IM EOR

pulmonary neoplasm

2 major categories Small cell lung cancer (SCLC), about 15% of cases (BAD) Non-small cell lung cancer (NSCLC), about 85% of cases, four subtypes include adenocarcinoma, squamous cell carcinoma, large cell carcinoma and carcinoid tumor Non-Small Cell (85% of cases) Grows more slowly and is more amenable to surgery Adenocarcinoma: 35-40% of cases. The most common type of bronchogenic carcinoma Patient presents → as a non-smoker, with an incidental finding, with a small peripheral lesion Squamous cell carcinoma: 25-35% of cases. Bronchial in origin and centrally located mass. More likely in smokers, more likely to have hemoptysis, central bronchus solitary tumor (cancer that started in the lung tissue has invaded the bronchus and this is why they are now coughing up blood). CCCP= central, cavitary lesions, hyperCalcemia, Pancoast syndrome Patient presents → as a smoker with hemoptysis and an abnormal chest X-Ray showing a large central solitary tumor. Large cell: rare (only 5%), fast doubling rates, responds to surgery rare Carcinoid tumor: 1-2% of all primary lung cancers lack glandular and squamous differentiation Small Cell (15% of cases) SCLC is highly aggressive and almost always occurs in smokers. It is rapidly growing, and roughly 80% of patients have metastatic disease at the time of diagnosis. Is more likely to spread early and rarely is amenable to surgery. Associated with ACTH and ADH - hyponatremia and hypercalcemia Lambert-Eaton myasthenic syndrome: characterized by muscle weakness of the limbs caused by ACTH/ADH SVC syndrome SCLC= Smoking, Central, Lambert-eaton, Chemo (responsive to chemo best option) CXR findings can help w/ diagnosis but BRONCHOSCOPY + BIOPSY for central lesions or FINE NEEDLE TRANSTHORACIC ASPIRATION will provide the most useful information New lesions > 0.5 cm carry a higher rate of malignancy, especially in a smoker. A biopsy is needed to evaluate a pulmonary nodule for malignancy unless the lesion is calcified or has been stable for years Associated Syndromes and paraneoplastic phenomena Carcinoid syndrome is specific to carcinoid tumors caused by the release of serotonin --> increased peristalsis and diarrhea and bronchoconstriction causing asthma Small cell lung cancer is commonly associated with ectopic ADH secretion and hence SIADH. Thus hyponatremia is a common finding in small cell lung carcinoma Small cell carcinoma of the lung may secrete ACTH causing Cushing syndrome Pancoast tumors are masses in the upper region of the lung that compress the nerves and blood vessels located there. They are most likely squamous cell and adenocarcinoma Superior vena cava syndrome if the tumor pushes on the superior vena cava this causes facial/arm swelling Pancoast's syndrome = shoulder pain + Horner's syndrome + bony destruction Shoulder or chest wall pain (due to tumor) Horner's syndrome - miosis (excessive constriction of the pupil of the eye), ptosis (lid droop) and anhidrosis (the inability to sweat normally) Bony destruction secondary to release of parathyroid hormone from squamous cell carcinoma which depletes calcium and causes brittle bones Tx- Non-Small Cell can be treated with surgery Treatment depends on staging: Stage 1-2 surgery Stage 3 Chemo then surgery Stage 4 palliative Small Cell: CAN NOT be treated with surgery will need chemotherapy PPx- USPSTF annual low dose CT for 55-80 who have a 30 PPY smoking Hx who currently smoke or have quit within 15y.

intracranial tumors

A cancerous or noncancerous mass or growth of abnormal cells in the brain 1/3 are glial cell origin; 1/3 meningioma, other: vestibular schwannoma, pituitary adenoma, neurofibroma, CNS lymphoma Most glial = malignant Astrocytoma: grade 4 = glioblastoma ⇒ MC with poor prognosis GlIOBLASTOMA patho/etiology: most common & aggressive primary malignant CNS tumor in adults. glioblastoma is a grade IV astrocytoma (heterogenous mixture of poorly differentiated astrocytes). RF include male >50 y/o, HHv-6 & cytomegalovirus infections, ionizing radiation. Types: primary most common (60%). seen in adults >50y/o. most common and aggressive type. secondary 40%. most common <45y/o. d/t malignant progression from a low grade astrocutoma (grade II) or anaplastic astrocytoma (grade III). May transform as early as 1 year or >10 y. Variants: classic 97%. presence of extra copies of the EGFR. TP53 is rarely mutated in this type (others are). mesenchymal high rates of mutations & alterations including the gene encoding for neurofibromatosis type 1. TP53 often mutated. an alteration of MGMT (a DNA repair enzyme). S/S: focal deficits depend on the location of the tumor; most common in the frontal and temporal areas of the cerebral hemisphere. General Sx include HA (worse in AM, wake patients up at night, positional), CN deficits, altered mental status, neurological deficits, ataxia, vision changes, weakness. Dx: Brain MRI with contrast initial study of choice-- finds heterogenous lesion with variable ring of enhancement with central necrosis, surrounded by edema and irregular margins. Mass effect may cause hydrocephalus. may cross the corpus callosum (butterfly glioma). Histology usually post-surgical: malignant astrocytes + necrotizing, hemorrhagic center surrounded by pseudo palisading (tumor cells lining the area of necrosis). Tx: surgical excision when possible, radiotherapy and adjuvant chemotherapy with temozolomide (alkylating agent). combination therapy with lomustine and temozolomide Ependymoma: occurs in ependymal cells that line the ventricles / spinal canal Medulloblastoma: MC primary malignant in children (long term survival with tx = 70%) MENINGIOMA patho/etiology: usually benign, slow growing tumors arising from arachnoid meningothelial cells of the meninges (covering the brain & spinal cord). Most commonly arises from the dura or sites of dura reflection (venous sinuses, falx cerebri). RF: females (estrogen receptors on tumor cells), radiation exposure.S/S: often asymptomatic (incidental finding) or causes Sx due to compression and displacement. seizures or focal neurologic signs depending on location. CNIII palsy common. Dx: MRI with contrast preferred to show extra axial intensely enhancing, well defined lesion often attached to the dura (snowball!) may have increased calcifications. Histology shows spindle-cells concentrically arranged in a whorled pattern. Psammoma bodies (concentric round calcifications) Tx: if asymptomatic, observation of small. Symptomatic, surgical excision when possible (transarterial embolization may be performed prior to Sx). radiation therapy may be used if not a surgical candidate or as adjuvant treatment in some. MC source of intracranial metastasis = lung, breast, kidney, GI tract DX: Head CT or MRI with contrast medium may detect the lesion, define its location and size, evaluate the extent to which the normal anatomy is distorted, and the degree of any associated cerebral edema or mass effect Arteriography may demonstrate stretching or displacement of normal cerebral vessels as well as the presence of tumor vascularity EEG may demonstrate a focal disturbance resulting from the neoplasm or a more diffuse change reflecting altered mental status Tx: complete superficial removal of the tumor with radiation/chemotherapy Steroids to help reduce cerebral edema, anticonvulsants

