to be also removed so then he had post-op low parathyrodism that needed treatment with supplementation (oral calcium and calcitriol (active form of Vit D). His high phosphate was treated with avoidance of phosphate rich foots and can be treated with oral phosphate binders ****BEWARE!!! YOU NEED TO MONITOR SERUM Ca and Phosphate levels very carefully when pt has post-op Hypo-parathryoidism. If the Ca-phosphorus product (serum calcium x serum phosphorus) > 55, then that increases the risk of soft tissue calcification. - Example: Serum calcium of 7.8 times serum phosphorus of 7.4 = 57.7, so this pt is at risk of soft tissue calcifications. This could mean deposits of calcium (induced by the high phosphorus, which makes sense bc if you have too much phosphorus your body thinks you have too much calcium in the serum so need to put it somewhere else, in the soft tissues ) in the basal ganglia...uh-oh. bc basal ganglia controls your movement... so if you get calcification of the basal ganglia, that leads to movement disorders. Could also get calcified kidneys and cataracts.

abscess over the upper or lower eyelid? what's it called?

Hordeolum.

Pt is in her 40s and comes in for resent mood instability (sad to irritable). She has mild forgetfulness. Is convinced she is going to die bc her father hd similar symptoms around this age and died subsequently. She has writhing movement of the extremities. What does she have?

Huntington's disease: It's AD inheritance and affects both sexes equally. Presents age 30-50. Presentation: mood disturbances (depression, apathy), dementia, choreiform movements (facial grimacing, ataxia, dystonia, tongue protrusion, writhing movements of extremities) Symptoms are progressive and will disable the patient.

When do you see Howell-Jolly bodies with basophilic remnant of RBC nucleus?

Hx of splenectomy or functional asplenia (like SCD)

What is Job Syndrome?

Hyper-IgE syndrome: rare immunodeficiency that causes recurrent skin and lung infections. Skin lesions can resemble eczema.

What is the relationship between TMP-SMX and hyperkalemia?

Hyper-K tends to happen in HIV infected pts who get higher doses of TMP. But even normal doses can cause elevation in K serum concentration. So be mindful and monitor electrolyte levels (esp. K levels) in HIV patients who are getting high doses of TMP

Elderly pt with constipation... you see one of their electrolytes is elevated, which one are you looking at?

Hypercalcemia may be asx with calcium <12, or you can also commonly see fatigue, CONSTIPATION and depression. Think about MM in that pt.

75 yo pt with T2DM has 2 days of progressive lethargy and confusion. He just got dx with polymyalgia rheumatica and started exogenous glucocorticoids. Oral mucous membranes are dry. His glucose is 830. Trace ketones in his urine. Why is he altered?

Hyperosmolality. (He's got HHS) Labs: Glucose >600 Bicarb will be >18 (bc had time to compensate and increase) Normal AG Negative or ***Small*** serum ketones Serum osmolality > 320 mOsm/kg HHS is Hyperosmolar hyperglycemic state -see hyperglycemia -high serum osmolality d/t relative insulin deficiency Can be caused by infection (Most common), meds (GLUCOCORTICOIDS!!!, Thiazide diruetics, pentamidine, atypical antipsychotics), interruption of insulin therapy, and trauma/acute illness (ex: stroke, MI) Severe hyperglycemia --> glycosuria and osmotic diuresis --> hypovolemia and dehydration. As hypovolemia worsens, the GFR declines --> reduced renal glucose excretion and worsening hyperglycemia. Older pts are at risk for altered perception of thrist and restricted fluid intake. Neuro sxs range from confusion --> coma and are d/t to the high osmolality (>320 mOsm/kg).

What is Lichen simplex chronicus?

Hyperplastic response to repetitive scratching and irritation. Will see thickened, leathery textured skin.

What is an indictor of severe heart failure?

Hyponatremia indicates severe heart failure. Hyponatremia in pts with CHF usually parallels the severity of heart failure and is an independent predictor of adverse clinical outcomes. Note: don't give more digoxin bc higher digoxin levels have increased risk of toxicity with NO EVIDENCE of improvement in sxs or outcomes for those with decompensated CHF.

What are signs of relatively mineralocorticoid deficiency? (ex: aldo)

Hypotension Hypo-natremia Hyper-kalemia Elevated plasma renin activity (since low aldo will upregulate RAAS so Renin will be high)

If you have a female athlete who is muscular and how has amenorrhea for 5 months and mild facial acne, what are you thinking about?

Hypothalamic amenorrhea. Pt who is doing strenuous exercise, relative calorie deficiency, stress fractures, amenorrhea, infertility. think about this. Labs: decreased GnRH, decreased LH/FSH, decreased Estrogen (the whole HPO axis is decreased) Long term consequences: decreased bone mineral density, increased TC< increased TG. Tx: eat more, Estrogen, Ca and Vit D supplements.

Mom is 35 weeks gestation and she is GBS positive, what do you want to give her as she is imminently delivering?

IV Penicillin to prevent GBS infection. Note: Mg sulfate for neuroprotection is only for fetuses <32 GA (Memory tool: Mg++ so 2 cations to remind you it's thirty-TWO weeks GA as cut off for mag)

What is the med for thrombolysis therapy that is recommended in pts with acute ischemic stroke sxs within 3-4.5 hrs of symptom onset?

IV alteplase

Pt has malignant (necrotizing) otitits externa. Severe infection of external auditory canal with edema and purulent dischare and granulation tissue in the floor, but the TM is clear. What do you treat them with?

IV cipro. Caused by pseudomonas. An infection spread beyond the external auditory canal can cause osteomyelitis of the skull base or tempormandibular joint involvement and present with pain by chewing. CNs can also be involved. Given the severity of MOE, tx with IV cipro.

Tx for Guillain-Barre?

IV immunoglobulin or plasmapheresis Monitor autonomic and respiratory function

Complications of chronic hypo-parathyroidism?

If calcium x phosphorus > 55, worried about soft tissue calcification deposits; in the basal ganglia --> movement disorder calcification in kidneys cataracts

How do you tell the difference between Primary (autoimmune most common cause) and central adrenal insufficiency (secondary/pituitary; tertiary/hypothalamic)?

If it's the adrenal gland itself that has the lesion, primary autoimmune adrenal insufficiency ("autoimmune adrenalitis"): then you have severe symptoms bc the organ that's making the hormones doesn't work. -Aldo and cortisol are both down, which makes ACTH go up bc of negative feedback. -You have symptoms of: Low Aldo (mineralocorticoid deficiency): hyponatremia, hyperkalemia, hypotension High ACTH: Low Cortisol (glucocorticoid deficiency) hyperpigmentation (bc of melanocyte stimulating hormone is also secreted with ACTH) If the lesion is central, somewhere in the brain, then Aldo is normal since Aldo is controlled by RAAS, but ACTH will be down (bc ACTH is from the brain), and cortisol will be subsequently decreased as well. Symptoms are less severe, there is not hyper-pigmentation, there isn't hyperkalemia (bc Aldo is working fine), There may be hyponatremia.

When do you finally decide to use Clozapine (not a 1st line med bc of agranulocytosis SE)?

If pt fails to respond to 2 FGAs or SGA. NEVER use as 1st line tx.

When older pt has FNDs and it seems like a stroke, when do you suspect lacunar stroke?

If pt has hx of HTN, hyperlipidemia, diabetes, is older, smokes, and then has either a pure motor hemiparesis (most common, means the internal capsule is involved), pure sensory stroke, ataxic hemiparesis, or a dyarthria (clumsy hand: example of can't hold pen right) and there is absence of cortical signs (aphasia, agnosia, neglect, apraxia, hemianopia, seizure, mental status changes) If it says no abnormalities detected on non-contrast CT (since small lacunar stroke won't show it right away).

When a Confidence Interval (CI) contains the null value of 1, what does that mean?

If the CI contains the null of 1 (in the case of RRr and ORs), then the association is NOT statistically significant.

Relative Risk (RR) is calculated in cohort studies by comparing incidence (risk) of disease among exposed and unexposed individuals. Odds Ratio (OR) is the measure of association in Case-control studies, since case-control studies don't follow people and so you can't calculate a RR. However, there is a scenario where the OR generally approximates the RR, what is that scenario?

If the disease is rare (low disease prevalence), disease incidence (number of new cases) is typically low, and th OR generally approximates the RR. This is called the "rare disease assumption."

Just know that a bunch of drugs can cause SIADH. So if you see a stem with pt with low serum Na and they are taking some drugs.. think about SIADH. What would you expect for serum osm, urineosm, and urine Na?

If they have SIADH, they're holding on to free water. urine osmol: low <275 (bc too much free water held on) urine osmol: high >100 (bc all the free water is in serum, not in urine so the urine is concentrated) urine sodium: high >40 (bc the water is in the serum, so the urine Na is concentrated)

Asthma, who gets a daily low dose ICS (inhaled corticosteroid)? (beclomethasone, fluticasone.. "-sone" ending)

If they have day time symptoms > 2x/week or nighttime awakenings >2x/month

What are Bartter/Gitelman's syndromes and when should you think about them?

If you have a pt with hypokalemia, alkalosis and normotension, that's when you think about -Surreptitous vomiting -Diuretic abuse -Bartter syndrome -Gitelman syndrome So think of Bartter & Gitelman as having about the same electrolyte and metabolic imbalances as someone who is vomiting alot, except you tell the difference by looking at the URINE CHLORIDE concentration, which is going to be low in someone who is vomiting (Bc they lose Chloride int he vomit and so their body isn't trying to pee out the chloride), but the urine chloride will be high in Bartter/Gitelman's. Note: Pts with diuretic abuse may give hx of diuretic abuse and have positive urine assay for diuretics.

What's a cause when you suspect Lambert-Eaton that you must rule out?

If you suspect Lambert-Eaton bc the pt has strength and reflexes that improve following isometric contractions, then you must rule out small cell lung cancer (so get a CT Chest) About 50% of pts have underlying cancer (mostly small cell lung cancer), so if pt has risk factor for lung cancer (ex: smoking) get a CT Chest.

During the window period of Hep B infection, what may be the only detectable marker for acute Hep B you find?

IgM anti-HBc (antibody to core) Note: both HBsAg and anit-HBc are the most appropriate dx tests for acute Hep Bc infection as they are both elevated during initial infection and anti-HBc will remain elevated during the window period.

PT has hypercalcemia of 12.9 and sx of hypercalcemia (nausea, polyuria) 4 weeks after he is dx with quadriparesis. What is the likely cause of his hypercalcemia?

Immobilization. Immobilization --> hypercalcemia from increased osteoclastic bone resportion --> suppressed parathyroid hormone. Onset of hypercalcemia is usually around 4 weeks after immobilization (risk increased in pts with preexisting high rate of bone turnover - younger pts, Pagets dz). In renal pts, hypercalcemia can occur in as little as 3 days. Note: Bisphosphonates inhibit osteoclastic bone resorption and are effective in treating hypercalcemia of immobilization and reducing the associated bone loss.

Toddler with blood in urine, week of cough and nasal congestion, hx of ear infections and pneumonia. Has has skin rash (sounds like eczema), and scatter petechiae and plts are 31,000 (low) and peripheral smear shows small plts size (micro-plts). What's the dx?

Immune problem (recurrent infections), blood problem (specifically reduced size and number of plts; micro-platelets), and eczema, think about Wiskott-Aldrich syndrome. Etiology: X-linked recessive defect in WAS protein gene. Impaired cytoskeleton changes in leukocytes, platelets. (It's a cytoskeleton problem in the plts, WBC, and T cells so T cells don't work so they have increased/recurrent infections. Plts don't work so they have petechiae and purpura and can even have severe bleeding). Tx: Stem cell transplant.

What is ITP? When does it usually occur?

Immune thrombocytopenic purpura (ITP): caused by autoantibodies acting against plt antigens and usually occurs after a viral illness.

Young female patient has hx of MS and she has acute mono-ocular vision loss saying there is a smudge in the center of her left eye and the colors appear "washed out," she has eye pain with movement and theres is paradoxical pupillary dilation of the affected eye with swinging flashlight test (afferent pupil defect). What does she have? How to dx? how to tx?

Immune-mediated demyelination known as optic neuritis. Dx with MRI of orbits and brain. Tx with IV corticosteroids. 35% of cases recur.

Pt with hx of multiple GSW 1 year ago that required emergency surgery (so assume he has splenectomy) now has a really high fever, confusion, cough, malaise, crackles, dullness to percussion. You find gram positive cocci on blood cultures. What is wrong?

Impaired antibody-facilitated phagocytosis bc of presumed splenectomy so he can't handle encapsulated organisms (ex: strep pneumo, which is gram positive cocci).

Pt with hx of multiple GSW to abdomen 1 year ago, think about what organs he likely had removed. How he presents with 2 days of fever, cough, malaise and is now confused with temp of 104.9, BP 80/50, HR 110 RR 32 and dullness to percussion and crackles over left lower chest. Bounding peripheral pulses. Blood cultures show Gram + cocci. What is the underlying mechanism leading to this pt's presentation?

Impaired antibody-facilitated phagocytosis. Multiple abdominal GSW likely means splenectomy. High fever, hypotension, tachypnea, tachycardia in setting of bacteremia with gram + cocci suggests strep pneumoniae infection. Encapsulated organsims (Strep pneumoniae, Haemophilus influenzae, Neisseria meningitidis) have a polysaccharide exterior that conceals antigenic epitopes and resists innate phagocytosis. So these pathogens are largely eliminated by the humoral immune response with antibody-mediated phagocytosis (opsonization) and antibody-mediated complement activation. Much of this depends on splenic macrophages and generation of splenic opsonizing antibodies. So an asplenic pt is at high risk for FULMINANT infection with encapsulated organisms. So these pts should be immunized with penumococcal, meningococcal, and H. influenzae type B vaccines and take oral antibiotics early in the course of any febrile illness.

What's another way to say AV block? (for example, pt who passes out and EKG shows Wenchebach, Mobitz type I second degree AV block)

Impaired atrioventricular node conduction. (just read the answer... it's basically saying AV block; don't pick something that say SA node if you know it's AV block)

What are Beau lines?

Impaired cellular proliferation in the nail matrix (ex: trauma, local or systemic illness, medications) that lead to horizontal ridges that move outward as the nail grows (called Beau lines)

Overflow incontinence: what is the etiology aka another way to describe it?

Impaired detrusor contractility, bladder outlet obstruction.

Chromium deficiency presentation

Impaired glucose control in diabetics

Basis pontis (basilar pons) infarcts: what s/sx do you see

Impaired motor function (ex: hemiparesis, dysarthria-clumsy hand syndrome) - Memory tool: "can't pick up the ponpons... and dysrthria... cuz it's POMPOMs, not ponpons... can't pick them up and can't say it either.. think basilar pons infarct).

DDX for pain-less penile ulcer

In >60yo smoker or HPV hx, and ulcer has been there for several months, think penile cancer In sexually active, think primary syphilis chancre (tx with penicillin but otherwise resolves spontaneously in 3-6 weeks)

When is Fetal Blood Sampling done? What does it get? How is it physically done?

In Rh isoimmunization and when fetal CBC is needed. Place needs through the abdomen into the uterus and get blood from the umbilical cord and sample blood from the umbilical cord. This allows you to get the baby's CBC.

If you dx Medullary thyroid cancer (calcitonin), and you suspect MEN2A or 2B, why is it important to test for the MENs?

In addition to association with Medullary Thyroid Cancer, MEN2A and 2B are also associated with pheochromocytoma, which can be asymptomatic initially but cause severe hypertensive crisis during surgical resection of the thyroid masses of medullary thyroid cancer (MTC). So for pts with MTC, it's important to test them for the RET mutation (testing for MEN2A & MEN2B) and if positive, test for pheochromocytoma with a plasma fractionated metanephrine assay before doing surgery on the MTC, to avoid the hypertensive crisis from a catecholamine surge.

Why is bone scan the wrong answer for Multiple Myeloma?

In multiple myeloma, the osteolytic lesions are from osteoclast (crash... lytic) so a skeletal survey is needed instead. Bone scans are for detecting osteoblastic activity (ex: in metastatic solid tumor), bone scans are not for detecting osteoclastic activity. The answer to the question for next step in management for MM is serum protein electrophoresis, since MM is a plasma cell neoplasm, it is a problem from bone marrow infiltration (fractures, hypercalcemia, anemia) and monoclonal protein production (renal insufficiency). Serum protein electrophoresis (SPEP) is a common screening test for MM and detect elevated serum monoclonal protein (M-spike).

Where is the stenosis/occlusion in subclavian steal syndrome?

In the subclavian artery itself! don't get off track and think yourself out of this one, it's that easy, the name indicates where the occlusions/stenosis is.!! Subclavian steal syndrome = severe atherosclerosis of the subclavian artery, proximal to the origin of the vertebral artery. The proximal subclavian has a stenosis/occlusion. So the distal subclavian will steal blood from the ipsilateral vertebral artery. Note: the Left subclavian is more commonly affect than the right because of the sharper curve and more turbulent blood flow, leading to atherosclerosis. Subclavian artery stenosis can be asymptomatic, or pts can have ischemia in the affected upper extremity (pain, fatigue, paresthesias). If there is concurrent atherosclerosis in the circle of Willis, pt may have vertebrobasilar ischemia (dizziness, ataxia, dysequilibrium). Exercising the affected limb may cause arterial vasodilation and further lowering of distal pressure, which may exacerbate vertebrobasilar symptoms. PhyEx often shows significantly lower brachial systolic BP (>15mmHg) in the affected arm and a systolic bruit in the supraclavicular fossa on the affect side. A 4th heart sound may be present d/t LVH from systemic HTN. Dx: made by doppler u/s or magnetic resonance angiography. Tx: lifestyle management (ex: lipid lowering interventions, smoking cessation) and sometimes stent placement.

Serosanguineous drainage and incisional pain from surgical site that may cause incisional separation and potential infection (bc can be nidus for bacterial growth). RFs for this include inadequate surgical hemostasis, obesity, hypo-coagulability. What is it?

Incisional hematoma. Tx: for large symptomatic hematomas, open the incision and evaculate the clot, and get hemostasis, and then re-close the incision.

What do you expect to see in hemolysis cause of anemia? (Ex: in pts with mechanical valve replacement but now has hemolysis and SOB and fatigue when climbing stairs or walking at fast pace... and Hgb of 7.1. LDH of 1,200)

Increased LDH (bc it's released from hemolyzed RBCs) Decreased haptoglobin (bc binding hgb released from hemolyzed RBCs) Increased indirect bili (d/t macrophage breakdown of heme) Note: thrombocytopenia may also be present d/t mechanical destruction of plts. Periperhal smear typically demonstrates RBC fragments and schistocytes. Note: you can distinguish mechanical prosthetic heart valve dysfunction that is leading to IV hemolysis that is causing hemolytic anemia from anemia d/t impaired RBC production or excessive RBC loss by looking at the LDH (which is increased only in hemolysis bc it's released from RBCs that are hemolyzed)

What do you expect to find on labs with HS?

Increased MCHC (since the RBCs are spherical), increased RDW, increased osmotic fragility on acidified glycerol lysis test (since they'll pop since they're spherical), and abnormal eosin-5-maleimide binding test.

Reasons for increased vs decreased MS-AFP

Increased MS-AFP -Open NTD (anecephaly, open spina bifida), ventral wall defect (omphalocele, gastroschisis), multiple gestations (pay attention to where the fundus is inches compared to weeks GA), and less commonly in fetal congental nephrosis and benign obstructive uropathy. Decreased MS-AFP -Aneuploidies (ex: Trisomy 18, 21)

When do you see Cysteine stones?

Increased excretion of cysteine, which is an inborn error of metabolism. (Positive family hx may be seen)

Why do pts with thyrotoxicosis (hyperthyroid) have HTN?

Increased myocardial contractility (note: it has nothing to do with catecholamines) Thyrotoxicosis causes positive inotropic and chronotropic effect, leading to hyperdynamic CV state characterized by tachycardia, systolic HTN, and widened pulse pressure. Arrhythmias are common and may include sinus tachycardia, a.fib, a. flutter, and atrial/ventricular ectopy. Valvular abnormalities like MVP and TR are also associated.

24yo with pressure-like substernal CP occurs with exercise, no other symptoms. just started working out to lose weight 6 months ago. Has murmur as child. BP uneven between left and right. Palpable thrill in suprasternal notch, loud midsystolic murmur best heard at 1st right ICS. Likely cause of chest pain?

Increased myocardial oxygen demand. Supravalvulvar aortic stenosis (AS) is 2nd most common type of AS, usually a congenital LV outflow tract obstruction d/t discrete/diffuse narrowing of ascending aorta. Causes systolic murmur similar with valvular AS but this murmur is best at FIRST right ICS, higher than where the valvular AS is best heard. So with the AS and increased oxygen demand during exercise, the subendocardial and myocardial tissue can get ischemic. So that explains anginal symptoms during exercise in a young pt.

What do you expect to see in a pt with Guillain-barre's CSF? Protein, WBC count, RBC count, glucose. Gold standard tx?

Increased protein (CSF protein level may be elevated bc of increased permeability to the blood-nerve barrier) bc otherwise everything else is normal. (bc i don't think the camplylobacter jejuni goes into your CSF bc it's not a meningitis disease.. but i guess it causes increased permeability of the blood-nerve barrier so more protein is in the CSF; elevatd protein with normal cell count is called "albuminocytologic dissociation") Gold standard tx: IV immunoglobulin or plasmapheresis. Monitor closely d/t risk for respiratory failure.

Side effect profile: Ziprasidone

Increased risk for QT prolongation; avoid in pts with conduction defects Memory tool: Q ZZZZZZZ T, prolonged QT interval with Ziprasidone

HIV pt with pneumonia, what do you think the most likely organism is?

Increased risk of community acquired pneumonia. Strep pneumo is most common implicated organism. d/t increased rats of colonization and impaired immunity against encapsulated bacteria.

Fasciculations

Indicates lower motor neuron damage

How do you identify atypical Mycoplasma pneumonia?

Indolent HA, malaise, fever, persistent dry cough. (just feel kind of crappy), pharyngitis (nonexudative sore throat), macular/vesicular rash -Highly infectious but minimally virulent Note: lower pulmonary sxs of dyspnea and wheezing can occur after several days. Dx: normal WBC ct, subclinical hemolytic anemia (cold agglutinins), interstitial infiltrate (on CXR) (so basically stem wilil show young guy who feels crappy, seems like he has pneumonia on CXR but his labs look pretty normal; his WBCs aren't elevated... so it doesn't seem too alarming... if you see that think about atypical pneumo and pick a Macrolide as the tx, Azithromycin!!)! Usually with young people in close quarters (school, military), in fall/winter spread by resp. droplets. Tx empiric tx with macrolides (AZITHROMYCIN) or respiratory fluoroquinolones. Note: mycoplasma pneumoniae does NOT have a cell wall so don't try to use penicillins or cephalosporins bc those act by inhibiting bacterial cell wall synthesis and so if there is no cell wall in this atypical cause of pneumonia, then that's a useless tx.

How do you read a TB skin test for different categories of people?

Induration is positive if: >5 mm - high risk pts >10 mm - mod risk pts >15 mm - low risk pts

What should you think about when distinguishing inevitable abortion from cervical insufficiency?

Inevitable abortion: when you have a dilated cervix (that's it, that's the difference between inevitable and threatened abortion, whether the cervix is dilated). Spontaneous abortions are <20 weeks GA so thats going to be in the 1st trimester Cervical insufficiency is 2nd trimester when the weight of the baby is too much for the incompetent cervix to handle. Note: if they have lower abdominal pain (from uterine contractions), then it's not cervical insufficiency.

What's the pathology in statin-induced myopathy and polymyositis?

Inflammation of muscle fascicles. Pt presents with proximal muscle weakness (ex: difficulty getting up form chair), mild tenderness of both upper and lower extremities.

What is tenosynovitis

Inflammation of the tendon and its synovial sheath. Usually seen in hands/wrist, often due to overuse or following a bite/puncture wound. Patients have pain and tenderness along the tendon sheath, particularly with flexion and extension movements.

What is Episcleritis?

Inflammation of the whites of the eyes (no involvement of the uveal tract) -Most associated with RA and inflammatory bowel disease.

What can high platelet count, ferritin, CRP or ESP indicate?

Inflammation/stress. These are all inflammatory markers: ESR, CRP, ferritin, high platelet count.

Associate spondylarthritis/sacroilitis (prolonged stiffness and low back and buttock pain that improves with activity) with what diarrhea problem?

Inflammatory bowel disease (IBD) IBD (Crohn's and UC) has extra-intestinal manifestations, including arthritis, eye (uveitis, episcleritis) and skin (pyoderma gangrenosum) involvement, and hepatobiliary disease (primary sclerosing cholangitis)

breast that is diffusely warm, red with dimpling, what are you thinking about?

Inflammatory breast cancer Edema, Redness, Peau d'orange (superficial dimpling, fine pitting), painful. Retracted nipple Enlarged lymph nodes (axillary LA suggests mets) May also be present: itching, palpable breast mass, nipple changes (flattening/retraction) Next step in eval: mammography and u/s. Tissue biopsy to confirm the dx.

What does infliximab treat? what class is it it?

Infliximab is a anti-tumor necrosis factor agent and treats rheumatoid arthritis, psoriasis, ankylosing spondylitis and Crohn's

Reheated rice and then pt starts having lots of episodes of vomiting and abdominal cramps. What is causing these symptoms?

Ingestion of preformed enterotoxin in the food. -Bacillus cereus enterotoxin (likes to grow in starches like rice that is reheated or left at room temperature for extended periods of time. Vomiting usually started within 1-6 hours of ingestion. Usually self limiting and resolves completely in 1-2 days.

What is induction therapy?

Initial dose of tx to rapidly kill tumor cells and send the patient into remission (<5% tumor burden). Ex: induction chemotherapy for acute leukemia.

What's are 2 meds you can use to temporarily lower serum K by driving K into the cells? Used to treat hyper-kalemia.

Insulin & Albuterol (selective beta-2 agonist )

INSULIN RESISTANCE TYPICAL FOR PTS WITH CENTRAL-TYPE OBSEITY IS KEY PATHOGENIC FACTOR IN DEVELOPMENT OF T2DM AND ASSOCIATED ABNORMALITIES (HTN, DYSLIPIDEMIA)

Insulin resistance!!! <-- key pathogenic reason for metabolic syndrome (HTN, impaired fasting glucose, dyslipidemia)

46 yo obese man with hx of T2DM and HTN, now with acanthosis nigrans and hepatomegaly. He's been obese since he was a teenager. He doesn't drink or use any elicits substances. He has sensation of RUQ fullness. Labs show: AP 100, AST 122 (high), ALT 131 (high) and fasting BG (168). Viral hepatitis serology, antimitochondrial antibodies, antinuclear antibodies, serum ceruloplasmin, and transferrin saturation are normal. What is likely the pathophysiologic mechanism for this pt's increased liver enzymes?

Insulin resistance. He's got hepatocellular injury even though he doesn't have viral hepatitis or an autoimmune disease, meaning he has non-alcoholic fatty liver diseae (NAFLD). These people are usually middle-aged, obese, and have metabolic syndrome (central obesity, HTN, DM, HLD). NAFLD can range from bland steatosis to inflammation and necrosis (steatohepatitis) to fibrosis and cirrhosis. NAFLD is d/t increased transport of FFAs from adipose tissue to the liver, decreased oxidation of FFA in the liver, or decreased clearance of FFA from the liver (bc of decreased VLDL production). It's frequently related to peripheral insulin resistance leading to increased peripheral lipolysis, triglyceride synthesis, and hepatic update of fatty acids. Think about this person with metabolic syndrome. and now he has increased AST and ALT. The AST/ALT ration is <1, indicating steatohepatitis. Treat with diet and exercise, and if their BMI >35, think about bariatric surgery.

What is Lichen sclerosus?

Intense burning, itching with "cigarette paper" skin around the introitus and perianal skin, sclerosis (ex: retraction) of normal anatomical markers of the genitals.

What is the most appropriate next step in the management to alter the course of a pt's diabetic nephropathy? He has uncontrolled DM and HTN and proteinuria.

Intensive BP control. The most beneficial tx to reduce the progression of diabetic nephropathy is strict blood pressure control. Pt with diabetic nephropathy should be treated toward a target BP of 130/80!!!!! BP CONTROL TO MANAGE DIABETIC NEPHROPATHY!!!! - best choice is manage the BP.

What are the symptoms of carcinoid syndrome? Initial dx test? Tx?

Intermittent diarrhea. Flushing Wheezing Cardiac abnormalities on right side of the heart. Initial test: urinary 5-HIAA Tx: Octreotide is a synthetic somatostatin (-eotide) and it helps control the diarrhea (intermittent diarrhea with carcinoid syndrome)

Pure motor deficit in lacunar stroke, what part of brain likely affected?

Internal capsule Picture: driving (motor) and you've got a helmet (capsule) on.

What causes alveolar spaces filled with fibroblasts?

Interstitial lung disease (ILD) PFTs: should show restrictive pattern with FEV1 <80% & low FVC & normal to high FEV1/FVC ratio Would also see reticular opacities on CXR

58yo man presents with skin discoloration, anorexia, unintentional wight loss (13lbs) over the last 3 months. His urine is dark and stools are pale. He has scleral icterus. Gallbladder is enlarged, nontender and palpated below the right costal margin. No abdominal pain. What do you think imaging would reveal?

Intra- & extra-hepatic biliary tract dilation. This pt most likely has pancreatic cancer. Most are at the head of the pancreas. These tumors expand and compress the pancreatic duct and CBD (leading to painless jaundice) and sometimes you see the "double duct sign" on imaging. The bile backs up and leads to intra- and extra-hepatic biliary duct dilation and a non-tender, distended gallbladder at the right costal margin (Courvoisier sign). Jaundice can also --> pruritis, pale stools, and dark urine. Note: cancers in the body or tail of pancreas usually present with abdominal pain without jaundice. Remember that pt from wilmington that came in with painless jaundice and we were worried she may have pancreatic cancer.

Pt has Allergic Rhinitis (runny nose, nasal congestion, sneezing, nasal itching, cough 2/2 postnasal drip, eyes itchy and tearing, allergic shiners (infraorbital edema and darkening), allergic salute (transverse nasal crease), pale/blue/enlarged turbinates, pharyngeal cobblestoning, allergies facies (high arch palate, open mouth breathing). What kind of meds do you give them?

Intranasal corticosteroids (nasal sprays like fluticasone and memetasone... the -sone endings are steroids) are the single more effective agents -initial response see within hours of administration but max benefit may require continuous tx for several days or weeks. Also, avoid the allergens.

What is trichiasis?

Inversion of the eyelashes. Can lead to repeated or chronic infection --> scarring of eyelids --> ulceration & blindness.

Pt undergoes AAA repair and postop has LLQ abdominal pain and bloody diarrhea. CT abdomen shows thickening of colon at rectosigmoid junction. Colonoscopy shows ulcers in the same area and the colon above and below the lesion is completely normal. What is the likely cause of these sxs?

Ischemic colitis s/p AAA repair! -rectosigmoid area is a watershed area more vulnerable to ischemia. CT will show colon wall thickening and fat stranding and endoscopy will show edematous, friable mucosa. -Management: IV fluids, bowel rest, Abx with enteric coverage, colonic resection if necrosis develops.

What is the complication of Isoniazid that I should know related to the liver?

Isoniazid can cause idiosyncratic liver injury with histo findings similar to those seen in pts with viral hepatitis (but the Hepatitis panel will all be negative)

First line treatment for Beta-blocker overdose? Bradycardia, hypotension, ***wheezing***, hypoglycemia, delirium, seizures, cardiogenic shock.

Isotonic IV fluids and atropine are fist line tx options. IV Glucagon should be given to pts with profound or refractory hypotension.

What s the only crystalloid solution you can give for IV fluid resuscitation in kids?

Isotonic cyrstalloid. So pick 20mL/kg of NS IV

What happens if you have hypertensive hemorrhage in the cerebellum?

It can push the cerebellum through the FORAMEN MAGNUM --> cerebellar tonsillar herniation. S/sx: neck tilt, flaccid paralysis, coma, BP instability, respiratory arrest

What is Beta-interferon used for (med)?

It's a disease modifying drug used for chronic maintenance for pts with MS. IT can decrease the frequency of relapses and reduce the development of brain lesions.

What is oral Leukoplakia?

It's a mucous membrane disorder that presents as white patches or plaques over the oral mucosa that usually cannot be scraped off. The RFs for developing this are similar to those for SCC (tobacco - esp smokeless like chewing tobacco - and alcohol use). This is a reactive pre-cancerous lesion that represents hyperplasia of the squamous epithelium. 1-20% of these lesions will go on to progress to SCC in 10 years. Fortunately, most resolve if you stop using tobacco. If there are ulcers or indurations, need to rule out malignant transformation of this lesion.

What is albuterol's relationship with K?

It's a selective beta-2 agonist. It is used to LOWER serum potassium by driving K into the cells. (Remember that like insulin, albuterol is a quick way to push K into the cells to manage hyper-K quickly)

26 yo with 1 episode of seizure. 2 days of fever and HA. NSAIDS don't provide relief. She starting acting strangely today. Temp 102. HR 110. RR 18. Lethargic, confused, hyper-reflexia. CBC and CT Head unremarkable. CSF shows: normal opening pressure, Increased protein (100), normal glucose (55), increased WBC (150), Lymphocyte predominance (90%), and increased RBC (200). Most likely dx?

It's a virus. bc of Lymphocyte predominance (virus), elevated protein (virus is in there) but normal glucose (so not eating up the glucose). The fact that there are RBCs points towards hemorrhage, and the one virus I know can cause hemorrhage causes temporal hemorrhage --> HSV encephalitis. Note: MRI is generally preferred to CT bc CT can be normal in up to 50% of patients even though herpes encephalitis is the most common cause of fatal sporadic encephalitis in the USA. Presentation: acute onset (<1 week duration) of focal neurologic findings (AMS, FND, ataxia, hyper-reflexia, focal seizures). Fever in 90% of pts. Behavioral changes (hypomania, Kluver-Bucy syndrome - hyperphagia, hypersexuality - and amnesia) Dx: Gold standard is PCR analysis of HSV DNA in CSF (highly sensitive and specific) - has replaed brain biopsy. -MRI preferred over CT (which can shows normal in 50% pts); but should show temporal lobe lesions -Focal EEG findings of prominent intermittent high amplitude slow waves occur in >70-80% of patients and can be used as corroborative evidence of herpes encephalitis. Tx: IV acyclovir (tx of choice)

How does fat necrosis of the breast present?

It's benign. presents post trauma or surgery with firm, IRREGULAR mass, +/- ecchymosis and skin/nipple retraction.

When would you suspect conus medullaris syndrome?

It's similar to cauda equina syndrome (CES), but instead the pt has early onset bowel/bladder disturbance Numbness confined to the perianal area Symmetric motor weakness (vs: asymmetris in CES) Hyperreflexia (since it's UMN lesion) (vs hyporeflexia in CES since it's spinal nerve root lesions)

Non-white male starts TMP-SMX (sulfa drug) 4 days ago and then has 1 day of fatigue, sudden onset back pain, and dark urine. There's conjunctival pallor, hemolysis (Hgb 7.5, Tbili 3.5, Dbili 0.8 so it's mostly direct bili = hemolysis, decreased haptoglobin, increased LDH) and bite cells. G6PD activity assay is WNL. Why?

It's still dx of G6PD deficiency. -hemolytic anemia s/p oxidative stress (here it's sulfa drugs, also infection and fava beans can dod it). -usually seen in men bc X-linked (Asian, African, Middle eastern descent) -G6PD deficiency may be normal during attack so check it in 3 months after an attack. (Most RBCs that are severely G6PD deficient are hemolyzed early in a hemolytic episode and reticulocytes, which hae normal G6PD levels are circulating at abnormally high levels. So it may appear that G6PD is normal during an acute attack when the pt is in-fact G6PD deficient)

Preconception counseling for couple who has mediterranean ancestry. Pt's mother and sister have anemia. What is the initial screening test for thalassemia anemia for this pt?

Just get her CBC and look for anemia and decreased MCV. However, if that is normal, then you're good. stop there, no further testing needed.

75 yo man w/ progressive hearing loss & ringing in his ears. Decline in ability to hear social conversations, esp with competing background noise. Difficulty tolerating loud sounds others in the room can handle. Subjective continuous high-pitched ringing in both ears. No vertigo or disequilibrium. Weber & Rinne shows BL sensorineural hearing loss. Otoscopic exam and auscultation over both periauricular areas unremarkable. Neuro exam normal. What is the dx?

Just hearing loss of old age. So presbycusis Think about grandpa not being able to hear in a loud room (like in a coffee shop) but when your'e at home and you talk with him one-on-one, he can hear you well. He's got ringing in his ears and can't tolerate loud sounds, "he's sensitive" - think sensorineural hearing loss. - Presbycusis.

multicentric, red/purple/brown macule/plaque/nodule on the trunk/extremities/face in a immunocompromised (ex: AIDS) patient.

Kaposi Sarcoma, due to HHV8.

Pt with rheumatic fever Mitral stenosis now has A.fib (irregular irregular heart rhythm with absent P waves), what is causing the abnormality?

LA dilatation. (Think about the pulmonary veins - which we think is where the A.fib comes from - are all stretched and weird with MS causing blood to back up into the LA so the LA get all dilated, causing the A.fib.) Pressure in the LA can be greatly elevated in order to compensate for the high resistance of the stenotic mitral valve. This cuases the LA to dilate, which predisposes to the development of A.fib. (~70% of pts with MS develop A.fib; A. fib causes a lack of "atrial kick" which could cause worsening flow through the stenotic mitral valve and increased congestion in the lungs, thus leading to the patient's acute onset of dyspnea. Auscultation: Loud S1 and mild diastolic rumbling murmur at the apex - classic for mitral stenosis.

What lab studies are consistent with acute liver failure?

LIVER: prolonged PT (means synthetic function is affected) with INR > 1.5 Acute liver failure is characterized by triad of: elevated aminotransferases, hepatic encephalopathy, and prolong PT (INR >1.5) without underlying liver disease (aka no cirrhosis). -So basically your AST & ALT go up all of a sudden and affect your mentation (somnolence, disorientation, asterixis), and then your synthetic function is also affects so PT prolongates. Note: acute renal insufficiency with elevated Cr can happen in up to 70% of ALF cases and is likely d/t decreased renal perfusion (and direct renal tubular toxicity if there is Tylenol OD) but it points to the kidnyes, and is not specific for acute LIVER failure.

Post MI (up to 3 months) and pt starts throwing arterial clots, what are you thinking they have?

LV aneurysm

Common complications after acute MI and their timelines

LV aneurysm: 5 days - 3 months (think about as late complication, think of this if pt starts to throw arterial clots) Pericarditis: 1 days - 3 months (think of this as late complication) Papillary muscle rupture: 2 days - 1 week Post-infarction angina: hrs - 1 month Fee wall rupture: hrs - 2 weeks Ventricular septal rupture: hrs - 1 week Re-infarction: hrs - 2 days.

What enzyme does someone with lactose intolerance lack? What does that enzyme usually do to the lactose?

Lactase; brush border enzyme that hydrolyses lactose.

What kind of infarct makes neurologic deficits over min-hrs and symptoms follow a stuttering course?

Lacunar infarcts.

Pt has stroke symptoms that are pure motor hemiparesis, or pure sensory stroke, they have ataxic hemiparesis, or they have dysarthria & a clumsy hand. But they don't have any cortical signs (like aphasia, agnosia, neglect, apraxia, hemianopia), seizure, or mental status changes (stupor, coma). Hx of HTN (or DM, older age, increased LDL, or smoking). What is the most likely cause of the pt's symptoms? What areas does it affect?

Lacunar stroke aka hypertensive vasculopathy. Small penetrating artery occlusion d/t hypertensive arteriolar sclerosis. Affects: basal ganglia, subcortical white matter (ex: internal capsule, corona radiata), pons.