cryptococcus

AIDS-defining illness, diagnose with CSF and serum serology Transmission is through inhalation. Budding yeast found in soil contaminated with pigeon/bird droppings India ink may be positive Treat with amphotericin B + flucytosine for two weeks followed by fluconazole for 10 weeks Prophylaxis in HIV: Fluconazole if CD4 < 100

gastroenteritis

AKA infectious diarrheaDefinition: inflammation of the GI tract (primarily stomach & small intestine) S/s: include some combination of diarrhea, anorexia, vomiting, and abdominal pain. Fever, lack of energy, myalgia, and dehydration may also occur. typically lasts less than two weeks. It is unrelated to influenza though it has been called the stomach flu Exposures: foreign travel, playing in creek, daycare, poultry Causes: Gastroenteritis is usually caused by viruses. However, bacteria, parasites, and fungus can also cause gastroenteritis. If the stool is bloody, the cause is less likely to be viral and more likely to be bacterial TYYYPPPESSSS: Viral: In children, rotavirus is the MCC of severe disease. Norovirus (#1 in adults), adenovirus, enterovirus Parasitic: cryptosporidium, giardiaBacterial: campylobacter (Reactive arthritis occurs in 1% of people following infections with Campylobacter species), e. coli, clostridium, salmonella (reptiles). Some foods commonly associated w/ illness include raw or undercooked meat, poultry, seafood, and eggs; raw sprouts; unpasteurized milk and soft cheeses; and fruit and vegetable juices. Dx: Gastroenteritis is typically diagnosed clinically, based on a person's S/S ⇒ Determining the exact cause is usually not needed as it does not alter the management of the condition Stool cultures should be performed in those with blood in the stool, those who might have been exposed to food poisoning, and those who have recently traveled to the developing world. It may also be appropriate in children < 5, old people, and those w/ poor immune function Labs: Electrolytes and kidney function should also be checked when there is a concern about severe dehydration. CBC: WBC, bands. BMP/CMP: CO2, BUN/Cr. Stool: Culture, O&P, virus (GE panel). UA: dehydration Concerns: Presence of blood or mucus, Weight loss, Low BP, sunken fontanelle, dry MM ⇒ want to know if crying, peeing. Decreased urine output Traveler's diarrhea: e-coli Diarrhea after a picnic and egg salad: Staph aureus Diarrhea from shellfish: Vibrio cholerae Diarrhea from poultry or pork: Salmonella Diarrhea in a patient post abx: C. Difficile Diarrhea in poorly canned home foods: C. perfringens Diarrhea breakout in a daycare center: Rotavirus Diarrhea on a cruise ship: Norovirus ⇒ vomiting and horrible muscle cramps Diarrhea after drinking (not so) fresh mountain stream water: Giardia lamblia - incubates x 1-3 weeks, causes foul-smelling bulky stool and may wax and wane over weeks before resolving Tx: FLUIDS! mild- moderate cases, drink oral rehydration solution (a combination of water, salts, and sugar). In those who are breastfed, continued breastfeeding is recommended. For more severe cases, IV fluids may be neededViral: symptomatic, fluids. Children infected w/ rotavirus usually make a full recovery within 3-8d. rotavirus vaccine recommended for kiddos Bacteria: abx are recommended for young children with a fever and bloody diarrhea: Cipro, Doxy, Azithro, Bactrim INFLAMMATORY V. NONINFLAMMATORY Patho/etiology: Non-inflammatory: small bowel enteritis (E. coli, Staph aureus, Bacillus cereus, Clostridium perfringens; virus; giardia. Inflammatory: shigellosis, salmonellosis, campylobacter, C. diff, E. coli. S/S: Non-inflammatory watery, high volume, nonbloody, with periumbilical cramps, bloating, nausea, vomiting. Inflammatory fever and bloody diarrhea in low volume(dysentery) LLQ pain bc mainly colon involved. Testing: Non-inflammatory shows NO fecal leukocytes, + metabolic acidosis, hypokalemia, dehydration. Inflammatory shows fecal leukocytes.

addison's disease

AKA primary adrenal insufficiency. E.O.D: Deficiency of cortisol and mineralocorticoid from destruction of the adrenal cortex. Weakness, vomiting, diarrhea; abdominal pain, arthralgias; amenorrhea. Increased skin pigmentation, especially of creases, pressure areas, and nipples. Hypovolemic hypotension, small heart.Hyponatremia; hyperkalemia (may be absent with vomiting and diarrhea); hypoglycemia; eosinophilia. Elevated plasma ACTH level; cosyntropin unable to stimulate serum cortisol to 20 mcg/dL (550 nmol/L) or more.causes: caused by dysfunction or absence of the adrenal cortices. It is distinct from secondary adrenal insufficiency caused by deficient secretion of ACTH. S/S: can occur suddenly but usually develop gradually over months or years. fatigue, reduced stamina, weakness, anorexia, and weight loss. Over 80% of affected patients present with symptoms of orthostatic hypotension (aggravated by dehydration caused by nausea or vomiting), lightheadedness with standing, salt craving, and eventually hyperpigmentation of skin and gums. Abdominal pain, nausea, and vomiting eventually develop in most patients; diarrhea can occur, aggravating dehydration and hypotension. Fevers and lymphoid tissue hyperplasia may also occur. Patients often have significant pain: arthralgias, myalgias, chest pain, abdominal pain, back pain, leg pain, or headache. Psychiatric symptoms include anxiety, irritability and depression. Cerebral edema can cause headache, vomiting, gait disturbance, and intellectual dysfunction that may progress to coma. Hypoglycemia can occur and worsen the patient's weakness and mental functioning. Hyperpigmentation of the skin and gums eventually occurs in most patients with Addison disease. Sun-exposed areas darken the most, but nonexposed areas darken as well. Undiagnosed adrenal insufficiency can cause intrauterine growth retardation and fetal loss. Pregnant women with undiagnosed adrenal insufficiency can experience shock from adrenal crisis, particularly during the first trimester, concurrent illness, labor, or postpartum. Labs: mild anemia, moderate neutropenia, lymphocytosis, and eosinophilia (total eosinophil count over 300/mcL). Among patients with chronic adrenal insufficiency, the serum sodium is usually low (88%) and the potassium usually elevated (64%). However, patients with vomiting or diarrhea may not be hyperkalemic. Fasting hypoglycemia is common. Hypercalcemia may be present. plasma cortisol less than 3 mcg/dL (83 nmol/L) at 8 AM is diagnostic, especially if accompanied by simultaneous elevation of the plasma ACTH level greater than 200 pg/mL (44 pmol/L). diagnosis is confirmed by a simplified **cosyntropin stimulation test: (1) Synthetic ACTH1-24 (cosyntropin), 0.25 mg, is given intramuscularly. (2) Serum cortisol is obtained 45 minutes after cosyntropin is administered. Normally, serum cortisol rises to at least 20 mcg/dL (550 pmol/L), whereas patients with adrenal insufficiency have stimulated serum cortisol levels less than 20 mcg/dL (550 pmol/L) (hydrocortisone must not be given for at least 8 hours before but pred and dex are ok) Treatment: glucocorticoid replacement 15-30 mg of hydrocortisone (or if better then pred/methylpred) orally daily in two or three divided doses at lowest dose possible. If partial ACTH deficiency (basal morning serum cortisol >8mg/dL) require hydrocortisone replacement in lower doses. If mild illness or surgical stress, 2-3x the dose. If severe illness, trauma, or surgical stress, hydrocortisone 100 mg IV. mineralocorticoid replacement Fludrocortisone acetate has a potent sodium-retaining effect; 0.05-0.3 mg orally daily or every other day **For 8-9 AM cortisol levels between 3 and 15 mcg/dL, a cosyntropin test is often required.patients should hold any corticosteroid replacement for at least 18-24 hours.8-9 AM, blood is drawn for serum cortisol, ACTH, and dehydroepiandrosterone (DHEA); then cosyntropin 0.25 mg is administered intramuscularly or intravenously. Another serum cortisol is obtained 45 minutes after the cosyntropin injection; a stimulated serum cortisol of less than 20 mcg/dL (550 nmol/L) indicates probable adrenal insufficiency.The baseline serum ACTH level is low or normal in secondary hypoadrenalism, distinguishing it from primary adrenal disease.

pertussis

AKA whooping cough. infection with bordetella pertussis. rarely seen d/t vaccination so MC in kids <2 years old. spread by respiratory droplets during coughing fits. 7-10d incubation period. S/s: catarrhal phase: MOST CONTAGIOUS! URI Sx x1-2 weeks. paroxysmal phase: severe paroxysmal coughing fits w/ inspiratory whooping sound after. post-cough emesis. lasts x2-4 weeks convalescent phase: resolution of the cough (coughing stage may last for up to 6 weeks). Dx: clinical. when available order throat culture AND PCR. lymphocytosis. throat culture will be most sensitive during first 2 weeks, but PCR of NP swab will be sensitive up to 4 weeks. Tx: supportive (oxygenation, nebulizers, mechanical ventilation, droplet precautions). antibiotics to shorten contagiousness; macrolides best. choose one--5 days of azithromycin, 7 days of clarithromycin, 14 days of erythromycin (not in neonates) or TMP/SMX if older than 2 months.

salmonellosis

Although there are many types of Salmonella, they can be divided into two broad categories: those that cause typhoid and enteric fever and those that primarily induce gastroenteritis: Enteric fever (salmonella typhi): a flu-like bacterial infection characterized by fever, GI symptoms, and headache. Transmitted via the consumption of fecally contaminated food or waterGI symptoms may be marked constipation or "pea soup diarrhea"Rose spots may be present (2-3 mm papule on trunk usually)More common in the developing world (usually immigration cases) Gastroenteritis (Salmonella Typhimurium, Enteritidis, and Newport): results from improperly handled food that has been contaminated by animal or human fecal materialIt is estimated that 1 in 10,000 egg yolks is infected with Salmonella enteritidis Treat with Ceftriaxone or other medications based on the sensitivity

sickle cell anemia

African American, pain, family history of blood disorder Hemoglobin electrophoresis: Hemoglobin S, Blood smear: Sickled RBCs, Howell-Jolly bodies, target cells Chronic hemolytic anemia occurs almost exclusively in black people Hemolysis, jaundice, splenomegaly, priapism, poor healing, pain/swelling hands and feet, acute chest syndrome, pigmented gallstones Sickle-cell shaped RBCs clog capillaries causing organ ischemia (crises) A very high reticulocyte count can be used to monitor event (decreases as pt improves) Dx: Diagnosis requires (+) HgbS on hemoglobin electrophoresis → is definitive Reticulocytosis; mildly increased WBCs Blood smear: sickled RBCs, Howell-Jolly bodies, target cells Hgb 8-10, HCT 20-30RBCs = normochromic, normocyticHb SS = diseaseHb SA = traitTwo parents with sickle cell trait have a 1 in 4 chance of having a child with Hb SS disease. Tx: High flow O2, pain control during a crisis, supportive transfusion when Hgb <6 Vaccines (meningococcal, pneumococcal, H. influenzae, influenza), prophylactic antibiotics, and aggressive treatment of infections prolong survival Hydroxyurea may decrease the frequency of crises. Infection, bone marrow aplasia, lung involvement can develop acutely and be fatal Complications that occur more commonly in sickle cell anemia splenic sequestration osteomyelitis (salmonella) stroke cholecystitis lung infection (Pneumonia) urinary tract infection arthritis delayed growth and puberty Causes of, presentation of, GENERAL treatment of sickle cell crisis causes: painful vaso-occlusive crisis triggered by hypoxia, cold weather, infection, dehydration, EtOH, pregnancy. S/S: associated with abrupt onset of pain. acute chest syndrome fever, cough, tachypnea, oxygen desat, chest pain. back, abdominal, bone pain. Renal or hepatic dysfunction. prapism common. Treatment: pain control w/ IV hydration and oxygen. do not give meperidine. folic acid supp for RBC production and DNA synthesis. RBC transfusion in some crises like acute chest syndrome, splenic sequestration, preoperative transfusion. If severe vasocclusive crisis (acute chest syndrome, stroke, priapism, retinal infarction leading to visual changes), exchange transfusion therapy. Only potentially curative Tx is allogenic stem cell transplant.

acute renal failure

An abrupt or rapid decline in renal filtration function Elevated serum creatinine and decrease GFR Azotemia a rise in blood urea nitrogen (BUN) concentration PRERENAL patho/etiology: decreased renal perfusion issues; renal volume loss (diuretic), GI loss (diarrhea. vomit), blood loss. Afferent arteriole vasoconstriction (NSAIDs, IV contrast). Efferent arteriole dilation (ACE-inhibitors, ARBs). Hypotension, relative hypovolemia (CHF w decreased EF). Dx: BUN:Cr >20:1. high gravity, low urine Na and FeNa. Tx: fluids, cardiac support, treat shock INTRINSIC ACUTE INTERSTITIAL NEPHRITIS inflammatory or allergic response in the interstitium with sparing of the glomeruli and BV. "ALWAYS INVOLVING NSAIDS." drug HS (NSAIDs, penicillins, sulfa). infections (strep, legionella, CMV, EBV, HIV), idiopathic, autoimmune. S/S include fever, eosinophilia, maculopapular rash and arthralgia. WBC CASTS and eosinophiluria on UA. modest proteinuria (esp if NSAID induced) increased serum IgE and eosinophils. ACUTE TUBULAR NECROSIS (ATN) acute destruction and necrosis of renal tubules; most common type. can be ischemic (hypotension, hypovolemia) or nephrotoxic (contrast dye--immediate! or aminoglycosides, vanco, cyclosporine, NSAIDs. tumor lysis syndrome leading to uric acid precipitation, myoglobinuria d/t rhabdo, lymphoma, leukemia, bence-jones proteins from MM).UA shows renal tubular EPITHELIAL CELL CASTS & granular MUDDY CASTS d/t sloughing off of tubular cells into the nephrons. LOW urine specific gravity, osmolarity. increased FENA >2%, increased urine sodium >40, BUN/Cr <15:1. ACUTE GLOMERULONEPHRITIS immune inflammation of glomeruli leading to HTN, hematuria (RBC casts), azotemia, proteinuria <3, and edema. can be post infectious, Berger's dz/IgA nephropathy, membranoproliferative, RPGN.S/S include hematuria (cola or tea colored), edema, fever, abdominal or flank pain, malaise, oliguria. HTN. RBC CASTS VASCULAR microvascular like TTP, HELLP, DIC. macrovascular like aortic aneurysm, renal artery dissection, thrombosis, malignant HTN, artheroembolic disease (ischemic digits/blue toe syndrome or livedo reticularis) ALL LABS Decreased GFR with intrinsic kidney dysfunction. Typically have high FENa (> 1-2%) (Loss of tubular cells ability to reabsorb sodium). elevated BUN/Cr. POSTRENAL obstruction of the passage of the urine. rare cause bc obstruction has to be bilateral.kidney stone, tumors, BPH/prostate cancer, sloughed off renal papillae, neurogenic bladder (cauda equina, DM), anticholinergic drugs. Dx: varies with time; initially high urine osmolality, low urine sodium, high BUN:Cr, low FeNA. after several days, kidneys start to fail and cant concentrate urine; isotheuria. urine sediment usually bland or regular RBCs