What is it when they say "episode of fetal HR decreased to 120/min that began after the peak of contraction and lasted for a minute"

Late deceleration = placental insufficiency (esp. suspect this if it's a late term (41 wks GA) or post-term (42 wks GA) pregnancy; or if there is also evidence of oligohydramnios on the BPP (amniotic fluid index < 5cm and the deepest vertical pocket is <2 cm on u/s) VEAL CHOP

Good prognosis features for schizophrenia?

Late onset, rapid course, positive sx (rather than the negative sx), absence of family hx, lack of structural brain abnormlaities So the positive symptoms are a good prognosis for schizophrenia, whereas the negative symptoms are bad prognosis for schizophrenia

Where do you expect to find pain with iliotibial band syndrome? What causes it?

Lateral knee. It's an overuse injury with pain at the lateral knee. Exam shows tenderness at the lateral femoral condyle during flexion & extension.

What position do you put a pregnant woman in to displace the uterus off the aortocaval vessels and maximize cardiac output?

Left lateral decubitus position (think about my bed... and if anthony were with me and I were preggers, then i have to lie on my left side to hit the snooze button on the night stand.. left lateral decubitus position)

Cataracts are opacification of what structures?

Lens opacification

When pt has Parkinsons or Huntingtons disease, and they have EPS signs (rigidity, bradykinesia, tremors, chorea), where is the pathology of that?

Lesions of the subcortical nuclei (basal ganglia) --> EPS signs.

Hypomania:

Less severe than mania, change from baseline but does not markedly impair pt's social and job functioning. Sxs not bad enough that you would hospitalize them. Not quite one week, but more than 4 consecutive days. ("only a few days") NO psychotic features. Bipolar II is defined as hypomania and MDD (need at least 1 episode of each to dx bipolar II) Hypomania is less severity and functional impairment than mania (bipolar I)

What do you expect to see on urine dipstick for positive UTI? What do they present?

Leuk esterase & Nitrites Leuk esterase: indicates pyuria (since it's WBCs) Nitrites: signifies presence of Enterobacteriaceae, which converts urinary nitrates into nitrites. (most likely UTI organism is E.coli)

Pt with massive hemorrhage gets 2units pRBCs and 2 hours later, gets fever, chills and malaise. You stop the transfusion and they get better in 6 hours. What could have prevented this reaction?

Leukoreduction: He has febrile nonhemolytic transfusion reaction, the most common adverse reaction that occurs within 1-6hrs of transfusion. When red cells and plasma are sepaated from whole blood, small amounts of residual plasma or leukocyte debris may remain on the red cell. During storage, the leukocytes release cytokines that can also be transfused to the patient --> transient fever, chills, malaise without hemolysis. Stop the transfusion, give antipyretics, and leukoreduce blood products in the future. (Note: also reduces risk of HLA alloimmunization and transission of CMV that typically resides in leukocytes).

Patient with purple, flat-topped papules or plaques that are pruritic, planar, and polygonal. Common occur on flexural surfaces of the extremities, trunk, and genitalia. What is that?

Lichen planus (the P's). Purple, Papule, Plaque, Pruritic, Planar, Polygonal, can be on Penile (genitalia), otherwise on flexural surfaces of extremities and trunk.

Young pt with chronic LBP that is worse at night but improves with physical activity. You are thinking inflammatory spondyarthritis (ankylosing sponydlitis, psoriatic arthritis, reactive arthritis, or arthritis associated with IBD). The spondyarthropathies are immune-medaited d/os that are most common in pts <40yo and affect sties of ??

Ligamentous insertion (enthesitis)!! leading to gradual onset of LBP and progressive stiffness. AS eventually leads to destruction of the articular cartilage, esp at the SI joints and apophyseal joints of the spine So the question could describe a pt with AS and ask what most likely accounts for his symptoms, and the answer would be "inflammation at ligamentous insertions"

When do you see spur cells (acanthocytes), irregularly sized and spaced projections on RBCs

Liver disease

When do you see Burr cells (echinocytes), spiculated RBCs with serrated edges?

Liver disease and ESRD. (liver and renal disease (end stage))

How do you treat Gastrinomas (Zollinger-Ellison Syndrome)?

Local disease, just cut it out (surgical resection) Metastatic disease: unresectable and treated with lifelong PPIs to block acid production (since that's what gastrinomas do, they create too much acid... that causes ulcers)

What should you know about candida when you are evaluating it, what should you find?

Location: intertrigous regions (under breasts, axillae, groin, fat folds) Usually caused by candida (but can be caused by other organisms like staph aureus) Risk factors: -Obesity: friction/ribbing cause skin barrier to break down -Moisture: occlusive clothing, high heat/humidity -HIV/Glucocortoid therapy: impaired immune function -DM with hyperglycemia: local environment conducive to microbial growth. See red plaques on symmetric "kissing" pattern across skinfold. Candida intertrigo forms satellite lesions (vesicles, papules, pustules) near the primary infection. Dx: based on clinical features, and KOH prep or fungal cultures of skin scrapings can confirm the dx. -See PSEUDOHYPHAE with BUDDING YEAST FORMS (blastoconidia) Tx: topical antifungals (nystatin, miconazole) with good skin hygiene and measure to keep affected area dry.

Features of Borderline personality disorder?

Long standing pattern of identity disturbance, mood liability, recurrent suicidal and self-mutilating behavior, abandonment fears.

Non-compliant schizophrenic patient, what IM meds can you chose?

Long-acting antipsychotics (SGA) -Ex: Risperidone, Paliperidone are the 1st line treatment Note: Haloperidol (FGA) and fluphenazine (FGA) are still used but they have more side effect, so if given the option, chose SGAs.

62yo pt with normal S1 and S2, with a 4th heart sound (S4) just before S1, and pt has DOE. What likely explains these findings? (TEN-nes-see)

Longstanding HTN S4 in adults indicates a stiff left ventricle, occurs bc of restrictive cardiomyopathy of LVH from prolonged HTN. S4 is atrial contraction, occurs at end of diastole, its the sound from blood striking a stiffened left ventricle. Exertional dyspnea + S4 sound likely means diastolic HF from long standing HTN causing LVH. Note: S3 vs S4 S3 (ken-tuc-KEY) is sigh of LV failure (sloshing blood) S4 (TEN-nes-see) is sight of stiff left ventricle (stiff heart)

Case control studies:

Look at Diseased and non-diseased control CASES and compare what their RFs were (compared RF frequency)

If the vignette has a pt with both COPD descriptions and hx of Asbestos exposures (Ex: shipyards), then how do you tell if their lung disease is from COPD of Asbestosis?

Look at the FEV1/FVC COPD will be obstructive pattern so FEV1/FVC < 70 Asbestosis is restrictive lung disease, so FEV1 and FVC will both decreased, so there will be a normal FEV1/FVC ratio (and low DLCO bc the lung has fibrosis and so gas can't exchange well)

s/sx Rett syndrome

Loss of communication skills (with previously normal baby girl), deceleration in head growth, hand clapping without evidence of purposeful movement, and gait abnormalities. -Usually normal development for the first 6 months but may ahve deceleration of head growth prior to this point. Loss of communication and fine motor skills follow around 12-18 months and may be sudden or slow in onset. -Stereotypical hand movements: hand-to-mouth licking or hand clapping, autistic features (lack of eye contact and social reciprocity, restricted interest), sleep disturbance (waking up crying or screaming), seizures (remember that little girl would curl up to her mom and seize), gait disturbance, periodic breathing abnormalities common sign. Mutation: MECP2 gene.

What is going on in Narcolepsy? Features? Treatment?

Loss of hypocretin leads to inability to regulate sleep. Features: sleep attacks (irresistible sleepiness and refreshed on waking), cataplexy (cata- means "down" so... loss of o muscle tone - considered pathognomonic; loss of tone/cataplexy may be preceded by loud noise or emotions), Hypno-go-gic and hyponopompic hallucinations, sleep paralysis (usually on awakening, pt can't move but is awake) Decreased REM latency (falls asleep fast; < 8 minutes), at least 2 sleep onset rapid eye movement periods (SO-REM-Ps), true Cataplexy (loss of tone) is pathognomonic for Narcolepsy Tx: manage with forced naps during the day. -Modafinil: used to maintain alertness -Methylphenidate and dextroamphetamine can be used -Gamma-hydroxybutyrate (GHB) given at bedtime to induce sxs of narcolepsy in attend to contain them at night

What do you expect to find in neurogenic shock?

Loss of vagal tone. CNS injury --> reduction in SVR. Bradycardia bc of impaired sympathetic response and no underlying infection.

Trisomy 18, what do you find with MSAFP, estriol, beta-HCG, and inhibin A?

Low MSAFP, very low estriol, very low beta-HCG Normal Inhibit A levels.

How does Hypothryoidism affect FSH and LH?

Low T3/T4 increases TRH via feedback mechanism. Increased TRH stimulates prolactin to increase, that has in inhibitory effects on GnRH, which then decrease FSH And LH.

When would you see: Low LH, Low T, low DHEAS?

Low androgen with low LH level is hypopituitarism with hypogonadotrophc hypogonadism, which can cause amenorrhea but would have other manifestations of ovarian insufficiency (hot flashes, vaginal dryness).

Side effect profile: Quetiapine

Lower incidence of mvt disorders; appropriate use for pts with existing movement disorders Memory tool: think.. you're "quiet" if you don't move... so Quetiapine doesn't cause movement disorders as much so appropriate to use in pts who have movement disorders

How do you distinguish between a pt with pre-eclampsia and lupus nephritis (since both present with edema, HTN, and proteinuria)?

Lupus nephritis will have associated s/sx of SLE (joint pain, malar rash) and have RBC casts on UA. (THIS IS A BIG CLUE, bc pre-eclampsia doesn't have RBC casts) You'll also see DECREASED COMPLEMENT LEVELS AND INCREASING ANA or Anti-DS DNA TITERS!!! YOU CAN TELL IF SLE PT IS HAVING A FLARE BY LOOKING AT HOW MUCH THE COMPLEMENT LEVELS DECREASE. And ANA or Anti-DS DNA will rise during a flare. so if those things are happening, you can say with confidence that it's a lupus flare.

pt has swelling and redness on the forearm and you see a red streak extending from forearm to elbow. Epithrochlear lymph nodes are enlarged. Exam of distal radial aspect of the right upper extremity has an 8x13 cm warm, erythematous area of edema that is tender to palpation; there is warm, tender red streak extending from this area to the elbow. No wound, ulcer, fluctuance, or palpable cord. Whats the likely dx?

Lymphangitis (think about lymphangitis when they mention enlarged lymph nodes... and this is in the upper extremities.. vs when you think about superficial thrombophlebitis, think about the lower extremities)

What is this a description of? Small and shallow ulcers, Large, painful, coalesced inguinal lymph nodes ("buboes")*** Intracytoplasmic chlamydial inclusion bodies in epithelial cells and luekocytes Initial lesion Not painful

Lymphogranuloma vernereum (Chlamydia trachomatis)

What are features of methanol poisoning aside from AG metabolic acidosis?

M for Methanol (think of the M as two arrows pointing up towards your eyes so Methanol poisoning damages the eyes): -Blurred vision -Hyperemic optic disc -Epigastric pain/Vomiting

HIGH YEILD: Major toxicity for mycophenolate (reversible inhibitor of inosine monophosphate dehydrogenase IMPDH, the rate-limiting enzyme in de novo purine synthesis)

M or mycophenolate and bone Marrow suppression. Major toxicity for Mycophenolate is bone Marrow suppresion

Pt in hypertensive emergency, at what rate do you want to lower their BP

MAP should be lowered by 10-20% in the 1st hour Then another 5-15% over the next 23 hours. IF you drop the BP too quickly, they can get cerebral ischemia with AMS and/or generalized seizure. So basically in the first day, you can lower his BP by max of 35%. Drop from in the first 24 hours from 220 to 176 is fine.

77yo F bought in by daughter. She's feeling progressively tired and weak. Hx of breast cancer with treatment (surgery, radiation, chemo 15 years ago). She has mild anemia. Takes a daily multivitamin. No LA. Labs show anemia (MCV 108), low plt, low leuks (so all 3 are low) There are some precursor cells seen as well... including 1% blasts. Peripheral smear shows PMNs with decreased segmentation and decreased granulation. What is the most likely dx?

MDS (myelodysplastic syndrome) - pancytopenia DESPITE hypercellular marrow. -Suspect MDS in pt >60yo with previous chemo/radiation, with pancytopenia (all 3 cell lines are down). This is a pre-leukemia disorder. Most pts don't develop AML bc complications of bleeding and infection get them first (dead). -the anemia is a macrocytic anemia and this is also related to the sideroblastic anemia... the only way sideroblastic is macro-cytic anemia is with MDS, and the RBCs are also nucleated. (Remember that MDS is a macro-cytic anemia.. since it's the M in the high MCV mnemonic: "Fat Men Always Have Lunch, Meds, and Cold Sandwiches: Folate/B12, MDS, Alcoholism, Hypothyroid, Liver dz, Meds (AZA, 6MP, Hydroxyurea, Zidovudine, Phenytoin), Cold agglutinins, Siderblastic) -the PMNs count is down, and the segments in them are also down. (Pelger-Huet cells are the most distinct lab value of MDS: the HYPO-segmented/bi-lobed PMNs) -There are small number of blasts. Note: the severity of MDS is based on the percentage of blasts. Usually present with asx pancytopenia on routine CBC. Sometimes there's splenomegaly. Peripheral smear: has dysplastic red cell (ovalmacrocytosis) and granulocytes (reduced segmentation - Pelger-Huet). Dx: BM biopsy needed to dx. Tx: -Transfusion -Epo -Azacitidine or decitabine (to decrease transfusion dependence and increase survival) Memory tool: "Lena, lend me 5 quid!, I lost (deleted) mine!" -Lenolidomide to tx pts with 5q deletion in order to decrease transfusion dependence. has excellent response in those with 5q deletion. -BMT for pts <50 yo.

What is the mutation that causes MEN1?

MEN1 is also the name of the mutation

Make sure I know the MENs before walking into the exam.

MEN1 is the Ps straight down: Pituitary tumors (prolactin, visual defects, acromegaly from GH producing pituitary adenoma) , Pancreatic tumors/GI (gastrinomas), Parathyroid (primary hyperparathyroidism; hypercalcemia) MEN2A: Medullary thyroid cancer (calcitonin), Pheochromocytoma, Parathyroid hyperplasia MEN2B: Medullary thyroid cancer (calcitonin), Pheochromocytoma, Marfanoid habitus/Mucosal neuromas

PAD is a strong predictor of what?

MI 20% 5year risk of nonfatal MI and stroke 15-30% reisk of death from CV cause.

Pt has B-12 deficiency (with all the symptoms of symmetric polyneuropathy, degeneration of dorsal spinal column --> numbness, paresthesias, impaired proprioception/vibration sense, gait ataxia). What lab value do you expect to be elevated in this patient?

MMA! (Methylmalonic acid should be elevated in B12 deficiency; that's the more sensitive test to do, more sensitive than detecting serum vitamin levels alone)

Optic neuritis is an inflammatory demyelinating disease with acute or subacute painful vision loss with abnormal pupillary response to light in the affected eye. Usually associated with what condition?

MS

32 yo female with moved to Arizona in the summer to take care of her mom. Now has paresthesias, occasional HA, dizziness, fatigue, poor sleep, blurry vision. Decreased sensation & pain n BL distal upper extremities. Right optic disc hyperemic and swollen. What do you think she has? what is the next step?

MS, get MRI of brain/spine. -T2 weighted imaging shows multifocal, ovoid, subcortical hypo-/hyper-intense lesions in the white matter, particularly the periventricular and subpial white matter of the cerebrum (corpus callosum), optic nerves, brainstem, and spinal cord. (If you are not sure of the dx, you can get LP after you do the MRI to document oligocloncal IgG bands in the CSF) MS symptoms: onset 15-50, optic neuritis, Lhermitte sign (sensation of electric shock that goes down back with neck flexion), internuclear ophthalmoplegia, fatigue, heat sensitivity (Uhthoff phenomenon, symptoms started after she moved to Arizona in the summer and had exposure to high temperatures - heat sensitivity), paresthesia, paraparesis/spasticity, bowel/bladder dysfunction.

What heart problems do you expect in Marfan pts?

MVP (mid-systolic click murmur) AR (early diastolic decrescendo murmur best heart at LSB at 3rd or 4th ICS with pts sitting up, leading forward and holding the breath after full expiration)

What is the most common cause of chronic severe MR in developed countries? & would show up as displaced apical impulse, holosystolic murmur, and 3rd heart sounds.

MVP: most common cause of MR in developed countries. mPV happens bc of myxomatous degeneration of mitral valve leaflets and chordae and causes the Mid-systolic click followed by mid-to-late systolic murmur. As the severity of the leaflet dysfunction and MR worsens, the murmur becomes holosystolic and the click may no longer be audible. 3rd heart sound is from LV volume overload and does not necessarily represent CHF. Chronic severe MR can cause LA dilation, which eventually leads to a.fib (symptoms of palpitations) TL:DR: Findings of displaced apical impulse, holosystolic murmur, and 3rd heart sound: all represent MVP --> chronic severe MR. Stem: 38yo F with occasional palpitations, fast/irregular heart beat, 3 episodes in last 2 months, each lasting about 2 hours. & you have the physical exam findings above. Most common cause of MR is MVP that has been really chronic and severe (so myxomatous degeneration of the mitral valve). -Note: Rheumatic heart disease can also cause MS, MR, and AR, but it is much less common cause of chronic MR than MVP.

What are 2 Abx meds that can cause cholestasis and so shouldn't be used in neonates who are at high risk of developing cholestasis?

Macrolides & Ceftriaxone.

Loss of central vision, think about

Macular degeneration

Elderly (67yo) pt has progressive visual loss in right eye over several months. He's asked to cover his left eye and look at a small spot on a grid of vertical and horizontal lines. He describes the vertical lines as being bent and wavy. What is this likely due to?

Macular degeneration Visualization of straight lines is a task that requires fine visual acuity, which is controlled primarily by the centrally-located macula.

HIGH YIELD Majority toxicity for azathioprine (purine analog that is enzymatically converted to 6-mercaptopurine. Acts primarily by inhibiting purine synthesis)

Major toxicity of azathrioprine is: gut, blood & liver. -dose-related diarrhea, leukopenia, and hepatatoxicity

How do you tell the difference between malignant (necrotizing) otitis externa that is d/t pseudomonas infection and needs IV cipro. vs cholesteatoma, the keratinized epithelial growth in the middle ear that needs surgical management?

Malignant otitis externa is more likely in pt with severe pain (one sided ear pain that is unrelenting and esp. sever at night and worse with chewing), fever, and elevated ESR.

What is the self limited esophageal tear associated with vomiting? What is the associated location?

Mallory-Weiss tear. It's self limited bc it's an incomplete mucosal tear. usually at the gastroesophageal junction due to protracted vomiting (think mallory-weiss is a hyphenated name... and so it's location is at a "junction" which is also kind of like a hyphen... so at the gastroesophageal junction is mallory-weiss tears) .

54yo postmenopausal woman you feel a breast mass, her mammogram 6 months ago with normal. What do you do next?

Mammogram again. (breast cancer is common in post-menopausal women so need evaluation of this new mass. Mammogram is gold standard and first-line modality even if recent mammogram was negative. Still get the mammogram no matter how recent a prior negative mammogram was)

How does Toxoplasma encephalitis present and what does it look like on MRI?

Manifests when HIV+ pt's CD4 count is <100. Symptoms of HA, confusion, fever, FND, and seizures. Imaging: multiple ring-enhancing lesions on MRI.

Uterine inversion, what do you need to do right away?

Manual replacement of the uterus. -If the placental is still attached, leave it attached. Put the uterus back in place first bc if you take the placental off, you are risking massive hemorrhage since the uterus is still inverted and wouldn't be able to clamp down. If you need you can use uterine relaxants (nitroglycerine, terbutaline) to help you if the initial attempt is not successful. DO NOT give uterotonics before replacing the uterus since that could make uterine replacement impossible to do.

Pt between age 40-60 who has disorientation and memory loss, but the prominent change is a personality change and loss of social restraints. Eventually, that patient will have profound dementia and become mute, immobile, and incontinent. What do you expect to see on this patient's CT Head?

Marked atrophy of frontal and temporal lobes. when personality change and social inhibition are the main symptoms, you are thinking this is ***Frontotemporal dementia***

Which thyroid cancer has (parafollicular) C-cell Calcitonin levels as marker?

Medullary Thyroid cancer (part of the MEN2A & 2B, with the RET oncogene picture)

Mass in the cerebellar vermis in a peds patient and presents with ataxia, truncal instability from hydrocephalus, and mass effect.

Medulloblastoma

Symptoms of B9 (folate) deficiency

Megaloblastic anemia Hypersegmented PMNs

What is this? (pic) Discoloration of right index fingernail. The discoloration has been there for 10 months and has progressively enlarged. Not sure if he injured his nail at work. 25 year pack year history.

Melanoma arising from nail matrix. Don't ignore a enlarging pigmented nail lesion. Nail melanomas are long bands in the nail plate (longitudinal melanonychia) d/t the presence of pigment int he nail as it grows outward. Unpigmented melanomas can also occur and present as nodules or irregularities int he nail plate. Longitudinal melanonychia that involves multiple nails, is stable over years, or is <3 mm wide is usually benign and may be observed with regular follow up. However, lesions that are large, have indistinct borders, change appearance over time or extend into the nail folds suggest possible MELANOMA!!!

What if you have an older, fragile patient with MM that can't handle adverse effects of dexamethasone (glucocorticoid) with chemo (lenalidomide, bortezomib)? What do you treat that patient with?

Melphalan (think Mel is a frail/"phal" old guys, Melphalan for fragile older pt with MM)

Mesangial hypercellularity suggests what kidney problem?

Membranoproliferative glomerulonephritis (most commonly presents with nephritic syndrome rather than nephrotic syndrome; so not as much proteinuria and more hematuria)

Thickened basement membrane and subepithelial "spikes" is pathonomonic for which kidney problem?

Membranous glomerulonephritis (most common nephrotic syndrome in adults)

Cutaneous Systemic Scleroderma: If you start seeing a pt with systemic scleroderma and the have sudden HYPERTENSIVE CRISIS are hemolyzing, think about: -Scleroderma renal crisis can occurs in 1st 5 years of SSc dx. Likely mechanism: increased vascular permeability, activation of coag cascade, increased renin secretion. Pts typically develop suden onset renal failure (w/o previous kidney diseae) and malignatn HTN (HA, blurry vision, nausea). UA can be normal or show mild proteinuria.. Peripheral blood smear can show MAHA (similar to HUS or TTP) or DIC with fragmented RBCS (ex: schistocytes) and thrombocytopenia What are their normal SSc sxs?

Memory Tool: CREST for systemic sclerosis. Calcinosis - calcium deposist in skin Raynaud's Esophageal dysfunction Sclerodactyly - thickening and tightening of skin on hands but also on face especially around lips. Telangiectasias

Twisting trauma of knee, acute to subacute symptoms, medial joint line tenderness, and catching sensation during extension of the knee. what are you thinking?

Meniscal injury

For antipsychotic meds, what are the effects on the following pathways: Mesolimibic, NIgrostriatal, Tuberoinfundibiular

Mesolimbic: how the antipsychotics have their effect (efficacy) Nigrostriatal: EPS sx: acute dystonia, akathisia, parkinsonsim (memory tool: oh No for Nigrostriatal... you got EPS sxs) Tubuloinfundibular: hyperprolactinemia (Memory tool... sexual SEs are "no fun" "in-fun-dibular") (SE: amenorrhea, galactorrhea, gynecomastia, sexual dysfunction)

Salicylate (aspirin) intoxication.

Metabolic Acidosis (AG) Respiratory Alkalosis (tachypnea) Tinnitus*** Fever Nausea GI irritation

What electrolyte and metabolic imbalances does someone with chronic diarrhea have?

Metabolic acidosis (pewping out bicarb which is alkaline so you get acidic), and hypokalemia (excess K loss from GI tract)

Pt has symptoms of PCOS, what should you also screen them for?

Metabolic syndromes (like diabetes and HTN) -Gold standard for diagnosing T2DM in PCOS pt is doing an oral glucose tolerance test (OGTT) bc it is more sensitive in detecting glucose intolerance than other screening tests (ex: fasting glucose, Hb A1c) Due to obesity and metabolic syndrome, PCOS pts are also at risk for developing: - Obstructive Sleep apnea -Nonalcoholic fatty liver disease -Endometrial cancer

When someone comes into the hospital, why does everyone want to stop metformin?

Metformin can cause lactic acidosis in AKI and sepsis (sick patients) and should be withheld until renal function improves.

Pt is already on metformin. He's is having increased beta cell failure so his prior dose drug tx with them meformin that was controlling his A1c is not not working; his A1c is now 8% and he notices that his BGs are around 156. He's overweight and has hx of MI 2 years ago. what medication do you want to add? Which ones are not options, explain why with their SEs.

Metformin is the preferred initial drug in pts without contraindications such as renal insufficient. Pts with suboptimal control need a 2nd drug. The choice depends on the side effect profiles. Since he's overweight, has hx of heart disease, and needs about 1% A1c reduction: -GLP-1 agonists (ex: exenatide) is a good choice since it can lower weigh and BG. Note the SE of acute pancreatitis is possible. Note: they are also injected. Do not want to add: -SU: since they cause weight gain -Insulin: since it's associated with weight gain (remember it's an anabolic hormone), and guidelines say add insulin when HbA1c is >8.5% -Thiazolidinedione (ex: pioglitazone): used when pt can't take SU, but don't want to use in this pt bc can cause weight gain and possibly induce CHF in this pt who already has heart disease. -DPP-4 Inhibitors: which increase endogenous incretins.. bc they do not affect weight; they are weight neutral so not as helpful with the weight loss as GLP-1 agonists

How do you distinguish ethylene glycol and methanol poisoning? Both are ingested as substitute for ethanol, both cause AG metabolic acidosis and increased osmolar gap. But what organs do they damage differently?

Methanol: damages eyes (M: looks like two arrowing pointing up.. towards your eyes so Methanol damages your eyes) Ethylene glycol: damages kidneys (E: looks like a kidney sitting there.. so Ethylene glycol damages your kidneys)

Pt with cyanosis and bluish discoloration of skin and mucous membranes. What are you concerned about?

Methemoglobinemia

Question with a pts with ectopic pregnancy on adnexa is 3cm. She presents with 12 hrs mild right lower abdominal pain but doesn't mention anything about her HDS. What do you do next for initial management, Methotrexate therapy or Salpingectomy?

Methotrexate since she has an ecoptic <3.5cm, you can try the methotrexate since there isn't increased risk of failure since it's under 3.5cm.

Pt with RA & there is progressive erosion of the bone and cartilage and significant joint destruction/deformity. Indomethacin NSAIDs control her symptoms but symptoms recur if she skips a done. What do you prescribe next?

Methotrexate. (Preferred initial DMARD in mod-severe active RA d/t efficacy and long-term safety profile. Need to test pts for Hep B, Hep C, and TB before starting tx. Use DMARDs ASAP bc joint damage begins early in the course of RA) Contraindications: pregnancy or planning for pregnancy, renal insufficiency, liver disease, excessive ETOH intake. If pt doesn't respond after 6 months, they may need a biologic DMARD (there are non-biologic and biologic DMARDS.. and methotrexate is a non-biologic), such as TNF-alpha inhibiotrs (etanercept, infliximab) as the next stage in tx.

Once someone has torsades, what do you tx them with?

Mg sulfate (if they are hemodynamically stable) Immediiate defib (if they are hemodynamically unstable)

What is the cut off GA to give Mag. sulfate?

Mg++ (think of these 2 cations.. to remember): thirty-TWO weeks GA for fetal neuroprotection.

PT has fever, confusion and stiff neck. Mechanism of meningitis infection?

Microbial invasion into CNS

What do you expect for MCV in iron deficiency?

Microcytic anemia (low MCV)

Pt with CXR findings of hilar mass in setting of weight loss, cough, and significant smoking history, thinking about small cell lung cancer. This can cause SIADH, which presents with hyponatremia, serum osmolality <275 mOsm/kg, and urine osmolol >100 mOsm (inappropriately elevated) in an euvolemic patient. Pt presents with lethargy, confusion, and forgetfulness (so mild symptoms). What is the treatment you give these pts? What if they have more severe symptoms of seizure and coma, or they have Na <120? What do you treat those patients with?

Mild/mod symptoms of nausea, confusion, forgetfulness: treat with fluid restriction and salt tablets. Severe symptoms like seizure, coma (these symptoms signal increased risk of cerebral edema and brainstem herniation, requiring more urgent increase in their serum sodium concentration): treat with hypertonic (3%) saline for severe hyponatremia

If you have mild elevation of prolactin in the context of an otherwise normal pituitary function, what do you think the cause would be? (Prolactin ~45 when <15 is normal, normal LH, normal TSH)

Mildly elevated prolactin with normal pituitary function: think antipsychotic medications, hypothyroidism, or renal failure (kdney disease elevates prolactin). Note: cirrhosis/liver disease also elevated prolactin.

1 month old full term baby has blood streaked stools. He's exclusively breastfed. He also has diffuse eczema. Fecal occult blood test positive. Likely cause? Management?

Milk protein-induced enterocolitis -presents at age 2-8 weeks. -regurgitation/vomiting, painless bloody stools, eczema Breastfeeding moms should eliminated all milk and soy products from their diet (bc of cross reactions) and then continue to BF. Formula fed infants should be switched to hydrolyzed milk. Visible bleeding should stop in 3 days but complete resolution may take up to 2 weeks. Prognosis is excellent: almost all affected infants can tolerate dairy and soy products by age 1.

What kind of kidney disease has "normal light microscopy" findings?

Minimal change disease

What is anti-Scl-70 (anti-topoisomerase) antibody good at detecting?

Mod sensitivity and high sensitivity for systemic sclerosis (scleroderma) and associated with extensive skin involvement and interstitial pulmonary fibrosis

Risks d/t HTN in pregnancy?

Mom: superimposed pre-eclampsia, pp hemorrhage, GDM, placental abruption, C-section delivery Fetus: growth restriction, perinatal mortality, preterm delivery, oligohydramnios.

Older woman (65yo) comes in with a month of back pain, mostly in lumbar and thoracic spine that is only partially relieved with acetaminophen. Worse with activity. She has hx of DM, HTN, osteopenia. She take OTC calcium and Vitamin D. Annual physical 4 months ago with normal labs. Thin but appears well. No focal tenderness over the spine. Today, Hgb 10.2 (slightly low), Calcium 10.9 (slightly low), BUN 30 (high), and Cr 2.5 (high). Urine dipstick is bland except it shows a few granular casts. What is causing her condition? What does she have?

Monoclonal proteins. she has multiple myeloma. Usually presents with constitutional symptoms (fatigue, weight loss) and bone pain. They make too much monoclonal proteins that can then deposit in the kidneys and damaging them, explaining the increased Cr and BUN. Also causes bone destruction, so you see anemia and hypercalcemia. and too much monoclonal proteins are made and they deposit int he kidney --> kidney damage. Urine dipstick usually picks up protein like albumin, not immunoglobulins, so the urine dipstick will look bland.

Pain between 3rd and 4th toes on plantar surface with ***clicking*** sensation (Mulder sign) that occurs when simultaneously palpating this space and squeezing the metatarsal joints. What does this pt have?

Morton neuroma.

Pt has HTN (160/90), she has a bunch of things she's doing wrong: she eats out for dinner every night, drinks 4-5 glasses of wine daily, her TC is 205. DEXA shows osteoporosis. What is the most appropriate recommendation for this patient?

Most appropriate. Tell her to decrease ETOH use. She drinks too much and that affects primary HTN. So if there is a pt with HTN and they drink too much, the answer is to decreased ETOH. Note: I picked decreased sodium intake, but that's not as important as decreasing her drinking I suppose. Uptodate lists excessive ETOH as a cause of primary/essential HTN so pick ETOH reduction if pt drinks too much. (note: weight loss wasn't on there as an option since her BMI was relatively normal at 26)

how do newborns with polycythemia present?

Most are asx but have ruddy/plethoric appearance (like in the face). As the Hct rises, the viscosity of the blood also rises and impairs blood flow to organs. So you can see lethargy, irritability, jitteriness, respiratory distress, tachypnea, cyanosis, poor feeding. Increased RBC mass --> hypoglycemia and hypocalcemia d/t increased cellular intake by those cells (they're eating up all your glucose and calcium). can also have hyperbili (since there are more RBCs to get rid of) Asx babies just need hydration by feeds or parenteral fliuds. Sx babies need partial exchange transfusion, where you remove blood in exchange for NS to normalize their HCT. Give glucose if they have low glucose.

What is anterior uveitis?

Most common extra-articular manifestation of Ankylosing spondylitis; -caused by inflammation of the iris (aka iritis), ciliary body and choroid and presents with unilateral occular pain and photophobia Inflammation of the uveal tract (iris, ciliary body, and choroid). Intense pain and photophobia in one eye.

Most common and then other causes of sideroblastic anemia? (microcytic)

Most common: ETOH's suppressive effect on the bone marrow Other causes that are less common: lead poisoning, isoniazid and B6 deficiency.

Presentation of early disseminated lyme disease. Treatment?

Multiple erythema migrans (bulls eye rash), unilateral/bilateral CN palsy (ex: CN VII), meningitis, carditis (AV block), migratory athralgias (so starting to get more specific and not just nonspecific symptoms is early disseminated disease) Timeline: weeks-months Tx: IV ceftriaxone

Older man with constipation now needs laxatives to help him poop. He has back pain and lab evidence of anemia and hypercalcemia. Cr is 2.2. Stool occult blood is negative. What are you concerned the dx may be? Therefore, what is causing his constipation?

Multiple myeloma is suspected in pt with constipation, back pain (bc osteolytic bone lesions), lab showing anemia (bc bone marrow infiltration), renal insufficiency, and hyperCA (bc bone marrow infiltration) The constipation is due to the hypercalcemia (although hyperCa can be asymptomatic if <12), hypercalcemia can also cause fatigue, CONSTIPATION, and depression. So the constipation is bc of the electrolyte abnormality of hyperCa.

What is the cause of bilateral Trigeminal Neuralgia?

Multiple sclerosis: demyelination of nerve nuclei. -Demyelination of the trigeminal nerve or nerve root leads to improper signaling of the nerve and paroxysms of severe pain.

When should you suspect Gastrinoma (aka Zollinger-Ellison Syndrome)??

Multiple, large (1-2 cm) ulcers past the duodenum (weirdd that they would be past the duodenum) that recur even with eradication of H.pylori (weirdd that they would keep recurring even after you get rid of H.pylori) If those are present, think about Gastrinoma (Zollinger-Ellison Syndrome) Also think of it when pt has symptoms of diarrhea (since the acid that the gastrinoma secretes inactivates lipase, so pts have diarrhea)

Negative psychotic symptoms, related with these kind of receptors

Muscarinic receptors

Side effect profile: Risperidone

Mvt disorder Memory tool: Think about a person "Whispering" and moving around in the movie theater... they can't help but move and make noise... whispering is making noise.. so think Risperidone has greater incidence of movement disorders

38yo F has muscle fatigue halfway through meals: can't chew and swallow food. Has episodes of this. .. We are shown a chest CT and looks like there is an anterior mediastinal mass. What is the likely cause of the pt's symptoms?

Myastenia Gravis... has related bulbar muscle fatigue and dysarthria... need to scan for thymoma. -MG has to do with autoantibodies to the Ach-receptors. so that means there are decreased available Ach-Rectpors (bc the antibodies have bound them up) Note: autoantibodies (come from thymus) are directed against NICOTINIC acetylcholine receptors at the NMJ. The antibodies binding leads to complement activation with receptor degradation, causing impaired APs and muscle weakness.

What are s/sx of opioid withdrawal?

N/V, abdominal pian, cramping, MUSCLE ACHES, Dilated pupils, YAWING, piloerection!, lacrimation! hyperactive bowel sounds.

What condition is pheochromocytoma associated with (outside of the MEN association)?

NF1 (Neurofibromatosis type 1) presents with cafe-au-lait spots, neurofibromas, axillary freckling, intracranial tumors, and skeletal abormalities

MG where is the site of pathology?

NMJ. Autoantibodies against Ach-receptors in the motor end plate. Pts have ptosis, fatigable proximal muscle weakness that worsens with prolonged use (ex: after work, while holding up head when sitting/standing, while brushing hair). Fluctuating and fatigable extraocular and bulbar muscle weakness and symmetric proximal muscle weakness.

Do you do a LP on pts with symptoms of increased ICP (nausea vomiting, headache, AMS) and confirmed CT scan of acute intracerebral hemorrhage?

NO! Avoid doing LPs on pts with acute intracerebral hemorrhage bc this has a risk of herniation as a result of the increased ICP.

Pt with LBP takes OTC meds to treat them He has fatigue and you get UA that shows trace proteins, moderate blood, negative leuks esterase, negative nitrates, 20-30/hpf WBCs, 2-3/hpf RBCs, White blood cell casts. Cr is 2.2 and BUN 34. What is the likely cause?

NSAID/analgesic induced tubulointerstitial nephritis. Think about this whenever someone is using OTC analgesics too much. and then they have painless hematuria, sterile pyuria, WBC casts, trace proteins, then think non-glomerular d/o affecting tubulointerstitium or lining of the urinary tract. D/t papillary necrosis.

Pt loses her 1 month old baby and is in grief and wants her lactation to stop. What meds are most appropriate to give her?

NSAIDS. DA agonists are NOT FDA approved currently. Also, breast engorgement will lead to cessation of lactation by itself when there is negative inhibition of prolactin release. So even thought she's grieving, prescribe meds unnecessarily. Have her wear a comfortable supportive bra, avoid nipple stimulation, and apply ice pack to the breast and use NSAIDS to reduce inflammation and pain. (Breast binding not recommended bc risk of mastitis, plugged ducts, and increased pain; tight bra may also lead to nipple stimulation, which you don't want)

Pregnant woman with epilepsy is taking carbamazepine, what is her baby at risk for?

NTDs. Carbamazepine is a anticonvulsant with folic acid antagonist properties, placing her at increased risk for inadequate folic acid levels. High risk patients (NTD in prior pregnancy, anticonvulsant meds) require additional folic acid supplementation (ex: 4mg daily) rather than the 0.4mg daily recommendation for average-risk patient.

When you dx Gastrinoma (Z-E syndrome), what else do you want to make sure to do in the management of that patient?

Need to rule out metastatic disease. First get a CT/MRI of abdomen (even though it has poor sensitivity, jut do it first). If the CT/MRI abdomen is normal, then you need to go another step further bc you still haven't ruled out metastatic disease. Need to do Somatostatin receptor scintigraphy (a nuclear octreotide scan) combined with endoscopic ultrasound. If that is negative, then you have ruled out mets. (You do the somatostatin receptor scintigraphy because gastrinomas are associated with massive increase int he number of somatostatin receptors in the abdomen so that's how you catch metastatic disease)

Sickle cell pts are essentially asplenic so they need vaccination against what organisms? which what kind of vaccines?

Need vaccination against encapsulated organisms: Strep penumoniae, H. influenzae, N. meningitidis. Use vaccines with a conjugate capsular polysaccharide. Can also give BID prophylactic penicillin in kids with SCD until they reach age 5.

Pt feels feels nausea and warmth spread over he body before passing out while standing in line at a supermarket. Pulse was weak at 40/min. Not confused afterward. What most likely caused her episode?

Neurocardiogenic syncope aka vasovagal syncope. Triggers: prolonged standing (like during surgery), emotional distress, painful stimuli. Prodromal: Nausea, warmth, diaphoresis. This happens bc of excessive vagal tone. The excess tone causes a transient profound hypotensive reaction and bradycardia due to activation of the autonomic reflex. Benign and self limited, lasts about 10 sec to a few minutes.

Missionary, 46yo man, presents to ED with generalized tonic-clonic seizure, first occurrence. Spent 3 months in rural Bolivia with pig farmers. EEG shows epileptiform activity. Brain MRI shows several intraparenchymal, 5- to 10- mm cystic lesions with surrounding edema. HIV test is negative. What is the likely cause?