rabies

Caused by a ribonucleic acid (RNA) rhabdovirus affecting mammals, including humans. Transmission via dogs, raccoons, skunks, bats, fox, coyote Hydrophobia (inability to swallow water) is a classic symptom. Pharyngeal spasms, aerophobia (fear of drafts of fresh air) and hyperactivity DX: Negri bodies (eosinophilic inclusion bodies in the cytoplasm of hippocampal nerve cells) are considered pathognomonic and are found in the brain of dead animals TX: Post-exposure treatment: Rabies immunoglobulin + inactivated vaccine (4 doses over 14 days) Fatal when there are neurological symptoms

testicular torsion

Caused by a twisting of testicle around the cord supplying blood to the scrotum S/s: Asymmetric high riding testicle "bell clapper deformity"; negative Prehn's sign (lifting of testicle will not relieve pain). Teenage males. Sudden, severe pain and swelling in the testicle are symptoms. Associated with nausea and vomiting. Very tender to palpation. Cremaster reflex absent. Blue dot sign: Tender nodule 2 to 3 mm in diameter on the upper pole of the testicleDx: USN and radionuclide study (gold standard) Tx: Surgical emergency; Repair both testes within 4-6 hours. A longer wait may cause infertility

anemia of chronic disease

Causes: anemia of inflammation IBD, rheumatoid disorders, chronic infections, malignancy via hepcidin primarily elevating iL-6 resulting in reduced iron uptake in gut and transfer to bone marrow. Also decreased response to erythropoietin. anemia of organ failure CKD, liver failure, endocrine gland failure. erythropoietin is reduced and RBC mass decreases in response to the diminished signal for RBC prod; serum iron is normal except in CKD. anemia of older adults present in 25% of people 85+ in whom a thorough explanation of anemia is negative. consequence of decrease in erythropoietin production relative to nephron mass, relative resistance to RBC production, negative erythropoietic influence of higher levels of chronic inflammatory cytokines in older adults, the presence of various somatic mutations in myeloid genes typically associated with myeloid neoplasms. S/S: clinical features are those of the causative condition. diagnosis should be suspected in patients with known chronic diseases. In cases of significant anemia, coexistent iron deficiency or folic acid deficiency should be suspected. Decreased dietary intake of iron or folic acid is common in chronically ill patients, many of whom will also have ongoing gastrointestinal blood losses. Patients undergoing hemodialysis regularly lose both iron and folic acid during dialysis. Labs: hematocrit rarely falls below 60% of baseline (except in kidney failure). The MCV is usually normal or slightly reduced. RBC morphology is usually normal, and the reticulocyte count is mildly decreased or normal. inflammation serum iron and transferrin values are low, and the transferrin saturation may be extremely low, leading to an erroneous diagnosis of iron deficiency. In contrast to iron deficiency, serum ferritin values should be normal or increased. A serum ferritin value <30 indicates coexistent iron deficiency. Anemia of inflammation has elevated hepcidin levels; however, no clinical test is yet available. anemias of organ failure and older adults iron studies are generally normal. The anemia of older persons is a diagnosis of exclusion. Treatment: In most cases, no treatment is necessary and the primary management is to address the condition causing the anemia of chronic disease. If anemia is severe or is adversely affecting the quality of life or functional status, then treatment involves either RBC transfusions or parenteral recombinant erythropoietin (epoetin alfa or darbepoetin). The FDA-approved indications for recombinant erythropoietin are : Hgb <10 g/dL and anemia d/t RA, IBD, HCV, zidovudine therapy in HIV-infected patients, myelosuppressive chemotherapy of solid malignancy (treated with palliative intent only), or CKD. there is concern that recombinant erythropoietin is associated with reduced survival in patients with malignancy. For patients with ESRD receiving recombinant erythropoietin who are on hemodialysis, the anemia of chronic kidney disease can be more effectively corrected by adding soluble ferric pyrophosphate to their dialysate than by administering intravenous iron supplementation.

peripheral neuropathies

Causes: can be d/t systemic disease (#1 cause is DM &impaired glucose tolerance, AIDS), toxic exposures, B12 deficiency, multiple myeloma or other immunoglobulin disorders (check SPEP), inflammatory demyelinating diseases (AIDP), drugs (Li, chemo), alcoholic neuropathy, liver/kidney Dz, HIV/neurosyphilis, CT disease.Effects: if severe can lead to steppage gait, sensory ataxia, imbalance, falls. Feet are more prone to injuries, ulcers, deformation (Charcot foot). Autonomic effects include orthostasis, bladder and ED. S/S: can affect sensory, motor, or autonomic nerve pathways. Distal weakness, atrophy, sensory disturbances, pain, hypo or areflexia. Often most marked distally (usually starts in feet then eventually upper extremities) then ascends in stocking glove pattern. Workup PE should eval sensation (light touch, pain, vibration, position sense). Motor strength and muscle stretch reflexes. Gait, cerebellar function.Labs: CBC, ESR, SPEP, plasma urea, lytes, LFT, TSH, RA/ANA, HBsAG, RPR, FBS, Urinary heavy metals, CSF, CXR.EMG: Measures denervation caused by loss of motor units. Can determine site, extent, severity of neuro lesion. Tests will tell if the abnormality is in one or more nerves (plexopathies); nerve root (radiculopathy); muscle (myopathy); neuromuscular junction (myasthenia gravis). Determine if problem is sensory, motor, or both. Determine if it is demyelinative or axonal. Acute or chronic. Tx: ASA, NSAIDs, gabapentin for neuropathic burning pain. SNRIs especially for painful diabetic neuropathy. Opioids if sever hyperpathia or pain induced by minimal stimuli.gabapentin, pregabalin, carbamazepine, or TCAs for stabbing pains episodically. Fludrocortisone reduces postural hypotension but high doses are needed for patients with DM and can lead to recumbent HTN. Midodrine is an alpha-agonist that could be helpful at 2.5-10mg. Neuropathic bladder may respond to parasympathomimetic drugs like bethanechol chloride.