Neurocysticercosis: parasite eggs from contaminated food and water. Taenia solium (pork tapeworm) eggs. Fecal-oral human transmission. Central/South American, Sub-saharan Africa, Asia. Has prolonged incubation time (months to years), presents with adult onset seizure, or symptoms of increased ICP (headache, vomiting, AMS; bc of obstructed CSF flow). CT/MRI shows 1 or more cysts (hypodense, enhancement/edema, or calcified) Tx: Seizure/ICH managment, antiparasitic tx (albendazole), and corticosteroids

Pt started an antipsychotic med and now they have fever (>104), confused, has generalized muscle rigidity, and autonomic instability (abnormal VS, sweating). What is going on?

Neuroleptic malignant syndrome (NMS): autonomic instability (notably high fevers), delirium, generalized rigidity (often sever) rhabdo (with increased serum creatine kinase) and leukocytosis. Happens after initiation of antipsychotics (ex: risperidone). Can be life-threatening. Usually seen with high-potency 1st gen. antipsychotics (ex: haloparidol), but can be seen with all antipsychotics. First manifestation usually delirium.

What are signs of TCA toxicity/overdose?

New onset seizure, ***anticholinergic toxicity*** signs (dilated pupil, hyperthermia, flushed skin, decreased bowel sounds), QRS widening, mental status changes (sedation, delirium), tachycardia, hypotension, cardiac conduction delay. Note: QRS prolongation is d/t inhibition of fast-sodium channels, with values >100 msec associated with increased risk for ventricular arrhythmia and seizures. Note: TCAs have anticholinergic properties.. so with OD you'll see dilated pupils, hyperthermia, flushed skin, decreased bowel sounds.

Presentation of Endocarditis

New or changed murmur, fever (bc infection), and then the complications: splinter hemorrhages, janeway lesions (flat, painless), osler nodes (raised, painful), Roth spots in eyes, Brain (mycotic aneursym), Kidney (hematuria, glomerulonephritis), conjunctival petechiae, splenomegaly, septic emboli to the lungs.

Patient with Alzheimer's presents >60yo with memory loss that progresses over time. Initially short term memory is affected, then long term memory and cognitive abilities. Daily activities and normal life is disrupted. They have difficulty with word finding and loss of visuospatial skills and executive function. Confusion and disorientation shows up as wandering and urinating in inappropriate places. What will CT Head of these patients show?

No changes seen in early disease. Late stage of disease will show corticol and subcortical atrophy. Atrophy may be more prominent in the ***parietal and temporal lobes** atrophy, particularly in the ***hippocampus.***

Symptoms of B-vitamin toxicity

No such thing since B vitamins are water soluble

Symptoms of Vitamin C toxicity

No such thing since Vitamin C is water soluble

Pt has hx of recent use of systemic glucocorticoids (ex: methylprednisolone) and now you see Leuks 16,000, PMN % increases to 82%, there are bands 3%, and lymphocytes are decreased to 13%, and eosinophils are decreased to 0%. Are you concerned?

No, that is a medication side effect. -Mobilization of marginated PMNs into the blood stream. Can also stimulate release of immature PMNs from bone marrow, so you can also see bands. There's also inhibition of PMN apoptosis. -There is also a decreased number of circulating lymphocytes and eosinophils bc there is increase apoptosis of those cells and increased emigration into tissues and decreased production.

Do cataracts tend to recur once removed? What may be a situation that occurs following cataract surgery?

No, they don't tend to recur. some patients may develop posterior capsule opacification (thickening of capsule holding the artificial lens), which can cause cloudy vision and can be treated with a laser without resulting in longterm vision problems.

Do you expect splenomegaly in bone marrow aplasia aka aplastic anemia?

No, you do not. Splenomegaly is very unlikely in aplastic anemia and suggests an alternative diagnosis that is not aplastic anemia (since that is more a problem with decreased RBC production rather than destruction and sequestration of RBCs by the spleen)

Can cross-sectional studies establish causation?

No. Cross-sectional studies just demonstrate a observation at a single point in time so they can show association, but CANNOT establish causation

46yo presents with 1 week fever, chills, productive cough with yellow-white sputum, and SOB. He got a renal transplant 6 months prior and takes maintenance immunosuppressives. T 102.9. HR 110 RR 22. Left upper lung crackles and bronchial breath sounds heart. Chest imaging; left upper lobe nodular density with cavitation and nodular infiltrates in right lung. Sputum Gram stain and cx are negative. BAL shows light growth of branching, filamentous rods that are partially acid fast. Causative organism?

Nocardia Microbiology: Gram + rod (beaded or branching), Partially acid fast, Aerobic Found in soil, disease for inhalation or traumatic inoculation into skin, or in immunocompromised or elderly patients. Presentation: Pneumonia (similar to TB except TB is strongly acid fast), CNS involvement (brain abscess), skin involvement Tx: TMP-SMX, surgical drainage of abscess (Think of Sketchy picture card game table. He's drawing the gun "fast" so partially acid fast. The guy has a covering on his legs that low like cows (so cutaneous involvement), his hat/head is getting shot at (brain involvement) and i think his chest is also shot at (pneumonia) and there is a can of sulfa eggs (sulfa drugs like TMP-SMX as Tx). and there is a potted plant in the back, so it comes from soil.

Pt has acute exacerbation of COPD (AECOPD). You already tried the initial management of inhaled SABA, glucocorticoids and abxs. She continues to have sxs despite the medical management. What do you do next?

Non-invasive ventilatory support (basically full face CPAP as "non-invasive positive-pressure ventilation (NPPV)). Deliver the ventilatory support via facemask before intubating the pt. NPPV decreases work of breathing and improves alveolar ventilation and is preferred in pts with AECOPD bc it is associated with decreased in mortality, intubation rate, treatment failure, length of hospital stay, and incidence of nosocomial infections. If the patient fails trial of NPPV after 2 hours (is hypercapnic, has poor mental status, hemodynamically unstable, has profound acidemia with pH < 7.1), then you would intubate them. But this pt can do trial of NPPV before you intubate them bc advanced COPD may make weaning and extubation more challenging.

List of Meds that can cause high K (hyperkalemia)

Non-selective beta blockers (Interferes w/ beta-2-mediated intracellular K uptake) ACE inhibitors/ARBs, K sparing diuretics (Blocks Aldo or ENaC channel) Digitalis (Blocks Na-K-ATPase pump) Cyclosporine (blocks Aldo activity) Heparin (blocks Aldo production) NSAIDs (Decreases renal perfusion --> decreased K delivery to collecting ducts) Succinylcholine (Extracellular leak of K through Acetylcholine receptors)

Severe hypercalcemia (>14), what is the best initial therapy?

Normal Saline!!! (0.9% saline) plus calcitonin is the immediate short term treatment. -use aggressive hydration with normal saline to restore IV volume and promote urinary calcium excretion. -calcitonin quickly reduces serum calcium and can be given with saline, inhibit osteoclast-mediated bone resorption Long term tx: use bisphosphonate (zoledronic acid) -Bisphosphonates (pamidronate, zoledronic acid) inhibit bone resorption and provide a sustained reduction in calcium levels. But this takes a while, 2-4 day to take affect. so usually given after initial hydration.

What do you expect to see in the CSF for viral meningitis?

Normal or slightly elevated protein (something is in there but it's not a protein-y as bacteria being in there) Normal glucose (since virus doesn't eat up glucose) Elevated WBC (since your body does try to fight the virus) Normal RBCs. The only exception is in herpes meningoencephalitis which can have high RBC and protein levels bc of the temporal lobe hemorrhage.

65 yo obese female with progressive worsening memory, usually independent is now forgetting to pay her bills. It's causing her some distress. She has mild urinary incontinence, broad-based shuffling gait, right sided carotid bruit, 2/6 systolic ejection murmur, and MRI shows significantly enlarged ventricles. What is the most likely dx?

Normal pressure hydrocephalus (NPH) is a triad of gait disturbance, dementia, and urinary incontinence (wet, wacky, wobbly; urinary incontinence, dementia, gait disturbance). Memory impairment is slow and progressive. CT/MRI will show dilated ventricles. Dx is made clinically or with radionucleotide CSF studies. If repeated spinal taps lead to an improvement in symptoms, then ventriculo-peritoneal shunts can be considered as definitive treatment. Note: it's really that MRI finding that points you in the direction of NPH rather than some other diagnosis, such as multi-infarct dementia (since that would show MRI with multiple areas of increased T2 weighted density in the periventricular areas. Also the onset of dementia tends to be more abrupt in these cases)

What is normal pupillary size? (to help you distinguish pinpoint pupils, they would have to be smaller in diameter than this number)

Normal pupil size: 2-4 mm in bright light (so 3mm is normal)

Derm: "peripheral scaling" what does that characteristic of?

Not SCC, but rather tinea corporis. (ring-shaped inflammatory skin lesions with peripheral scaling)

What are the non-seminomatous germ cell tumors?

Not the serminoma (which has elevated beta-hCG and normal aFP) We are talking about yolk sac tumor, choriocarcinoma, and embryonal carcinoma. Mix of all of them is mixed germ cell tumor. Most of these non-seminomatous germ cell tumors have elevated AFP, with considerable number having elevated beta-HCG.

Side effects of thionamides (Antithyroid drugs): Propylthiouracil (PTU) and Methimazole (MMI)?

Note: most common side effect is allergic reaction. PTU: Hepatic failure: -PTU is usually not the preferred drug d/t the black box warning of sever eliver injury and acute liver failure. However, PTI us preferred during the 1st Tri of pregnancy since MMI has fatal teratogenicity. MMI: Agranulocytosis (0.3% of pts) <-- most serious SE. -Need to tell all pts getting MMI that they could have agranulocytosis. If you get a sore throat and fever, stop the drug and get your WBC ct checked. Routine monitoring of WBC ct is not needed since agranulocytosis is so rare. but know it as a MMI SE. Note: about 30-40% of pts treated with antithyroid drugs for 1 year go into permanent remission. But there are side effects so know those side effects.

What would you hear with a hematoma?

Nothing, would not hear a bruit. May or may not be a mass.

33 yo F has dyspeptic sx, she uses OCPs and has nausea and bloating. Stopped taking OCPs a few months ago but still has episodic postprandial fullness, upper abdominal discomfort, and nausea. Otherwise healthy. Abdominal u/s shows 4cm solitary lesion in right hepatic lobe. CT shows enhancement of mass during hepatic arterial phase and CENTRAL STELLATE SCAR. You treat her dyspepsia with PPIs. What do you do with the liver mass?

Nothing. This is a focal nodular hyperplasia (FNH): associated with anomalous arteries (so that's when there is enhancement of mass during hepatic arterial phase) There's arterial flow and central scar**** on imaging. ("central stellate scar") FNH is a a benign common nonvascular liver lesion. Normally asx and most cases are discovered incidentally during eval of other abdominal problems (ex: gallstones, dyspepsia). Commonly small (<5cm), solitary lesion. More common in women. May be estrogen sensitive so pts on OCPs tend to have large more vascular ones. Usually stable and don't result in complications. So just manage conservatively. Some providers tell women to stop their OCPs and do serial exams with larger (>8cm) masses.

Pt who clearly has PCOS, what additional test do you want to do for them?

OGTT. screen for T2DM since they are at risk for co-morbid metabolic syndrome; OGTT is gold standard in dx of T2DM in PCOS pts.

You are in the USA and get bit by your neighbor's dog, it has not been vaccinated against rabies but appears healthy, the neighbors and dog are there with you at the doctor's office. What do you do?

Observe the dog for 10 days for signs of rabies; no immediate prophylaxis for patient bitten because the dog is available for testing.

Pt has severe HA with N/V, that came on suddenly when she was running in the park. She has hx of migraines, but this HA became unbearable in seconds. Her vision became blurry and caused her to stumble and fall. In the ED she feels nauseous and continues to have a SEVERE headache. BP is 148/86. What's the next best step for this pt?

Obtain noncontrast CT scan of head. She may be having a Subarachnoid hemorrhage "WORSE HEADACHE OF YOUR LIFE"/thunderclap headache. Usually d/t ruptured saccular ("berry") aneurysm with severe, sudden onset different from previous HAs. N/V, brief LOC, FND, and meningismus as presentation. RF: smoking, HTN, mod-heavy ETOH use, family hx, sympathomimetic drugs. Dx: noncontrast head CT > 90% sensitive within 2-6 hrs of SAH onset. -LP is needed to exclude SAH definitively in pts with negative head CT (classically SAH will have elevated opening pressure, with CSF showing xanthochromia - yellow/pink discoloration d/t hemoglobin breakdown and continued high levels of RBC from 1st to 4th tube of CSF collection) -Xanthochromia confirms dx (usually >6hr from SAH onset) -Cerebral angiography to ID bleeding source

Prior heroin addict gets in MVC. How do you treat their pain?

Obvious trauma will have acute nociceptive pain. Initial management options for acute pain include opioids are generally similar for all pts regardless of substance abuse hx. However, if pt has current/recovering opioid addition and you give them opioids for pain, closely follow them to monitor pain relief and avoid addiction relapse. IV morphine is appropriate treatment and should be offered following discussion of risk/benefits.

What is selective survival bias? when does it occur?

Occurs in case-control studies when cases are selected from the entire disease population instead of just those that are newly diagnosed. Ex: A study on cancer survival that is not limited to newly diagnosed pts will contain a higher proportion of relatively benign malignancies as these pts generally live longer.

Pt complains of eye discomfort, says for last 3 weeks it feels like he has had feeling of "dirt in my eyes" with associated redness and tearing. You also see increased redness of conjunctivia, red/scattered papules on the nose and cheek. What's going on?

Ocular rosacea. Eye symptoms associated with red, pustular rash of central face, think rosacea. Note: ocular rosacea can lead to vision loss and most patient need an ophthalmologic consult. Mild sx are treated with lid scrub, topical abx (metronidazole, erythromycin) and ocular lubricants. More severe cases may need systemic abx and topical immunosuppressive agents (ex: glucocorticoids, cyclosporine) 4 primary manifestations of rosacea: -Erythematotelangiectatic: red facial flushing, telangiectasias, rough/sclaing, burning discomfort -Papulopustular: small papules/pustules resembling acnes -Phymatous: chronic irregular thickening of skin, usually involves nose -Ocular rosacea: involves the cornea, conjunctiva and lids with burning or ***foreign body sensation***, blepharitis (inflammation of eyelid margin), keratitis, conjunctivitis, corneal ulcers, and recurrent chalazia (lump on eyelid)

Tell me about cytomegalovirus (CMV) colitis.

Often presents with bloody diarrhea and usually develops in pts whose CD4 < 50. The anti-CMV agents are toxic, so the specific therapy for CMV should not be started empirically, instead you should make sure to establish a diagnosis before giving the CMV treatments.

Pt has anorexia nervosa, What med is most effective?

Olanzapine if no response to CBT and nutritional rehab. Memory tool: think of the people who don't eat at all being a little crazier... than bulimics... so since they're a littler crazier...who doesn't like food? that's crazy... so give then antipsychotic - Olanzapine.

Who gets screened for AAA?

Older men (age 65-75) with any hx of smoking; one time screening with abdominal ultrasound.

What are some names of PPIs (so you don't mistake them for fungal medications)

Omeprazole, pantoprazole, lansoprazole -ends with -prazole (note: don't just see the -azole part and think it's an anti-fungal medications; these are PPIs)

Gradual loss of peripheral vision (pd of years) and consequent tunnel vision. Dx?

Open-angle glaucoma

Gradual loss of peripheral vision in both eyes, leading to tunnel vision. Thinking about

Open-angle glaucoma

How does topical pilocarpine work to treat acute glaucoma?

Opens the canal of Schlemm to allow aqueous humor to drain, decreasing the intraocular pressure

Pt presents with: Hx of IV heroin daily, and track marks. GI: N/V/D, cramps, increased bowel sounds CV: increased pulse, BP, sweating Psych: insomnia, yawning, diaphoresis MSK: myalgias (feel miserable, aching muscles), arthralgias (aching joints) HEENT: lacrimation, rhinorrhea (nasal congestion/runny nose), mydriasis (dilated pupils) Extremities: piloerection What doe they have? How do you treat them?

Opioid withdrawal. Tx: Methadone (preferred) or buprenorphine

Pt with depressed mental status, decreased RR, bradycardia, and small constricted pupils (miosis). What drug did they take?

Opioids (remember the i's in opioids look like little pinpoint pupils), and it can be a respiratory depressant (so decrease RR, and also depressed mentation)

Central scotoma "smudge", eye pain with movement, afferent pupillary defect (dilates instead of constricts when you shine light into it), and color vision abnormalities, think about what dx?

Optic neuritis in multiple sclerosis.

26yo female pt complains of a "smudge" in the center of her left vision that started 2 days ago. The smudge has gradually enlarged and now almost involves the entire left visual field. Colors appear "washed out" and she has mild ocular discomfort with eye movement. Vision is 20/200 in that affected eye. When you move the light from right to left eye, the left eye dilates. What's the dx?

Optic neuritis see in young women, associated with MS, could be the 1st sign of it. Manifestation to know about optic neuritis to distinguish it from other things: -Acute, peaks in 2 weeks -Monoocular vision loss -Eye main with movement -"Washed out" color vision -Central scotoma (the "smudge" in the vision) -Afferent pupillary defect (paradoxical pupillary dilation of the affected eye with swinging-flashlight test.. normally when you shine light into someone's eye it should constrict... but these affected eye in optic neuritis will dilate when light is hone into it. ) Get a brain and orbit MRI to dx and look for other areas of inflammation. Tx: IV steroids.

Pt with DM, immunodeficiency, or use of Abx or inhaled glucocorticoids. Now they have white plaques on oral mucosa, tongue, or oropharynx with underlying erthyma that can be scraped off with a tongue depressor. Thoughts?

Oral candidiasis.

If there is extensive impetigo - red papules/vesicles with overlying adherent honey-colored crust, what do you want to tx with?

Oral clindamycin

Infection of the fat and extraocular muscles surrounding the eye and is a medical emergency. Infection posterior to the orbital septum. Unilateral infection common in kids with paranasal sinus infection. Present with abrupt onset of fever, proptosis, restriction of extraocular eye movements, and swollen, red, tender eyelids.

Orbital cellulitis

Pt stands up and then passes out. What kind of syncope?

Orthostatic syncope. Postural changes in HR/BP after standing suddently

Pt with the flu, when do you give oseltamivir and when do you just do symptomatic tx?

Oseltamivir: If present within 48 hr of sx onset, or they have RF for flu complications (>65yo, chronic medical problems, pregnancy). Supportive care: for everyone else, and if they present laster than 48hs from sx onset, then oseltamivir is no good.

Pt with hx of SLE (lupus) and takes glucocorticoids is now complaining of hip pain that increases with weight bearing. She has a normal hip x-ray. What do you think she has? what's the next step in management?

Osteonecrosis (avascular necrosis) of the femoral head. MRI is the most sensitive so get her an MRI. (Osteonecrosis of the femoral head is characterized by gain in groin, thigh, buttock that worsens with activity. In the first few months x-ray will be normal (so may have a normal hip x-ray) and MRI is more sensitive and can show the boundary between normal and ischemic bone. In advanced disease, plain x-ray can show a subchondral lucency (crescent sign) and deformities of the femoral head. This is a common complication of SLE And the risk is increased when pts take glucocorticoids.

What is a patient with RA at greatest risk for?

Osteopenia, Osteoporosis, and bone fractures RA's pro-inflammatory cytokines, corticosteroid therapy, and lack of physical activity may contribute to local or generalized loss of bone mass. The degree of bone loss generally correlates with disease activity. Strategies to prevent bone loss (adequate physical activity, optimization of Vit D and calcium intake, minimization of glucocortoid dose) should be implemented. Most experts suggest low threshold for starting bisphosphonate therapy in RA pts. Risk of osteoporosis is up to 2-fold with one study showing prevalence of 22%.

What does a dysgerminoma secrete?

Ovarina tumor most commonly in women <30 yo and can secrete LDH or beta-hCG. (note: does NOT cause precocious puberty bc does NOT secrete estrogen like granulosa cell tumors)

What are features of Narcolepsy:

Overnight Polysomnogram and multiple sleep latency tests (5 opportunities to nap) will show: -Decreased sleep latency (shortened time between being awake and sleep onset) -Decreased REM latency (narcolepsy pts enter REM sleep within 15 minutes of sleep onset; whereas people w/o narcolepsy will take about 90 minute before they enter REM sleep) -Increased REM density (frequency of rapid eye movements during REM sleep) In summary: pts with narcolepsy have decreased latency (sleep and REM) bc they fall asleep faster and enter REM faster. and they also have increased REM density bc they have more REMs during REM sleep) Clinically, they have recurrent lapses into sleep or naps (>3x/week for 3 months) and also have at least one of the following: -Cataplexy (brief loss of muscle tone precipitated by strong emotion - laughter, excitement -low CSF levels of hypocretin-1 -Shortened REM sleep latency Associated features: hypnagogic or hypnopompic hallucinations, and sleep paralysis.

Pt is having acute COPD exacerbation (increased SOB< cough, and sputum production). What do you need to give them?

Oxygen (target Spo2 88-92%) Inhaled bronchodilators Systemic glucocorticoids** (Ex: methylprednisolone) Abx if >2 cardinal symptoms Oseltamivir if evidence of influenza NPPV if ventilatory failure. (Intubate if that fails) Note: systemic glucocorticoids decrease inflammation associated with COPD exacerbation, improve lung function and hypoxemia, and are shown to decrease risk of relapse, tx failure, and length of hospital stay. Usually given for 5 days as oral prednisone or IV methylprednisolone. IV is more often used in severe exacerbation but doesn't' have more benefit over oral administration. (Note: don't pick the inhaled ICS for COPD exacerbation bc inhaled ICS ex: fluticasone inhaler is for managment of persistent asthma. In COPD pts, you want to do systemic glucocorticoids)

Pt with impaired judgement, tachycardia, aggressive behavior, ataxia, mild HTN, multidirectional nystagmus. What drug did they take?

PCP (phencyclidine)

Pt with severe hyper-TG is started on niacin. 1 week later he has intense generalized itching and flushing. What is causing this?

PG related reaction. Cutaneous flushing and intensive generalized itching are well known SEs of high-dose niacin therapy (high dose required to tx lipid abnormalities) This is d/t Niacin-induced peripheral vasodilation. Note we know it's PG related reaction bc low dose ASA can reduce and prevent the skin flushing and itching if taken 30 min before giving niacin. So niacin is frequently prescribed with ASA. The flushing and itching usually improve after being on Niacin for 2-4 weeks.

Kid with musty odor, eczema, albinism, impaired cognition, microcephaly, can be boy or girl. What do you think they have?

PKU: phenylketonuria (Think... PHEW.. that smesll bad... PKU... that's a musty odor.. )

What are features of paroxysmal nocturnal hemoglobinuria? What category of problems is it?

PNH is an autoimmune hemolytic disorder. - autoimmune - hemolytic It has Intravascular AND extravascular hemolysis (so see labs showing hemolysis). and hemoglobinuria (so pee is dark) This is a diseased that occurs bc lack of glycosylphosphatidylinositol anchor, which connects proteins, including CD55 and CD59 to the cell surface. these proteins normally INHIBIT the activation of COMPLEMENT on RBCs, but since they aren't there, the complement membrane attack complex (MAC) forms and causes hemolysis. Pts usually have symptoms in the 4th decade of life with -Hemolysis --> hemoglobinuria (see dark urine) -Cytopenias (see fatigue, dyspnea, anemia) -Hypercoagulable states (ex: portal vein thrombosis) - acute abdominal pain may be d/t severe hemolysis or portal vein thrombosis. Tx: Iron & folate supplementation. Eculizumab (monoclonal antibody that inhibits complement activation) for hemolysis and thrombosis treatment. -Prednisone is best initial therapy for hemolysis. BMT is only way to cure (since this is a clonal stem cell defect) Memory tool: (ECU Liz likes to go out at night.. noctural (paroxysmal noctural hemoglboinuria).. is tired/fatigued, anemia, has dark pee (hemoglobinuria) and clots. (venous thrombosis).. those are all sx of PNH and tx is Eculizumab)

What's the description of mesenteric ischemia?

POOP: Pain out of proportion. RF: older age, a. fib (since it's basically a MI of your gut), CHF, atherosclerotic vascular dz. CT: will show focal and segmental bowel wall thickening, small bowel dilation and mesenteric stranding.

What makes a pt more susceptible to C.diff infection rather than just recent abx use?

PPI use: gastric acid suppression with PPIs are thought to alter the colonic microbiome and increase the risk of C.diff growing too much. Hospitalization: that's where people get C.diff. Advanced age: older pts have decreased colonic immunity and greater exposure to abx, PPIs, and hospital environments, putting them at increased risk for C.diff.

What is someone is allergic to penicillin, what do you do for H.pylori triple therapy?

PPI, clarithromycin, replace amoxi with metronidazole

What are renal complications that can happen in pts with sickle cell trait?

Painless hematuria UTIs Renal medullary cancer

Pt presents with painless jaundice and scleral icterus, weight loss, and AP 890, TBili 14.6, D.bili 10.9. AST ALT are only mildly elevated. Likely cause?

Painless jaundice with mostly direct (conjugated) bilirubin elevation, then thinking malignant biliary obstruction (like cholangiocarcinoma, pancreatic or HCC, or metastatic cancer). Next step is to get abdominal U/S or CT. MRCP or ERCP if imaginig is non-diagnostic. This is NOT chronic pancreatitis bc in chronic pancreatitis, the LFTs are usually normal and it would give more of a hx of recurrent bouts of abdominal pain and symptoms of fat malabsorption with steatorrhea.

24 yo F with hyperthyroid symptoms (heat intolerance, increased appetite, weight loss, tachycardia) and mildly enlarged, mobile and non-tender thyroid. Mild lid-lag. RAIU is <5% (normal is 8-25%). Thyroid gland is NOT visualized on thyroid scan. likely dx?

Painless thyroiditis (aka silent thyroiditis: has acute thyrotoxicosis with mild thyroid enlargement and suppressed TSH. Thyroid scintigraphy shows decreased RAIU. - this is autoimmune. - RAIU is decreased, which suggests preformed thyroid hormone. (which is different from Graves which shows diffuse RAIU, signifying hyperthyroidism d/t increased synthesis of thyroid hormone). - Not Graves bc Graves has diffuse uptake. - Not subacute thyroiditis bc that one hurts. (aka De Quervain thyroiditis. Also causes hyperthyroidism, suppressed TSH, and decreased RAIU. But it hurts!) (also think of this one as post-viral inflammatory process, so elevated ESR, CRP, fever and it hurts) - Not toxic nodular goiter bc will have increased uptake (focal uptake in toxic adenoma and heterogenous uptake in toxic multi-nodular goiter) - Not struma ovarii because this is a young pt (struma ovarii is a rare cause of thyrotoxicosis d/t production of thyroid hormone by ovarian teratoma. Typically presents in women >40yo with pelvic mass, ascites,or abdominal pain. The thyroid gland is not enlarged in struma ovarii bc the source of the symptoms is the teratoma) - Not Hashimoto thyroiditis (chronic autoimmune thyroiditis) bc Hashimoto is hypothyroidism.

What is amaurosis fugax? What is the cause of this usually?

Painless, transient monocular blindness that lasts a few seconds. Usually vascular (ex: embolus to ophthalmic artery) in origin.

Which thyroid cancer types arise from thyroid epithelial cells?

Papillary and follicular cancers

Pt is s/p MI in the first week and then they have severe MR --> hypotension and pulmonary edema, what complication are you thinking happened?

Papillary muscle rupture

What might cause and enlargement of your blind spot?

Papilledema. (increased ICP --> pappilledema --> enlarged blind spot)

What kind of kidney disease has "Hyalinosis" that affects both the afferent and efferent arterioles?

Pathognomonic for DIABETIC nephropathy. Memory tool: Hiya! Diabetes... (Hyalinosis = Diabetic nephropathy)

Best way to confirm diagnosis of fibroids?

Pelvic Ultrasound Yes, you can see it on ultrasound!

Pregnant mom has lots of vomiting (hyperemesis gravidarum), her uterus is also larger than expected size (12 week size for 8 week gestation. what do you want to do?

Pelvic Ultrasound (to look for multiples or molar pregnancy) If you see hyperemesis gravidarum, first think to think about is multiples or hydatidiform mole (both are associated with markedly elevated beta-HCG).

Dull and ill-defined pelvic ache that worsens with standings. Dyspareunia

Pelvic congestion

Pt with skin sores. Painful ulcers in mouth 3 weeks ago. diffuse onset, large painful blisters on trunk and extremities. Exam: oral mucosa with several erosions and ulcers. Skin with scattered, large erosions and few FLACCID bullae. light rubbing of the skin causes easy separation of epidermis (pushing on the bullae pops it and now you have an ulcer; bc the is separation of the epidermis). Punch biopsy of skin and immunofluorescence microscopy shows ***intercellular*** deposits of IgG. What's the dx? What's the autoantibody target?

Pemphigus Vulgaris (looks vulgar.. all these oral lesions and large erosions on the skin and skin that pops easily - Nikolsky sign) Targets Desmosomes.

60 yo man has ***persistent*** glans penis ulcer, began ***several months ago*** and has slowly enlarged. No pain, fever, dysuria.. Smoker for 40 years. 2cm ulcer on penis with superficial slough and hard, indurated base. Several enlarged, hard, mobile inguinal lymph nodes BL. Most likely cause of ulcer?

Penile cancer Painless penile nodule or ulcer on distal penis (glan, coronal sulcus, foreskin), think penile cancer (primarily in men > 60yo). Most cases are d/t SCC. Lymphatic spread (or inflammation) may lead to inguinal LA. Distant mets are not typically present until later in the course. Biopsy needed for dx. RFs: HPV infection, phimosis, cigarette smoking. Tx: excision, chemo (depending on stage)

Pt tries to commit suicide with organophosphate insecticide. On arrival, he's afebrile, BP 80/60, RR 12, HR 75, he has lots of vomiting, diarrhea, and copious oral secretions. What receptor site is most likely responsibel for his clinical manifestations?

Peripheral muscarinic receptors. (not central cholinergic receptors)

Symptoms of B6 (Pyridoxine) deficiency

Peripheral neuropathy (B6 must be given when you give INH bc INH will cause a B6 deficiency)

Clinical findings for congenital infection with CMV

Periventricular calcificiations

Pt has malaria... what is the most likely cause for recurrence of symptoms?

Persistent dormant infection. YIKES malaria can lie dormant in your liver... (Plasmodium vivax; dominant species in non-African countries). Dormant and then can recur weeks to months after initial infection. So want to make sure you treat with Cloroquine for the erythrocyte phase AND Primaquine for the dormant hepatic phase. If you don't treat with primaquine, most patients will relapse. Patient initially has fever, chills, flu-like sx with lower severity but possibility of reactivation. Memory tool: Vivax has 2 V's so have that help you think.. it can lie dormant in the liver and then come back an recur, the second V... and also think this is outside of Africa (since Katie Fridel went to Africa and her sxs were really bad but it infection didn't recur... so the one in Africa is more severe but doesn't lie dormant and recur) (vs Plasmodium falciparum is primarily in Africa. Has more severe sxs: fever, chills, flu-like sx, but also AMS and organ failure. But no dorman phase. Tx with Chlororquine)

High pulmonary vascular resistance results in R--> L shunting and hypoxia. Tachypnea and severe cyanosis. CXR shows clear lungs with decreased pulmonary vascularity.

Persistent pulmonary HTN. of the newborn should be suspected in all term and post-term neonates with cyanosis. High pulm. vascular resistance results in R-->L shunting of deoxygenated blood through foramen ovale and ductus arteriosus --> hypoxia. Dx is rare in very low birth weight infants.

How does Creutzfeldt-Jakob disease, the prion disease present?

Personality change, dementia, and (often) myoclonus.

Point tenderness over medial aspect of knee joint just distal to the joint line. What is that?

Pes anserinus pain syndrome (also known as anserine bursitis) -Pain is worse by pressure form contralateral knee while ling on the side.

How does HSV1 acute pharyngitis present?

Pharyngeal edema and exudates. Associated mucocutaneous ulcerative lesions typically present.

How does strep throat (pharyngitis) from GAS present?

Pharyngeal exudates, tender cervical LA, Lower abdominal pain

How is Pick's disease different form Alzheimer's?

Pick's disease is similar to Alzheimer's except it presents at an early age (around late middle age). Seen more in females and frequently causes personality changes due to involvement of frontal lobes.

AD d/o that has patchy absence of melanocytes, noticed at birth and confined to head and trunk

Piebaldism Memory tool: think of it as looking like a piece of a pie is missing... and theyre balding since the color is missing. (looks like Storm form the comics)

10 yo boy has headache, vomiting, visual disturbances. He has 2 weeks of persistent headache that isn't improved with OTC analgesics. He also has daily vomiting, BL upper eyelid retraction, and limitation of upward gaze with preference for downward gaze. Pupils react sluggishly to light but appropriately to accommodation. What kind of mass does he have?

Pinealoma The pineal gland is located kind of posteriorly, in the quadrigeminal cistern and make melatonin. A tumor there can have serious complications of mass effect (Parinaud syndrome, obstructive hydrocephalus) Parinaud syndrome (dorsal midbrain syndrome): d/t pressure on the pretectal region of the midbrain near the superior colliculus and CRANIAL NERVE III (If Cranial 3 is out, then all that's left is SO4, LR6 so you get a down and out gaze) You also get BL eyelid retraction (ex: Collier sign, sclera visible above superior corneal limbus), and light-near dissociation (ex: pupils that react to accommodation but not to light) Pineal gland masses can also block CSF flow in the aqueduct of Sylvius, causing obstructive hydrocephalus and sx of HA and vomiting.

Worried patient may have cancer in the spine? Do you do MRI first or Pain film x-ray?

Plain film X-ray. MRI spine is reserved for pts with significant neurologic deficits, features of cauda equina syndrome, or suspected epidural abscess. X-ray is useful in pts with elevated risk of malignancy*** DING DING DING, if you're thinking cancer in spine, go with plain film x-ray first. Note: inflammatory markers (ex: ESR) can increase sensitivity in such patients.

Concerned about ototoxicity in what kind of chemotherapy? examples? So what should you do before giving these drugs?

Platinum-based chemotherapy (ex: cisplatin, carboplatin) Get baseline audiometry before initiation of platinum based-chemotherapy that can cause ototoxicity

Facial plethora (ruddy cyanosis), splenomegaly, Aquagenic pruritis (itching after bathing), increased blood viscosity (HTN, erythromelalgia - burning cyanosis in hands/feet, transient visual disturbances), gouty arthritis (increased RBC turnover), bleeding. What does this person have? what do you expect to see on labs? complications? tx?

Polycythemia vera. So expect elevated hemoglobin, leukocytosis, and thrombocytosis (so RBC, WBC, and platelets are all elevated), low epo levels (since you have enough RBCs, too many infact), and JAK2 mutation positive (think.. Jack is 2 itchy... polycythemia vera has JAK2 mutation, which is constitutively active instead of just in response to tissue hypoxia so pt has erythrocytosis and low EPO levels.) Complications: thrombosis, myelofibrosis and acute leukemia. Tx: phlebotomy, hydroxyurea (if increased risk of thrombus)

Macrosomic babiy of diabetic mom. What is that baby most at risk of developing?

Polycythemia. Persistent maternal hyperglycemia --> fetal hyperglycemia --> fetal hyperinsulinemia. Fetus is in constant anabolism so the placenta is not able to meet the increased metabolic demands --> fetal hypoxemia. In attempt to increased oxygen carrying capacity of RBCs, increased EPO production --> polycythemia in up to 1/3 of babies of diabetic moms. Polycytemia is dangerous as the viscous blood is at risk for sludging, ischemia and infarction of vital organs. Newborns need close monitoring of CBC and signs of hypoperfusion. Hypocalcemia: bc of parathyroid hormone suppression. Neonates are usually asymptomatic but should be watched for sx of neuromuscular irritability (ex: seizures, tetany) Hypoglycemia: bc they leave moms steady high glucose supply but they are still making their own hyperinsulin so at risk for profound hypoglycemia. Monitor their BG and give IV glucose infusion until oral feedings can maintain euglycemia.

45yo woman with progressive weakness for several months. Difficulty lifting her kids and getting out of the car (proximal muscle weakness), Difficulty swallowing and has several episodes of choking when drinking water (esophageal muscle involvement). No medical problems. Denies pain. Strength 4/5 in deltoids and quadricep muscle groups. No limitation to ROM. ESR 50 (high), Serum Creatine Kinase elevated. TSH normal. Best initial treatment? What does she have?

Polymyositis: Presentation: proximal muscle weakness (ex; difficulty getting out of car and also lifting kids), mild/absent pain. Peaks incidence at age 40-50. If esophageal muscles are involved, pt can have dysphagia with regurgitation and aspiration. Dx: - Elevated muscle enzymes (ex: creatine kinase, aldolase, AST). -auotantibodies to ANA and anti-Jo-1. -Inflammatory markers (ex: ESR) can be elevated. -Biopsy is how you make the definitive dx: would show endomysial infiltrate and patchy necrosis. Tx: Initial remission can be induced with glucocorticoids (ex: prednisone) and most pts also get glucocorticoid-sparing agents (ex: methotrexate, azathioprine) to minimize long-term adverse effects of tx. Screening: Since polymyositis frequently occurs as a PARANEOPLASTIC syndrome, pts should also receive age appropriate cancer screening

Dysarthria & clumsy hand in lacunar stroke, what part of brain likely affected?

Pons Picture: someone whose so clumsy, they can't hold even soft PomPoms.

What physical exam finding suggest cardiac cause of edema?

Positive hepatojugular reflux: putting firm/sustained pressure for 10-15 seconds over the upper abdomen. Positive response if there is sustained elevation of JVP >3cm during continued abdominal compression. Reflects a failing RV that cannot accommodate an increased in venous return with abdominal compression. Most common causes of positive hepatojugular reflux: constrictive pericarditis, RV infarct, and restrictive cardiomyopathy. Note: Hx of TB is suggestion of constrictive pericarditis as the likely cause. Note: hepatic congestion with hepatomegaly d/t constrictive pericarditis can eventually lead to cirrhosis (called cardiac cirrhosis.. but if the stem doesn't' say that has happened yet, look for cardiac cause first rather than hepatic cause.. hepatic cirrhosis is a sequelae)

Predictors of favorable prognosis in schizophrenia

Positive psychotic symptoms (ex: hallucinations, delusions) Female gender (possibly r/t later age onset) Acute onset (lack of prodrome) Identifiable precipitant Older age of onset Presence of positive psychotic symptoms

Pt has pericarditis (pain worse with deep inspiration, improved by leaning forward, diffuse ST elevations on EKG, reciprocal depression in aVR), 2 weeks after MI. When does post-MI acute pericarditis typically occur timeline wise? What do you think this pt have? What do you give this pt?

Post-MI acute pericarditis usually occurs in first several days s/p MI. This pt Most likely has Dressler syndrome, which can have pericarditis weeks after MI. Dressler syndrome is d/t immune phenomena. -Malaise, Fever, Elevated ESR, Pericarditis weeks s/p MI. -Mainstay tx for Dressler's syndrome: NSAIDS. Can also use corticosteroids if refractory or NSAIDS are contraindicated. ***NSAIDS IS THE TX OF CHOICE!!***

What are you thinking of you see pt with hyperthryoidism (elevated free T4, suppressed TSH), fever, neck pain, tender goiter, elevated ESR, and recent hx of URI?

Post-viral inflammatory process: Subacute (de Quervain, subacute granulomatous) thyroiditis. Note: Thyrotoxicosis in subacute thyroiditis resolves spontaneously within a few weeks and may be followed by a hypothyroid phase lasting a few months. Most pts recover with euthyroid state. Tx: beta blocker to control thyrotoxic symptoms. NSAIDS for pain relief (glucocorticoids can be used for severe thyroid pain not responsive to NSAIDS)

What's a reasonable way to decrease post-op pneumonia in a pt?

Pre-op PT (getting him to do aerobic exercise, inspiratory muscle training) significantly reduces post-op incidence of atelectasis and pneumonia and shortens length of stay post-op. Smoking cessation should happen >8 weeks b4 surgery bc immediately after cessation you have increased broncho-secretion. Note: do NOT pick inhaled corticosteroids bc that actually increases the risk of pneumonia.

Pt with COPD... you're worried about him having post-op pneumonia since he needs a CABG. What intervention will most likely decrease the risk of postop pneumonia?

Pre-op PT. Doing aerobic exercise, inspiratory muscle training can significantly reduce the post-op incidence of atelectasis and pneumonia and shorten post-op hospital LOS in pts undergoing elective cardiac surgery. Smoking cessation also helpful to reduce peri-op pulmonary risk, but the benefit may be present only when smoking is stopped > 8 weeks post op (bc there is increased bronchosecretions right after you stop smoking... so should stop smoking at least 8 weeks before surgery)

Pt has MI and now is in cardiogenic shock, what do you expect his preload, CO, and afterload to be?

Preload: high (heart muscle not pumping well so blood backs up) CO: low (heart muscle is damaged so not pumping well, decreased stroke volume) Aterload: high (SVR constriction in response to low CO to try to maintain BP)

Late lyme disease presentatin Tx?

Presentation: arthritis, encephalitis, peripheral neuropathy. Timeline: months-years Tx: IV ceftriaxone

Analgesic abuse nephropathy: What is happening in the kidneys?

Primarily a tubulo-interstitial disease characterized by focal glomerulosclerosis.

When a PCR of the CSF shows EBV DNA, what are you thinking the pt has? (MRI also shows ring-enhancing mass that is solitary and periventricular)

Primary CNS lymphoma - that finding is specific for this condition.

HIV+ pt with AMS, disoriented, lethargy, loss of recent memory. He's on TMP-SMX, taking his antiretroviral, and azithromycin. Temp 99.8. CD4 count 40. Viral load 25,000. Non-focal neuro exam. MRI shows solitary, irregular, weakly ring-enhancing mass in periventricular area. Serology for toxo is positive. PCR of CSF with EBV DNA. likely dx?

Primary CNS lymphoma. Ring-enhancing, you think toxo (but he's taking TMP-SMX ppx and it's not multiple of the ring enhancing lesion, also the serology for toxo means nothing bc that's really common in normal people in the USA). So the next thing you should think for ring enhancing lesion is CNS lymphoma!!! PCR with CSF showing EBV DNA is specific for primary CNS lymphoma. MRI for this is weakly ring-enhancing mass that is usually solitary and periventricular and can cause mass effect in a HIV pt. Note: it's not abscess bc he's afebrile. It's not AIDS dementia bc that would have cortical and subcoritcal atrophy and secondary ventricular enlargement. It's not progressive multifocal leukoencephalopathy bc those are non-enhancing, multi-focal and do not produce mass effect.

25yo HIV+ pt with CD4 count of 40. He has 1 month of AMS, disorientation, lethargy, and loss of recent memory. He is taking antiretrovirals, TMP-SMX (treats toxoplasmosis), and azithromycin. He is afebrile. Non-focal neuro exam. MRI shows "a solitary, irregular, weakly ring-enhancing mass" in the periventricular area. Serology for toxoplasma is positive. PCR of CSF shows EBV DNA. What is the most likely diagnosis?

Primary CNS lymphoma. - The presence of EBV DNA in the CSF is specific for this condition!! MRI reveals a weakly ring-enhancing mass that is usually solitary and periventricular. Note: Toxoplasmosis is a good ddx, however this pt is on TMP-SMX so it's unlikely for him to get toxoplasmosis even if his CD4 count is <100. MRI usually reveals MULTIPLE ring-enhancing, spherical lesions in the ***basal ganglia*** (not the periventricular area... which is more CNS lymphoma). Also Note: A POSITIVE TOXOPLASMA SEROLOGY IS QUITE COMMON IN NORMAL SUBJECTS IN THE USA. and is therefore not specific for toxoplasmosis. (don't get tricked by that)

When do you see calcium phosphate stones?

Primary Hyper-Parathyroidism & Renal tubular acidosis.

44yo M 6mo hx progressive fatigue and pruritis. Yellowing of eyes and dark urine. Scleral icterus, skin excorations. BUN 20. T bili 7.3, D bili 5.3, AP 580. AST 62, ALT 99. MRCP with multifocal short narrowing of bile ducts and segmental dilation.. dx? what else is likely in presentation?

Primary Sclerosing Cholangitis -fatigue, itchy -asymptomatic at time of dx -ABOUT 90% of pts have underlying IBD!!!!!, mainly UC This is a cause of liver disease. So get LFTs (serum aminotransferases <300) -Labs will have a cholestatic pattern of liver injury: predominately elevated AP, direct hyperbili, and increase LFTs (but <300) Imaging: will see strictures/dilations and intrahepatic &/or extrahepatic bile ducts on cholangiography Liver biopsy: fibrous obliterations of bile ducts with concentric replacement by CT in "onion skin" pattern Dx confirmed with ERCP or MRCP showing multifocal narrowing and intra- and extra-hepatic duct dilation. (PSC is the only cause of liver disease where you don't need to biopsy the liver.. you can just do ERCP or MRCP to dx bc you'll see the narrowing and dilation) Complications: -Intrahepatic &/or extrahepatic biliary stricture. -Cholangitis & Cholelithiasis (cholesterol &/or pigment stones) -CholangioCA (10-15% lifetime risk) -Cholestasis (ex: decreased fat soluble vitamins, osteoporosis) -Colon cancer ***PSC should be associated with IBD - recurrent bloody diarrhea and anemia, abdominal pain, tenesmus, and systemic symptoms (fever, fatigue, weight loss)

Complains of dysphagia to solids & liquids and a dilated esophagus with smooth tapering of distal esophagus. What does this suggest?

Primary achalasia (loss of peristalsis in distal esopahgus with lack of lower esophageal sphincter relaxation ) - or - Pseudoachalasia d/t esophageal cancer (supporting pseudoachalasia would be significant weight loss, rapid symptom onset and presentation at age >60; those things ponit to malignancy) Note: tobacco is major RF for esophageal adenoCA and SCC; ETOH use is also RF for esophageal SCC. tumor mets (mediastinal lymph nodes) or local involvement may give radiologic appearance similar to that seen in widened mediastinum (so CXR may say "widened mediastinum). -Want to evaluate with endoscopic evaluation to differentiate between achalasia and pseudoachalasia. In achalasia, you'd seen normal appearing esophageal mucosa and a dilated esophagus with possible residual material and it's usually possible to easily pass the endoscope through the lower esophageal sphincter (unlike in malignancy that would not be the case) DO ENDOSCOPY to EVALUATION!! if it's pseudo-achalasia (cancer) or just achalasia.

If pt has hyperpigmentation, and symptoms of fatigue, weight loss, lethargy, decreased appetite, dizziness, orthostatic hypotension, what are you thinking the dx is?

Primary adrenal insufficiency. They have injury to all 3 layers of the adrenal cortex so have features of glucocorticoid and mineralocorticoid (orthostatic hypotension) deficiency. Note: women may also have sx of adrogen deficiency (low libido) as adrenals are the major source of androgens in women.

Pt with chronic sinopulmonary infections, nasal POLYPS!!, bronchiectasis, digital clubbing. Situs inversus (50% of cases), infertility d/t immobile spermatozoa, normal growth (normal percentiles on the growth chart). What do they have?

Primary ciliary dyskinesia

Pt is 31yo female with 3 months burning upper abdominal pain that is only partially relieved by ranitidine or antacids. She has recent onset constipation and excess urination. Her father had hx of "many stomach ulcers and multiple kidney stones." VSS. Tender epigastric region. Stool positive for occult blood. Labs: calcium 11.4 (high), phosphorus 1.8 (low bc normal is 3-4.5), BUN 21 (high). What is the the dx?

Primary hyperparathryroidism. (as part of the MEN1 3P's) I was thrown off by the excess urination, but the hyperCa will cause the pt to go through diuresis so you have excess urine explained. Constipation is also d/t the parathryoid (not sure how). The burning upper abdominal pain is explained by GI/Pancreatic endocrine tumors (ex: gastrinomas aka Zollinger-Ellison syndrome with severe PUD d/t gastrinomas which are gastrin-producing tumors) since you are thinking this may be a MEN1 pt with the family hx of GI ulcers and kidney stones (likely d/t hyperCa). MEN1 is the 3P's: Pituitary adenoma, Parathyroid adenomas (so hypercalcemia), Pancreatic/GI endocrine tumors,

75 yo AA diabetic hypertensive comes in and you look at his fundus and see cupping of optic disc and the exam shows constricted peripheral vision. What's the likely dx?

Primary open angle glaucoma. -Gradual loss of peripheral vision over pd of years and eventual "tunnel vision" think about primary open angle glaucoma. -Intraocular pressure is high. -May be cupping of the optic disc with loss of peripheral vision. Tx: annual exams, tx with Timolol beta-blocker eye drops as initial management. Then Laser trabeculopasty as adjunctive measure. If there is continued increased in intraocular pressure, surgical trabeculectomy is done. Note: more common in AAs, increased prevalance in pts with family hx of glaucoma and DM.

Chronic disease with cholestatic pattern on liver tests. Pts may be asx or have chronic fatigue, pruritis on presentation.

Primary sclerosing cholangitis. See Short, annular strictures alternating with normal bile duct.

How does Rabies present?

Prodrome: fever, chills, malaise, HA (feeling crappy) Then comes the hydrophobia (water fear), pharyngeal spasm, hyperactivity, coma, and death.

What are features of complicated pyelonephritis?

Progression of initial pyelo to renal corticomedullary abscess, perinephric abscess, emphysematous pyelo, or papillary necrosis. Sepsis, multiorgan failure, shock, RF. Complicated pyelo is more likely to happen in pts with DM, kidney stones, immunosuppression, or other anatomic abnormalities of the urinary tract. These pts usually require imaging to evaluate for complications, urologic eval and prompt therapy (med/surgical)\ vs. uncomplicated pyelo doesn't need imaging unless they don't improve in 72 hours (which would push you to think they might have features of complicated pyelo...bc they are not getting better.. and then it's worth doing imaging)

what's the presentation for Riedel thyroiditis (Riedel struma)

Progressive Fibrosis of the thyroid gland and surrounding tissue. Fibrotic mass may resemble malignancy but sx are chronic and slowly progressive (not acute) Slow progression .. (think riding this to the end.. so going slow.. "Riedel").. so slow you start to fibrose... may look like malignancy but sx are chronic.

What is happening in ALS? (Amytrophic Lateral Sclerosis)

Progressive degeneration and death of motor neurons. Present with both UMN and LMN signs. -UMN signs: spastic weakness, hyperreflexia -LMN signs: atrophy, fasciculations.

Pt with CD4 count <200, now has mental status changes, motor deficits, ataxia, and imagining shows "multiple non-enhancing brain lesions with no mass effect (edema). What is that? "several asymmetric, hypodense, nonenhancing white matter lesions with no edema"

Progressive multifocal leukoencephalopathy (caused by JC virus reactivation when CT count is <200) Slowly progressive, confusion, paresis, ataxia, seizure.

You have a 56yo man with 7mo hx HA, loss of libido, ED, and visual disturbances (temporal field defects on in both eyes), atrophic testes. MRI shows 1.5cm pituitary tumor and you want to dx prolactinoma, what do you expect his prolactin level (normal is <15), LH (high/low/normal) and TSH (high/low/normal) to be? Tx?

Prolactin >200 is diagnostic. LH low bc feedback mechanism suppresses it TSH should be normal (r/o thyroid issues) Tx: DA agonists (cabergoline) since DA suppresses Prolactin. or do trans-sphenoidal surgery. Note: Younger women are dx earlier bc of effects on menstration, infertility and galactorrhea, but men and postmenopausal women don't present with those so they come later with visual field defects and HAs (compressive symptoms). The magnitude of the prolactin elevation correlates with the size of the prolactinoma and a level >200 is virtually diagnostic of prolactinoma. Note: very large pituitary masses will cause a low TSH and LH due to compression of thyrotrophs and gonadotrophs, along with the mildly elevated prolactin (around 45) d/t compression of the DA pathways in the pituitary stalk. <-- would be characteristic of "nonfunctioning" pituitary macro-adenoma (which is not the case in this pt with the 1.5cm mass)

Pt has Prolactinoma which is causing small temporal field defect. GU shows atrophic testes. MRI shows 1.5cm pituitary tumor. What do you expect to find with Prolactin levels (Nl is < 15), LH, and TSH levels?

Prolactin levels should be high (often >200) - since it's big enough to cause compressive sx causing a visual field defect. The magnitude of prolactin elevation correlates with the size of the prolactinoma and a level >200 is virtually dx of prolactinoma. LH should be low (bc of negative feedback to LH) -Note: also see hypogonadotropic hypogonadism (small testes) bc of suppression of GnRH from hypothalamuc by prolactin. Gynecomastic can also present in 1/3 of men. -TSH should be normal or low (note: hypothyroidism can cause prolactin to be evelated bc feedback of low thyroid hormone to TRH can also stimulate lactotrophs. There may be a relationship with prolactinoma --> TSH but it's not a not a stimulation/feedback thing, but rather it's physical compression effect on thyrotroph cells could cause the TSH to be low.. or the compression could not be there and so TSH could be normal) Note: VERY LARGE pituitary masses will cause low TSH and LH d/t compression of the thyrotrophs and gandotrophs, along with mildly elevated prolactin d/t compression of the DA pathways in the pituitary stalk. This would be more characteristic of "nonfunctioning" pituitary MACROadenomas (which usually secrete biologically inert gonadotrophin alpha subunit; so they would have just a mildly elevated prolactin level of 45 (instead of the >200 see with prolactinoma; note: prolactin levels can be as high as 1,000 in 2cm prolactinomas)

How does prolactinoma affect FSH and LH?

Prolactinoma means elevated prolactin levels --> negatively inhibits GnRH secretion, leading to decreased FSH and LH.

32 yo female ot has livedo reticularis (transient red/purple blotchy, latticelike rash on heir lower extremities). She also has 3 day hx of pain and swelling in left leg. Pain is moderate. Hx of migraines, IBS, recurrent miscarriages. Left calf and ankle are swollen and palpation of left thigh and calf elicits tenderness. What are you likely also to find on labs?

Prolonged PTT Livedo reticularis (LR) is caused by impaired blood flow in the superficial venules. Often a benign finding but can be a sign of vasculitic (ex: polyarteritis nodosoa, SLE) or vasooclussive (ex: choleserol embolization, antiphospholipid syndrome, cryoglobulinemia) disorder. it's the most common dermal manifestation of antiphospholipid syndrome. Combined with DVT and hx of recurrent miscarriages, the LR points to antiphospholipid syndrome. -In APL syndrome, the PT T is prolonged; d/t binding of phopholipid reagents in the assay by the lupus anti-coagulant (antiphospholipid antibodies). Mixing of patient plasma containing anticoagulant with normal plasma will not correct the partial thromboplastin time (PTT) in contrast to pts with clotting factor deficiencies. TL:DR: pt with livedo reticularis, DVTs, and recurrent miscarriages, think about antiphospholipid syndrome and they have Lupus anticoagulant that shows prolonged PTT. (Memory tool: think lupus anticoagulant.. is SLE.. with 3 letters, so it's PTT with the 3 letters that's prolonged)

27yo woman with 1 day CP and SOB. CP increases with inspiration. Right leg swollen. Rash on face that worsens in sun, recent painful swelling in both knees and had 2 previous early miscarriages. CT shows PE. What additional finding will you see with her blood lab work?

Prolonged PTT (d/t presence of Lupus anticoagulant) This pt sounds like she has lupus and she also has several miscarriage. Antiphospholipid antibody is associated with SLE. Now she has a VTE. She likely has Lupus anticoagulant, which will cause a prolonged PTT (in vitro; it does not correlate with prolonged bleeding in vivo, it's just a sign that someone has the lupus anticoagulation (LA)) APS characterized by: -VTE or recurrent early miscarriages (prior to 10 weeks) -Presents of antiphospholipid antibody, like Lupus anticoagulant (LA), anticardiolipin antibody, or beta-2 glycoprotein 1 antibody. LA occurs in 10-30% of patients with SLE. In vitro, you see prolonged PTT as it binds to phospholipids used in most assays. Does not correlate with bleeding in vivo. PT may also be prolonged. PTT will not correct if mixed in 1:1 dilution with normal plasma. Prolonged PTT is ***indirect indicator*** for presence of LA & highly suggestive in correct clinical setting. Specific tests include diluted Russell viper venom test & kaolin clotting time. -Memory tool: think SLE is lupus with 3 letter, so with lupus anticoagulant, it's the PTT (3 letters) that is prolonged.

Pt with lupus and early miscarriages, now has a DVT and VTE. What do you expect on blood labs?

Prolonged PTT: indicator that pt has Lupus anticoagulant (LA), which will have prolonged PTT (in vitro; doesn't correlate with increased bleeding in vivo). This pt has antiphospholipid syndrome, which is associated with SLE, early miscarriages, and VTE (DVT, PE): -10-30% of pts with anti-phospholipid syndrome will have LA.

Pt presents with acute liver failure, what labs do you want to check?

Prolonged prothrombin time (PT) with INR (>1.5) A prolonged PT with INR >1.5 tells you that there is synthetic liver dysfunction. Note: acute liver failure is characterized by triad of elevated aminotransferases, hepatic encephalopathy, and prolonged PT in pt without underlying liver disease.

What is the heparin reversal agent?

Protamine sulfate!!! Heparin, Protamine sulfate, heparin, protamine sulfate, heparin, protamine sulfate, heparin, protamine sulfate.

What kind of organism causes Chagas disease?

Protozoa - Trypanosoma cruzi - organism is common in Latin America. Think about this in symptomatic pt who recently comes from latin america. 2 primary manifestations are megacolon/megaesophagus and cardiac disease. -Megacolon/megaesophagus (focal GI dilatation) occurs 2/2 destruction of nerves controlling GI smooth muscle -Heart issues: pathophys not well understood but probably d/t prolonged myocarditis 2/2 protozoa infection (CHF sx of pedal edema, JVD, S3, cardiomegaly)

Pt has a PE, what is the most likely origin of the embolus?

Proximal/thigh veins: Iliac, femoral, popliteal veins (these are the sources of >90% PEs, probably d/t larger caliber and proximity to the lungs) They come from DVTs (deep vein thrombosis), but proximal/thigh clots are more likely to travel than distal/calf clots. -So femoral/iliac/popliteal clots are a more likely source of acute PEs than distal calf emboli. UGHHH I KNEW THIS but still got it wrong. Note: DVT stands for DEEP vein thrombosis, the D is not distal. So think about how proximal DVTs in the lower extremities are actually the ones that become PEs. And remember clinically we would watch distal clots.. and were more concerned if they moved more proximally.

Pt with UTI gets treated (presumably with TMP-SMX that is a sulfa drug that can cause oxidative stress), and he feels better but now his urine is dark. You stain the urine with Prussian blue, and it stains positive. What does the Prussian blue tell you, what does this pt have?

Prussian blue indicates presence of hemosiderin, which is found in the urine during hemolytic episodes. This pt has hemolysis after oxidative stress, so he has G6PD deficiency. Hemolytic episodes in these pts are most commonly precipitated by infections or medications that increase oxidative stress (like sulfa drugs, antimalarials and nitrofurantoin) In normal pts, G6PD is responsible for catalyzing the reduction of NADP to NADPH, the 1st step in hexose monophosphate shunt. This is the only source of NADPH in RBCs. NADPH is necessary to form reduced glutathione, which protects RBC from oxidative injury. If you don't have G6PD and there is oxidative stress (sulfa drugs, bacterial toxins), the hemoglobin becomes oxidized to make methemoglobin, denatured globin, and sulfhemaglobin. These molecules form insoluble masses (Heinz bodies) that attach to the RBC membrane, decrease membrane pliability, and promote RBC removal in the spleen's reticuloendothelial system (RES) Prussian blue = hemosiderin.

Pt wants to get pregnant so bad but hasn't been able to and how they have what seems like physical changes that are in line with pregnancy... but two office urine pregnancy tests are negative. Whats the dx?

Pseudocyesesis (think "pseudo" as in it's not a real pregnancy..their body has fooled them into it) Somatization of stress affects HPO axis to cause early sxs of pregnancy or when bodily changes are misinterpreted. Non-psychotic pt who thinks she's pregnant. This is a form of somatization so needs psych eval and tx.

Malignant otitis externa presents in elderly uncontrolled diabetic pt who can't keep food from dropping when she eats and her face droops asymmetrically. Left ear canal shows granulations and discharge. Fever. What is the likely organism? what is the treatment?

Pseudomonas aeruginosa. tx: ciprofloxacin (systemic treatment bc topical abx is not effective)

Young (<45yo) obese female has HA, transient vision symptoms, and pulsatile tinnitus. Exam shows papilledema, visual field loss, and 6th nerve palsy. Dx?

Pseudotumor cerebri (idiopathic intracranial HTN)

Pitting, distal onycholysis (painless detachment of nail bed) and hyperkeratosis (abnormal thickening). What might this be? Would also have red plaques with silvery scale over extensor surfaces (ex: knees, elbows) and the scalp. Note: this is a T-cell mediated immune d/o characterized by keratinocyte hyperproliferation.

Psoriasis

what is NON-classic congenital adrenal hyperplasia?

Pt has decreased 21-hydroxylase activity (but not complete deficiency in the enzyme) -so they present in adolescence or early adulthood with irregular menses, severe acnes, hirsutism, virilization (clitoromegaly, deepening of voice; rare). The enzyme is mildly deficient in nonclassic CAH so they have enough glucocorticoids and mineralocorticoids made so there is no mention of aldo (Na and K electrolyte problems) or cortisol problems. So pts don't have the salt wasting like in classic CAH, and electrolytes and BP remain normal. Dx confirmed by an exaggerated 17-OHP response on ACTH stimulation test.

elderly female patient with polymyalgia rheumatica has frequent HAs, recent weight loss, stiff shoulder muscles in morning, and tender cord palpated at right temporal area. ESR 85. Likely complication of this condition?

Pt has giant cell arteritis, which can involve the branches of the AORTA!! and so aortic aneurysm is a well-known complication. So she should be followed with serial CXRs. Sxs: HA, jaw claudication, muscle fatigue, visual disturbance Exam: scalp tenderness, decreased temporal artery pulse. Labs: ESR >50 mm/hr.

Description of ruptured popliteal (Baker) cyst?

Pt who doesn't exercise then goes and exercises and then has a weird exam finding..bulg behind knee that diminshes with flexion, posterior knee pain, swelling stiffness. Popliteal cysts are often asx and present as chronic painless bulge behind the knee. But when they rupture, following strenuous exercise, they can cause posterior knee and calf pain, with tenderness and swelling of the calf that resembles a DVT. an "arc of ecchymosis" is often visible distal to the medial malleolus ("crescent sign").

When do you see Target cells; RBC with central density with Bull's eye appearance?

Pt with Hemoglobinopathies (ex: thalassemia) or chronic liver disease (esp. obstructive liver disease)

What's functional hypothalamic amenorrhea?

Pt with low caloric intake (ex: low BMI) and they have decreased GnRH secretion which leads to low FSH and LH and suppression of ovarian function.

When and who do you screen with low-dose noncontrast chest CT?

Pts age 55-80yo with >30 year pack history or active smoking in last 14 years. Screen them for lung cancer. Note: that is correct for lung cancer screening, but if pt presents with productive cough and dyspnea, first do spirometry to see if they have COPD.

What's the thing with cirrhotic patients and temperature?

Pts with cirrhosis are often relatively hypothermic so any temperature > 37.8c (100F) warrants investigation

What group of patients do you think about PEs originating from the right atrium of the heart?

Pts with intracardiac devices (ex: Pacemakers); that doesn't tend to happen spontanously

What group of patients do you think about PEs originating from renal veins?

Pts with nephrotic syndrome. (Prevalence of PE with nephrotic syndrome is 10-30%)

What's a big key distinguishing factor between patients with pseudodementia (from depression) and Alzheimer's?

Pts with pseudodementia are frequently distressed by their impaired memory. Those with Alzheimer's are often relatively unconcerned and confabulate. Also, look at timeline. Does pt experience cognitive impairments (forgetfulness, difficulty recognizing relatives) before onset of depressive-like symptoms (social withdrawal, decrease interest)? If so, that's more in line with Alzheimer's. Also look to see if they meet criteria for MDD SIGECAPS criteria. If you suspect depression with pseudodementia (bc there is SIGECAPs components present), treat with anti-depressants first and should expect improvements in cognitive symptoms (improvements in the MMSE).

If a young pt (ex: 35 yo) has s/sx of scleroderma (CREST syndrome; with hx of tight skin, GERD, Raynaud's, telangiectasia) and now they are having dyspnea on exertion, think about what?

Pulmonary HTN (bc of intimal hyperplasia of pulmonary arteries) --> RV hypertrophy and possibly even RH failure. Symptoms: But they have dyspnea, fatigue, weakness Exertional angina, syncope Abdominal distention/pain -They're too young to have these symptoms from MI or AS, so think about PAH, esp since they have CREST syndrome. Signs: -Left parasternal lift, RV heave (bc RV is hypertrophied) -Loud P2, right sided S3 -Pansystolic murmur of TR -JVD, ascites, peripheral edema, hepatomegaly.

What is a life-threatening complications of severe pre-eclampsia where the pt gets SOB, is tachypneic, has bibasilar crackles, is using accessory muscles to breathe, and has 2+ pitting edema., has drop in arterial oxygen sat and SpO2 is 91% on RA?

Pulmonary edema. Caused by increased SVR, cap. permeability, pul. capillary hydrostatic pressure, and decreased albumin. Sudden onset SOB, hypoxia, crackles most likley d/t acute pulmonary edema (rare, life-threatening complication of severe pre-eclampsia). Preeclamptic pts have generalized arterial vasospasm --> increased SVR and high cardiac afterload. Heart becomes hyperdynamic and tires to overcome the systemic HTN. Other factors that lead to pulmonary edema: decreased renal function, decreased serum albumin, and endothelial damaged leading to increased capillary permeability. Management: oxygen, fluid restriction, diuresis in severe cases. Be careful with fluid restriction and diuresis since plasma volume is decreased through 3rd spaced and placental perfusion can be compromised.

What's another way to say PE?

Pulmonary infarction. -Pleuritic CP s/p long distance flight, hemoptysis, SOB, tachypnea, tachycardia, OCP use, all concerning for PE. *YES! They can have pain that is increased with inspiration with PE. The small peripheral thrombi are more likely to cause pleuritic CP and hemoptysis d/t inflammation and irritation of the lung parenchyma and adjacent visceral and peritela pleura.

What is the big category of symptoms you would expect to see in a sarcoidosis patient?

Pulmonary symptoms (ex: cough, dyspnea, wheezing or chest pain) -Sarcoidosis is a rheum disease with fever, cough, weight loss, arthritis. CXR shows BL hilar adenopathy with interstitial infiltrates. Erythema nodosum, tender red nodules on shins, are the typical skin manifestations.

Normal changes during pregnancy:

Pulmonary: pH 7.45 (chronic respiratory alkalosis with metabolic compensation, increased PaO2 and decreased PaCO2; Progesterone directly stimulates central respiratory centers to increased tidal volume and minute ventilation) PaO2: 110 (high: more tidal volume.) PaCO2: 30 (low; tachypnea bc increased minute ventilation) Bicarb: 20 (low; bc of metabolic compensation of the respiratory alkalosis) Renal: Increased CO and renal blood flow d/t P with increased renal excretion. GFR: increased BUN: decreased Cr: decreased Urinary frequency, nocturia (increased UO and sodium excretion) Mild hyponatremia: (increased ADH released from pituitary) Heme: Dilutional anemia (increased plasma volume and RBC mass) Prothrombic state (Hormones decrease total protein S antigen and activity, increased fibrinogen and coag. factors) CV Increased CO and HR (increased blood volume, decreased systemic vascular resistance) In pregnancy, P rises during 1st Tri and changes homeostatic set points in medullary respiratory centers of the brain. P directly stimulates respiratory centers to increase ventilation. Medulla is thought to become more sensitive to changes in PaCO2 and respond with exaggerated respiratory effort. Pregnancy --> hyperventilation, increased TV and minute ventilation, and Chronic respiratory alkalosis -PaO2: 100-110 (increased TV) -PaCO2: 27-32 (increased minute ventilation) -pH: 7.4-7.45 (resp. alkalosis) -Bicarb: decreased (bc of metabolic compensation)

18yo comes for physical for college. She has mild dyspnea when climbing stairs. Younger sister was born with hold in the heart that closely spontaneously in infancy. During expiration, ther'es an extra high-pitched sound after S1. There is 3/6 systolic < > murmur loudest at LUSB. S2 is split throughout the respiratory cycle and splitting increases with inspiration. Murmur does not increase with standing. DP pulses 2+. Most likely mechanism of the murmur?

Pulmonic stenosis. Usually an isolated congenital defect. Rarely acquired in carcinoid. Presentation: < > murmur, increases on inspiration (tells you it's a right heart murmur; and pulmonary valve in in the right heart) systolic ejection clic (best heard during expiration) & widened split S2 (bc stenosis causes pulmonic valve to close later than usual) (different from fixed S2 of ASD. pulmonary valve stenosis has widened S2 split) Mild: symptoms like dyspnea on exertion in early adulthood Severe: right-sided HF in childhood. Dx: echo Tx: percutaneous balloon valvulotomy (preferred). Surgical repair in some cases

Pt with a.fib loses their pulses and has agonal breathing, what do you do?

Pulseless electrical activity (PEA) means start CPR (need to get their heart pumping, do it manually by pushing on their chest). CPR + give EPI (as vasopressor) to achieved adequate cerebral and coronary perfusion. CPR should be done uninterrupted while attempts are made to ID and treat the reversible causes of PEA: -5Hs & 5Ts: Hypovolumia, hypoxia, H ions (acidosis), hypokalemia/hyperkalemia, hypothermia, Tension pneumo, Tamponade (cardiac), Toxins (Narcotics, benzos), Thrombosis (PE or CAD), Trauma

Asymptomatic pt with neck artery stenosis, you see 60% and 40%, waht do you do?

Put then on anti-platelet and statin medication. -Also manage DM, obesity, smoking aggressively. Careful BP control. If symptomatic (TIA or stroke in the previous 6 months), and stenosis is between 70-99%, then do carotid endarterectomy (CEA) If asymptomatic (no TIA/stroke), there is evidence that suggest benefit with CEA for lesions between 80-99% stenosis. Asympatmic lesions <80% are managed medically with anti-plt and statin meds.

Hikers are lost in the woods. Their food supply ran out 16 hour ago. Their glycogen stores are becoming depleted and their bodies are upregulating gluconeogenesis. Alanine is concerted to what intermediate?

Pyruvate. Liver maintains glucose levels in the blood iva gycogenolysis and gluconeogenesis. During fasting states, glycogen reserves drop dramatically in the 1st twelve hours and gluconeogenesis starts to play an important role. After 24 hours, gluconeogenesis is the sole source of glucose production (So think of it as your body takes what's already there... glycogen and breaks it up easily to use as glucose - think of people taking bread off the shelf and breaking (-lysis) it into pieces to eat easily, that's like glycogenolysis) (And then you run out of your pre-formed glycogen that is easily broken up to glucose.. so then you have to start making glucose... gluconeogenesis... - think of people starting to scrounge up food to make (-neogenesis) a meal...so you're using what you can find to make it into a meal.. need to do the citric acid/kreb cycle) the main substrates of gluconeogenesis are gluconeogenic amino acids (from breakdown of muscle protein), lactate (from anaerobic glycolysis) and glycerol 3-phosphate (from triacylglycerol in adiopse). Alanine is the major gluconeogenic amino acid in the liver and is converted to PYRUVATE! by alaline aminotransferase. Pyruvate is eventually converted to glucose through a series of reactions, and free glucose is then released into the bloodstream.

What is cyclic citrullinated peptide antibody used to dx?

RA (>50% sensitivity, >90% specificity)

What's the problem when you have hematuria, HTN, proteinuria, dysmorphic RBCs, RBC casts?

RBC casts, think glomerular problem = Acute glomerulonephritis.

Pt left sided varicocele that doesn't empty when pt is lying down, he has flank pain, hematuria, and blood stuff is weird (anemia or erythrocytosis, increased plts) could also have fever, hypercalcemia, cachexia. What does he most likely have? What test are you going to do?

RCC. Get CT scan to look fo rthe renal mass. Classic triad of RCC: flank pain, hematuria, palpable abdominal renal mass (only found in about 10% pts and that means it's likely advanced or metastatic disease). -Hematuria means tumor has invaded the collecting system. -Scrotal varicocele (most are left sided) are seen in about 10% pts. Varicoceles that fail to empty when the pt is recumbent d/t tumor obstruction of the gonadal vein when it enters the renal vein. This finding should ALWAYS raise suspicion for mass obstruction to venous flow, as seen in RCC. -May see constitutional symptoms: fever, night sweats, anorexia, weight loss, easy fatigability -Ectopic production of EPO by the tumor can --> polycythemia, although most advanced tumors are associated with anemia (so RBC can be up or down) Most sensitive and specific dx test: CT scan of abdomen

What symptoms would you expect if someone had a lesion in the brain or spinal cord (aka upper motor neuron findings)

REMEMBER THAT SPINAL CORD INJURY, LIKE BRAIN INJURY, would result in UMN findings. -Hyperreflexia -Hypertonia -Spasticity -Babinski reflex Note: acute CNS lesions can also present with areflexia or flaccidity (d/t cerebral or spinal shock). Note: remember this so you don't pink a spinal cord injury answer when they are describing cauda equina syndrome, which is a "spinal nerve root compression" injury, which is not part of the CNS but part of the peripheral NS. Radiculopathy is suggestion of peripheral localization, such as a nerve root.

Osteoarthritis: RFs? Hx? PhyEx? Imaging?

RF: >50yo (older), obesity (heavier), prior joint injury Hx: chronic, insidious symptoms (over years), minimal or no morning stiffness (joint pain is worse at end of the day after activity) PhyEx: OA affects the big weight bearing joints (hips/knees) as well as the cervical and lumbar spine, and the small peripheral joints in the hands. There may be hard, boney enlargements of the joints (causing tenderness over medial tibial condyle; or crepitus and pain with movements, limited ROM, small joint effusions w/o redness or warmth, varus/valgus angulation of the tibia, and popliteal (Baker's) cyst behind the knee joint may also be associated. Imagining: X rays will show narrowed joint space, osteophytes, and subchondral sclerosis.

What does a RR = 0.71 show about the drug's decrease in risk of mortality (as outcome)

RR = 0.71 means the drug decreases risk of mortality by 29% (1.0 - 0.71 = 0.29 = 29%)

Pt with sudden onset chest pain, sweating, elevated jugular venous pressure, positive Kussmaul' sign. Lungs are clear. and now they have ST elevation in II, III, and avF and ST segment depressions in I and aVL. What is the cause of their hypotension of 80/50?

RV infarct. Inferior MI (II, III, avF) is due to occlusion of RCA proximal to the origin of the RV branches. Their JVD and Kussmaul's sign (increased JVD with inspiration) along with clear lung fields

What can be associated with development or worsening of opthalmopathy in Graves disease pts?

Radioactive iodine

Most sensitive test for screening for nephropathy?

Random urine for "microalbumin/creatine" ratio.

What is the strongest (gold standard) kind of study for looking at efficacy of a tx or procedure?

Randomized control trial. Has the least amount of bias and provides strongest evidence for a causal relationship

What do you do for acute rejection of renal transplant (presents with oliguria, HTN, increased Cr/BUN)?

Rapid institution of anti-rejection therapy, including HIGH DOSE IV STEROIDS!!!!

How does Peripartum cardiomyopathy present?

Rapid-onset systolic HF (fatigue, SOB, cough, pedal edema) at >36 weeks GA or early puerperium. So symptom onset at about 36 weeks GA, you're thinking peripartum cardiomyopathy.

what is the presentation for primary thyroid lymphoma?

Rapidly growing thyroid that compresses surrounding structures. It's an uncommon disease but has a 60x incidence in pts with pre-existing Hashimoto's (chronic lymphocytic thyroiditis)

What kidney disease has "crescent formation" on light microscopy?

Rapidly progressive glomerulonephritis Memory tool: the moon's crescent shape comes and goes very quickly... every day of the month it's different... so "crescent formation" is "rapidly progressive" glomerulonephritis.

What is stiff person syndrome

Rare autoimmune d/o with rigidity, stiffness, muscle spasms involving the axial muscles. Autonomic instability can also occur, mental status changes are not typically seen.

What is ataxia-telangiectasia?

Rare, progressive neurodegenerative disease: can present with increased sinopulmonary infections, but pts will have severe ataxia, abnormal eye movments, and telangiectasias, particularly o the face.

What kinds of infections and conditions do you see with people who have decreased IgG, IgA, and IgM? What is this condition called? What is the immune problem that causes this condition? What age do these pts usually get diagnosed?

Recurrent respiratory and GI infections. Can see chronic lung disease (ex: bronchietasis), and autoimmune disease (RA, pernicious anemia, thyroid, hemolytic anemia), and also GI disorders (chronic diarrhea, IBD-like conditions - Crohns, UC - presents with blood diarrhea). Decreased IgG, IgA, and IgM is called "Common Variable Immunodeficiency (CVID)" The immune problem is that they have ***Impaired B cell differentiation and hypogammaglobulinemia*** Get diagnosed in adulthood (ex: age 20-45)

What do you do if you suspect DRESS syndrome? Pt with rash on face and torso spread to body, facial edema, LA,and eosinophilia!! and elevated transaminases, started after taking A drugs - ***allopurinol***, antiepileptics (phenytoin, carbamazepine)

Remove the offending drug. (most pt recover completely) DRESS syndrome is a rare but potentially life-threatening drug reaction: Drugs: most commonly allopurinol and antiepileptics (ex: phenytoin, carbamazepine) Reaction (rash): morbilliform eruption that stats on face and upper trunk and becomes diffuse (often >50% body surface area) and confluent; facial edema is common. Eosinophilia Systemic Symptoms: fever, malaise, and diffuse LA; approximately 90% of patients have involvement of >1 organ system (ex: liver transaminitis, kidney, lung) Note: unlike other drugs reactions, DRESS syndrome has an unusually long latency (2-8 weeks) between starting the drug and manifestation of symptoms. Pathogenic mechanism is unclear but majority of pts have antibody evidence of HHV6 reactivation Some studies suggest cross-reactivity between herpesvirus lymphocytes and drug antigens. Dx: largely clinical, tx involves immediate CESSATINO OF THE INCITING DRUG and supportive care (ex: fluids, electrolytes, nutrition support). Most pts recover completely within weeks-months but relapses may occur.

Farmer tried to kill himself. No prescription meds at home. Body and clothes are soiled with vomit. He's SOB, agitated, pulse 50, RR 20, SpO2 86%, watering eyes, 1 mm pupils BL, widespread rhonchi with prolonged expiration. Increased bowel sounds. Muscle fasciculations. Most appropriate next step?

Removes all his clothes and wash his body so the organophosphates don't keep soaking through the skin. Can counteract effects of organophosphate poisoning with atropine (should be given immediately)

Kiddo (23month old toddler) with first UTI or kiddo of any age with recurrent UTIs, you know it's from E.coli this time. What is the next step?

Renal & bladder u/s. to eval for anatomic abnormalities that might predispose the kiddo to UTIs. U/s should be performed after improvement of fever and sx to minimize false positive results from acute inflammation. If pt has persistent or worsening sxs, an ultrasound should be performed immediately to assess for renal abscess. Note: don't choose voiding cystourethrogram quite yet bc it should be considered if you see hydronephrosis or scarring on renal ultrasound (so need to do the renal ultrasound 1st). It would be indicated in newborns <1 mo or kids <2 years with recurrent UTIs or 1st UTI from organism other than E.coli.

What kind of patients do you see EPO deficiency?

Renal failure.

Kiddo has hx of lots of ear infections and he seems inattentive but socially is affectionate with parents. what do you want to do?