cholelithiasis

Cholelithiasis is stones in the gallbladder. RF: women>men, increase in incidence with age (highest 60+). Rates are higher in Mexican-Americans and native americans than in whites and AA (although common in those with sickle cell). also high in Crohn dz. S/S: frequently asymptomatic and is discovered in course of routine radiographic study, surgery, or autopsy. Biliary pain in some, acute cholecystitis in some. Risk factors for development of Sx or complications include female sex, young age, awareness of having gallstones and large, multiple, and older stones. Can lead to small intestinal obstruction due to gallstone gallstone ileus. Testing: USN is the initial test of choice. CT or MRI may also be used. Treatment: NSAIDs for biliary pain. laparoscopic cholecystectomy is treatment of choice for symptomatic gallbladder disease. Usually outpatient; patients may go home within 1 day of the procedure and return to work within days; good for those even with acute cholecystitis. Sometimes necessary to convert to open cholecystectomy. ursodeoxycholic acid 8-13mg/kg is a bile salt that when given orally x2 years will dissolve some cholesterol stones and may be considered if someone refuses cholecystectomy Choledocholelithiasis is a stone obstructing the CBD. S/s: RUQ or epigastric pain, N/V, Jaundice. Labs: elevated AST and ALT. Increased alk phos + GGt. imaging USN first. ERCP better as it can be diagnostic and therapeutic; usually obtained after USN. MRCP + EUS may be used in patients with intermediate risk. Treatment: ERCP stone extraction. SURGICAL RECALL: Which artery is susceptible to injury during cholecystectomy? Right hepatic artery. proximal to cystic artery and calot's triangle. What makes up calot's triangle? the cystic duct, the common hepatic duct, and the cystic artery (not the liver edge). What is biliary colic? Pain from gallstones usually at the cystic duct. RUQ, epigastrium or right subscapular region. min-hours and goes away, postprandial esp after fatty foods.

shock

Classified into four categories by ETIOLOGY: Hypovolemic (Blood VOLUME problem) Cardiogenic (Blood PUMP problem) Distributive (neurogenic, anaphylaxis, septic) (Blood DISTRIBUTION problem) Obstructive (extra cardiac obstruction to blood flow) BY SEVERITY:mild, moderate, severe (depends on amount of blood loss, duration of shock) by STAGE initial, compensated, decompensated, refractory Symptoms include weakness, hypotension, tachycardia, tachypnea, sweating, anxiety, and increased thirst Malfunction of organ systems: lactic acidosis, renal (anuria/oliguria), CNS dysfunction (AMS) TX: ABC assessment Initial steps: stabilize patient hemodynamically, determine the cause Fluid bolus (500-1000 L NS or lactated Ringer's solution) CBC, CMP, Creatinine, PT/PTT, continuous pulse oximetry EKG, CXR Vasopressors (dopamine or norepinephrine) if hypotensive despite IVF Types of shock: Cardiogenic: Heart is unable to generate cardiac output Post-acute MI → Cardiac tamponade, tension pneumothorax, arrhythmias, PE, CM, myocarditis, valvular defects SBP <90 Urine output <20 mL/h Altered sensorium, pale cool skin, hypotension, tachycardia JVD Pulmonary congestion DX: EKG: ST elevation (most common) Echo Hemodynamic monitoring TX:ABCsIdentify underlying causeVasopressors: Dopamine (initial) +/− dobutamineNTG or nitroprussideIVF—harmful if LV pressures elevated (may need diuretics) Hypovolemic Decreased circulatory blood volume → decreased preload and cardiac output Hemorrhage (trauma, GI bleed, retroperitoneal) Nonhemorrhagic—vomiting, diarrhea, dehydration, burns, third space loss Vital signs and clinical picture DX: Central venous line or pulmonary artery catheter: decreased CVP/PCWP, decreased cardiac output and increased SVR TX:AB: intubation, mech ventCirculation: direct pressure if acute bleedIV Hydration: class II (optional), class III/IV (required) Neurogenic Failure of sympathetic NS to maintain vascular tone SCI, head injury, spinal anesthesia, drug blockade DX: Vasodilation with decreased SVR (warm, flush skin); UOP: NL to LOW; Bradycardia, hypotension TX:Judicious use of IV fluidsVasoconstrictors to restore venous toneSupine or Trendelenburg positionMaintain temp Septic Hypotension induced by sepsis, persistent despite adequate IVF → Multi-organ system failure Pneumonia, pyelonephritis, meningitis, abscess, cholangitis, cellulitis, peritonitis Severe decrease in SVR due to peripheral vasodilation (flush, warm skin) Signs of SIRS Signs of shock: hypotension, oliguria, lactic acidosis Fever or hypothermia DX: Decreased EF—reduced contractility; Clinical DX: (+) blood cultures × 2 Source of infection TX: IV Antibiotics (broad-spectrum) at max doses IVF:Increase mean BP Pressors: Maintain BP