Repeat audiometry testings to make sure his hearing is okay. Multiple ear infections can affect hearing.

14yo kid with 2 days fever, nasal discharge, malaise, fatigue, myalgia. No family hx of kidney disease. Urine dipstick shows 2+ proteinuria, no hematuria, otherwise normal. Cr is normal. What is the next appropriate step?

Repeat the dipstick testing 2 more times. urine dipstick can be positive in up to 10% of school-aged kids. Proteinuria in kids can be transient (intermittent), orthostatic, or persistent. Transient is the most common cause and can be due to fever, exercise, seizure, stress, or volume depletion. Orthostatic is common in teen boys and is defined as increased protein when pt is in upright position that goes to normal when they're recumbent. The UA that shows no hematuria and is otherwise normal (aside from the proteinuria), should be repeated at least 2 more times. If it's negative the next couple of times, you dx with transient proteinuria. If you get another positive test, refer to nephrologist for further eval. (Don't just straight to doing a 24 hr urine protein collection in a teenage boy, get proteins again because it could be transient or orthostatic and not be a big deal)

One of your physician colleagues is not practicing appropriately, you confront them and they say, it's fine and they're just them being absent minded in their old age. You recommend that they get an assessment done but they assure you that everything is okay. What should you do?

Report your concerns to hospitals's physician health program. An impaired doc who has a medical, psychiatric, or substance use problem that affects their ability to practice according to accepted and safe standards that has already resulted in a prescribing mistake that could have caused a pt harm, then you are ethically and legally obligated to report them if they are an impaired colleague. Most hospitals have designed hospital committee, commonly called physician's health programs (PHP) <--- this PHP gathers facts and arranges comprehensive assessment with intervention and tx if necessary. With tx, many impaired docs are ble to return to full or modified practice. If such a body does not exist or if the doc doesn't accept the PHP's recs, then the state licensing board should be contacted.

Surfactant deficiency results in alveolar collapse and diffuse atelectasis. Pt has severe respiratory distress and cyanosis after premature birth. CXR shows diffuse, reticulogranular (ground glass) appearance, air bronchograms, and low lung volumes.

Respiratory distress syndrome (premature baby, doesn't have enough surfactant) Tx: give this baby early continuous positive air pressure ventilation.

Pt sees light flashes and floaters or a curtain across the visual field that starts from the periphery and is generally not painful. what do you think they have?

Retinal detachment (think about the "retinal" performing on a stage, people are taking pictures (flashes of light) but now it's the end of the show and the retinal is detaching.. and peacing out..floating away during curtain call, light are flashing with people taking pictures; so there are flashes of light, floaters and curtain across the periphery of the visual field with retinal detachment)

What does having cyclic citrullinated peptide antibodies clue in in on?

Rheumatoid arthritis.

Clinical findings for congenital infection with Syphilis

Rhinorrhea, abnormal long-bone radiographs, desquamating/bullous rash (snuffles, bones, rash that desquamates: think syphilis)

Symptoms of Vitamin D deficiency

Rickets in kids.

64yo woman comes to the office bc she's confused. She has hx of cirrhosis and ascites d/t PSC (which remember is associated with IBD). She's had several hospitalizations for hepatic encephalopathy. She's been confused and slow since yesterday. She's got asterixis and is incoordinated. Can't spell "world" backwards. Electrolytes and Cr are normal. She is already taking lactulose. What is the most appropriate additional treatment?

Rifaximin therapy. (since she's already taking lactulose) She has hepatic encephalopathy- want to get rid of the ammonia that she's building up (as evidenced by changes in sleep patterns, AMS, ataxia, asterixis) -want to decrease the blood ammonia concentration: can do that with lactulose or rifaximin -Or if there are other causes (like infection, GI bleed, 'lyte distubances), you can correct those (ex: fluids, abx). Note: the Abx are thought to act by decreasing ammonia producing bacteria in the colon. Note: TIPS is performed when the pt with ascites does not respond to medical tx (ex: diuretics) or ongoing active or recurrent bleeding from varices even after appropriate tx with upper endoscopy. TIPS can worsen hepatic encephalopathy due to ammonia-rich blood being shunted past the liver. SO DO NOT choose TIPS in pt with asterixis and AMS suggesting too much ammonia, instead choose lactulose or rifaximin.

Pt smokes crack has HTN (176/98) and now is unresponsive to deep sternal rub, right pupil is widely dilated and unresponsive to light. There is intermittent extended posturing of the left arm and leg. DTRs 4+ in left extremities. Babinski present on left side. What is likely cause of his sxs?

Right basal ganglia hemorrhage. Big clue is he used crack and then had HTN-sive vasculopathy - most common cause of spontaneous intracranial HEMORRHAGE. Know the basal ganglia is the most common (~50%) site of hemorrhage.!!! Potential consequence of basal ganglia hemorrhage is uncal herniation. -Mass effect pushes part of the temporal lob (uncus) lateral and down against tentorium cerebelli. This compresses the 3rd CN and results in a dilated, non-reactive ipsilateral pupil. Further displacement causes midbrain compression with contralateral extensor posturing, coma, and respiratory compromise. -FURTHER displacement causes: midbrain compression with contralateral extensor posturing, coma, respiratory compromise.

When does endometriosis pain peak?

Right before menses. Associated dyspareunia, infertility. pain with exercise.

Gross dysfunction of autonomic NS with severe orthostatic hypotension in pt of Ashkenazi Jewish descent.

Riley-Day syndrome (familial dysautonomia) -AR inheritence in Ashkenazi Jews

What are the SGAs?

Risperidone (long acting IM for noncompliant pts), Olanzapine (short acting, IM in emergency), Quetiapine, Ziprasidone (short acting, IM in emergency), Aripiprazole, Paliperidone (long acting, IM for noncompliant pt), Asenapine, Iloperidone, Lurasidone (can be given 3rd T.. but baby may have EPS sx) Short acting, for emergency IM administration: Olanzapine, Ziprasidone Long acting, IM administration for noncompliant pts: Risperidone, paliperidone

sudden onset severe unilateral lower abdominal pain immediately after strenuous or sexual activity and there is pelvic free fluid, what is the dx?

Ruptured ovarian cyst. Note: HDS, conservative managment with pain meds. Hemodynamically unstable will need surgical intervention.

3rd heart sound (S3) that shows up later in life, along with Hx of T2DM new SOB, HTN, high RR, and SpO2 of 87%. What are you thinking? (Ken-tuc-KEY)

S3 later in life is sx of LV Failure. Several signs consistent with left HF (SOB, tachypnea, hypoxemia, S3). Most appropriate thing to do right now is diuresis.

Asthma tx regiment

SABA (albuterol) Low dose ICS Low dose ICS + LABA *** or *** Medium dose ICS Medium dose ICS + LABA High dose ICS + LABA & consider omalizumab for pts with allergies High dose ICS + LABA + oral corticosteroids & consider omalizumab for pts with allergies.

What is it when pt has abdominal distention, high pitched hyperactive bowel sounds (and later no sounds), dilated loops of bowel with air fluid levels on imaging and no or minimal air in colon and rectum?

SBO

The vast majority of head and neck cancers is what kind of cancer? What kind of history is concerning for head and neck cancer?

SCC (squamous cell carcinoma) Hx of older patient with hx of smoking and a hard submandibular or cervical region lymph node is highly concerning for head and neck cancer. so concered it's SCC.

SIADH vs DI, how is the relationship with sodium (Na)? What is the relationship to urine osm?

SIADH: holding onto free water. -low sodium (hypo-natremia; < 135) -urine mOsm and urine Na are both high aka concentrated (be you're holding on to all the water in your serum) DI: peeing out all your free water -high sodium (hyper-natremia; > 145) -urine mOsm is low (around 100 or so), it's dilute bc you're peeing all the water out (vs. psychogenic polydipsia has concentrated urine >600 mOsm/kg bc your ADH in that is still working so you're not peeing out as much free water; so your urine is more concentrated)

What kind of injury to the kidney does SLE cause? how does that present?

SLE --> glomerular injury. Presents with proteinuria & hematuria.

What does SLE have to do with heart disease?

SLE is a know RF for accelerated atherosclerosis and premature coronary heart disease.

What's the diff between sensorineural (SN) hearing loss and conductive hearing loss?

SN: d/o of the inner ear, cochlea, or auditory nerve -Presbycusis (hearing loss of old age - can't hear social conversation with competing background noise) -Meniere disease (too much endolymph: hearing loss, tinnitus, vertigo) -Barotrauma -Acoustic neuroma (tumor of schwann cells cover CN8) Cerebrovascular ischemia Conductive: any cause that limits sound from gaining access to the inner ear (aka sound can't get through to conduct) -Otitis externa or media -Cholesteatoma -Trauma -Cerumen (ear wax) -Tympanic membrane perforation

SPF of sunscreen you want?

SPF of 15-30 or higher Apply 15-30 minute before sun exposure Reapply q2 hrs.

What's 1st line tx for bulimia nervosa?

SSRI (fluoxetine) with nutrittional rehab and psychotherapy (CBT) Note: Fluoxetine is evidence-based tx for bulimia nervosa. However, there is little evidence to support the use of meds as primary tx for anorexia nervosa.

Atypical Depression (reverse vegetative changes, increased sleep, increased weight, increased appetite, super sensitive to interpersonal rejection, limbs feeling "heavy"). What meds do you use to treat them?

SSRI and MAOI. MAOI for atypical depression

What meds can cause serotonin syndrome? What is the antidote for severe cases?

SSRI, SNRI, MAOI, TCA, and pain med tramadol also has serotonergic activity. Cyproheptadine is serotonin antagonist used for severe cases.

How do you treat binge-eating disorder?

SSRIs, Lisdexamfetamine, topiramate CBT, behavioral weight loss therapy. Memory tool: so this is also a condition where someone eats alot... so think about giving SSRI.

Who gets acalculous cholecystitis?

SUPER STRESSED pts: the SEVERELY ILL pt. -ex: in ICU with multiorgan failure, severe trauma, surgery, burns, sepsis, prolonged TPN. D/t cholestasis and gallbladder ischemia leading to 2ndary infection by enteric organisms and resultant edema and necrosis of the gallbladder. This is a serious condition that can lead to sepsis and death if undetected. Oh no!!! So it's actually an infected gallbladder. So sx of disease (fever, leuks) think about this in a non-communicative sick pt. Best way to dx is high index of suspicion and confirm with imaging: gallbladder wall thickening and distention and presence of PERICHOLECYSTIC FLUID. Immediate tx in critically ill pts includes Abx followed by percutaneous cholecystostomy under radiologic guidance. Cholecystectomy w/ drainage of any associated abscess is definitive tx once pt's medical condition improves.

Side effect profile: Lurasidone

Safer for use in pregnant patients (note: baby may have EPS sx if used in 3rd Trimester) Memory tool: think Lu for "Lu"rasidone and "Lu"llaby for baby..

HIGH YIELD: Major toxicity of tacrolimus (macrolide antibiotic made by fungi)

Same MoA as cyclosporine and has similar toxicity profile: nephrotoxicity and hyperkalemia. Higher incidence of neurotoxicity, diarrhea, and glucose intolerance *** No hirsutism or gum hypertrophy *** (Think about how my pt EH, she didn't have weird gums or extra hair. But she did act funny, complain of her head hurting and not wanting to do her homework (neurotoxicity) and diarrhea. Think about monitoring her renal function and electrolytes (hyper K) and watching her glucose while she was on the tacrolimus)

What causes chronic inflammation and noncaseating granulomas?

Sarcoid. Pulmonary HTN is a potential complication of sarcoidosis. PFTs typically show: restrictive pattern and CXR with hilar adenopathy possibly in combo with interstitial infiltrates

Young African American woman has cough, dyspnea and chest pain. She has skin lesions, anterior/posterior uveitis, Lofgren syndrome. You see BL hilar adenopathy and pulmonary reticular infiltrates. Labs shows hypercalcemia and hypercalciuria, elevated serum ACE levels. Biopsy shows noncaseating granulomas that stain negative for fungi and acid-fast bacilli. What does this patient have?

Sarcoidosis

Pt with HTN, but you only have one measurement bc he hasn't seen the doctor is like 6 years. You get him to start dietary modifications. What do you do next?

Schedule a follow up exam in 1 moth since you need to get another BP measurement to confirm he has HTN and not just white coat HTN and then you also want to give the diet/exercise a chance to control his HTN... so don't start him on ACE inhibitor just yet. (I made the assumption that he doesn't come to the doctor so let's just start him on a med... but that's the wrong line of thinking; think about letting diet/exercise work and also need a 2nd measurement to confirm HTN)

previously healthy 13 yo boy comes in for being short. His bone age is of 10-year-olds. Growth chart shows normal length at birth and quickly goes to the bottom of the growth chart and continues to trend along but at bottom of the growth curve as he gets older. What is the next best step?

Schedule follow up visit in 6 months. This is constitutional growth delay, most common cause of short stature and pubertal delay in teens. They have normal birth weight & height, but between 6mo-3years, height growth velocity slows and the child drops percentiles on their growth curve. Around age 3, the kid regains normal growth velocity and follows the growth curve at 5th - 10th percentile. Puberty and adolescent growth spurts are delayed, but eventually occur. They will have normal growth spurts and reach normal adult height. Bone age radiographs show a bone age that is delayed compared to the chronological age. (So just wait a while..they'll get there.. follow up in 6 months)

Pt with nephrotic range proteinuria (>3.5 g/L in 24 hours), what do you want to do in the next step of management?

Schedule kidney biopsy (need to established a clear dx before you start treating them. so get the kidney biopsy first)

IF pt has a hx of endometrial infections (ex: endometritis) or instrumentation with D&C, and all their hormone levels are normal but they have amenorrhea, what could be the cause?

Secondary amenorrhea d/t intrauterine adhesions, which is Asherman syndrome (structural cause of amenorrhea)

Kid drinks some caustic chemical. What do you do?

Secure airway: breathing, circulation Decontaminate: remove any clothing that is contaminated or has visible chemicals, irrigate the exposed skin so the chemical doesn't keep getting absorbed. CXR if resp. symptoms Endoscopy within 24 hours. (upper GI endoscopy is recommended within 24 hours to assess the extent of the injury, which may not be apparent if performed immediately, and delayed endoscopy increases perforation risk) Note: do not do anything that could cause them to vomit bc that would make the extent of the injury worse. Don't play chemist (don't try to neutralize or lavage since that can trigger vomiting and may further damage the mucosa) Interventions are just to secure airway, decontaminate, and see what the damage is (CXR, endoscopy) Complications: Upper airway compromise, perforations, strictures/stenosis in the next 2-3 weeks (so barium contrast study at that time would be helpful to assess for strictures/stenosis), ulcers, cancers.

What is internuclear ophthalmoplegia? when s it seen?

Seen in MS. If your right eye has the pathology and you are trying to look to the left, your right eye isn't able to adduct and look to the left, and your left eye is able to look to the left but it has nystagmus.

What causes bronchial wall thickening and mucous plugs?

Seen in bronchiectasis, which causes 2ndary pulmonary HTN d/t chronic hypoxia. Pulmonary function tests would show obstructive pattern with FEV1/FVC < 70%

Pt with hx of recurrent pneumonia, atopy (ex: asthma, eczema) and anaphylactic reaction during blood transfusion. What do they have?

Selective IgA deficiency. They have low/absent IgA & Normal IgG, IgM and B cells

55 yo truck driver has impaired vision last 6 months. Increasing difficulty looking sideways and has to turn his neck to look to the side. Intermittent HAs that worse in the morning. Decreased libido. BMI 32. Decreased vision in temporal fields on both sides. Likely dx?

Sellar mass: ex: ***craniopharyngioma,*** pituitary adenoma, meningioma -Craniopharyngiomas are benign tumors from Rathke's pouch and commonly occur in kids but 50% are in people > 20, esp. between55-65 yo. bc of of the bitemporal hemianopsia, vision loss, and HA, and hormonal changes (causing decreased libido d/t hypogonadism )

Kid has hx low grade fever and runny nose about 1 week ago. Now with Fever 101F, doesn't weight bear, leukocytosis >12,000, elevated ESR, elevated CRP, refuses to walk, cries when you move his right leg. Right hip is abducted and externally rotated and screams in pain with movement of the hip. What are you thinking about? How did that happen?

Septic hip: Hematogenous spread of bacteria into the joint space. -Septic arthritis often follows an Upper resp. tract infection or skin infection where there can be intermittent bacteremic showers, allowing for hematogenous spread of the bacteria into the synovial fluid. Most commonly in kids d/t Staph aureus and strep. Want to eval and tx right away because delays can results in AVN of femoral head. Bacteremia is the most common cause of joint infection, so blood cultures should be obtained. U/s guided arthrocentesis typically shows purulent synovial fluid with >100,000 leuks. Prompt surgical drainage and lavage are needed to decompress the joint space and remove inflamm. debris. Treat: empirically with IV abx (ex: Vancomycin) immediately after cultures of the synovial fluid and blood are obtained.

Pt has hx of c-section and prolonged labor. now POD3 and she has intermittent fevers and BL lower quadrant tenderness. Nothing really else. What is it?

Septic thrombophlebitis. Complications associated with pelvic surgery or PP period. Bc of thrombosis of deep pelvic or ovarian veins (note: BL lower quadrant tenderness) that becomes infected. Bc most common etiology of fevers puerperal is endometritis so pts are given abx but then the fevers persist so you know it's not endometritis bc that responds to abxs. So this is a dx of exclusion, unresponsive to abx, negative infectious eval on blood and urine, Treat with anticoagulation and broad spectrum antibiotics.

Pt has BL facial nerve palsy with mild flu-like symptoms and hx of time spent in Rhode Island and spending time outdoors. What is likely to be seen?

Serology positive for Borrelia burgdorferi Can also see lymphocytic meningitis, CN palsies, radiculoneuritis. When you see rapid onset facial weakness that is BL, then think about Lymdisease. Make dx with ELISA, then Western Blot with B. burgdorferi serology. most pts recover completely after oral or IV antibiotics (ex: doxy, ceftriaxone)

Meds that can cause serotonin syndrome.

Serotonergic drugs (SSRI, SNRI), MAOIs, TRAMADOL (pain med with serotonergic activity)

What's the difference between serotonin syndrome and NMS?

Serotonin syndrome: d/t serotonergic drugs (SSRI, SNRI, MAOI, TCA, tramadol). -more prominent NM hyperreactivity (tremore, hyperreflexia, myoclonus) -Tx: Stop serotonergic agent, supportive care, cyproheptadine for severe cases. NMS: d/t anti-psychotics (FGA, SGA) -more diffuse muscular rigidity, and brady-reflexia -Tx: stop offending antipsychotic agents, ICU, supportive care with hydration and cooling; if refractory, give Dantrolene, bromocriptine (which are DA agonists)

What establishes dx of malignant HTN?

Sever HTN: >180/120 associated with retinal hemorrhage, exudates, &/or ***papilledema.*** Note: HTN emergency is marked severe HTN with malignant HTN or HTN-sive encephalopathy (associated with cerebral edema d/t breakthrough vasodilation from failure of autoregulation) Note: the definition of Malignant HTN includes BP >180/120 as well as eye findings.

What is HTN urgency?

Severe HTN >180/120 with no sx of acute end organ damage

What is HTN emergency

Severe HTN with acute, life-threatening end organ complications -Malignant HTN: with retinal hemorrhage, exudates, pappilledema -HTN encephalopathy: with cerebral edema and non-localizing neuro s/sxs

S/sx of urine dehiscence (of hysterotomy repair)

Severe abdominal pain, peritoneal signs, hemodynamic instability, vaginal bleeding

Pt has confusion and GI sxs and hypercalcemia (>14). What is the most appropriate next step?

Severe hypercalcemia >14 or symptomatic, as in this pt, you need IMMEDIATE, short term tx: Normal Saline hydration + calcitonin Long term tx: bisphosphonates (but take a while, 2-4 days, to kick in, so need to give normal saline with calcitonin first) Note: hemodialysis is effective tx for hyperCa but is reserved for pt with renal insufficiency or HF where you can't safely do what you would normally do, which is aggressive hydration.

How does Legionella infection presents?

Severe pneumonia: high fever, with GI symptoms.

If pt has features of glucocorticoid (fatigue, loss of appetite, weight loss) and mineralocorticoid (orthostatic hypotension) deficiency, and you are concerned they have adrenal insufficiency, what are features that make you think primary adrenal (lesion in the adrenals themselves) insufficiency (usually d/t autoimmune disease)? What should you add?

Severe symptoms Hyper-pigmentation (bc the ACTH is high and byproduct is more pigmentation) Low Aldosterone (so hyperkalemia and hyponatremia) Hypotension (from loss of mineralocorticoids) Women: can also have sx of androgen deficiency (low libido; since adrenals are the major source of androgens in women) Will aos have high renin activity (since the mineralocorticoids are low) Addition of FLU-DRO-Cortisone (fludrocortisone) is advised to correct this deficiency bc it has more mineralocorticoid action.

Mania:

Severe symptoms, markedly impairs social and occupational functioning, hospitalization needed. >1 week May have psychotic features. Bipolar I: is Mania + MDD (episode of depression not necessary to make dx of bipolar I)

19yo sexually active female comes in with persistent sore throat, fever, mild lower abdominal discomfort for the past few days. Started college 4 months ago and lives with 3 roommates. She has 2 new sex partners, uses OCPs. Temp 101F, otherwise VSS. Pharyngeal arches are red without exudate. BL nontender cervical LA. Abdomen is tender to deep palpation int he lower quadrants. Urine pregnancy test negative. Most likely responsible pathogen?

Sexually active female with lower abdominal discomfort, worried about PID & Neisseria. she could also have oral sex with these infected people and that is what's causing her sore throat symptoms (gonococcal pharyngitis) CMV and EBV are not the right answer bc those don't cause lower quadrant abdominal pain, which this question is painting the picture more for PID with the young sexually active female.

IF a pt is on her 2nd pregnancy and she got all the RhoGam at the appropriate times.. but her anti-D antibody titer is 1:32... what happened?

She had inadequate dose of anti-D immune globulin (RhoGam) after her first delivery. You gotta do the Kleihauer-Betke (KB) test to see what dose of RhoGam she needs. -The standard dose is 300 ug at 28 weeks GA but about 50% of pts will need higher dose after delivery, placental abruption, or procedures. The KB test helps determine the dose. -Put RBCS from mom's circulation on a slide and expose to acidic solution and the adult hgb lyses, leaving "ghost" cells. The dose of anti-D immune globulin is calculated from % of remaining fetal hgb.

64 yo woman (elderly) comes in with fever, confusion, lethargy. She started having N/V/watery diarrhea yesterday on vacation. Also has myalgias, HA, photophobia. Hx HTN and CLL. Fever. nuchal rigidity. LP with CSF showing neutrophilic pleocytosis. Blood cultures show gram positive bacilli. What could have prevented this conditions?

She has Listeria, which is a gram positive bacilli that causes meningitis in the elderly - transmitted via diary products Note: strep pneumo causes about 70% of community acquired bacterial meningitis (suggested by CSF neutrophilic pleocytosis). However, in pts 50yo or immunocompromised pts (ex: heme malignancy), you have to also think about the gram positive bacilli - Listeria monocytogenes. Listeria is foodborne illness: raw meats/veges, unpasteurized milk products, prepackaged meats (hot dogs, deli meats). Healthy adults are rarely symptomatic but may have self-limited febrile gastroenteritis if large inoculation occurs. But pts at extremes of age (<2, >50), pregnant or immunocompromised are at greater risk of invasive disease, which can happen shortly after gastroenteritis (within hrs to days of exposure) or can have prolonged incubation period (up to months following exposure)

26yo F 6 months postpartum, has breastfed for 5 months, anxiety and worried for first 2-3 months after giving birth. Unusually fatigued and irritable, worsened over the last several weeks. Constipated, gained 6lbs in the last 3 months. BL lower extremity edema. -Sodium: 130 (low) -Potassium is normal. What's the next best step? What does she have?

She has Postpartum thyroiditis: occurs in 7-8% women after childbirth Brief hyperthyroid phase: release of preformed thryoid hormone (usually just mild sxs like anxiety, palpitations) Then Hypothyroid phase: tired, gain weight, constipation. PheyExa

54 yo white Caucasian woman comes in with fatigue. She says she has dizziness and palpitations after physical activity. Her feet feel "numb" and are less sensitive to cold. She has pale conjunctivae and a shiny tongue. Ankle reflex is decreased BL. Hgb 7.6 (low), MCV 110 (high), MCHC 36 (normal), WBC 3,900 (low), Plt 150,000 (low, just right there at cut off). What long term complication should this pt be monitored for? What does she have?

She has pernicious anemia, which is showing up as B12 deficiency. She has the classic signs of B12 deficiency (macrocytic anemia, glossitis, neuro changes with peripheral neuropathy) Pernicious anemia is an autoimmune problem that leads to B12 deficiency in 2 ways. 1) Anti-intrinsic factor (anti-IF) antibodies decrease the amt of functional IF available to facilitate B12 absorption (IF needed for B12 absorption). 2) Pts develop chronic gastritis w/ decreased production of IF by gastric parietal cells. This atrophic gastritis increases the risk of intestinal type cancer and gastric carcinoid tumors by 2-3 x the overall general population. So, pts with pernicious anemia need to be monitored for development of gastric cancer (periodic stool testing for presence of blood) tl;dr She has pernicious anemia --> B12 deficinecy. Monitor for gastric cancer bc pernicious anemia's decrease in IF creates atrophic gastritis, which results in 2-3 fold higher risk for gastric cancers

58yo woman has left sided HA, N/V, blurred vision, seeing halos around lights. Has hx of hand tremors and started taking a new medication. She is in severe distress, phyexam shows left eye circum-corenal injection with dilated and sluggish pupil. Visual acuity decreased in left eye. Resting hand tremor and increased resistance to passive movements of the extremities. What's causing her current symptoms?

She took Trihexyphenidyl, and anticholinergic medication that is used to tx Parkinson disease symptoms (ex: resting tremor, cogwheel rigidity). But it caused angle-closure glaucoma (ACG) as seen by the HA, N, blurry vision, sluggish/dilated pupil. Need urgent ophthalmologic consultation bc untreated acute ACG can damage the optic nerve and result in permanent vision loss in 2-5 hrs of symptom onset. TL:DR so Trihexyphenidyl is an anticholinergic med used to treat symptoms of parkinson's that can end up with Acute-closure glaucoma. So think about that when you see pt with headache, N, blurry vision, sluggish/dilated pupil with hx of parkinson's symptoms that just started a new medication for the sxs.

How do infants with hypoplastic left heart syndrome present?

Shock d/t impaired systemic perfusion. They may have some cyanosis depending on the degree of obstruction, but they usually appear pale or mottled instead of straight up cyanotic like the "T" heart conditions. Note: Like hypoplastic left heart syndrome, kiddos with coarctation of the aorta also has shock... and more pale/mottled appearance.

Emergency situation with schizophrenic pt, you need IM medication, which one do you chose?

Short acting SGA (Olanzapine or Ziprazidone) over FGA (Haloperidol; still used but has more SEs) If given a choice, pick the SGA bc they have less side effects

What do you expect to find in septic shock? (Pt with hypotension, tachycardia, tachypnea, mental status changes, and source of infection)

Should have a source of infection. -Decreased SVR (cardiac afterload will decrease) d/t overall peripheral vasodilation. -PCWP (preload) will be low-normal (leaky capillaries cause decreased pre-load) -SVR will be low -CO will increase initially (heart is trying t fight the low SVR) (In late septic shock, CO can decrease) -High mixed venous oxygen saturation (ex: 82% when normal is 60-80%) (this is bc of hyperdynamic circulation; as CO increases in response to reduced SVR to maintain the peripheral tissue perfusion, with inability of tissues to adequately extract oxygen, may develop lactic acidosis from tissue hypo-perfusion)

Pt with Parkinsonism experiences orthostatic hypotension, impotence, incontinence, or other autonomic symptoms. They may have fatal bulbar dysfunction and laryngeal stridor. Anti-parkinsonism drugs are ineffective. 1) Parkinsonism 2) Autonomic dysfunction (postural hypotension, abnormal sweating, disturbance of bowel/bladder control, abnormal salivation or lacrimation, impotence, gastroparesis) 3) Widespread neuro signs (cerebellar, pyramidal, LMN) What do you think they have?

Shy-Drager syndrome (multiple system atrophy): degenerative disease.

Pt passes out after sinus pause and EKG shows increased PR or QRS duration. What is cause of syncope?

Sick sinus syndrome, bradyarrhythmias, or AV block

What can impaired SA node automaticity lead to?

Sick sinus syndrome: often d/t degeneration and/or fibrosis of the SA node and surrounding atrial myocardium. May present with fatigue, lightheadedness, palpitations, pre-syncope or syncope. EKG often shows bradycardia, sinus pauses/arrest, SA exit block, alternating bradycardia and atrial tachyarrhythmias (tachycardia-bradycardia syndrome)

Spasticity, bulbar symptoms, exaggerated deep tendon reflexes

Signs of upper motor neuron damage

Tacrolimus compared to cyclosporine.

Similar toxicity profile (including renal toxcity and hyperkalemia) -but not gum hypertrophy or hirsutism -More likely to have neurotoxicity, diarrhea, and glucose intolerance

Young pt in the fall or winter has this kid of indolent HA, malaise, fever, persistent dry cough.. may just be kind of tired and have exertional dyspnea but it doesn't really sound severe, some scattered wheezes heard on exam. May have pharyngitis (non-exudative), may have macular/vesicular rash, Subclinical hemolytic anemia (ex: Hgb 12.2 bc of cold agglutinins), reticulocytes 2.2%, leuks are not elevated (normal leuk ct). CXR shows diffuse reticulonodular opacities (interstitial infiltrate on CXR). What do are you thinking?

Since it just sounds like of like this vague thing with viral-like prodrome then they have lower pulmonary symptoms of SOB and wheezing. and they labs are pretty normal but they have CXR findings and they're tired, think about ATYPICAL PNEUMONIA!!! WITH MYCOPLASMA PNEUMONIAE!!! -Tx with with macrolide or respiratory fluoroquinolone. Note: the subclinical hemolytic anemia is bc of antibodies that cross-react with RBCs (cold agglutinins). The mycoplasma lack a cell wall, gram stain is ineffective and cultures are not sent. Treat empirically with Azithromycin (or respiratory fluoroquinolone)

If you have a study with reported risk calculations (relative risk or odds radios) with the following 95% CIs, what does this mean? Cigarette smoking: -Breast cancer: 1.10 (1.02 -1.14) -Endometrial cancer: 0.81 (0.74 - 0.88)

Since the confidence intervals do not include 1.0, then this info is statistically significant. For relative risk (RR) and odd ratio (OR): >1 is positive association (increased risk, higher odds) <1 is negative association (decreased risk, lower odds) So since Br CA is 1.10, which is >1, there is an increased odds/risk but Endometrial CA is 0.81, which is <1, there is a decreased odds/risk of endometrial cancer with cigarette smoking. -that may be true, but that doesn't outweigh the risks of cigarette smoking.

When you do radioactive iodine (RAI) therapy with Grave's disease (symptomatic hyperthyroidism with low TSH and high T4 and elevated titer of thyroid-stimulating immunoglobulins, but without Graves opthalmopathy), what is the most likely outcome? IF the pt has Graves opthalmopathy, do you treat them differently?

Since there is DIFFUSE uptake of the radioiodine in Grave's disese, you get development of hypothyroidism over months to years. (DIFFUSE uptake of radioiodine eventually leads to permanent hypothyroidism within months in >90% of patients) Note: In contrast, when RAI is used to treat toxic nodular goiter and toxic adenoma, the radioisotope is taken up ONLY by the autonomous thyroid tissue and the function of the remaining normal tissue is usually adequate to prevent permanent hypothyroidism. If pt has Graves opthalmopathy, RAI can actually worsen the opthalmopathy bc of increased titers of thyroid stimulating immunoglobulins (autoantibodies). So for those pts with bugged eyes, thyroidectomy is preferred.

Pt with gout, but now the stem says they are already on an anticoagulant like ASA, plavix (clopidogrel), apixaban for some reason. What do you treat their gout with? .. and who should you not use this med in?

Since they are already on a anti-coagulant, giving them NSAIDs like indomethacin is contraindicated bc it can acutely worsen their HF. So give them colchicine instead. Colchicine usually results in resolution of gout sxs. Colchicine should NOT be used in elderly pts or those with severe renal dysfunction.

Pt has MI of anterior wall and then now they have what seens like HF symptoms (tachypnea, oxygen sat is only 90% on 4L oxygen, there's an S3 sound, basilar crackles halfway up lung fields BL). His HR is 60. You gave them ASA, plavix, and atrovastatin. What do you treat "flash pulmonary edema" with?

Since this pt has flash pulmonary edema, you need to give a diuretic to get the fluid off. -Given the choice between furosemide and spironolactone, give furosemide (stronger diuretic). Spironolactone is more for its aldo effect.. and it's a weak diuretic and a pt with flash pulmonary edema needs strong diuretic right now. Loop diuretic is a good choice in this situation, furosemide quickly relieves the pulmonary edema by decreased cardiac preload. Furosemide also causes venodilation, which further decreases preload. Note: be careful not to cause AKI. Note: Beta blockers are a standard of tx in MI but should be AVOIDED in pts with decompensated CHF or bradycardia. (don't want to slow their HR even more).

Pt coughs, pees, or poops and then passes out. What kind of syncope is that?

Situational syncope

Person who passes out when they cough, pee, or poop, what's going on?

Situational syncope with the above listed triggers: d/t reflex (neurally mediated) syncope. There is an alteration int he autonomic response and can lead to a "cardioinhibitory," "vasodepressor," or mixed response. Increased parasympathetic stimulation can lead to profound bradycardia, varying degrees of AV block, or asystole. Decreased sympathetic output can lead to vasodilation, hypotension or syncope. Older pt with BPH could also strain more when voiding, thereby exacerbating the "cardioinhibitory" syncope response. ... aka when you relax to pee.. you relax too much and get bradycardia, AV block and asystole and you pass out..

13yo boy with limp. BMI 31 (obese). Fell off his bike today. Leg is rotated externally with decreased ROM and pain with internal rotation of hip. No leg length discrepancy. BL anterioposterior and frog-leg x-rays of hips are obtained. What do you expect to see?

Slipped Capital femoral epiphysis. Note: minor trauma can sometimes make the pain worse and bring the kid to medical attention. Tx: gold standard: immediate surgical screw fixation at the CURRENT degree of slippage to avoid the risk of AVN.

How do you tx scleroderma?

Slow underlying disease process in pts with limited scleroderma (CREST syndrome): with Methotrexate (the DMARD) Then treat the manifestations: Renal crisis: ACE inhibitors (use even if Cr is elevated) Raynauds: CCBs Esophageal dysmotility : PPIs for GERD Pulmonary fibrosis: Cyclophosphamide improves dyspnea and PFTs (but remember it causes renal cancers) Pulmonary HTN: Bosentan ambrisentan (endothelin antagonist), sildenafil, Prostacyclin analogs: iloprost, treprostinil, epoprostenol. Thromboembolic disease: riociguat (cGMP stimulator)

What predisposes someone to calcium oxalate crystals (stones)?

Small bowel disease, surgical resection or chronic diarrhea can all lead to malabsorption of fatty acids and bile salts; this predisposes to the formation of calcium oxalate stones. Fat malabsorption leads to increased absorption of oxalic acid bc of the unabsorbed fatty acids chelate calcium, making oxalic acid free for absorption.... so it more has to do with more oxalic acid.. (don't not pick calcium oxalate stones bc the serum calcium is normal; you're more at risk for calcium oxalate stones bc of fat malabsorption --> fatty acids that aren't absorbed chelating calcium and so there's more free oxalic acid around so that creates the increased risk for calcium oxalate stones)

What do you expect to find as the description of a Echinococcus liver lesion?

Smooth, cystic mass on U/s or CT Normally w/o sxs unless they're large (>10 cm)

In kids/adults, you know that eczema is on the flexural creases, but where is it in kids?

So know that in kids, it can be on extensor surfaces, the trunk, cheeks and scalp. So if an infant has itchy red scaly lesions but it's in the wrong areas (when you're thinking flexural creases), just know that's okay because for infants, it can be kind of everywhere.

Suicide attempt with TCA (ex: imipramine). Give them Sodium bicarb. Why?

Sodium load will alleviate the depressant action on myocardial sodium channels. Cardiac toxicity causes most deaths in TCA overdose. TCAs inhibit fast sodium channels in the His-Purkinje system and myocardium. This decreases conduction velocity, increases duration of repolarization and prolongs absolute refractory period. So these TCA OD pts have QRS prolongation and ventricular arrhythmias (VTach, VFib). QRS Interval >100 msec in setting of TCA overdose is an indication for Sodium Bicarb, which increases serum pH and extracellular sodium. pH goal of 7.50-7.55 decreases drug avidity for sodium channels. Elevated extracellular sodium concentration increases the electrochemical gradient across cardiac cells and affects the ability of TCA to bind to the fast sodium channels.

30 yo woman with intermittent dizziness, unsteadiness for 2 weeks. yesterday her sx were getting worse and had several near syncope esides. Mild SOB. She's obese, has asthma, and chronic cough. Had uveitis 6 months ago. HR is 36 (marked bradycardia) EKG with 2:1 AV block and LBBB. CXR with "BL midfield lung opacities" Most likely dx?

Sounds like CXR with BL hilar adenopathy so I went with Sarcoidosis. This is sarcoid with cardiac involvement. Autopsy would see cardiac noncaseating granulomas in at least 25% of sarcoid pts. Only 5% have s/sx of cardiac involvement. Suspect sarcoid in young pt (<55yo) with unexplained 2nd or 3rd degree heart block or with EKG changes in pt with known or suspected systemic sarcoid. Combo of her imagining findings, EKG and hx strongly suggests sarcoid.

64 yo, sharp, stabbing back pain that radiate to back of legs. Falls frequently for last 2 weeks. Increasing difficulty initiating urination and has pain in saddle region with associated paresthesias. Hx of prostate cancer with radiation tx. BL lower extremity proximal and distal muscle weakness, more pronounced on right. BL absent knee & ankle reflexes. Anal sphincter tone decreased. Sensations reduced asymmetrically in most of the dermatomes of lower extremities. Location of lesion?

Sounds like cauda equina syndrome due to mets from his prostate cancer that are now compressing the ***spinal nerve ROOTS.*** ESPECIALLY look for the the asymmetric part (did not know that. CAUDA EQUINA SYNDROME HAS ASYMMETRIC MOTOR WEAKNESS)... sensation is decreased in cauda equina syndrome (ex: saddle hypo/anesthesia)., he has BL severe radicular pain, and late onset bowel/bladder issues Note: vs conus medullaris syndrome has symmetric motor weakness (and sudden onset severe back pain, peri-ANAL hypo/anesthesia, hyper-reflexes, and early onset bowel/bladder dysfunction) He has both CT and ST and spinal cord issues (lack of reflexes).. so i'm thinking spinal lesion... but the CT and ST should make me think about spinal nerve roots? but how do you tell the difference from a lumbar spinal cord and spinal nerve root lesion.

Pt had cholecystectomy but now is having those symptoms again... u/s shows mildly dilated CBD but no stones. What's going on?

Sphincter of Oddi dysfunction. -a functional biliary d/o d/t dyskinesia or stenosis of the sphincter of Oddi. Note: opioid analgesics (Ex: morphine) can cause the sphincter to contract and precipitate symptoms.

If it sounds like cauda equina syndrome, but the pt also has BL lower extremity weakness, what do you think it is?

Spinal cord compression. Get MRI and neurosurgery involved.

How do you dx COPD?

Spirometry: FEV1/FVC < 0.70 Do this in pt > 40 yo who has significant smoking hx and chronic cough (productive or nonproductive) and progressive DOE. Note: pt may have 4th heart sounds. Severe COPD may lead to pulmonary HTN --> RVH --> right sided 4th heart sound.

How do splinter hemorrhages (microemboli from infectious endocaritis) that disrupt the capillary nail bed compare to nail melanoma?

Splinter hemorrhages are small*** linear or flame-shaped streaks under the nail. (vs nail melanoma is a long dark strip on the nail)

12yo boy with several months back pain. Bed wetting recently. Note palpable "step-off" at lumbosacral area. Straight leg test negative. Perianal sensation with pinprick test is decreased. Anal reflex is normal. Likely dx?

Spondylolisthesis. Back pain in kids usually has an organic cause so you need to investigate that complaint (vs. in adults, back pain is usually is benign in nature). Slowly developing back pain and neuro dysufnction with "palable step-off" at lumbosacral area is typical for high grade spondylolisthesis: developmental d/o with forward slip of vertebrate (usually L5 over S1). This displacement results in chronic back pain and neuro dysfunction if significant.

Pt with cirrhosis and ascites presents with low-grade fever, abdominal discomfort, AMS. You do a Reitan trail test (timed connect-the-numbers test) and detect subtle mental status changes. What do you suspect? How to dx? Tx?

Spontaneous bacterial peritonitis (SBP) Dx: PMNs > 250/mm3, positive culture (often gram negatives like E.coli or Klebsiella), Protein < 1 g/dL, SAAG > 1.1 g/dL Tx: empiric Abx with 3rd get cephalosporin (ex: cefotaxime), Fluoroquinolones for SBP prophylaxis.

Hx of ulcerating lesion in sun exposed area Histo with invasive cords of squamous cells with keratin pearls. What does that describe?

Squamous cell carcinoma (SCC)

What kind of cancer are you thinking of if the pt presents with significant smoking hx, hyper-Ca, and a hilar mass? (And also has anorexia, constipation, increased thirst, easy fatiguability)

Squamous cell carcinoma of the lung Memory tool: "sCa++mous" for squamous cell carcinoma of the lung and hyper-Ca++ Hyper-Ca usually results from effects of parathyroid hormone-related protein (PTHrP), which binds the PTH receptor and results in increased calcium resorption from the bones and increased renal calcium resorption int he distal tubules.

Scaly papules/plaques/nodules in sun-exposed areas. May present as non-healing ulcers.

Squamous cell carcinoma. (2nd most common skin cancer)

Pt that smokes and drinks a lot. Now you find a persistent nodular, erosive and ulcerative lesion with surrounding erythema or induration. May see some lymphadenopathy as well. What are you thinking?

Squamous cell carcinoma. Make rule to evaluate for malignant transformation since this has very concerning features (ulceration, induration)

Most likely organisms responsible for deep infection (ex: osteomyelitis) following puncture wounds? What's more likely if you have a puncture wound through the sole of a shoe, think warm, moist environment? Tx?

Staph aureus & Pseudomonas aeruginosa. Pseudomonas more likely for a puncture wound that goes through the sole of a shoe. Tx with IV antibiotics (ex: cipro or pip-tazo) & surgical debridement.

Foodborn illnesses.

Staph aureus or Bacillus cereus: quick onset (1-6 hrs) bc you ingest the enterotoxin, vomiting predominant. C. diff, Clostridium perfringens, ETEC/STEC, Vibrio cholerae: delayed onset (>1 day) bc the enterotoxin is made in the intestine, you get watery/bloody diarrhea. Campylobacter jejuni, Nontyphyoid salmonella, Listeria monocytogenes: Variable onset, watery/bloody diarrhea,***FEVER***, systemic illness (with listeria) bc of bacterial epithelial invasion.

Pt presents with changing FNDs that get better on their own, has pronator drift and MRI brain shows hyperintense white matter lesions (particularly at the periventricular and subpial white matter of the cerebrum - corpus callosum - and the optic nerves, brainstem, and spinal cord), she clearly has MS (multiple sclerosis) What is the tx?

Start steroids (methylprednisolone) pt with acute attacks and disabling symptoms are treated with high-dose IV glucocorticoids (like methylprednisolone). Can do plasma exchange in pts who do not respond to glucocorticoids. Other immunomodulators (interferon beta, natalizumab, glatiramer) can be used for long-term disease suppression

What are some etiologies for avascular necrosis of the hip? How does it present?

Steroid use, Alcohol abuse, SLE (lupus), antiphospholipid syndrome, hemoglobinopathies (ex: sickle cell), infections (ex: osteomyelitis, HIV), renal transplant, decompression sickness Presentation: groin pain on weight bearing, pain on hip abduction and internal rotation, no redness, swelling, or point tenderness. Labs/Imagining: normal WBC count, ESR, and CRP (so seems normal.. plain x-ray can also be normal early on). But with advanced disease, can see crescent sign on X-ray and MRI is more sensitive test.

Pt has all the hyperthryoid sx and also proximal muscle weakness, what do they have?

Still thyroid disease. Can get acute thyrotoxic myopathy. presents with severe distal or proximal muscle weakness usually without bulbar or respiratory muscle involvement. Chronic hyperthyroid myopathy presents with proximal muscle weakness weeks to months after the onset of hyperthyroidism. Objective findings: muscle atrophy. Tx of hyperthyroidism usually improves the myopathy. So don't get misled by a pt having proximal muscle weakness or A. fib, those are still symptoms that are pointing you to hyperthyroidism.

50 yo has family hx of brother with pancreatic cancer, he smokes and drinks and has diabetes and takes metformin. His BMI is 29 and random blood glucose is 190. What is the intervention with greatest impact to decrease his risk for pancreatic cancer?

Stop smoking (most significant environmental risk) -can also lose some weight, be more active. but smoking cessation is the biggest thing.

Serotonin Syndrome treatment?

Stop the SSRI Give a serotonin antagonist (Cyproheptadine) -Memory tool: Sketchy picture in the serotonin syndrome office and the guy is holding a sign that say "Pranks ProHibited" -Cy-Pro-Hibit-ed... "Cyproheptadine"

Helminth that causes mild intermittent skin, GI, and pulmonary symptoms over the course of years. Diarrhea and abdominal pain may occur.

Strongyloides stercoralis.

If you have different BPs in your 2 arms, what is on the differential?

Subclavian steal syndrome (BP will be lower in the affected arm that has the stenosis/occlusion in the ipsilateral subclavian artery) Aortic dissection

what kind of herniation happens at the falx cerebri?

Subfalcine herniation.

50yo with worsening jaundice, anorexia, general malaise, RUQ abdominal pain over past 3 days. Has scleral icterus and tender hepatomegaly. MCV 102 (high), Leuks 13,000 (high), Cr 1.2 (high), Albumin 3.4 (low), TBil and Dbili both elevated, AP 105 (high). AST 212, ALT 99 (so AST:ALT ratio is >2:1). INR 1.2 (high). What are you going to look at to establish a dx?

Substance abuse hx, LOOK AT AST: ALT RATIO!!! and think alcoholic hepatitis. AST & ALT usually <300 AST:ALT ratio >2 Elevated GGT, bilr, INR Leukocytosis (mostly PMNs) Decreased albumin if malnourished. Imaging may show fatty liver.

Parkinson's disease is problem with what part of the brain? what is missing?

Substantia nigra decreased dopaminergic activity, increased cholinergic activity.

57 yo woman with 2 day hx of localized tenderness and swelling of her left calf. Pain at rest that increases with weight bearing. 40 pack year history. Exam shows superficial varicosities BL. There's tenderness, induration, and erythema and thickening in a linear distribution approximately 1cm wide along the medial aspect from just below the left knee to the ankle. Pedal pulses are normal BL. Most likely dx?

Superficial thrombophlebitis. (think about this in the lower extremities, also there is no mention of lymph nodes so you're not thinking lymphangitis. There's no mention of an abnormal bulge in the calf after exercise or ecchymosis so not thinking ruptured popliteal cyst. There is no mention of cyanosis of hands/feet in the medium vessels so not thinking Beurger disease aka thromboangiitis obliterans)

How do you treat cholesteatoma, a keratinized epithelial growth int he middle ear that can present with hearing loss and discharge?

Surgical management..

You dx papillary thyroid cancer (the slow growing one), what do you do next?

Surgical resection as primary tx. After surgery, do adjuvant therapy with radioiodine ablation for pts with increased of tumor recurrence (large tumor, extrathyroid invasion, lymph node mets, incomplete resection). Note: TSH can stimulate growth of occult residual or metastatic disease, so you want to stop that from happening so for pts with increased risk of recurrence, give them adequate doses of thyroid replacement to suppress TSH secretion (so that that TSH doesn't then encourage any remaining cancer to grow)

What do you want long-term home oxygen therapy to be at for pts with advanced COPD?

Survival benefit in these pts if -Resting arterial oxygen tension (PaO2) < 55 mmHg or -Pulse ox (SaO2) < 88% on RA Note: dose of supplemental oxygen should be titrated so SaO2 is maintained at >90% during sleep, normal walking, and at rest. Survival benefit of home oxygen therapy are significant when it is used for >15 hours a day. Note: wantPaO2 < 59 or SaO2 <89% in pts with cor pulmonale, evidence of right heart failure, or Hct > 55%

Older patient has CHF but does not have history of HTN. Now she has unexplained CHF, proteinuria, and LVH... what is going on?

Suspect Amyloid aka restrictive heart disease. Amyloidosis can cause multi-systemic disease d/t fibril deposits in tissues. Cardiac amyloidosis is form of restrictive cardiomyopathy; suspect this in pt with CHF with LVH, esp. in absence of HTN. RHF sxs predominate. Other things that suggest amyloid: asx proteinuria or nephrotic syndrome, waxy thickened skin, shoulder pad enlargment, anemia, easy bruising with ecchymosis (thrombocytopenia), hepatomegaly, GI bleeding, early satiety, subQ nodules, enlarged gone, and peripheral autonomic neuropathy, stroke, peripherla edema, dysmotility, malabsorption, pulm. nodules, tracheobronchial infiltration, pleural effusions.

Pt with DVT is put on warfarin but they're busy and their eating changes alot so their INR was okay at 2.2 (goal 2-3) but on recheck , their INR is 1.3 (low so more likely to clot) and doppler u/s shows right popliteal vein thrombus that extends to femoral vein (so higher than knee) and is worse than the previous lower extremity DVT. He has moderate pre-tibial edema but is HDS. What do you want to do next? Is there a class of patients you wouldn't do that next step with?

Switch the pt from warfarin to rivaroxaban (Direct Factor Xa inhibitor), which is as effective as warfarin in tx of acute DVT or PE but doesn't increase risk of bleeding complications. He needs immediate anticoagulation bc the proximal DVT has higher risk for PE than a distal DVT. These direct factor Xa inhibitors have rapid onset of action and don't need INR monitoring and no requirement for overlap with heparin. Note: just don't use these with pts with impaired renal function or who have DVT/PE 2/2 malignancy. (don't initiate thrombolytic therapy, bc that is usually reserved from hemodynamically unstable pts with PE, it can also be used for massive DVT w/ significant swelling or limb ischemia)

How do you characterize digoxin toxicity, what is a drug that can interact with it and cause dig toxicity in pt who was stable before?

Symptoms: GI- N/V/abdominal pain, anorexia. MSK: weakness. fatigue AMS, color vision changes. LIFE THREATENING ARRHYTHMIAS. Note: recommended to decreased digoxin by 25-50% when starting amiodarone therapy; with close monitoring of digoxin levels once weekly for next several weeks after starting amiodarone.

Pt has SVT (HR 240/min, BP 65/40, diaphoretic, cold extremities, EKG shows regular narrow complex tachy), What do you do?

Synchronized cardioversion. This pt is hemodynamically unstable with hypotension and signs of poor perfusion (pool extremities). - manage unstable pts with immediate synchronized direct current cardioversion d/t risk of rapid clinical deterioration. Note: if pt is HDS, then you can do adenosine or vagal maneuvers (ex: bearing down, squatting, breath holding).

What is this a description of? Single, indurated, well circumscribed ulcers. Clean base. Thin, delicate, corkscrew shaped organism on dark field microscopy Initial lesion Not painful

Syphilis. (Treponema pallidum) Ex: pt with 2cm-ulcer with non-exudative base and a raised, indurated margin. No tenderness to palpation. Moderate, painless BL inguinal LA present.

What's the difference between primary syphilis lesion and chancroid from haemophilus ducreyi?

Syphilis: -Single ulcer -clean base -NOT painful Chancroid/Haemophilus ducreyi: -multiple/deep ulcers (plural) -yellow-gray exudative base (not a clean base) -IS painful

Uveitis, diminished visual acuity, and symptoms of syphilitic meningitis

Syphilitic chorioretinitis.

What can cause central cord syndrome (weakness in upper extremities BL, shoulder cape like distribution where they loss of pain and temp. vibration and proprioception is preserved)?

Syringomyelia: fluid filled cavity in the central spinal cord.

What does having anti-Scl-70 (anti-topoisomerase) antibodies clue you in on? (moderate sensitivity & high specificity for...)

Systemic sclerosis (scleroderma) & are associated with extensive skin involvement and interstitial pulmonary fibrosis.

What kind of sound would you hear with pseudoaneurysm? what would you feel?

Systolic bruit: blood forced through arterial wall during systole so systolic bruit is heard at the site of the psuedoaneursym Bulging, pulsatile mass Strongest RF: inadequate post-procedural aterial compression. Should confirm dx of pseudo-aneursym by ultrasound.

IVDU gets Tricuspid valve endocarditis, how does that usually manifest?

Systolic murmur (holosystolic) that is accentuated with inspiration. Note: cardiac conduction abnormalities are uncommon in tricuspid valve endocarditis... should just be murmur.

Pt with fibromyalgia who doesnt' respond to regular exercise sand good sleep hygiene can be tried on what med?

TCA!!!! YESSS IT'S TCA!!! (Know this confidently; I thought it was a antidepressant but I thought it was kind of intense to start with a TCA), but that's right! TCA (ex: amitriptyline) are preferred 1st-line drugs for fibromyalgia. (Think about it as it's so bad the pain.. no one see... that you're willing to try TCA as 1st line med). Note: SSRI ad ANRI and pregabalin are alternative therapies that can be sued in pts who don't respond to TCAs.

31 yo man HIV+ only takes antiretrovirals. with 2 weeks daily HAs and progressive confusion. Slowly worsening behavior changes, inappropriate suspicions and aggression. Temp 101.4. unkempt, disoriented, Ataxia, right sided hemiparesis. MRI shows multiple ring-enhancing lesions. What could have prevent this pts condition?

TMP-SMX HIV pt with neuro sxs (HA, confusion, focal deficits), fever, evidence of ring-enhancing lesions on MRI, strongly suggest toxo. Likely caused by reactivation of toxo. HIV pts are at risk when CD4 count is <100. and should take TMP-SMX as prophylaxis. Pts newly dx with HIV should be tested for latent infection with serology for T gondii IgG antibody (basically have they had it before?). If serology is positive and CD4 count is <100, prophylaxis with TMP-SMX reduces the risk of toxo dramatically (to 0-2%). Can d/c TMP/sMX when CD4 is >200 for 3 months and there is adequate viral suppression with antivirals. (Note: TMP-SMX is also used for primary prophylaxis against PCP)

Abx to treat PCP

TMP-SMX works for Pneumocystis pneumonia, Gram negative and Gram positive agents. (do NOT work for anaerobes)

Homeless HIV man with fever, SOB, nonproductive cough, BL patchy opacities in lower lungs. started on Azithromycin, Ceftriaxone, TMP-SMX, Prednisone, and albuterol. His Cr bumps up from 1.2-1.5. and his K bumps from 4.2 - 5.9. Which med is likely responsible for these lab changes?

TMP-SMX. TMP worse by blocking epithelial sodium channels int he collecting tubules (similar to action of K-sparing diuretic amiloride). This occurs commonly in HIV pts treated with high doses of TMP, but can happen even in normal doses; can produce modest elevation in plasma potassium concentration. Pts treated with high dose TMP require serial monitoring of POTASSIUM to avoid serious complications. TMP also competitively inhibits renal tubular creatinine secretion and may cause an artificial increase in serum creatinine; however, GFR is unchanged. TL:DR: when giving high doses of TMP-SMX, esp to HIV pts to treat PCP, be watchful for K+ and Creatine bumps.

If TSH is increased AND thyroid hormones are increased, that's super weight bc there should be feedback mechanisms that make them opposite. So if they are both increased, what is going on?

TSH secreting pituitary adenoma (coming up from up top to make everything elevated; called "central hyperthyroidism") Note: these can also present with tumor mass effect: HA, visual symptoms, impaired production of other pituitary hormones (so can have sx like amenorrhea) Note: most TSH secreting pituitary adenomas are macro-adenomas. Pts with this condition typically have a goiter d/t the effects of TSH on growth of thyroid follicles. They do not have extrathryoidal manifestations of Graves disease like infiltrative ophthalmopathy or pre-tibial myxedemal.

How does opiate withdrawal present?

Tachycardia, hypertension, diaphoresis, restlessness, irritability

Cross-sectional studies:

Take RFs and compare disease prevalence (looking at right now aka "cross-section in time," who has the disease aka disease prevalence)

Pt with HHS comes in with AMS & with glucose 800 and it looks like they have hyponatremia of 128. But first you have to correct the their serum sodium. How do you calculate a corrected serum sodium? Is this person's Na level contributing to their AMS?

Take the measured serum sodium and then + 2 for every 10 mg/dL that their glucose is above 100 mg/dL. glucose of 800 is above 100 seven times. So 128 + 2 (7) = 128 + 14 = 142 So this pt's sodium is actually okay and it's just pseudohyponatremia and you can't get neurologic symptoms form pseudohyponatremia. So this pt's Na level is not contributing to their AMS AMS due to hyponatremia is due to cerebral edema caused by mvt of water into brain cells from low osmolar extracellular fluid ("high to low, your brains will blow" - cerebral edema).

Clinical trials:

Taking tx and control groups and looking at ***outcomes***

Pre-menopausal woman gets ER+ breast cancer, what med do you use? what are you concerned about? so what do you check before starting this drug?

Tamoxifen. increased risk of VTE. Since pts with Factor V Leiden mutations are at increased risk for VTEm make sure to test the pt for factor V Leiden mutation before starting tamoxifen so that you're not giving them really bad risk for getting VTE.

What do you expect to see on peripheral smear for someone who has thalassemia?

Target cells and teardrop cells. (think of Kim... and she probably has teardrop and target cells in her blood if she really has thalassemia)

Absence of hexosaminidase and common in Ashkenazi population. Development is normal for 6 months and then there is mental deterioration. Infants are usually macrocephalic d/t accumulation of gangliosides in the brain. Cherry red spot on macula. Death at age 3-5. Dx?

Tay-Sachs

Meckel's what is the best modlaity to confirm the dx?

Technetium-99m pertechnetate scan

Pt has 2 days fever, chills, dysphagia, and drooling. He can't eat or drink bc of pain in mouth and neck. Temp 101.8. HR 108. RR 22. Appears toxic with drooling and muffled voice. Tongue displaced posteriorly and superiorly d/t swollen area on floor of mouth. Tongue is displaced posteriorly and superiorly d/t swollen area on floor of mouth. BL submandibular area is tender, indurated, and non-fluctuant with palpable crepitus. What is likely source of infection in pt?

Teeth roots. He has Ludwig angina: rapidly progressive cellulitis of the submandibular space. Most cases arise from dental infections in mandibular molars that spread contigously down the root into the submylohyoid (and then sublingual) space. The infection is usually polymicrobial and mixture of oral aerobic (ex: strep viridans) and anaerobic bacteria. Pts develop sxs rapidly with systemic (fever, chills, malaise) and local compressive (mouth pain, drooling, dysphagia, muffled voice, AIRWAY COMPROMISE) manifestations. PhyExam: often striking d/t mass effect from edema. Submandibular area is usually tender and indurated and floor of mouth is often elevated, displacing the tongue. Anaerobic, gas producing bacteria may cause crepitus. Confirm dx with CT scan of neck and rule out abscess. Tx with IV Abx (ex: ampicillin-sulbactam, clindamycin) and REMOVE THE INCITING TOOTH!! Drainage and surgery rarely required as the process is cellulitis and typically non-suppurative. Impaired respiratory statue requires prompt attention & early intervention with mechanical airway.

Stressed out so much your hair falls out. What is that called?

Telogen effluvium. -one of the most common causes of adult hair loss -"telogen" phase is the shedding phase of a hair follicle. So in TE, they are in this phase more. So pts have widespread thinning of hair but the scalp and hair shafts appear normal. -Hair pull test: small tracts of hair (50-60 fibers) are pulled firmly and extraction of >10-15% of fibers is abnormal and suggests TE. Acute, diffuse, non-inflammatory hair loss. Scalp and hair fibers appear normal. Hair shafts are easily pulled out (hair pull test). Triggered by: severe illness, fever, surgery, pregnancy, childbirth, emotional distress/psych trauma, endocrine and nutritional disorders, weight loss Manage: address the underlying stressor. reassure pt this is a self-limited disorder (may take up to a year to resolve)

Pt travels to South American, has 4 weeks hx of diarrhea with foul smelling stools, abdominal cramps, and bloating. 3-day course of cipro didn't help. He has increased bowel sounds. What do you do?

Test for Giardia with stool antigen assay (direct immunofluorescence of ELISA) Could also do stool microscopy for oocysts and trophozoites in resource poor setting. Metronidazole is the preferred treatment.

Young man with painless unilateral testicular nodules - ovoid, firm, hard, fixed, does not transilluminate. What's going on?

Testicular germ cell tumor - most common solid organ malignancy in med age 15-35. Workup: get serum tumor markers (AFP, beta-hCG) and BL scrotal u/s. Tx: radial orchiectomy with lymph node diessection is usually needed for histo dx and staging. Most pts get chemo and cure rates are as high as 95%.

Failure of closure of processus vaginalis causes?

Testicular hydrocele - collection of fluid between parietal and visceral tunica vaginalis. Causes testicular swelling but not acute pain.

Pure sensory deficit in lacunar stroke, what part of brain likely affected?

Thalamus Picture: The-mouse running over your foot and you don't feel it.

If someone has anemia with low MCV... but they have a really high number of RBCs.. you're thinking the cause of the anemia is?

Thalassemia. (reduced production of globin chains) You want to look at the Mentzer index, which is MCV/RBC and you want that <13. If the RBC number is in the millions (ex: 5 million), then your Mentzer index will be very low. The RBC number helps you come up with the Mentzer index. Also, look at the Hct which is usually >30% in pts with thalassemia minor (ex: 31%) Peripheral smear: in thalassemia, will show target cells and teardrop cells. Note: be careful to exclude iron deficiency bc giving unnecessary iron in someone who is not iron deficient can lead to hemochromatosis.

What is the expected Mentzer index in iron deficiency anemia?

The MCV willb e low and the pt will be anemic. However, there is also a decline in RBC count bc you're having a deficit in the material you are using to make the RBCs so Mentzer index = MCV/RBC and with a decreased RBC count, your Menzter index will be high, Menzer index > 13. You'll also see increased RDW bc the size of the RBCs are changing as you run out of the supplies used to make the RBCs.

Pt with 7cm AAA. He also has inoperable pancreatic cancer. What do you do about his AAA?

The aneurysm should not be repaired because of the patient's poor prognosis. Wow, okay.

Pt with TIA (transient symptoms) and smoking and HTN hx. Doppler u/s shows 75% stenosis of proximal left internal carotid artery. what is most appropriate intervention?

The choices were referral for carotid endarterectomy (correct) and adding clopidogrel (incorrect; bc ASA is the 1st-line therapy for those undergoing carotid endartectomy and you can use clopidogrel if the pt cannot tolerate aspirin) Medical management is initial intervention for all pts with carotid artery stenosis: with aspirin, statin, BP control. and couseling on lifestyle changes (exercise, smoking cessation)

What is Ischemic optic neuropathy?

The feared complication of temporal arteritis. -results from vasculitis of the retinal artery and may cause blindness (not enough blood supply to the optic nerve)

Pt with high BMI (40), and one week after c-section, she has increasing pain around the incision, no redness or induration near the surgical site, but has serosanguineous discharge that is expressed from a 5-mm opening left of midline. Exploration of the defect with a sterile swab meets resistance at a depth of 3cm. What is going on?

The key here is that it's at the edge of the incision. So this is incisional hematoma. -Post-op serosanguineous drainage and incisional pain are consistent with incisional hematoma, an abnormal collection of blood at the incision site d/t inadequate surgical hemostasis. RFs for incisional hematoma: obesity and hypo-coagulability (ex: anticoagulation, coagulopathy). Hematomas can reopen surgical potential space (ex: incisional separation and create a collection of stagnant fluid. So they can be niduses for bacterial growth and increase risk of surgical site infection like cellulitis or abscess. Tx large symptomatic hematomas by opening the incision, evacuating the clot, and getting hemostasis and then reclosing the incision) Note: this is NOT fascial dehiscence: which is a re-opening of the fascial incision, that presents with a "popping" sensation followed by lots of sero-sanguineous drainage and an incisional bulge. Note: the resistance encouraged during probing of this pt's incision suggests her fascia is intact (meets resistance at dept of 3cm, so the fascia is intact in this pt so this is note a dx of fascial dehiscence)

Why do we give Sodium bicarb to suicide patients who use TCAs (ex: imipramine)- in TCA overdose?

The sodium bicarb is used to support the pt and prevent further QRS widening and ventricular arrhythmias. In short: a sodium load will alleviate depressant action on myocardial sodium channels. Explanation: TCAs are cardiotoxic. Cardiac toxicity cause most deaths in TCA overdose. TCA inhibits the fast sodium channels in the His-Purkinje system and myocardium. This therefore decreases the conductive velocity, increases duration of repolarization and prolongs absolute refractory period. The result is hypotension, QRS prolongation, and ventricular arrhythmias (ventricular tachycardia, ventricular fibrillation). QRS interval >100ms in the setting of TCA overdose is an indication for sodium bicarb therapy. Sodium bicarb increases the serum pH and extracellualr sodium. Increased pH (goal 7.5-7.55) decrease drug avidity for sodium channels (ITS ALL ABOUT THE SODIUM CHANNELS WHEN YOU GIVE SODIUM BICARB). Elevated extracellular sodium concentration increases the electrochemical gradient across cardiac cells and affects the ability of TCAs to bind to the fast sodium channels.

Testicular torsion. What is twisting?

The whole testes. So it's d/t inadequate fixation of the testis to the tunica vaginalis. -Abrupt onset scrotal pain with swelling and DIFFUSE tenderness. The pampiniform plexus of the testicular vein is compressed and there is reduced venous outflow. This is a surgical emergency as irreversible damage to the testis can occur quickly d/t impaired blood flow. Dx: made based on clinical findings. -shortened spermatic cord -high riding scrotum with long axis oriented horizontally (bell-clapper deformity) -Cremaster reflex is absent*** (so no retraction of testes on pinching or stroking of inner thigh) -If uncertain, can confirm dx with Doppler u/s that shows lack of blood flow in the testicle. *Note: don't get tricked by the testicular appendix, that's jsut a little thing off of the teste so that's not what's being twisted.

How do you dx Gastrinoma (Zollinger-Ellison Syndrome)?

There are 3 ways to do it. The single most accurate test is always a functional test, looking at the response to secretins. 1) Persistent high gastrin levels despite injecting secretin 2) High gastrin levels despite a high gastric acid output 3) High gastrin levels off antisecretory therapy (PPIs or H2 blockers) with high gastric acidity. -so basically having high gastrin levels despite things that say you shouldn't have a high gastrin level (ex: secretin injection, high gastric acid output, high gastric acidity). There should be some signaling feedback telling your G cells to stop making so much gastrin... but that's not happening since you have a tumor making the gastrin so the gastrinoma will just keep putting out gastrin and the normal feedback mechanism will not work.

If you're not sure what is causing a pt to have nephrotic syndrome, then you need to do a kidney biopsy. why is that?

There are a number of causes so need to get kidney biopsy to establish a clear dx and so you don't delay appropriate treatment. Ex: pt with T2DM and now has peripheral edema and nephrotic range proteinuria (>3.5 g/L in 24 hours), suggesting nephrotic syndrome. Diabetic nephropathy is one of the most common causes of nephrotic syndrome in adults. But if the pt also has normal renal function recently, relatively well controlled blood glucose, hematuria and RBC casts (suggests glomerulonephritis), that is a bit confusing as to what the cause is, so should get kidney biopsy to establish a clear dx

Why is there an increased false-positive response for TB skin test in the USA?

There is high likelihood of exposure to non-tuberculous mycobacteria in several parts of the southern USA. (so someone who is low risk, healthy person not exposed to TB could have a TB skin test induration of 12mm even though they don't have TB bc they may have been exposured to non-TB mycobacteria)

Multiple myeloma: what is happening in the kidneys?

There is renal insufficiency in about 50% of MM pts. This is bc of obstruction of the distal and collecting tubules by large laminated casts consisting mainly of Bence-Jones proteins. Amyloid deposits and infiltration of the kidney by plasma cells are commonly seen.

What should you know about anaplastic thyroid tumors?

These are bad, happens in old people, grows quickly and kills you because they grow into everything and choke you out

Are spleen and reticuloendothelial system considered intra- or extra-vascular? What is the special case?

They are extra-vascular . So autoimmune hemolytic anemia in patients with chronic lymphocytic leukemia (CLL) is extravascular

Big babies of moms with DM are at risk for polycythemia, why?

They are in a constant anabolic state... so the placenta can't meet their increased metabolic demand so they have fetal hypoxemia. So then their EPO production increases so that causes polycythemia, which is dangerous bc it makes blood more viscous (sludging, ischemia and infarction of vital organs can occur)

Tell me about uric acid stones.

They are: -Radiolucent: can't see on Xray but CAN seen on CT Scan -Highly soluble in alkaline urine (alkalinize the urine to pH 6.0-6.5 with oral K citrate as tx of choice) Note: it's a clue that it's a uric acid stone when the urine pH is acidic (low) and you can treat these by alkalinizing the urine (increasing the pH with K citrate)

Why does a pt with lactose intolerance have a positive breath hydrogen test?

They don't have the brush border enzyme lactase to process the lactose in diary, so instead bacteria metabolizes the lactose carbohydrate, causes a rise in the measured breath hydrogen level after the person ingests lactose.

What is Chediak-Higashi syndrome?

They have albinism (skin and eyes), recurrent skin and soft tissue infections, peripheral neuropathy. It's a defect in lysosomal trafficking, leading to impaired phagocytosis. Affected pts have recurrent skin and soft-tissue pyogenic infections, albinism, and peripheral neuropathy.

Pt has rapidly progressive hirsuitism with virilization (clitoromegaly), and increased acne and confirmation of an adrenal mass. What is going on, what do you expect their LH, T, and DHEAS (note the S!!! sulfate) to be?

They have androgen producing tumor (in the adrenal gland) which is causing the hirsutism and virilzation. Expect LH to be low bc of negative feedback by T Expect Elevated T levels Expect Elevated DHEAS <-- ***Note: women normally made androgens: T, androstenedione (AS), DHEA, and DHEAS. -AS, DHEA, and T are made both by the ovaries and adrenals -DHEAS is special bc it's predominately made by the adrenal glands. So this question specifically asks about DHEAS (with the S; Memory tool: ***think S for special***). Since she has an adrenal tumor that is making androgens, her DHEAS will be high.

Pt from another country has hx of throat infections and now they are pregnant and they have a.fib with RVR. What is the reason?

They have rheumatic mitral stenosis (from untreated strep throat from GAS) and now they are pregnant and they have pregnancy related increased in HR and blood volume so they have increased transmitral gradient and LA pressure. . So they get fatigue, exercise intolerance, dyspnea when they were previously asx. They are at increased risk for develop Afib bc the loss of effective "atrial kick" and decreased diastolic filling times seen with AF and RVR (pulse >100/min is a clue!!!), further increased LA pressure with dramatic worsening of pulmonary congestion and pulmonary edema. Pregnant pt with hx of sore throat and now has Afib with RVR, think about hx of GAS strep throat and rheumatic fever with mitral stenosis.

What meds can trigger gout?

Thiazide and loop diuretics (d/t decreased clearance of urate) Other triggers: surgery, trauma, volume depletion, lifestyle factors (excessive ETOH use and high-urate diet)

Pt with corneal lesions and has ocular pain, tearing and discharge. What does he have?

Think about HSV keratitis.

Women on OCPs now has HTN. what do you do?

Think about OCP's SE of causing HTN. So just discontinue the OCPs and start a different method of birth control.

23yo Female with 3mo hx of hand stiffness and pain. She's excessively tired and has occasional episodes of knee pain and sharp chest pain. She sunburns easily and thinks it might be because of her acne minocycline medicine. She has BL hand joint and wrist tenderness and swelling. Mild BL lower extremity edema. Labs show Hgb 12, Plt 98k (low), and leuk 3,300 (low). She has UA that shows 2+ protein, 5-10 erythrocytes/hpf. What would you do to evaluate her next? What do you think she has?

Think about SLE (lupus) with this pt who MD SOAP BRAIN - She has: Serositis (CP), Arthritis, Photosensitivity (burns easily), Blood (pancytopenia: anemia, thrombocytopenia, leukopenia), Renal (protein losing nephropathy - edema, proteinuria, microscopic hematuria), ANA, Immune other.. (anti-ds DNA, anti-Smith; increased immune complexes, low complement levels) So check ANA titer (95-100% sensitivity) as the 1st test If that's positive, then you do the more specific anti-ds DNA or anti-SMOTH tests to confirm.

'Hemosiderin deposits and fibrosis'

Think about bleeding into the joint as a late complication of Hemophilia A or B. Bleeding into the joints is though to be d/t iron/hemosiderin deposits leading to synovitis and fibrosis within the joint. Presents with chronic worsening joint pain and swelling and can --> contractures of the joint and limited ROM. Most common in pts with recurrent hemarthroses. Early ppx tx with factor concentrates can significantly reduce the risk of developing arthropathy.

What's something you want to think about with a pt with scleroderma who suddenly has malignant HTN?

Think about renal failure with the HTN crisis and they might start hemolyzing with MAHA (schistocytes/fragmented cells on peripheral smear) or go into DIC (decreased plts)

acute complete vision loss. What are 2 possible diagnoses?

Think central retinal artery occlusion, or retinal detachment.

Coma and extensor posturing

Think intracranial hemorrhage with uncal herniation (dialted nonreactive same side pupil) with further midbrain compression causing extensor posturing on the opposite side, coma, and respiratory compromise.

Pt who is obese and has HA and transient vision changes and BL papilledema with normal brain imaging. What is the dx? What do you do to treat them?

Thinking pseudotumor cerebri Treat with acetazolamide, it's a carbonic anhydrase inhibitor that treats increased ICP as it reduces CSF production.

When you have someone with hx of taking aspirin d/t RA or migraines, and then they now have tinnitus, fever, tachypnea, nausea, GI irritation. What are you thinking they have? Now tell me what you expect to see their pH, PaCO2, and HCO3 to be?

Thinking they have ASA (salicylate) intoxication: So they have an AG Metabolic Acidosis with a Respiratory Alkalosis. So expect -Metabolic acidosis: HCO3 to be low -Respiratory alkalosis (bc tachypnea): PCO2 to be low (Bc blowing off the CO2 acid) -pH: expect it to be near normal bc the 2n primary acid-base disturbances are shifting the pH in opposite directions. NOTE: In Aspirin toxicity, you expect the ABG to have near-normal pH (ex: pH = 7.39) with mixed independent respiratory alkalosis and metabolic acidosis.

1 day old boy with MACROCEPHALY and jaundice. Mom had a bunch of different risks (school teacher, traveled to Zambia and got fever for 2 weeks, swollen glands, muscle aches that resolved spontaneously). Baby is weight/length are 25%tile, HC is >95%tile. VSS. Diffuse jaundice, liver palpable 4cm below costal margin. CT Head: hydrocephalus, diffuse INTRACRANIAL CALCIFCATIONS. LabS: Tbili 7.2, dbili 5.5. What maternal exposure most likely resulted in this condition?

This baby has toxoplasmosis: so undercooked/raw meat, unwashed fruits/veges, or cat feces. Clinical features of congenital toxo: macrocephaly (big head), diffuse intracranial calcifications, non-specific sx of congenital infection (jaundice, growth restriction, HSM, blueberry muffin spots). Note: majority of infants are asx at birth but may experience chorioretinitis in adulthood d/t reactivation of their infection Dx: with serology Tx: Pyrimethamine, sulfadiazine, folate.

Pt travels to endemic area (Central and South Americ) or eats pork that isn't cooked all the way. MRI shows mixture of enhancing and nonenhancing and calcified lesions, what do you need to treat them with?

This is neurocysticercosis (NCC) The MRI shows different things bc it depends on the stage of the cyst. Treat with Albendazole.

60 yo woman has 4 weeks of hoarseness of voice and progressively worsening difficulty in swallowing. She has fatigue, mild fever, and night sweats. She has long-standing hypothyroidism with anti-thryoid peroxidase antibody (TPO) in high titers. She also has hx of pernicious anemia. Thyroid gland is diffusely enlarged, firm, and mildly tender. She has facial congestion, cyanosis, and inspiratory stridor when she lifts her arms (weirdddd). What is the most likey cause of these syptoms?

This is super werid sounds. so she definitely has cancer with the B symptoms (fever night sweats, and weight loss). ***SPECIFICALLY LYMPHOMA!!!! B symptoms are a sign of lymphoma!!!!*** Dx: Thyroid lymphoma. These are uncommon but increased incidence (about 60x higher incidence) in pts with pre-existing chronic lymphocytic thyroiditis aka Hashimoto (as seen by the chronic hypothyroidism and high titers of TPO antibody). Typical presentation of thyroid lymphoma is rapidly enlarging, firm goiter associated with compressive symptoms (ex: dysphagia, hoarseness). Also, she has B symptoms = lymphoma. So think about B symptoms ad someone who has compressive symptoms on their neck.. that's Thyroid lymphoma, esp if there's that Hashimoto's hx. The mass is painful and tender and is fixed to the surrounding structure and doesn't move up when swallowing. Retrosternal extension of the tumor is common can cause lead to venous compression with distended neck veins and facial plethora and raising the arms compresses the subclavian (& right internal jugular) veins between the clavicle and enlarged thyroid, leading to more prominent venous distention and facial redness (Pemberton sign) Inflammatory markers (ESR) can be elevated but are nonspecific. CT will show diffuse enlargment of thyroid around trachea (doughnut sign). Core or excision biopsy may be required, and flow cytometry can confirm monoclonal lymphoma cells.

When do you think about Condylomata lata?

This is with secondary syphilis. This about this when they describe flat, velvety lesion with broader base and flatter surface and are lobulated or plaque-like.

Type 2 Diabetic comes in with AMS and really high glucose. Serum K looks normal (high even at 5.9). What are you not fooled by? Why does this happen? What do you need to do then?

This patient has normal serum K but they actually have total body K deficit. This happens in DKA and HHS. The insulin deficiency and hyperosmolality promotes movement of K out of cells and into the extracellular space, and the execssive urinary loss caused by osmotic diuresis induced by hyperglycemia causes these patients to have a deficit in total body potassium. So the clinical implication is that when you give these pt insulin therapy (to correct there hyperglycemia), you can abruptly lower their serum K levels and cause severe hypokalemia, so make sure to also give K.

Pt with 1 year of diarrhea. Stools watery with abdominal cramps. No fever, blood in rectum or foul smelling stool. He has frequent dizziness, flushing, wheezing, feeling of warmth. Also has 2/6 systolic murmur over LLSB that increases with inspiration. Abdominal exam with HSM 3cm below right costal margin and no abdominal tenderness. AP 400 AST 101 ALT 99. What's the deficiency?

This pt has Carcinoid syndrome with the skin flushing and secretory diarrhea, brochospasm, and cardiac valve abnormalities. So remember that on thanksgiving everyone is happy (serotonin) bc we eat turkies (tryptophan). So Serotonin in carcinoid syndrome is made from tryptophan (we get our joy for eating turkeys). But that means the turkey doesn't get to go and live its NICE (niacin) little life. Tryptophan also makes niacin. So by us eating the turkey and making serotonin instead, we're not making niacin. So you can have a niacin deficiency (deficiency of turkeys living nice lives). And Niacin is B3 so that cause sx pf B3 deficiency (pellegra): diarrhea, dermititis, dementia.