IBD

Crohn's disease v. Ulcerative Colitis Site of involvement Any area of the GI tract; the rectum is usually spared Only involves the colon; the rectum is usually involved Pattern of involvement Skip lesions Continuous Diarrhea Usually non-bloody Bloody Severe abdominal pain Frequent Rare Perianal disease 30% of patients No Fistula Yes No Endoscopic findings Aphthoid and deep ulcers; cobblestoning Erythematous and friable superficial ulceration Radiographic findings String sign of terminal ileum, RLQ mass, fistula, abscesses Tubular (lead pipe) appearance resulting from loss of haustral folds Histologic features Transmural, non-caseating granulomas Mucosa-only crypt abscesses Smoking Worsens course Protective Serology ASCA p-ANCA CROHN'S DZ S/s: abd pain, weight loss, diarrhea (non-bloody), & oral mucosal aphthous ulcers. Longer standing disease may have severe anemia, polyarthralgia, and fatigue. MC site is terminal ileum Distribution from mouth to anus and will commonly present with thickened bowel wall, cobblestoning and "skip" lesions Linear fissures and cobblestone appearance. Tends to be transmural vs. UC is limited to the mucosa and submucosa Complications include strictures identified by a string sign on barium study Presents with abdominal pain, weight loss, diarrhea, and oral mucosal aphthous ulcers Obstruction, abscess, fistula, and sinus tracts are common 1-3% cancer risk (low) Antibody test: +Anti-Saccharomyces cerevisiae antibodies (ASCA) ULCERATIVE COLITIS S/s: bloody puss-filled diarrhea, rectal/lower quadrant pain, fever, and urgency. Inflammation isolated to colon and confined to mucosa and submucosa (unlike Crohn's, not transmural) Most common site is the rectum Bimodal distribution of peak onset: age 15-25 and age 55-65 Labs: ↑ WBC, ESR, and anemia Dx by barium enema lead pipe appearance and colonoscopy with biopsy both show continuous inflammation starting from rectum and extending proximally with loss of haustral markings and lumen narrowing. +- pseudopolyps. Complications: Toxic megacolon, colorectal cancer Antibody test: Antineutrophil cytoplasmic antibodies (p-ANCA) Dx: CBC, ESR, CRP, albumin, electrolytes, ALT, AST, creatinine, urea nitrogen, fecal calprotectin, stool microscopy and stool cultures, along with testing for C.diff toxin. Colonoscopy with biopsy. shows transmural involvement in crohn's and granulomas. May have to do flex sigmoidoscopy in UC to prevent perf. LFTs ⇒ elevated alkaline phosphatase and γ-glutamyl transpeptidase levels in patients w/ major colonic involvement suggest possible primary sclerosing cholangitis. To detect nutritional deficiencies, levels of vitamin D and B12 should be checked every 1 to 2 yr. Tx: Sulfasalazine useful if the colon is involved. 5-ASA (mesalamine) is the active compound and is released in the colon—more useful in UC than in Crohn's disease. 5-ASA compounds block PG release and serve to reduce inflammation. There are preparations of 5-ASA that are more useful in distal small bowel disease. Metronidazole—if no response to 5-ASA Systemic corticosteroids (prednisone/budesonide)—for acute exacerbations and if no response to metronidazole Immunosuppressants (azathioprine, 6-mercaptopurine)—in conjunction with steroids if the patient does not respond to the above agents Bile acid sequestrants (cholestyramine or colestipol)—for patients w/ terminal ileal disease who cannot absorb bile acids Antidiarrheal agents generally not a good choice (may cause ileus) Nutritional supplementation and support—parenteral nutrition is sometimes necessary Surgical UC — often curative (unlike Crohn's disease) and involves total colectomy. Surgical Crohn's (eventually required in most patients) - Involves segmental resection of involved bowel Disease recurrence after surgery is high—up to 50% of patients experience disease recurrence at 10 years postoperatively SURGICAL RECALL: Extraintestinal manifestations: A PIE SACK Apthous ulcers Pyoderma gangrenosum Iritis Erythema nodosum Sclerosing cholangitis Arthritis, anklyosing spondylitis Clubbing of fingers Kindey (amyloid deposits, nephrotic syndrome) Whos high risk for iBD? jewish people (women Crohns, UC male) What meds are used for crohns but not UC? methotrexate, abx (flagyl/cipro)

hyponatremia

Definition: serum sodium of < 135 mmol/L S/s: Peripheral and presacral edema, pulmonary edema, JVD, hypertension, decreased hematocrit, decreased serum protein, decreased BUN/CR Presentation: Muscle cramps and seizures Causes: check serum osmolality Hypotonic= <280 mOsm Isotonic= 280-295 mOsm Hypertonic= >295 mOsm should always be hypotonic hyponatremia. If isotonic (normal serum osmolality) this is pseudohyponatremia d/t presence of XS protein, HLD. so the osmolality looks normal bc of other solvents but there is actually not enough sodium. If hypertonic this is d/t hyperglycemia or mannitol pulling water out of intracellular stores and into EC space. you will still have high serum osmolality because of the glucose, but not bc of sodium. hypotonic hyponatremia- most common, only "true" hyponatremia. water intake exceeds excretion capacity of kidney. NON-ADH causes include psychogenic polydipsia (suppressed ADH, low urine osmolality <100), beer potomania/tea and toast diet (malnourished, low protein & solute), renal impairment (GFR <15, cannot dilute their urine, prone to water retention/hyponatremia) ADH causes hpovolemic hyponatremia (renal or extrarenal volume loss leads to subsequent hypotonic fluid replacement. reduced BP leads to increased aDH secretion, limiting water excretion I.e. cerebral salt wasting; can lead to refractory hypotension). hypervolemic hyponatremia (edematous states of cirrhosis and HF; decrease effective arterial blood volume aka hypotension occurs despite overall increase in extracellular volume aka edema leading to ADH secretion. euvolemic: SIADH (ADH secreted w/o a stimuli; caused by CNS issues like cancer or infections, medications. Dx of exclusion). Reset osmostat (rare, patients regulate vasopressin ADH release around a lower or hypotonic set point) adrenal insufficiency and hypothyroidism (cortisol cannot have negative fdbk on ADH release so its secreted alot. in hypothyroid, myxedema coma causes this) nausea, pain, Sx (nausea, pain stimulators of ADH release. severe hyponatremia can develop after elective surgery in healthy patients d/t XS use of hypotonic fluids.) exercise-induced (during or after exercise esp. endurance) thiazide diuretics and other meds (thiazides esp. in older patients can cause hyponat d/t water Intake and diuretic-induced volume contraction leading to ADH secretion. NSAIDs increase ADH by inhibiting prostaglandin. MDMA, SSRIs can lead to hyponatremia. Hypervolemic hyponatremia - CHF, nephrotic syndrome, renal failure, cirrhosis Euvolemic hyponatremia - SIADH, steroids, hypothyroid Hypovolemic hyponatremia - sodium loss (renal, non-renal) Treatment: asymptomatic- free water restriction moderate hyponatremia- IV normal salineloop diuretics may be added severe hyponatremia- hypertonic (3%) saline Serum Na should be corrected slowly—by ≤ 10 mEq/L over 24 h to avoid osmotic demyelination syndrome

cluster headaches

Definition: severe unilateral pain in orbit or surrounding areas 15-180 minutes. More common in middle aged males. Recurring from once every other day to 8x per day. S/S: 1+ of these: ipsilateral conjunctival injection, lacrimation, nasal congestion, ptosis, miosis, attacks occur in series lasting for weeks or months separated by remissions lasting for months or years. Precipitating factors: EtOH, smoking, stress, nitroglycerin, chocolate. Treatment avoidance of triggers. Abortive therapy includes 100% O2 w/ nasal cannula in house x15 min. Sumatriptan, ergotamine NOT PO; rectal or dissolvable. Intranasal lidocaine. High dose prednisone (60-80 mg po daily until HA freq diminishes) if very severe and often Prophylaxis antidepressants, anticonvulsants (lithium, Topamax), ergotamine, CCB, SSRI, Verapamil.

dementia

Delirium vs neurocognitive disorders (dementia) Delirium is an acute, usually reversible syndrome caused by a medical condition versus neurocognitive disorder which is a long-term impaired memory disease process that is usually irreversible such as Alzheimer's disease Neurocognitive disorders (previously known as dementia) are described as those with a significant (major) or moderate (mild) impairment of cognition or memory that represents a marked deterioration from a previous level of function -Increasing age -Insidious onset, progressive -Preserved consciousness, rarely hallucinations present -No tremor unless due to Parkinson disease -Typically irreversible Alzheimer Disease (most common type) Progressive cognitive decline; MC >65 years Loss of brain cells, beta-amyloid plaques, and neurofibrillary tangles PE: Abnormal clock drawing test Treatment: anticholinesterase drugs (Tacrine, Donepezil) Vascular Disease (second most common type) Associated with arteriolosclerotic small vessel disease Multi-infarct, usually correlated with a cerebrovascular event and/or cerebrovascular disease Stepwise deterioration with periods of clinical plateaus May cause a sudden decline Treatment: Blood pressure control Frontotemporal lobar degeneration Language difficulties, personality changes, and behavioral disturbances Personality changes precede memory changes Lewy Body Disease Parkinsonian symptoms Gradual, progressive decline in cognitive abilities Hallucinations and delusions, gait difficulties, and falls Substance/medication use dementia Related to medication or non-prescription drug use HIV infection Cognitive decline associated with HIV infection Substantial memory deficits, impaired executive functioning, poor attention and concentration, mental slowing, and apathy Cerebral atrophy is typically evident on brain imaging

migraine headache

Demographic: females 15-18%, males 6%. Females more likely to consult provider. 85% of migraineurs report disability. Pathogenesis: characterized by increased sensitivity of the N.S, genetic factors, hyper-excitability of the occipital cortex (auras, scotomas), trigeminal vascular system activation. Serotonin plays a role, calcitonin gene related peptide CGRP plays a role, brainstem, hypothalamus involved. Variants and their S/S CLASSIC migraine w/ or w/o aura: Unilateral throbbing pain. Can be associated w/ anorexia, N/V, photophobia, phonophobia. Usually build up gradually and last several hours. Attacks may be triggered by emotional or physical stress, sleep disturbances, missed meals, certain foods, alcohol, hormones. EQUIVALENT patient has aura or other neurological Sx but without the headache. BASILAR ARTERY blindness or visual disturbances throughout both visual fields. Dysarthria, disequilibrium, tinnitus, perioral parathesias. Followed by unilateral headache, N/V. OPTHALMOPLEGIC headache, eye pain, third cranial nerve palsy. Dx if red flags present, Basic labs (CBC w/ diff, LFT, TSH, basic serum chem Na Cl K CO2 BUN Cr Glucose, ESR). EKG (consider if cardiac Hx, exam abnormal). EEG (not routinely used for headache workup). LP if suspicious of CNS infection, cancer, hemorrhage, or change in pressure. If mass lesion is suspected or pt has papilledema, defer LP until CT has been performed to reduce possibility of cerebellar herniation. Neuroimaging if high suspicion of bleed, trauma, or mass lesion. Patient w/ non acute headache and unexplained abnormal neuro findings. Avoid neuroimaging if they will not lead to change in management. Management GENERAL: establish Dx, patient education, establish realistic expectations, patient empowerment (diary, calendars), create formal management plan. NON DRUG THERAPY: eliminate triggers, biofeedback (takes a long time, though), relaxation, exercise, CBT, quite smoking, acupuncture, maintain regular eat/sleep pattern. PHARMACOLOGIC NONSPECIFIC: acute attack treatment can be ASA, NSAIDs, acetaminophen, caffeine; Triptans when OTC agents fail for mild-moderate attacks OR first line for moderate-severe attacks. Anti-nausea as needed like prochlorperazine, metoclopramide, Zofran. PHARMACOLOGIC SPECIFIC: ergotamine. Triptans (vasoconstrictor, enhance serotonin and/or dopamine blockade) more common i.e., sumatriptan, almotriptan, eletriptan, etc. Available in oral, rectal, nasal, sublingual, IM. Best if triptan is combined with naproxen. Prophylaxis: for people who have headaches >2-3x per month, migraines interfere w/ life. avoid triggers, sleep and eating hygiene, diary. ANTI-EPILEPTICS Topamax/Topiramate, valproic acid. CARDIOVASCULAR propranolol, verapamil, candesartan, guanfacine. ANTI-DEPRESSANTS amitriptyline, venlafaxine. MONOCLONAL ABYS v CGRP erenumab, fremanezumab, galcanezumab. ADJUNCTIVE Botox, riboflavin B2, butterbur. Guard against medication-overuse or rebound headache. Side effects or contraindications to Triptans and Ergots Triptans s/e include chest tightness from vasoconstriction, N/V, abdominal cramps, flushing, malaise. C/I: ischemic stroke or ischemic heart dz, uncontrolled HTN, pregnancy, hemiplegic or basilar migraines. Triptans should not be used within 24h of the use of ergotamines. Ergots older drug, effective but may cause rebound headache. selectively binds and activates serotonin (5-HT) 1D receptors located on intracranial blood vessels, including those on AV anastomoses, thereby resulting in vasoconstriction and reducing the blood flow in cerebral arteries that may lead to relieve of vascular headaches. C/I in pregnancy, CAD (cuz can cause coronary vasoconstriction), HTN, cerebrovascular or peripheral artery dz, hepatic or renal dz, migraines with prolonged aura.

bladder cancer

E.O.D.: Gross or microscopic hematuria. Irritative voiding symptoms. Positive urinary cytology in most patients. Filling defect within bladder noted on imaging. Epidemiology: men> women. mean age at diagnosis is 73 years. Cigarette smoking and exposure to industrial dyes or solvents are risk factors for the disease and account for approximately 60% and 15% of new cases. transitional cell carcinoma MC. S/S: Painless hematuria presenting symptom in 85-90% of patients w/ bladder cancer. Irritative voiding sx (urinary frequency and urgency) occur in a small % of patients as a result of the location or size of the cancer. Most patients w/ bladder cancer do not have signs of the disease because of its superficial nature. Abdominal masses detected on bimanual examination may be present in patients with large-volume or deeply infiltrating cancers. Hepatomegaly or palpable LAD may be present in patients with metastatic disease, and lymphedema of the lower extremities results from locally advanced cancers or metastases to pelvic lymph nodes.labs: reveals microscopic or gross hematuria in the majority of cases. On occasion, hematuria is accompanied by pyuria. Azotemia may be present in a small number of cases associated with ureteral obstruction. Anemia may occasionally be due to chronic blood loss or to bone marrow metastases. Exfoliated cells from normal and abnormal urothelium can be readily detected in voided urine specimens. Cytology can be useful to detect the disease initially or to detect its recurrence. Cytology is sensitive in detecting cancers of higher grade and stage (80-90%), but less so in detecting superficial or well-differentiated lesions (50%). There are numerous urinary tumor markers under investigation for screening or assessing recurrence, progression, prognosis, or response to therapy. imaging: Bladder cancers may be identified as masses within the bladder using ultrasound, CT, or MRI. However, the presence of cancer is confirmed by cystoscopy w/biopsy, with imaging primarily used to evaluate the upper urinary tract and to stage more advanced lesions. Treatments include surgery, biological therapy, and chemotherapy