HIV pt with 4 day hx of low-grade fever, profuse watery (non-bloody) diarrhea, and abdominal cramps. what do you want to do?

This suggests infectious etiology. Common AIDS-related diarrhea include Cryptosporidium, Mycobacterium avium complex (if CD4 <50), microsporidia, Giardia, or Isospora belli. Absnce of dysentery (bloody diarrhea) makes infection with many non-opportunisitic pathogens (Salmonella, Campylobacter, Entamoeba, Shigella) less likely. 1st step is to get a stool exam for culture, O&P, C. diff antigen, and acid-fast stain (for Cryptosporidium). AKA check the poo first.

Pregnant patient who is Rh positive has spotting, but exam shows the cervix is CLOSED and normal fetal cardiac activity, What is the dx? what do you do for them?

Threatened abortion (since cervix is closed) Just reassure them and follow up with ultrasound later. (management is just expectant with observation and repeated ultrasound) DO NOT DO NOT DO NOT pick hospitalize, bed rest, and obs bc bed rest and hospitalization do not improve outcomes are are not recommended, furthermore, bed rest is associated with increased risk of VTE since that would cause venous stasis if you're not moving around. Note: pts with threatened abortions frequently have uncomplicated pregnancies with normal outcomes. So manage threatened abortions with expectant outpatient observation. Serial ultrasounds can be performed until either the sxs resolve or there is progression to a complete abortion.

What is Buerger disease? How does it present? what is the other name? What do you do to treat it?

Thromboangiits obliterans (Beurger disease) Presents: Age <45, with ongoing or recent smoking hx, pt has distal limb ischemia, gangrene, and ulcers d/t nonatherosclerotic occlusion, thrombosis. (Young pt who smokes that has gangrene and painful ulcers of the distal lower extremities = Buerger disease, thromboangiitis obliterans) - usually in heavy smokers but can also be in pts who use smokeless tobacco or marijuana. More common in men. Peripheral pulses may be decreased, but normal ABI. Eval: ischemia on vascular studies (digital plethysmography), segmental occlusion of small/medium-sized vessels on angiography Tx: complete smoking cessation!!! STOP SMOKING AND the tips of your fingers and toes will stop getting ischemic and stop looking like they're rotting. Note: even low-level smoking or nicotine replacement therapy can cause progression of the disease

Selenium deficiency presentation

Thyroid dysfunction Cardiomyopathy Immune dysfunction

Pt with high T3 and T4, but low TSH. RAIU is high but in a diffuse pattern. So you think this patient has Grave's disease. What is the process responsible for this pattern of elevated thyroid hormone?

Thyroid-stimulating autoantibody-induced activation of TSH receptors on thyroid follicular cells.

Pt with difficulty walking, involuntary movements, imbalance that has gotten worse the past few months. HA and blurry vision. Hx of papillary thyroid CA treated with total thyroidectomy 10 years ago. He has resting hand tremor, increased muscle tone. Gait slow and unsteady. Skin dry and coarse. Funduscopic exam fullness of optic cups. Labs: Ca: 7.8 (low), phosphorus 7.4 (high), Cr 1.2 (high), CT head without contrast: extensive calcifications in basal ganglia BL. What is causing these symptoms?

Thyroidectomy often also takes out parathryoids so that would explain his low Ca and high phosphorus and permanent postop low parathryoidism. Need to monitor this condition closely. So if your calcium-phosphorus product (serum Ca x serum phosphorus) is >55, that increases the risk that you will deposit calcifications in your soft tissues. In this pt: Serum Ca x Serum phosphorus = 7.8 x 7.5 = 57.7, which is greater than 55, so increased risk of calcification deposits in the soft tissues. Deposits in the basal ganglia leads to extrapyramidal manifestations (movement disorders). Other potential complications of chronic hypoparathyroidism include nephrocalcinosis (so calcifications of your kidneys like Apoorve was talking about) and cataracts.

What conditions are associated with release of preformed thyroid hormone?

Thyroiditis (de Quervain thyroiditis, silent thyroiditis, transient hyperthyroid phase in some pts with chronic lymphocytic (Hashimoto) thyroiditis) - RAIU in these cases is markedly reduced.

What do you expect to have septate hyphae on KOH prep?

Tinea cruris- caused by dermatophytes, associated with septate hyphae. Presents with annular lesions with partial central clearing (may be absent) and scaly, raised border.

When do you give methylene blue?

To treat methemoglobinemia (in the setting of ingestion of drugs like dapsone or anesthetic agents). Note: Methemoglobinemia manifests as cyanosis and respiratory depression as a result of impaired oxygen delivery to the tissues.

Transient hemiplegia following a seizure. What's that called?

Todd paralysis.

What's the link with Hyperthyroid disease and bones?

Too much thyroid hormone --> increased osteoclast activity so you get more bone resorption, decreased bone density and increased fracture risk. You get hyper-Ca and hyper-calci-uria d/t increased bone turnover. If untreated, pts with hyperthyroidism can have rapid bone loss --> osteoporosis and increased fracture risk.

Tx for HPV condylomata acuminata genital warts

Topical trichloroacetic acid. Think about condylomata acuminata caused by HPV 6 and 11. when you see multiple pink or skin-colored lesions. Lesions can be smooth, flat papules or exophytic/cauliflower-like growths. Tx: Chemical: Podophyllin resin, Trichloroacetic acid Immunologic: Imiquimod Surgical Cryotherapy, laser therapy, excision Prevention: vaccination, barrier contraception

Prophylaxis meds for Migrains?

Topiramate (sounds like Tapir, think of the Tapir animal getting migraines all the time so you give them ppx with Topiramate) Divalproex sodium (sodium valproate), TCAs, and BETA BLOCKERS!! (Propranolol is #1)

Treatment of binge-eating disorder?

Topiramate. Memory tool: Tapir likes to eat... ALOT (so this med used to treat bing-eating disorder)and Tapir likes to sleep (also used as ppx for migraines)

Pt has syncope and labs show hypo-K, hypo-Mg, orthey use meds that increase QT interval. Cause of syncope?

Torsades de points (acquired long QT syndrome)

Eye pain & decreased vision. Retinal lesions appear in nonvascular distribution.

Toxoplasmosis chorioretinitis (YES, EYE PAIN WITH TOXOPLASMOSIS CHORIORETINITIS)

4yo boy in refugee camp with 10 days of mild rhinorrhea and cough now resolving. He has eye redness. 2 days ago started having mild eye redness with scant watery discharge. 6 yo brother has similar sx. Exam of the eye shows sever pale follicles and inflammatory changes in the tarsal conjunctivae BL. Conjunctivae appears mildly thickened. Visual acuity is 20/20. likely dx?

Trachoma Conjunctival injection, tarsal inflammation (that part under the eyelid), and pale follicles are concerning for trachoma. This is d/t Chlamydia trachomatis serotypes A, B,and C and is leading cause of blindness worldwide. C. trachomatis spreads effectively in crowded/unsanitary conditions (really contagious). Active phase: most common in kids and characterized by follicular conjunctivitis and pannus (neovascularization) formation in the cornea. Concomintant nasopharyngeal infection (runny nose, pharyngitis). Dx made clinically by looking at the tarsal conjunctivae. C. trachomatis may be visible by Giemsa stain exam of conjunctival scrapings. Tx: Oral azithromycin. The entire region (village, refugee camp) should be treated simultaneously bc this is very infectious. If pts have trichiasis (inversion of eyelashes that will cause repeated chronic infection --> scaring of eyelids; over time lashes rub on eye and cause ulcerations and blindness - cicatrcial trachoma), eyelid surgery is needed to preserve vision

What's the pain med that you could get during surgery that also has serotonergic activity so want to be careful if pt is already taking SSRI, SNRI, or MAOI.. bc you don't want to cause serotonin syndrome? What's the triad of serotonin syndrome?

Tramadol. Triad: Mental status changes (anxiety, restless, agitated delirium), autonomic dysregulation (sweating, tachycardia, HTN, hyperthermia), NM hyperactivity (hyper-reflexia, tremor, rigidity, myoclonus, ocular clonus (slow, continuous, horizontal eye movements), BL Babinski signs. There are also serotonin receptors in the gut, resulting in hyperactive bowel sounds and diarrhea. Management: d/c all serotonergic agents (including tramadol!!) and give supportive care (hydration), sedation with benzos. Severe cases may need cyproheptadine as serotonin antagonist (Sketchy: in the serotonin office, the signs says "Pranks prohibited" = cyproheptadine)

Pt with heavy menstrual bleeding, What might you try to treat them with?

Tranexamic acid (an antifibrinolytic agent) (Tran-exam-ic... you exam pt with heavy menstrual bleeding (HMB).. try tran-exam-ic acid to treat the HMB)

Respiratory distress & sxs of noncardiogenic pulmonary edema. Occurs within 6 hours of transfusion. Caused by donor anti-leukocyte (anti-WBC) antibodies.

Transfuion-related acute lung injury (TRALI)

pure red cell aplasia without macrocytosis. no associated congenital abnormalities. found in a kid.

Transient erythroblastopenia of childhood.

what is primary hypotension reaction?

Transient hypotension often in patients taking ACE-inhibitors. Happens within minutes of transfusion, caused by bradykinin in blood products (normally degraded by ACE)

Inadequate alveolar fluid clearance at birth results in mild pulmonary edema. Tachypnea beings shortly after birth and resolves by day 2 of life. CXR shows: BL perihilar linear streaking

Transient tachypnea of the newborn (think about this in full term infants; has no long term sequelae)

How do you treat pt with postnasal drip (hx of upper airway cough after recent URI that occurs primarily at night and is without expectorate)?

Treat empiricially with oral 1st Gen antihistamine (ex: Chlorpehniramine) or combined antihistamine-decongestant (ex: brompheniramine and pseudoephedrine) and see if they respond in the next 2-3 weeks.

How do you treat macroprolactinomas (>1 cm aka > 10mm) or symptomatic prolactinomas?

Treat with DA agonists (ex: cabergoline, bromocriptine) which can lower the prolactin levels and reduce tumor size. Try tahat frist before jumping to do transsphenoidal resection. Note: pts who fail to respond or have VERY large tumors (>3 cm aka > 30 mm) should be referred for transsphenoidal resection.

How do you treat symptomatic sarcoidosis?

Treat with systemic glucocorticoids (if pt has symptoms of sarcoidosis like cough, dyspnea, fatigue, hypercalcemia)

Sxs of Serotonin syndrome?

Tremor, clonus, hyperreflexia, tachycardia, agitation, sweating, autonomic instability, HTN, diarrhea, hyperactive bowel sounds, dilated eyes (mydriasis), mental status changes (anxiety, restless, agitated delirium), autonomic dysregulation (sweating, tachycardia, HTN, hyperthermia), NM hyperactivity (hyper-reflexia, tremor, rigidity, myoclonus, ocular clonus - slow continuous horizontal eye movements, BL Babinski signs), Hyperactive bowel sounds and diarrhea (bc there are also serotonin receptors in the gut) too much serotonin activity. Hx of serotonin drugs (SSRI, SNRI), MAOI, or ***tramadol (pain med that also has serotonergic activity) Manage: d/c all serototonergic agents, do supportive care (ex: hydration), sedate with benzo. Severe cases may need cyproheptadine *** (serotonin antagonist)

What are the sxs of Serotonin syndrome?

Triad: AMS, autonomic instability**, and neuromuscular excitability (tremor, hyper-reflexia, myoclonus)*** r/t too much serotonergic drug use.

fragility of hair with breaking of strands. fractured strands with splitting of fibers. Can be congenital or acquired (excessive heat, hair dyes, salt water).

Trichorrhexis nodosa

Behavior d/o with compulsive pulling of hair. Irregular patches of hair loss and broken fibers are seen. Typically affects front and sides of scalp, eyebrows, and eyelashes.

Trichotillomania

What does a serous cystadenoma secrete?

Trick question! They are common benign ovarian neoplasms. Hormonally inactive.

What does a mature teratoma secrete?

Trick question! it's a benign ovarian tumor (aka dermoid cyst) that is hormonally inactive

What are the methods of abortive migraine therapy?

Triptans (sumatriptan NSAIDs (naproxen) Acetaminophen Antiemetics (metoclopramide, prochlorperazine) Ergots (dihydroergotamine)

If pt has long term use of analgesics for chronic pain of some sort. They have WBC casts, painless hematuria, sterile pyuria (elevated WBCs but neg luek esterase, nitrates and bacteria), and trace proteins on UA. what are you worried about in terms of kidney damage, what kind of kidney damage? What would you see on UA?

Tubulointersitial nephritis ***THE INTERSTITIAL PART, and also affects the tubes... so tubulointerstitial nephritis --> WBC cast*** (Note: this is not the same as acute tubular necrosis with 'muddy brown casts', don't mix those up) Analgesic use can --> Tubulointerstitial nephritis (Pt has white blood cell casts) UA will show: painless hematuria, sterile pyuria, WBC casts, and trace proteinuria

WBC casts

Tubulointerstitial nephritis (Think AIN: acute interstitial nephritis)

What are the drugs that you are concerned for reactivation of latent TB and so should check a TB skin test before starting this drug on patients? What is the drug used to treat?

Tumor necrosis factor - alpha inhibitors (TNF-alpha inhibitors) are the drugs that tx rheumatologic disease and can cause reactivation of latent TB. so need to do TB skin test before starting these TNF-alpha inhibitors. Ex: infliximab, etanercept, adamimumab (DMARDS)

What an acoustic neuroma? What kind of hearing loss do you expect with this?

Tumor that arises from the Schwann cells covering the vestibular brach of the 8th CN. AS the tumor grows, you get symptoms of vertigo, unilateral tinnitus, and sensorineural (SN) hearing loss. Acoustic neuroma, tumor from Schwann cells cover CN8, SN hearing loss.

Fullterm newborn baby girl. She has a 2/6 systolic murmur best heart at the midback*** (didn't pay attention to this, what is this, it's important***), redundant skin at the nape of the neck and edema of the dorsum of the hands and feet. What is the likely diagnosis?

Turner syndrome (Gonadal dysgenesis 45 XO) Murmur best heard at the midback is coarctation of the aorta bc it's a systolic murmur best heard in the left infraclavicular area and under the left scapula aka at the mid-back., redundant tissue is the cystic hygroma (abnormal lymphatics), and edema of hands and feet is also part of turners (again because of abnormal lymphatics; so don't forget that clue, think through it)

What is neoadjuvant therapy?

Tx given ***before***the standard therapy for a particular disease. Ex: if radiation therapy was given before radical prostatectomy (the standard therapy)

What is maintenance therapy?

Tx given after induction and consolidation therapies (or initial standard therapy) to ***kill any residual tumor cells and keep patient in remission***. Ex: daily anti-androgen therapy for prostate cancer.

What is consolidation therapy?

Tx given after induction therapy with multidrug regimens to ***further reduce tumor burden*** Ex: multidrug therapy after induction therapy for acute leukemia

What is adjuvant therapy?

Tx given in addition to standard therapy. ex: if radiation was given in addition to radical prostatectomy (the standard therapy).

4yo girl comes to ED with fever for 9 days, reaching 102.2 each day. She has rash on trunk that spreads to extremities. Cranky, irritable but able to be calmed by mom. BL conjunctivae are injected. A 1.7cm tender, mobile anterior cervical lymph node is felt. CV reveals mild tachycardia. See blanching maculopapular rash on trunk & extremities. Hands & feet are red and edematous. Pharynx mildly injected without exudates or tonsillar hypertrophy. Next appropriate step?

Tx with ASA and IVIG Kid has Kawasaki disease (>5 days of fever and >4 mucocutaneous findings of: conjunctivitis, oral mucous changes (red, fissured lips, strawberry tongue), rash, hands an feed red/swollen/desquamation, cervical LA >1.5cm ode. "CRASH & Burn" -Conjunctivitis, -Rash -Adenopathy (cervical, unilateral) -Strawberry tongue -Hands & feet swelling & redness -Burning (fever >5 days)

What's the mutation in osteogenesis imperfecta?

Type 1 collagen mutation

What kind of adverse drug reaction is NMS?

Type B. It's a dose-independent med effect (another example would be SJS with lamotrigine) Note: in contract, Type A drug reactions are dose-dependent (example: respiratory depression with opioid use) Note: FGA (like haloperidol) are most frequently associated with NMS, but SGA are also implicated.

What kind of kidney disease has "linear deposits on immunofluorescence microscopy"?

Typical for anti-glomerular BM disease (ex: Goodpasture's syndrome).

What is physiologic jaundice? (what kind of bili, waht timeframe?)

UNconjugated hyperbili (so would be increased indirect hyperbili) that appears after 1st 24 hours of life and resolves within the 1st week.

When do you see Struvite stones?

UTIs with proteus.

MS symptoms worsen when exposed to hot temperatures, what is that called, the heat sensitivity in MS?

Uhthoff phenomenon (Memory tool: looks like someone saying "Uh it's Hott! off!")

Pregnant lady with fever, N/V, RLQ pain and tenderness to palpation without guarding. What is the next step?

Ultrasound the abdomen. She may have acute appendicitis; may result in ruptured appendix. Note that location may be higher than expected in a pregnant woman, up by the gravid uterus. U/S is the 1st dx test to confirm dx and r/o other causes. Use u/s with graded compression technique. Noncompression and dilation of the appendix is dx of appendicitis. U/s does not radiate the baby. If U/s is non-dx, then MRI can be done bc it also doesn't' radiate the baby.

What kind of herniation is it if the temporal lobe (uncus) is pushed laterally and down against the tentorium cerebelli?

Uncal herniation (of temporal lobe uncus) Manifests: dilated nonreactive ipsilateral pupil bc of CN 3 compression. If further displacement causes midbrain compression, then will have contralateral extensor posturing, coma, and respiratory compromise

Pt has hx of DVT and now her labs show elevated aPTT and new onset thrombocytopenia (76K when it was 246K at presentation 6 days ago) and arterial thrombosis. What kind of anticoagulation therapy do you think she's been using?

Unfractionated Heparin; since the pt is now presenting with heparin-induced throbocytopenia (HIT) - >50% drop in platelets count from baseline 5-10 days after starting heparin - thrombosis (arterial or venous) - thrombocytopenia

Pt has wasting of extremity muscles, weakness, difficulty swallowing/chewing/speaking, feels some movements in face and tongue, fasciculations, hyper reflex is in all extremities.Bulbar reflexes are decreased., What does pt have?

Upper and lower motor neuron lesions, indicates ALS (amyotrophic lateral sclerosis). UMN lesions: spasticity, bulbar sxs, hyperrelfexia LMN lesions: fasciculations Weakness and wasting of muscles may be due to both UMN and LMN lesions

What is the test used to dx adrenal insufficiency?

Use synthetic ACTH (so corticotropin simulation test)

Sickle cell TRAIT patients only have what potential issue?

Usually asymptomatic, but may have painless microscopic or gross HEMATURIA d/t sickling in the renal medulla. Isosthenuria (impairment in concentrating ability) is also common and can present as nocturia and polyuria. (May also have increased risk of UTIs during pregnancy. Splenic infarctions are uncommon but may occur at high altitudes)

How do pts with central (secondary/pituitary; tertiary/hypothalamic) adrenal insufficiency compare to pts with primary adrenal insufficiency?

Usually d/t chronic glucocorticoid therapy. See decreased ACTH and cortisol but aldo is normal. Sx: less severe, no hyperpigmentation (since ACTH is low), No hyperkalemia (since aldo is normal), may have possible hyponatremia

What's the presentation for Subacute (de Quervain) thyroiditis?

Usually follows an acute viral syndrome and presents with fever, neck pain, tender, diffuse goiter. Pts are commonly ***thyrotoxic d/t release of preformed thyroid hormone*** Inflammatory markers (ex: ESR) may be elevated. After virus, in thyrotoxic state, diffuse goiter fever, hurts.

What kind of kidney disease has "granular deposits"?

Usually immune complex glomerulonephritis (Ex: Lupus nephritis, IgA nephropathy, post-infectious glomerulonephritis)

postpartum pt has uterine atony, what do you do?

Uterine massage & pit (oxytocin), IV fluids, oxygen If that doesn't work, then you use uterotonics -Methylergonovine: causes smooth muscle constriction, which also means vasoconstriction so contraindicated in pts with HTN (Memory tool: think about how blood vessels are like vines... and so this Methyergono-"vine" also causes vasoconstriction of the blood vessels. so don't use in hx of HTN) -Carboprost (Hemabate): synthetic PG that causes bronchoconstriction, so contraindicated in asthmatics. (Memory tool: remember that Carboprost is HEEEEEEMAbate... sounds like someone wheezing if they are asthmatic and you give them this as uterotonic and now you caused bronchoconstriction)

What distribution does trigeminal neuralgia pain follow? What should you suspect if TN presents bilaterally?

V2 (maxillary) and V3 (mandibular) branches of the trigeminal nerve. suspect multiple sclerosis if TN presents bilaterally.

watery diarrhea, muscle cramps/weakness (hypokalemia), and decreased gastric acid secretions. Can see facial flushing. What are you thinking if I say there is a tumor in the tail of the pancreas?

VIPoma - with pancreatic tumor, watery diarrhea, hypokalemia, hypercalcemia, hyperglycemia, can have facial flushing (so don't get fooled to thinking only carcinoid with facial flushing, esp if they say the growth is in the pancreas)

What's the VSD murmur?

VSD: harsh holosystolic murmur with maximal intensity over left 3rd or 4th ICS, with a palpable thrill. VSD is the most common congenital heart defect and has spontaneous closer in about half of pts. A small (restrictive) VSD has a loud murmur bc there is high resistance of flow vs a large (unrestrictive) VSD is relatively soft bc there is little resistance to flow, which is prominent in early systole (d/t early equalization of RV and LV pressures during systole) Adults with persistent, small restrictive VSDs with L-->R sunting have favorable hemodynamics and normal right-sided heart pressures. They remain asx and the VSD is usually detected during routine clinical eval when cardiac auscultation reveals harsh holosystolic murmur with max intensity over 3rd or 4th ICS along left sternal border.

<1 day (acute) fever, severe HA and AMS. Nuchal rigidity present. What's the empiric treatment for bacterial meningitis?

Vanc & ceftriaxone.

IVDU now has IE , treatment?

Vanc (braod spectrum)

IV Drug user with track marks and hx of arm cellulitis now comes in with fever, fatigue, generalized weakness and holosystolic murmur at LLSB which increased with inspiration (tricuspid regurg.). She most likely has infective endocarditis from IVDU. What is the Abx tx you giver her?

Vancomycin - most likely d/t staph aureus. - empiric therapy in native valve should cover MSSA, MRSA, strep, and enterococci. So Vancomycin is the choice bc of its broad spectrum of activity.

IVDU now has fever, chills, generalized weakness, was in the hospital in the past for cellulitis 6 months ago, you se track marks on their arms. Now has holosystolic murmur at left sternum with increased intensity with inspiration. What initial tx should you do while you wait for blood cultures?

Vancomycin: want to cover MRSA, strep, and enterococci when dealing with this native valve endocarditis.

Pt with hx of CAD, MI, cardiomyopathy, or decreased EF passes out, What do you suspect as etiology of syncope?

Ventricular arrhythmias

What is Wolff-Parkinson-White syndrome due to?

Ventricular pre-excitation d/t an accessory conduction pathway that directly connects the atria and ventricle, bypassing the AV node. EKG will show short PR interval (<0.12 second), widened QRS complex, and "slurred" upstroke of QRS complex ("delta wave")

Pt with ankylosing spondylitis falls on their back and now they have back pain, what likely happened?

Vertebral fracture. They are at increased risk of vertebral fractures bc of osteoporosis associated with the disease bc of increased osteoclast activity in setting of chronic inflammation (mediated by TNF-alpha and interleukin-6). Spinal rigidity can increase risk of vertebral fracture, which often results from minimal trauma. May also find thoracic wedging and hyperkyphosis. Other complications include aortic regurg, and cauda equina.

42 yo pt with Ankylosing spondylitis (AS) has reduced ROM with thie spine. He also has a early diastolic murmur that suggests aortic regurg., which is a common finding with AS. He now has acute pain after a fall. Although a ground-level fall would be unlikely in a otherwise healthy man of this age, you suspect what int his pt with AS? Why?

Vertebral fracture. -bc pts with longstanding AS get osteopenia/osteoporosis d/t increased osteoclast activity in the setting of chronic inflammation (mediated by TNF-alpha and interleukin-6). The spinal rigidity in these pts also increases the risk of vertebral fractures after minor trauma.

How do pts with Androgenic steroid use (Athlete who is doping ) present?

Virilization (male pattern baldness, voice deepens, clitoromegaly) and yes, they do have HTN. But they also have aggressive behaviors and mood disorders. If you don't' see all of that, don't suspect androgenic steroid use in an athlete

When would you see: Low LH, high T, and normal DHEAS (with the S)

Virilizing ovarian tumors. They can release large amounts of T, leading to suppression of LH. But DHEAS would be normal as adrenal androgen secretion is regulated primarily by ACTH rather than LH.

Severe consequences of methanol intoxication

Vision loss and coma. (Fundoscopic exam shows: optic disc hyperemia) Damage to the eyes is what you would use to distinguish methanol ingestion/poisoning from ethylene glycol ingestion/poisoning (which is instead associated with kidney damage). Both may be ingested by homeless individuals instead of ETOH and both cause an AG metabolic.

What meds are usually in the hx of malignant hyperthermia?

Volatile anesthetics or Succinylcholine!!!

Kids presents with vomiting after a picnic where they ate potato salad and BBQ chicken. They also have a pet turtle. No diarrhea. What is the cause of their illness?

Vomiting predominant = staph aureus. Presents in 1-6 hrs bc s. aureus produces enterotoxins rapidly. Vomiting is predominant sx, usually self limiting in 1-2 days. (chicken and turtles can carry salmonella, but that would be diarrhea predominant, these kids are just vomiting, so it's the potato salad with staph aureus from people who prepped the food and have staph aureus in their nose, LIKE BRETT!!!!! He loves to cook and make fancy food but his culture of his nose was positive for s. aureus)

How does vitamin toxicity present?

Vomiting, confusion, polyuria, polydipsia.

How does Wernicke encephalopathy usually present? Tx? Is there a specific order to give things?

WE is Thiamine (B1) deficiency usually d/t ETOH use and causes thalamic neuronal loss --> ataxic gait, oculomotor dysfunction (ex: horizontal nystagmus, reacting slowly to light) and encephalopathy (AMS) Tx: give thiamine (B1) to prevent further complications. Thiamine is a cofactor in many enzymes required for energy metabolism and giving IV fluids with glucose prior to thiamine can precipitate or worsen WE. So thiamine should be given ALONG WITH or BEFORE giving glucose. Give THIAMINE BEFORE glucose.

When would you want to use Buproprion (NE and DA reuptake inhibitor), when would you NOT want to use it?

Want to use with for MDD when pt desires the favorable side effect profile of the drug: increased wakefullnes, energy, and concentration. Also helps with smoking cessation and weight loss. Does not cause sexual SEs. Do NOT want to use buproprion in pts with hx of seizures or eating disorders (bc lowers the seizure threshold) .

Pt with afib is already on warfarin, stable dose. Now he has started to exercise and has joint pain and take acetaminophen. He's eating more veges (spinach, brussel sprouts), and now he has extensive bruising and bleeding gums. What's causing this?

Warfarin + Acetaminophen interaction. Acetaminophen, NSAIDs, Abx (ex: metronidzole), Amiodaraone, Cimetidine, Cranberry juice, Ginkgo biloba, Vitamin E, Omeprazole, Thyroid hormones, SSRIs (fluoxetine) are all CYP450 inhibitors, and Warfarin is a CYP450 drug, so adding an inhibitor means that warfarin sticks around longer and the effect of warfarin is increased, leading to increased bleeding risk. Note: eating spinach and brussel sprouts would increased Vitamin K and would make pt more likely to clot (the oppose effect of Warfarin) so those pt would not be more likely to bleed, but more likely to clot bc warfarin is NOT working as it should.

When would you wash cells? When would you leukoreduce cells?

Wash cells for IgA deficient pts. Leukoreduction for normal pts to prevent febrile non-hemolytic transfusion reaction that can occur 1-6 hrs after transfusion is given. Pts get fever, chills, malaise without hemolysis.

When do you wash RBCs before transfusion?

Washed RBC for pts with IgA deficiency, complement-dependent autoimmune hemolytic anemia, or continued allergic reaction (ex: hives) with RBC transfusion despite anti-histamine tx.

If you suspect esophageal rupture (pt has acute chest pain, tachypnea, pleural effusion - usually left sided, subcutaneous emphysema) after endoscopy, it's an emergency and need eval through what method?

Water-soluble contrast esophagogram (less inflammatory to tissues), but a barium study has higher sensitivity and is advised if initial water soluble contrast study is not diagnostic.

What meds are used to tx Alzheimer's disease?

We think Alzheimer's disease may be due to selective loss of cholinergic neurons. So, the 1st line tx for cognitive symptoms of AD are cholinesterase inhibitors, which may improve QOL and cognitive functions. -Mild-mod Alzheimers: Donepezil, galantamine, rivastigmine (Sketchy: older people holding a "Alzheimer's Gala" (galatamine) with banner saying "Reverse the stigma" (rivastigmine) where they are doing puzzles "Done with puzzle!" (donepezil)) -Mod-Severe dementia: Memantine (N-methyl-D-aspartate receptor antagonist)

67yo mane with exertional syncope where he loses consciousness while shoveling snow or carrying heavy groceries. He's got progressive exertional dyspnea and fatigue and so has reduced his physical activity over the last year. What do you expect to find on physical exam?

Weak and slow rising carotid pulse. He's got a outflow tract obstruction (AS or HOCM). This pt likely has AS. He has a fixed outflow obstruction and so cannot increase cardiac output in response to exercise induced vasodilation --> hypotension, transient cerebral hypoperfusion, and decreased exercise tolerance, presyncope, or syncope. Physical exam findings of AS: -Delay (slow-rising) and diminished (weak) carotid pulse ("pulsus parvus and tardus"; remember Dr. Simpson asking me to feel that pt's AS who has "2 months to live" if she didn't get intervention.. he was asking me to feel for the slow-rising and weak carotid pulse on her neck and he said it's hard to feel bc it's so weak you to have just the right amount of pressure over the carotid) -Single and soft second heart sound (S2) -Mid- to late-peaking systolic murmur with maxial intensity at the 2nd right ICS radiating to the carotids.

Older pt with NPH, what is the problem? How does it present?

Wet, Wobbly, Wild: urinary incontinence, unstable/abnormal gait (slow, broad based shuffling gait), dementia (memory loss but no focal neuro change). (Note: fecal incontinence may also develop at advanced stages) You see increased ventricular size on imagining without elevation in ICP. This is d/t decreased CSF absorption at the arachnoid villi or obstructive hydrocephalus. Sx result from distortion of periventricular brain matter.

When you have a pt with a prosthetic joint infection, they have dull knee pain, mild swelling and tenderness of knee and skin over the joint is intact, but you get synovial fluid and they don't have high leuks, and he doesn't have a fever. what are you thinking about?

When it seems like it's not necessary infected, think about: the fact that it's a prosthetic joint... and they can get infected right away and have all the classic sxs of an infection, or it can have delayed onset in infection with less virulent organisms and seem not that bad. Prosthetic joint infection synovial joint lueks are usually elevated >1000 but lower than septic native joints (>50,000). Early Onset: Infections right away in 1st 3 months, think virulent organism (Staph aureus, Pseudomonas) with acute pain, feve,r leuks, overt local signs of infection (erythema, purulent drainage) Delayed Onset: Infection that start after 3 month but before 1 year, think of less virulent organisms (coag-negative staph, propionibacterium species, STAPH EPIDERMIDIS is the coag-negative staph common in delayed-onset PJI) Present with chronic pain, implant loosening, gait impariment or sinus tract formation. But Fever and leukocytosis usually absent. Late Onset: >1 year. usually not d/t the operation but infection that spread through the blood to the joint, like with a UTI. So tends to be staph aureus, gram negative rods, beta-hemolytic strep. You have actue sx in previoulsy asymptomatic joint. Recent infection at distant site.

When is it CREST syndrome (limited scleroderma) and when is it full blown Scleroderma?

When the internal organs are involved (hear,t lungs, kidneys), its scleroderma. Scleroderma is just CREST + internal organ involvement. Note: CREST can cause primary pulmonary HTN but you will see the lungs themselves are normal

When do you do a inferior vena cava filter for DVT?

When there is high risk of bleeding from anticoagulation (ex: recent surgery, hemorrhage) and so you don't want to medically anticoagulate the patient.

Follicular thyroid cancer, what do you want to do for these?

When you do FNA, it looks like "thyroid" and they spread hematogenously so it sounds bad, but they are actually easy to treat, you just use radioidodine ablation and it will get all the follicular thyroid cancer cells in your body, so it acts like a chemotherapy agent. So follicular thyroid cancer is not a bad one to have since it's easily treatable.

What is internal podalic version?

When you go int there and stick your hand in and grab the 2nd twin by the foot and pull them out to delivery them. It's breech extraction of a mal-presenting 2nd twin. (not done with singletons)

What is the presentation of Primary ovarian insufficiency?

When you have amenorrhea & vasomotor symptoms. -You have high serum FSH levels (which, remember high serum FSH is a sign of menopause)

50 yo white man has diarrhea, abdominal pain, weight loss, bulky-foul-smelling stools, abdominal distension, flatulence. He has arthralgias and chronic cough. Temp 100F. RR 18. Generalized LA, skin hyper-pigmentation and diastolic murmur in aortic area. Small bowel with villous atrophy and numerous PAS-positive material in lamina propria. Most likley dx?

Whipple's disease: Caused by Tropheryma whippelii. Mst commonly seen in white men in 4th-6th decades of life and presents with weight loss. GI sx. Extra-GI sx: migratory polyarthropathy, chronic cough, myocardial or valvular involvement --> CHF or valvular regurg. Later stages of dz may have dementia and other CNS findings (supranuclear ophthalmoplegia, myoclonus). Intermittent low-grade fever, pigmentation and LA may also be occasionally seen. PAS-positive material in the lamina propria of the small intestine is a classic biopsy finding. TL:DR: multi-systemic illness with arthralgias, weight loss, fever, chronic cough, CHF, and GI symptoms - abdominal pain, diarrhea, malabsorption w/ distention, flatulence, steatorrhea. ***PAS-positive material in lamina propria of small intestines*** is classic biopsy finding in Whipple's disease. (way too much going on to just be celiac although celiac has villous blunting)

What is leukocoria, what is it a sign of?

White reflex instead of the normal red reflex; sign of retinoblastoma. (Don't give radiation because that would cause the 2nd hit to the other eye if the other eye is normal; just surgically remove the affected eye. Then screen them for osteosarcoma (knee bone cancer) later in life.

2-5yo kid and mom finds an asx nontender mass in the left abdomen, there is blood in the urine. What is the likely dx?

Wilm's tumor (nephroblastoma) Note: less likely neuroblastoma bc that's usually in the 1st year of life and crosses midline WITH systemic symptoms. (Whereas Wilm's tumor is usually asymptomatic mass in kid that's 2-5 yo; so distinguish the 2 dxs by age and symptoms)

skin (eczema), blood (low plts), and immune problems (hypogammaglobulinemia): what is that?

Wiskott-Aldrich syndrome

Rh- woman and there is some kind of event where there could be mixing of blood between mom and fetus. (Ex: 1st trimester spontaneous abortion). You want to give RhoGam (Anti-D immune globulin) to the unsensitized woman within what time period?

Within 72 hours of any procedure or incident where there is any possibility of feto-maternal blood mixing.

When are you worried about ETOH withdrawal seizures?

Within the first 1-2 days (12 to 48 hours since last drink) Single or multiple generalized tonic-clonic seizures

When do you want to deliver the baby if mom has pre-eclampsia?

Without severe features: 37 weeks With severe features: 34 weeks Define pre-eclampsia -New onset HTN >20 weeks GA: >140/90 -& proteinuria &/or end-organ damage With severe features: -BP >160/110 2x in the last 4 hours -Low plts -Increased Cr -Increased LFTs -Pulmonary edema -Visual/cerebral sxs Note: at risk for eclamptic seizures, placental abruption, hepatic rupture, DIC Best way to get quick BP control: IV Hydralazine (vasodilator that works fast), IV Labetalol also works fast (note: don't use in bradycardic patients), Oral Nifedipine (CCB if able to tolerate oral meds)

Looking at relative risk (RR) as an estimate of association: does not account for random error. So it's always possible that the calculated RR occurred only by change. You look at the p-value to strengthen the results of the study and represent the probability of observing a given (or more extreme) result by chance alone, assuming the null hypothesis is true. So with RR 0.71 (p = 0.001), assuming the null hypothesis that hter is no difference in the end result between the tx and placebo groups, the probability of getting a RR = 0.71 or more extreme value d/t chance alone is 0.1% (p = 0.001 and you move the decimal point over 2 to get percentage of 0.1%). The commonly accepted upper limit (cut off point) of the p-value for results to be considered statistically significant is 0.05 ( p < 5% is statistically significant) So we can conclude there is a 0.1% possibility of observing the given RR (or more extreme) by chance alone assuming no difference in outcome (mortality) (aka assuming the null hypothesis)

Word.

Would you ever do a LP on a patient with suspected MS (multiple sclerosis)? What would you expect to find on LP?

Yes, do LP when the diagnosis of MS is suspected but not completely clear. LP would reveal ***oligoclonal IgG bands*** in the CSF.

Can thyroid stuff affect prolactin levels?

Yes. Primary hypothyroidism with High TSH can cause mild-mod hyperprolactinemia (prolactin ~ 90) d/t thyrotropin releasing hormone-induced stimulation of lactotrophs. LH in those pts may be normal or mildly low.

Pt has gout, but he also has CV problems and is on Plavix and Abixaban. What do you want to treat his gout with?

You don't want to give another NSAID on top of all his blood thinners, so not wanting to do the Indomethacin. (NSAIDS like naproxen or indomethacin are preferred, but if there are contraindications, you don't want to do the NSAIDs, and then you move on to 2nd line therapy) So next up is Colchicine. -Use Colchicine to resolve symptoms of gout in pts already on blood thinners (ASA, Plavix, Apixiban) since you don't want to do the 1st line NSAIDS (Indomethacin, Naproxen) since you would increase his bleeding risk . Note: Colchicine inhibits polymerization of beta-tubulin in microtubules, preventing migration and activation of PMNs. It can cause nausea, abdominal pain, diarrhea. ***Don't use in elderly pts or with severe renal dysfunction. Note: could also consider intra-articular glucocorticoid injections (thought want to be careful in diabetics)

What do you expect to find in terms of testosterone and LH, FSH lab values with myotonic dystrophy? Presentation?

You see testicular atrophy along with widespread muscular atrophy. So you have have lower than normal testosterone and therefore high FSH And LH levels. Patients present with muscle atrophy and weakness.

Know that Papillary thyroid cancer shows "orphan annie eyes" : large cells with ground glass cytoplasm and pale nuclei containing inclusio bodies and central grooving. (Memory tool: I think about Pappa having a baby... so thinking they are slow growing like kids, and then add to that story that kid is orphaned... so Orphan Annie nuclei with Papillary thyroid cancer)

You want to resect these. (Memory tool: ... if Pappa's kid was orphaned... you'd want to "take them out of the orphanage" aka resect Papillary thyroid cancer) Know that papillary thyroid cancers are the most common. Note: following surgery, adjuvant therapy with radioiodine ablation is warranted for pts with increased risk of tumor recurrence (ex: large tumors, extrathyroidal invasion, lymph node mets, incomplete resection). TSH can stimulate growth of occult residual or metastatic disease so pts at incrased risk of recurrence should also get adequate doses of thyroid replacement to suppress TSH secretion.

What would you see on imagining if there was a retained gallstone after cholecystectomy?

You'd see significant biliary dilation on imaging.

Where do you get zinc from? Who is at risk for zinc deficiency?

Zinc is in meat, nuts, and fortified cereal. Important for gene transcription and cell division. Pts on TPN are at risk for trace mineral deficiency (zinc, selenium, copper, chromium) bc of inadequate supplementation in their parenteral intake. Zinc is mostly absorbed in the duodenum and jejunum and so deficiency can be due to malabsorption (Crohns, celiac), bowel resection, gastric bypass, or poor nutritional intake. Diarrhea and malabsorption further increases the risk of trace mineral deficiency in pts on TPN due to excessive GI losses.

Pt with Crohns disease who has been on TPN for the past several weeks and just started oral feeds again. He says he has some non-bloody diarrhea. Food doesn't taste the same as before, he has patchy alopecia, and a pustular, crusting skin rash with scaling and erythema around the mouth and on his extremities. What would improve his current symptoms?

Zinc supplement. He has zinc deficiency: alopecia, pustular skin rash (perioral and extremities), and impaired taste. -other symptoms: hypogonadism, impaired wound healing, immune dysfunction

What's another name for hidradenitis suppurtiva (that' awful disfiguring condition in the intertriginous areas - axilla, inguinal and perineal areas that is d/t chronic inflammatory occlusion of folliculopilosebaceous units)?

acne inversa

What is transient erythroblastopenia of childhood (TEC)?

acquired red cell aplasia that happens to kids from 6mo to 5yo. Normocytic normochromatic anemia. Hgb can range from 3-8 with really low reticulocyte count. Presents at gradual onset of sx with pallor and decreased activity.

When the aldo/renin ratio is above this number is when you are thinking about doing adrenal vein sampling bc you're thinking of a primary hyperaldosteronism?

aldo/renin ratio >20

Rupture of popliteal cyst (Baker cyst) may cause posterior knee pain, more common in older adults and often associated with ____ of the knee.

associated with osteoarthritis of the knee. (may resemble DVT and get this confused with DVT)

What is the pathology in MS?

autoimmune demyelination of white matter tracts in CNS.

What is the mechanism of MS (multiple sclerosis)

autoimmune inflammatory demyelinating disorder of CNS

What are iron levels high in sideroblastic anemia?

bc the problem with sideroblastic is the iron can't be incorporated with the heme, so then the iron levels will be high.

What is a galactocele?

benign milk retentio cyst that occurs a few weeks-months after you stop breastfeeding, when the milk stagnates. Dx: initial: U/S Tx: No intervention for asx glactoceles. Needle aspiration for symptomatic galactoceles Ice packs and supportive well-fitting bra for symptomatic relief.

What is elevated in seminomas?

beta-hCG. (NO elevation of AFP) (think about seminomas being in the testes.. and that's where half of the pregnancy comes from to make a detection of beta-hCG possible... so elevation in beta-hCG in seminomas)

Copper deficiency presentation

brittle hair skin depigmentation Neuro dysfunction (ex: ataxia, peripheral neuropathy) Sideroblastic anemia Oseoporosis

How does torsion of vestigial testicular appendix present?

can have acute pain similar to testicular torsion but the associated tenderness is focal rather than diffuse, the cremaster reflex is preserved and the ischemic appendix may be visible as a dark area under the scrotal skin (blue dot sign)

How does Acetazolamide work to treat acute glaucoma?

carbonic anhydrase inhibitor, decreases further production of aqueous humor, decreasing intraocular pressure

What is Tarsal Tunnel Syndrome?

compression of the tibial nerve as it passes through the ankle. Usually caused by fracture of the ankle bone. Pts develop burning, numbness, and aching of the distal plantar (not dorsal) surface of the foot/toes that sometimes radiate up to the calf.

late complication of radiation therapy

constrictive pericarditis (10-20 years after mediastinal radiation) aka an inelastic pericardium ssx: fatigue, dyspnea, peripheral edema, ascites, increased JVP, pericardial knock (mid-diastolic sound), pulsus paradoxus, Kussmaul's sign, hepatojugular reflux (d/t RH failure)

What do you expect in right motor cortex infarct?

contralateral UMN signs (like Babinski sign, hyperreflexia) Note: consciousness generally preserved, pupillary response would be normal (start thinking about uncal herniation pressing on CN4 if you see a fixed, dilated ipsilateral pupil)

What are symptoms found if pt has right motor cortex infarct?

contralateral UMN sxs (Babinski sx, hyperreflexia). Consciousness is genearlly prefersed and pupillary responses are normal. ... so if pt is not responding to painful stimuli and is not conscious and their pupils are dilated and not reactive to light... and they're posturing (extensor), think about basal ganglia hemorrhage and not just motor cortex infarct

If OCP is causing HTN, what do you do

d/c the OCP and switch to another method of BC Note: women who develop HTN During previous pregnancy or have family hx of HTN are more likely to develop HTN From OCP use.

Orthostatic hypotension happens when you get older because of:

decreased baroreceptor responsiveness. Happens bc of insufficient constriction of resistance and capacitance blood vessels in lower extremities on standing, which may be due to defect in autonomic reflexes, decreased IV volume or medications. Some baroreceptor sensitivity is lost as normal part of aging. Arterial stiffness, decreased NE content of sympathetic nerve endings and reduced sensitivity of myocardium to sympathetic stimulation all contribute to tendency toward orthostatic hypotension with age. Defined as: decreased in BP systolic: 20 mmHg diastolic: 10 mmHg

What do you expect on UA for glomerulonephritis?

dysmorphic RBCs, subnephrotic/nephrotic range proteinuria (so more proteinuria than with tubulointerstitial nephritis's mild proteinuria), RBC casts!!! Glomeronephritis = RBC cast Tubularinterstitial nephritis = WBC casts, sterile pyuria Acute Tubular Necrosis (ATN) = Muddy brown casts

Greatest sensitivity for dx-ing HF?

elevated BNP >400 (90% sensitivity) whereras <100 ha high neg predictive value for CHF

When can mild ETOH withdrawal start?

first 6-24 hours since last drink. (so within the first day; but DTs are 2nd to 4th day since last drink) Anxiety, insomnia, tremor, sweating, palpitations, GI upset, they have intact orientation.

When do you use glucocorticoids (ex: prednisone) and NSAIDS (ex: naproxen)? Do you use it for fibromyalgia?

for inflammatory conditions with elevated markers (ESR, CRP) No, you don't use them for fibromyalgia bc FM is not an inflammatory condition so does not respond to steroids or NSAIDs. -Tx fibromyalgia with exercise, good sleep hygiene, and if that doesn't work, think about TCAs.

What's the prodrome of vasovagal syncope?

get pale, nauseous, lightheaded, weak, blurred vision, sweat, abdominal pain, and feel warm before passing out. (think of all the things that happen when I'm in the OR and staring at too much blood; and you look pale bc the OR techs will notice and ask you if you're okay or if you need to sit down)

What is Amantadine, what does it treat?

has dopaminergic and N-methyl-D-asparatate receptor antagonist properites. Used to tx Parkinson's disease.

ACA stroke

hemiparesis of contralateral leg and face.

You see portal vein thrombosis in a pt in their 40's... what else are you looking for? dx?

hemolysis and cytopenias, thinking about Paroxysmal noctural hemoglobinuria (PNH) which is an autoimmune hemolytic (intra- and extra-vascular) disease where CD55 and CD59 aren't available to stop the MAC complex from attacking RBCs and hemolyzing them.

What's the classic presentation of hereditary spherocytosis?

hemolytic anemia, jaundice, splenomegaly in a person of Norther European descent. Acute cholecystitis from pigmented gallstones is a common complication

PCA stroke

homonymous hemianopsia (bc it's in the back and goes to occipital lobe, which is in charge of vision and that side of your occipital lobe can't see) May have cerebellar stuff too since it's back there (ex: ataxia)

A. Fib can be a physical exam finding of _____ and so should be treated initially with ______ to control the HR and hyperadrenergic symptoms

hyperthyroidism; beta blockers (propranolol, atenolol). Note: Digoxin and calcium channel blockers (verapamil, diltiazem) are often used for rate control in pts with a.fib. However, unlike beta-blockers, they don't treat the hyperadrenergic drive in pts with hyperthyroidism and are not effectie for HR andsymptom control in pts with hyperthryoidism*** So if a pt with hyperthyroid symptoms (anxiety, insomnia, palpitations, heat intolerance, weight loss w/o decrease appetite) and physical exam findings (goiter, HTN, tremors, hyperreflexia, proximal muscle weakness, lid lag, a fib), treat with beta-blockers (shouldn't matter which beta blocker)

Pt presents with symmetric descending flaccid paralysis, blurred vision, areflexia and may include diaphragmatic paralysis Mechanism of clostridium botulinum toxin (Botulism)?

impairing pre-synaptic Ach release

What is intertrigo due to?

infection with Candida species. Presents with well-defined, erythematous plaques with satellite vesicles or pustules in intertriginous and occluded skin areas.

What is superficial thrombophlebitis?

inflammation or clot of the superficial veins (not a DVT)

What's the pathology in Guillain Barre?

inflammatory demyelination and/or motor axonal neuropathy

Unilateral bloody nipple discharge, dx? Management?

intraductal papilloma. -this is a benign condition Dx workup: start with mammogram to r/o carcinoma even without presence of plapable breast mass.

Burns

intubate Have low threshold for intubating if there is physical evidence of thermal damage of upper airways. Progressive airways edema can prevent intubation later on and may require surgical airway. Clues of upper airway injury or lung inhalation: singing of eyebrows, burns on face, oropharyngeal inflammation/blisterning, orophayrngeal carbon deposits, carbonaceous sputum, stridor, CarboxyHgb > 10% or hx of confinement in burning building. If 1+ of those exists, intubate early on to prevent upper airway obstruction by edema.

What is functional hypothalamic amenorrhea?

low weight/BMI/calorie intake/significant weight loss/chronic illness/stress/depression/anorexia/excessive physical training --> amenorrhea HPO axis is disrupted. There is decreased gonadotropin releasing hormone --> decreased LH, FSH, and estrogen. Note: Progesterone challenge would produce no withdrawal bleeding since low endogenous estrogen --> thin endometrial lining that will not shed. Note: in addition to secondary amenorrhea, pts also have secondary hypo-estrogenemia symptoms such as infertility, vaginal dryness, stress fractures. Tx: behavioral (increased calorie intake) but shoudl also include estrogen repletion for those unable or unwilling to tx the underlying etiology.

What do you expect to see with MCV in anemia of chronic disease (AOCD)?

microcytic or normocytic anemia. (trying to hide your iron from possible organisms that may be trying to get at your iron) AOCD usually causes normochromic, normocytic anemia.

What does controlling glucose better help with decreasing?

microvascular complications (ex: retiniopathy, nephropathy) Note: no change in prevention of macrovascular complications like MI, stroke, PAD have been established.

What's the murmur with MVP?

mid-systolic click followed by mid-late systolic murmur of mitral regug (best heard at cardiac apex)

How does portal-vein thrombosis (PVT) (aka clot in portal vein) usually present?

most often associated with cirrhosis. Acute PVT can present as gradual or sudden-onset abdominal pain. Chronic PVT: most often presents with variceal bleeding (i guess cuz the pressure builds up)

Cushing muscle weakness: think about it when pt has painless muscle weakness, weight gain, bone loss, HTN, hirsutism all points to cushing syndrome. So that muscle weakness is d/t?

muscle atrophy

What is thromboangiitis obliterans (Beurger disease)?

nonatherosclerotic, segmental, inflammatory disease that most commonly affects the small to medium-sized arteries and veins of the extremities. Highly cellular and inflammatory occlusive thrombus with relative sparing of the blood vessel wall. Patients are young smokers who present with distal extremity ischemia, ischemic digit ulcers or digit gangrene. The disease is strongly associated with the use of tobacco products and smoking cessation is important to decrease the risk for amputation. Raynaud's is a finding. Think hands. Memory tool: think of someone who doesn't like burgers.. you hold bergers with your hands to eat them..so think of this as person who doesn't like bergers bc their hands get all weird

gradual painless peripheral vision loss. with optic disc enlargement (increased cup disc ratio). what does pt have?

open-angle glaucoma.

PT with generalized tonic-clonic seizures can have transient what?

postictal lactic acidosis. just recheck it in a bit. Pts with generalized tonic-clonic seizures can have significantly raised serum lactic acid levels d/t skeletal muscle hypoxia and impaired hepatic lactic acid uptake. This is typically transient and self-limited and typically resolved within 90 minutes. (They have AG metabolic acidosis from increased lactic acid) So just observe & repeat chemistry panel in about 2 hours.

What's the pathology in ALS?

progressive motor NEURON degeneration --> upper (spastic paralysis) and lower (muscle atrophy, fasciculation) motor neuron signs. Pts typically have asymmetric limb and bulbar muscle weakness and fasciculations

What does a chi-squared test compare?

proportions. Chi-squared test compares proportions of a categorized outcome. A 2x2 table may be used to compared the observed values with the expected values. Ex: can use chi-squared test to assess the association between hormone replacement therapy (HRT in post-menopausal women and the level of serum C-reactive protein (CRP). If you see a 2x2 table, think about chi-squared test.

s/sx of fascial dehiscence?

re-opening of fascial incision: so has "popping" sensation followed by copious serosanguineous drainage and incisional bulge.

Pt gets blood transfusion and then a few minutes later starts to have wheezing, respiratory distress, low BP and loses consciousness. what happened?

sec-minutes = anaphylactic reaction. -rapid onset of shock, angioedema/urticaria and respiratory distress. Caused by recipient anti-IgA antibodies. IgA-deficient pts are at risk d/t presence of anti-IgA IgG antibodies. Stop transfusion immediately and give IM EPI. Hemodynamic and respiratory support with vasopressors and mechanical ventilation may be required. HIstamine blockers and glucocorticoids should be also given. Future transfusion should be with IgA deficient plasma and ***washed*** red cell products.

What is anti-histone antibody used for?

sensitive marker for DRUG-induced lupus.

How do you define acute liver failure (ALF)?

severe acute liver injury w/o underlying liver disease (ex: Tylenol/Acetaminophen OD) -Elevated aminotransferases (>1,000 U/L), hepatic encephalopathy, and synthetic liver dysfunction (prolonged PT with INR >1.5). Indicators of worsening ALF: -rising serum bili and PT (worsening synthetic function) -acute renal insufficiency (likely d/t decreased renal perfusion) is common and portends lower chance of recovery w/o liver transplant. -degree of hepatic encephalopathy is prognostic as grade III hepatic encephalopathy (marked confusion and incoherence) is associated with only 40-50% chance of spontaneous recovery. -Cerebral edema: complication of ALF that may lead to coma and brain stem herniation and is most common cause of death in ALF. Note: only half of pts with acute liver failure will survive w/o liver transplant. Liver transplant is firmly indicated in pts with grade III or IV hepatic encephalopathy, PT >100 seconds, and serum cr > 3.4. One year survival s/p liver transplant for ALF is about 80%.

Parkinsonism gait can be described as:

shuffling gait, festinating gait, or hypokinetic gait stooped posture, walk in series of short, accelerating steps with feet shuffling and scraping the floor. Arms are immobile and do not swing.

What is vitiligo?

skin condition: well-demarcated, depigmented macules involving face and distal extremities. Caused by regional destruction of melanocytes, likely due to an autoimmune cause. Often associated with other autoimmune disorders (ex: pernicious anemia, primary adrenal insufficiency, alopecia areata, RA, Sjorgren syndrome; Autoimmune thyroid disease (chronic lymphocytic [Hashimto] thyroiditis, Graves disease) is esp. common and should advise pt with vitiligo to be assessed for thyroid function.

What is nonbacterial thrombotic endocarditis (NBTE)?

sterile vegetation on the cardiac valves in pts with cancer. This can lead to systemic embolization with arterial occlusion and acute limb ischemia. Think of this with a pt with cancer who then starts throwing arterial clots.

What's the best therapy for a symptomatic sarcoid patient?

systemic Glucocorticoids!! (important to rule out infectious granulomatous diseases with similar presentations such as TB and histoplasmosis before you start glucocorticoids) Sarcoid pt: young AA, constitutional sx, ***cough***, ***dyspnea***, CP, extrapulmonary findings: skin lesions, anterior/posterior uveitis, Lofgren syndrome (arthralgia, erythema nodosum, BL hilar LA), ***BL hilar adenopathy***, pulmonary reticular infiltrates. Labs: hypercalcemia, hypercalciuria, elevated serum ACE level. Biopsy with ***noncaseating granulomas*** that stain negative for fungi and acid fast bacilli.

Elderly pt has polymyositis rheumatic and is is started on prednisone and now has AMS, severe hyperglycemia and high serum osmolality (due to exogenous glucocorticoid medication). What is causing the AMS in HHS?

the high serum osmolality (>320 mOsm/kg) is causing the AMS. severe hyperglycemia --> glycosuria and osmotic diuresis --> hypovolemia & dehydration --> decreased GFR --> reduced renal glucose excretion and worsening hyperglycemia. Elderly pts are at increased risk of altered perception of thirst and restricted fluid intake. Neuro symptoms can range from cofusion to coma and is primarily d/t the high serum osmo (>320 mOsm/kg)

What organ does acetaminophen toxicity mainly affect?

the liver! (not the kidneys). Remember with tynenol overdose, you are looking at the AST and ALT, so acetaminophen toxcity affects the liver and you see hepatitis and jaundice.

Where do the ectopic foci for Afib usually come from?

the pulmonary veins are the most common location of the ectopic foci that cause A.fib.

What is alteplase? What is it used for?

thrombolytic therapy used to improve neurologic outcomes in pts with acute ischemic stroke if given within 4.5hrs of symptom onset. (note: need to get non contrast head CT before giving thrombolytics to r/o hemorrhagic stroke). the sooner thrombolytic agents are given, the better chance for neurologic recovery of FNDs that pts got during ischemic stroke.

What do you have to have on physical exam if you think someone has serotonin syndrome?

tremor, hyperreflexia, and myoclonus (these are sxs of neuromuscular irritability) & Hx of serotonergic medication (SSRI or MAOI)

Pt has DVT and also renal failure, what meds do you put them on?

unfractionated heparin bridged to warfarin (Memory tool: -Un-fractionated heparin is okay with Ur-ine problems... (renal failure can use UN-fractionatl heaprin) (DO NOT use LMWH or rivaroxaban with renal pts. Aspirin has no role for DVTs that are formed)

What is the Berkson bias?

using hospitalized pts instead of the generalized population Solved by random selection

What does having anti-histone antibodies clue you in on?

usually a sensitive marker for Drug-induced lupus. (note: but anti-histone antibodies are significantly less sensitive for minocycline-induced lupus)

What is effect modification?

when an external variable positively or negatively impacts the observed effect of a RF on disease status. Ex: ASA use is associated with Reye's syndrome in kids but not adults. So age modifies the effect of aspirin on Reyes syndrome development. Stratification (ex: analyzing data by age) can help detect effect modification.

Symptoms of Vitamin A deficiency

-Poor night vision, eye dryness (xerophthalmia) -Hypo-parathyroidism -follicular hyperkeratosis (of hair follicles) -Immunity impairment

What's a MMSE score that suggests dementia?

24 out of 30 points suggests dementia.

Are AST or ALT more specific for hepatocyte injury?

ALT is predominately found in the liver and so it is more specific for hepatocyte injury.

Cluster HA. Periorbital, short and severe and keeps happening with pd of remission with autonomic symptoms (lacrimation, ipsilateral miosis), what's the Tx?

Abort with 100% facemask oxygen Prevent with verapamil

How would you describe how a patient experiences mumps orchitis?

Acute testicular pain and inflammation during acute viral illness.

If stem talks about someone who works with antique wood, pesticides, or drinks well water. & then they say they have garlic breath, or they have hyperkeratosis (of skin), Mee's lines (on nails), stocking-glove (hands and feet) neuropathy, and then their labs suggest that hemoglobin, WBCs, and platelets are all low (pancytopenia), and there may be slightly elevated LFTs, what are you thinking about? Mechanism of this problem and what does it affect on the cellular level? Dx? Treatment?

Arsenic poisoning Acute poisoning: garlic breath, vomiting, watery diarrhea, QTc prolongation (acute, severe: can see pancytopenia and hepatitis) Chronic poisoning: hypo/hyper-pigmentation, hyperkeratosis, stocking-glove neuropathy Mechanism: binds sulfhydryl groups. Disrupts cellular respiration & gluconeogenesis Dx: Hx & Physical exam, measure urine arsenic levels Treat with chelation with ***Dimercaprol*** (British anti-Lewisite), DMSA (meso-2,3-dimercaptosuccinic acid, succimer) (Menmonic: Think... I gave that sucker (succimer) a dime (dimercaprol) for the rat poison (to treat arsenic posioning))

Otherwise healthy middle-aged pt has elevated LFTs. AST is elevated more than ALT. What's the first thing you do?

Ask them about their drug/ETOH history. (Higher AST think: "S"omebody's been drinking) After you ask them all the social history questions, have them discontinue ETOH and drug use, and then repeat LFTs. If transaminases stay elevated over 6 months, then you can consider this a chronic condition. When you can label this as a chronic condition is when you want to start testing for viral Hep B, Hep C, hemachromatosis, and fatty liver disease. If those test don't give you the answer, look for muscle disorders (polymyositis) and thyroid disease as causes.

AG metabolic acidosis with tinnitus, fever, and hyperventilation. Think about:

Aspirin overdose

Bodybuilder has small testes and issues with infertility. What do you expect on his labs?

Assume he's using anabolic steroids (testosterone analog) so his serum testosterone should be normal since the exogenous testosterone is detected by our tests as testosterone. However, the feedback inhibition should make LH & FSH low. Sperm and testosterone production by the testes should then be decreased; thus the infertility. Can also expect to see acne, gynecomastia (d/t conversion of androgens to estrone), decreased testicular size, aggressivenessm and psychotic symptoms. Can see erythrocytosis (d/t erythropoiesis) with elevated Hemoglobin. Cholestasis, hepatic failure, dyslipidemia, and slightly elevated Cr (due to increased muscle mass)

pearly nodule with small telangiectasias in a sun-exposured area.

BCC (most common type of skin cancer)

Chronic alcoholic, is folate or B12 deficiency more likely?

Both can happen. However, folate is more likely because you can lose your folate stores within 5-10 weeks. Alcohol abuse is the most common cause of nutritional folic acid deficiency in the US bc alcohol abuse impairs the enterohepatic cycle of folate and inhibits its absorption. You'd see megaloblastic anemia (low Hemoglobin & High MCV)

Burning wood (ex: indoor bbq), automobile emission, furnace, or charchoal grill emission without proper ventilation can result in what kind of poisoning. (Basically smoke inhalation in confined space)

Carbon monoxide poisoning. CO is colorless, odorless gas. When inhaled, it prevents the body's tissues from utilizing oxygen effectively. So you get HA, N/v, abdominal discomfort, confusion, and coma. Pts often have pinkish-red skin hue. Dx confirmed with carboxyhemoglobin levels. Tx with hyperbaric oxygen administration.

What kind of organisms does cipro cover?

Cipro = Gram negative coverage.

What is the antibiotic choice for aspiration pneumonia (hx of poor dentition, foul-smelling sputum, endotracheal or NG tube, GERD, dysphagia, impaired conscious - aka alcoholic)?

Clean out that mouth! Clindamycin! Clindamycin for anaerobic organism. Other regiments: metronidazole + amoxicillin, amoxicillin-clavulante, and clindamycin.

Get bit by livestock or an unknown wild animal, what do you do?

Contact the public health department to direct how you would handle a concern about rabies.

How to dx a Zenker's diverticilum. Hx of dysphagia, regurgitation, foul-smelling breath (halitosis), and aspiration pneumonia in elderly patient, esp. men.

Contrast esophagram. (anything that you do to try to visualize the esophagus has high risk of complications like perforating the esophagus, so endoscopy is the WRONG answer)

fibroblast proliferation with isolated or multiple lesions, most commonly in lower extremities. Lesion is non-tender, discrete, firm, hyperpigmented nodule <1cm in diameter. Can "dimple" or "buttonhole" when pinched.

Dermatofibroma

AG metabolic acidosis with damage to the kidneys, think about

Ethylene glycol ingestion

presentation of cryptorchidism. what is associated with cryptorchidism?

Failure to palpate 2 testes in the scrotum in infancy. Increased risk of testicular cancer

What is Felty syndrome? Does it have anything to do with RA (if so, what is the relationship)? How do Felty syndrome patients present?

Felty syndrome: clinical disorder seen in patients with severe, long-standing (>10yrs) RA. It is characterized by ***neutropenia and splenomegaly***. You can only make the dx of Felty Syndrome if they have neutropenia.

Young/middle aged female patient with normal lab values but chronic widespread pain > 3 months. Tender points at costochondral area and trapezius. She's fatigued and has trouble concentrating. What do you think she has? What is the tx for this?

Fibromyalgia. Tx: Regular aerobic exercise and good sleep hygiene is recommended. -Patients who don't respond to conservative treatments may require medications: TCAs (ex: amitriptyline) are the preferred 1st line drugs. Serotonin and norepinephrine re-uptake inhibitors (duloxetine, milnacipran) and pregabalin are alternative therapies that may be useful for pts not responding to TCAs. If pt has persistent symptoms, may need combined drug therapy, referral for supervised rehab, pain management consultation, or cognitive-behavioral therapy.

What do you see with folate (B9) and cobalamin (B12) deficiency? What's the one thing you see in B12 deficiency that is different.

For both B9 & B12 deficiency: -Megaloblastic anemia (low Hgb, high MCV) -hypersegmented PMNs For B12 deficiency: -Peripheral neuropathy of the dorsal column tract.

Ascending paralysis, progressive motor neuropathy, decreased/absent DTRs.

Guillain-Barre syndrome

Warts on plantar, palmar, or genital area in a young sexually active patient or pt with decreased cellular immunity (ex: AIDs, organ transplant), what do you think is the causative organism?

HPV- enter through cuts or abrasions in the skin after direct contact with HPV infected person. They are hyperkeratotic papules (cutaneous verrucae) and can be painful when walking or standing on them. Dx made by looking at the location and appearance.

Symptoms of Vitamin D toxicity

Hyper-Calcemia Polyuria Polydipsia (think about calcium as increasing the osmolality)

Tx for carbon monoxide poisoning

Hyperbaric oxygen administration

You are in the USA and get bit by a pet animal (cat, dog, gerbil, ferret), what do you do?

If pet is available, watch it for 10 days and don't give rabies PEP if the animal is healthy. If the pet is NOT available, give rabies PEP.

Pt with subtotal gastrectomy. He has easy fatigability and exertional dyspnea for several months.He's got a shiny tongue (glossitis) and pale palmar crease. Hgb is 7.8 (low), bilirubin is high (2.3), and LDH is 190 (high). What is the cause of this anemia given this patient has had a gastrectomy?

If you see anemia and hx of gastrectomy, think B12 deficiency. You may think.. but B12 is absorption in the ileum. Well, gastrectomy means you lose intrinsic factor (IF) since IF is secreted by gastric mucosa and IF is needed to absorb B12 later in the ileum. And then B12 is a required cofactor to make thymidylate and purines for DNA synthesis. So if you have a total gastrectomy, you lose IF and therefore can't absorb B12 and so now you have ineffective erythropoiesis due to delayed nuclear maturation, so you have decreased maturation of immature megaloblasts in the bone marrow to mature RBCs, so you have tons of immature megaloblasts in the bone marrow. This causes increased intramedullary hemolysis of these megaloblasts and releases heme --> hyperbilirubin --> jaundice. Hemolysis also releases the intracellular enzyme LDH. Total RBC count and reticulocyte count will be low (bc of the hemolysis). Patients can also have thrombocytopenia, leukopenia, and hypersegmented PMNs. You can see glossitis in micronutrient deficiency (like B12, in this case. But also can be seen in riboflavin, niacin, folic acid, and iron deficiencies) TLDR: Gastrectomy --> B12 deficiency, which is required as cofactor of purine synthesis so not enough B12 --> defective DNA synthesis --> ineffective erythropoiesis and presents as megaloblastic anemia.

Symptoms of Vitamin K deficiency

Increased INR (prothrombin time) s/sx of mild-severe bleeding Analogous to warfarin therapy

Kid lives in an old house, having trouble with school, having lots of "tummy aches," problems with growth and development, sensorimotor neuropathy in stocking-glove distribution, microcytic anemia, basophilic stippling. What are you concerned for?

Lead poisoning. Make sure they have safe housing and not eating lead paint or getting lead from pipes of old house or parent who does pottery, etc. Severe lead poisoning: would chelate with dimercaprol and make sure they have adequate hydration to pee all that out.

What medicines raise concern for ototoxicity?

Loop diuretics (***furosemide***), risk is greater in patients taking high dose furosemide. However, patients with renal failure can have ototoxicity (hearing loss, deafness) at lower doses. Mnemonic: thinking.. loop me in! I can't hear bc loop diuretics --> ototoxcity! Other meds: aminoglycoside antibiotics, chemotherapeutic agents, aspirin (needs very high doses), loop diuretics. Note: HCTZ is a thiazide diuretic that can cause orthostatic hypotension, photosensitivity, hypercalcemia. Hearing loss is NOT an associated SE of HCTZ.

Elderly pt with fatigue, decreased appetite, dyspnea on exertion, firm enlarged cervical/inguinal/supraclavicular lymph nodes, LSB systolic murmur, palpable spleen, and anemia to 7. What do you think they have?

Lymphoproliferative disorder (ex: leukemia or lymphoma). The anemia here is due to RBC progenitor cells in the bone marrow being replaced with cancer cells. Treating the cancer will improve the pt's anemia (though many chemotherapeutic agents are myelosuppressive)

What are side effects of Methotrexate (MTX) as a treatment for RA? What can help reduce the incidence of some of these side effects without loss of drug efficacy?

MTX side effects: stomatitis (oral ulcers), hepatotoxicity, cytopenia. Other symptoms include GI symptoms, rash, alopecia, pulmonary toxicity, bone marrow suppression (macrocytic anemia, leukopenia, thrombocytopenia) Folic acid supplementation is recommended for all MTX pts to reduce incidence of MTX adverse effects.

Symptoms of B12 (cobalamin) deficiency

Megaloblastic anemia (high MCV so macrocytic anemia) Hypersegmented PMNs Peripheral neuropathy of the dorsal column tracts (loss of position and vibration sense, ataxia, spasticity, incontinence)

RA treatment that has side effects of oral ulcers. What class of drug? What other side effects does it have?

Methotrexate: DMARD (disease modifying anti-rheumatic drug), it is a folate antimetabolite and the preferred initial DMARD to use in pts with mod-severe RA bc of established efficacy and safety in long term use. Side effects of Methotrexate (purine antimetabolite): Hepatotoxicity (LFTs increased), Stomatitis (oral ulcers), Cytopenias

38 yo woman presents with 4 months muscle weakness. Has to rest when climbing more than a few stairs, can't keep her arms up when blow-drying her hair, and has double vision at the end of the day when watching TV. What do you think she has? How to dx? Tx?

Myasthenia gravis (fluctuating, fatiguable proximal muscle weakness that worsens with repetitive motions of the same muscle groups and improves with rest. Ocular (ptosis, diplopia), bulbar (dysphagia, dysarthria) and respiratory muscles (myasthenic crisis) can all be involved. Dx: with edrophonium (Tensilon) test, ice pack test (ptosis improves), ACh receptor antibodies (highly specific), or CT scan of chest to look for thymoma. Tx: Pyridostigmine (ACh-esterase inhibitors), may add immunotherapy (ex: corticosteroids, azathioprine), and thymectomy if there is a thymoma.

What are the muscles involved in MG? So how do patient present?

Occular (diplopia, ptosis), bulbar (dysarthria, dysphagia, fatiguable chewing), and proximal muscles (hip flexors, quadriceps, deltoids --> difficulty climbing stairs or blow-drying hair). Respiratory muscles weakness is a life-threatening complication that may lead to respiratory failure (myasthenic crisis). They will present with fluctuating and fatigable proximal muscle weakness worse later in the day, diplopia, ptosis, dysphagia, dysarthria, and possibly even respiratory failure. However, they will have normal reflexes, sensation, coordination and pupillary responses.

What are features that distinguish biliary colic from cholecystitis?

Pain resolved within 4-6 hrs, absence of abdominal tenderness, fever, leukocytosis.

Symptoms of B3 (Niacin) deficiency

Pellagra: Diarrhea, Dementia, Dermatitis (& Death)

Pt that is 55yo has stiffness in the shoulders and hip girdle and some pain but stiffness is the main complaint. What do you think they have? What lab values do you want to look for? how do you treat? What other problem is associated with this dx?

Polymyalgia rheumatica (stiffness in pt >50yo) Look for elevated ESR and CRP (since it's a rheum thing) Tx with glucocorticoids (rapid improvement) - Low dow prednisone!! (old man that is stiff, give him steroids, treatment of choice!) Associated with giant cell arteritis (which come with symptoms of HA, jaw claudication, vision loss, tenderness over temporal artery). (get biopsy and up the prednisone dose if they have these symptoms)

Pt with gradual-onset of weakness in the leg muscles. Over last several months, she has increasing difficulty climbing stairs and rising from a chair. She denies problems chewing, morning stiffness or joint pain. Thigh muscle strength is 4/5 BL and distal muscle strength is 5/5 BL. Repeated contractions doesn't make affect the weakness. Proximal thighs are mildly tender. Proximal muscle weakness is the main complaint. -Note: esophageal muscle involvement --> dysphagia What do you need to do to establish dx? What do you think she has?

Polymyositis. (inflammation of muscles so imagine the muscle enzymes (creatine kinse, aldolase, AST), and autoantibodies (ANA, anti-Jo-1) will be elevated and you can do a muscle biopsy as the most definitive dx and it will show mononuclear infiltrate surroudning necrotic and regenerating muscle fibers

AA pt with family hx DM and glaucoma. He has gradual loss of peripheral vision over a period of years with eventual tunnel vision. Intraocular pressure is high. You see "cupping of the optic disc with loss of peripheral vision." What does he have?

Primary open angle glaucoma. Usually asymptomatic in earlier stages and more common in African Americans.

Symptoms of Vitamin A toxicity

Pseudotumor cerebri Hyper-parathyroidism

Similar to RA with morning joint stiffness in hands, mostly at DIPs, but with soft tissue (well demarcated red plaques with silvery scale) and nail changes (nail pitting and separation of nail bed - onycholysis), sausage fingers (dactylitis). What is this? Tx?

Psoriatic arthritis

benign vascular skin tumor, that presents as a small red papule that grows quickly (weeks or months) into a pedunculated or sessile shiny mass. These most commonly occur on the lips or oral mucosa and can bleed with minot trauma.

Pyogenic granuloma

Patients with RA have a 2-fold increase in risk of what cancer? How does that cancer present?

RA pts have 2-fold increased risk of Lymphoma. May present with low-grade fever, fatigue, and palpable spleen.

Pt with ischemic stroke. He work up with FNDs and so wasn't given fibrinolytic therapy because of uncertainty of symptom onset. CT scan shows large left hemisphere infarction bc of occluded MCA. 2 days (48hrs) later, he gets progressively obtunded and has more signs of additional FNDs. What is the best next step in management?

Repeat CT Head. Ischemic stroke has a chance to turn into hemorrhagic stroke, especially when the ischemic stroke covers a large area, is due to embolic cause, or has been treated with thrombolytics. Hemorrhagic transformation usually occurs in less than 48 hours after the iniital even and shows up as deterioration in the pt's neuro status. You should get an ***emergent CT Head***B to evaluate if urgent surgical decompression is needed.

Symptoms of Vitamin C deficiency

Scurvy (ecchymosis, petechiae, bleeding gums) -think about unstable collagen.. and bleeding of gums and under the skin (ecchymosis and petechiae)

Sjogren syndrome vs Age-related Sicca Syndrome.

Sjogren: autoimmune d/o with dry eyes and dry mouth. Usually ***middle age onset (before age 65)***, and ***ANA will be positive*** in majority of patients, can be associated with systemic sclerosis (manifestation of that autoimmune disorder) Age-related Sicca Syndrome (ARSS): just age-related dry eyes. ***See in older patients (ex: 73yo)**. Stem may mention a negative ANA. Your exocrine output from your lacrimal and salivary glands (so dry eye and dry mouth) declines with age, associated with atrophy, fibrosis, and ductal dilation of the glands. Decreased blink rate, oxidative damage, excessive evaporation of tears (d/t meibomian dysfunction) and use of anticholinergic medications in older pts can also contribute to dry eyes. ARSS is more common in women, increased risk in pts with DM or thyroid d/os. Can also get corneal epithelial erosions and lead to impaired vision. Manage with artificial tears or other ocular lubricant. Cyclosporine drops can also be used to increase tear secretion.

Get bit by high risk wild animal (bat, raccoon, skunk, fox, coyote), what do you do?

Start rabies post-exposure prophylaxis if animal is not available. If animal is available, kill it and test the brains for rabies and start PEP if the animal is positive for rabies

Immunocompromised patient (hx solid organ transplant) who now has pulmonary symptoms (dyspnea on exertion, dry cough), GI symptoms (abdominal pain, diarrhea, hematochezia), pancytopenia, mild hepatitis, and interstitial infiltrates on CXR. What is most likely organism? How do you dx?

Suggests tissue invasive CMV disease (causing pneumonitis, gasteroenteritis, and hepatitis) Dx: confirm with CMV DNA in blood using PCR. Tissue biopsy rarely required. Tx: discontinue antimetabolite immunosuppression (ex: mycophenolate) and starting antiviral therapy. Ganciclovir is used for patients with severe disease (ex: pneumonitis, meningoencephalitis, high viral load, significant GI disease). Valganciclovir can be used with patient with minimal s/sxs.

Pt presents with sudden onset contralateral sensory loss involving all sensory modalities (pure sensory stroke). What region of the brain is likely affected?

Thalamus. Lacunar stroke of the thalamus.

Tinea versicolor, how does it present? what kind of organism is it? Dx? Tx?

Tinea versicolor is hypopigmented, hyperpigmented or mildly red lesions. Think of the hypopigmented circle on a kid's face after sun exposure tans the other areas. On teens and adults, see it more on trunk and upper extremities Tinea versicolor is the ONLY tinea that is NOT a dermophyte. It is Malassezia globosa. Dx: KOH prep will show hyphae and yest cells in "spaghetti & meatball" pattern. Tx: topical ketoconazole, terbinafine, or selenium sulfide.

Tetanus pt presents with muscle stiffness, trismus/lockjaw (can't open mouth completely), and painful muscle spasms. What is Mechanism in which tetanus causes muscle contractions?

Toxin-mediated neurotransmission blockage Get cut in skin and C. tetani enters the body. C tetani secretes tetanospasmin (toxin) that binds to the peripheral nerve terminals and uses retrograde axonal transport to get to the NMJ, where it blocks the release of inhibitory NTs (glycine & GABA) across the synaptic cleft. (Exocytosis proteins cleaved, inhibiting GABA, glycine release). So the motor neuron is then disinhibited, leading to increased muscle tone and spasms. This mechanism takes time, so symptoms occur in a few days-several weeks after inoculation. Sxs can include sweating, dysphagia, labile blood pressure, and tachycardia.

Pt with chronic low back pain due to trauma 20 years ago, takes OTC meds. He is now fatigued, with UA showing trace protein in urine, moderate blood (painless), 20-30 WBC/HPF (sterile pyuria), and WBC casts. Cr 2.2 and BUN 34 (both elevated). What do you think he has? Dx?

Tubulointerstitial nephritis caused by long-term use of analgesics (ex: ASA, ibuprofen). This is usually asymptomatic but can have chronic tubulointerstitial nephritis or hematuria due to papillary necrosis. Can have renal colic. Dx: elevated CR with UA showing hematuria or sterile pyuria. Can have mild proteinuria (<1.5 g/day). CT scan can show small kidneys with BL renal papillary calcifications.

"bag of worms" of testes

Varicocele

Older patient with progressively thickened lens. Blurred vision, problem with nighttime driving, and glare. What is wrong? How do you treat it>

cataract. Occurs bc of oxidative damage of the lens. Tx with lens extraction

Where is Clostridium tetani found? (organism that causes tetanus)

normally found in soil, enters body through breaks in skin (puncture wound, lower extremity abrasions/lacerations).