botulism

EOD: Recent ingestion of home-canned or smoked foods; recovery of toxin in serum or food. Injection drug use. Diplopia, dry mouth, dysphagia, dysphonia; muscle weakness leading to respiratory paralysis; normal sensory examination. Pupils are fixed and dilated in most cases. Botulism is a paralytic disease caused by botulinum toxin, which is produced by Clostridium botulinum, a ubiquitous, gram +, strictly anaerobic, spore-forming bacillus found in soil. Botulinum toxin is a zinc metalloprotease that cleaves a specific component of the synaptic vesicle membrane docking and fusion complex at the neuromuscular junction blocking release of the neurotransmitter acetylcholine. Naturally occurring botulism exists in three forms: food-borne botulism, infant botulism, or wound botulism. Food-borne botulism is caused by ingestion of preformed toxin present in canned, smoked, or vacuum-packed foods such as home-canned vegetables, smoked meats, and vacuum-packed fish. Commercial foods have been associated with outbreaks of botulism. Infant botulism (associated with ingestion of honey) and wound botulism (often occurs in association with injection drug use) result from organisms present in the gut or wound that secrete toxin. S/s: 12-36h post-ingestion, visual disturbances (diplopia and loss of accommodation, Ptosis, CN palsies w/ impairment of EOM, and fixed dilated pupils). sensory exam is normal. Other sx are dry mouth, dysphagia, and dysphonia. N/v may be present. sensorium remains clear and the temperature normal. Paralysis progressing to respiratory failure and death may occur unless mechanical assistance is provided. Dx: Toxin in foods and patients' serum can be demonstrated by mouse inoculation and identified with specific antiserum. clinical presentation of botulism is so distinctive and the differential diagnosis limited Tx: procurement of equine serum heptavalent botulism antitoxin within 24 hours of onset of Sx. its admin should not be delayed for lab confirmation of the dx. Respiratory failure is managed with intubation and mechanical ventilation. Parenteral fluids or alimentation should be given while swallowing difficulty persists. The removal of unabsorbed toxin from the gut may be attempted. Remnants of suspected foods should be assayed for toxin. Persons who might have eaten the suspected food must be located and observed. Exposure to moist heat at 120° C (248° F) for 30 min kills the spores. Toxins, on the other hand, are readily destroyed by heat and cooking food at 80° C (176° F) for 30 min safeguards against botulism Honey (no honey for babies) - it is recommended that you wait until your baby is at least 12 months before introducing honey Treatment: Botulinum antitoxin

shigellosis

Gram-negative bacteria shigella that results in watery diarrhea or dysentery (the frequent and often painful passage of small amounts of stool that contains blood, pus, and mucus) The illness starts abruptly with diarrhea, lower abdominal cramps, and tenesmus accompanied by fever, chills, anorexia, headache, and malaise Stools are loose and mixed with blood and mucus. The abdomen is tender; dehydration is common Treat with TMP-SMX or ciprofloxacin HUS is a condition that can follow diarrhea caused by E. coli O157:H7 or Shigella dysenteriae

lymphoma

Hodgkin's Disease Lymphoma HIGHLY CURABLE - Painless lymphadenopathy + Reed-Sternberg + Bimodal Age (20s/50s) + B sx Age: Bimodal peaks in 20's then in 50's Reed-Sternberg Cells are pathognomonic - B cell proliferation with bilobed or multilobed nucleus "owl eye" Painless LAD: Upper body lymph nodes: neck, axilla, shoulder, chest (mediastinum) Contiguous spread to local lymph nodes: usually localized single group of nodes B symptoms are common - fever, weight loss, night sweats Associated with EBV (40% of patients) Dx: CXR - mediastinal adenopathy Tx: chemo, radiation, highly curable Excellent 5-year cure rate (60%) Non-Hodgkin's Lymphoma HIV patient + GI sx + painless LAD > 50 years old, increased risk with immunosuppression (ex HIV) B cells and T cells Peripheral, multiple nodes; non-contiguous extranodal spread (GI and skin = MC) B symptoms not common Not associated with EBV S/s: SOB, intussusception, bowel obstruction, abdominal masses tx: rituximab, chemo, variable course Variable cure rate

hydronephrosis

Hydronephrosis is caused by a blockage in the ureter Causes include a kidney stone, an infection, an enlarged prostate, a blood clot, or a tumor Symptoms include difficulty urinating and pain in the side, abdomen, or groin. Treatment: antibiotics if there's an infection. In severe cases, the urine may need to be drained from the bladder or kidney.

hypervolemia

Iatrogenic (parenteral overhydration); Fluid retaining states: CHF, nephrotic syndrome, cirrhosis, ESR, hypoalbuminemia Total body water increased Total body sodium increased Weight gain, peripheral edema (pedal or sacral), ascites Signs: Jugular venous distention, pulmonary edema (pulmonary rales) DX: Pulmonary artery catheter (Swan-Ganz) to measure CVP (definitive): elevated CVP and PCWP Low hematocrit or hypoalbuminemia Serum sodium may be low < 135 mmol/L decreased BUN/CR TX: Fluid restriction Judicious use of diuretics Monitor urine output and daily weights, consider Swan-Ganz catheter See fluid and electrolyte disorders

acute glaucoma

Increased IOP (>22) with optic nerve damage; an impediment to the flow of aqueous humor through trabecular meshwork; canal of Schlemm's with increasing pressure in the anterior chamber Open-angle = more common ⇒ > 40 yo, African Americans + family history ⇒ Acute angle-closure glaucoma ⇒ ophthalmic emergency - complete closure of the angle Classic triad: injected conjunctiva, steamy cornea, and fixed dilated pupil Painful eye/loss of vision, tearing, nausea, vomiting, diaphoresis IOP acutely elevated TX: Immediately refer to ophthalmology - start IV carbonic anhydrase inhibitor (acetazolamide), topical b-blocker (timolol), osmotic diuresis; laser/surgical iridotomy Mydriatics (to dilate pupils) should NOT BE ADMINISTERED! ⇒ Open-angle: chronic, asymptomatic, potentially blinding disease Increased IOP, defects in the peripheral visual field, increased cup to disc ratio Asymptomatic until late in the disease, loss of peripheral vision = main symptoms DX: can have elevated IOP without optic disc damage or optic nerve damage without increased IOP TX: should be referred to an ophthalmologist for close monitoring Prostaglandin analogs are the 1'st line (ex. latanoprost), β-blocker (Timolol), α-agonist, a carbonic anhydrase inhibitor to decrease production Laser or surgical treatment

erectile dysfunction

Occurs when a man can't get or keep an erection firm enough for sexual intercourse Psychological Organic causes include hypertension, neurological problems from diabetes, and hormonal dysfunction Medication side effects Nocturnal penile tumescence used to evaluate sleep erections Do not use with nitrates may cause hypotension Treat with phosphodiesterase 5 inhibitors Sildenafil (Viagra), Tadalafil (Cialis), Vardenafil (Levitra) Weight loss, smoking and alcohol cessation, hormone replacement and vacuum erection devices, and surgery from current: Organic and psychogenic erectile dysfunction most frequently occur in tandem, given that erectile dysfunction can cause emotional stress and decreased quality of life. Psychogenic erectile dysfunction typically occurs in young men and can generally be differentiated by patient history, whereby men will describe normal nocturnal or morning erections and situational erectile dysfunction.A trial of treatment with oral medications (type 5 selective phosphodiesterase inhibitors) is indicated for most men and may provide insight into the etiology and severity of erectile dysfunction. Patients with inadequate response to oral medications may undergo further evaluation with direct injection of vasoactive medications into the penis. These medications (prostaglandin E1, papaverine, phentolamine or a combination) induce erections in men with an intact penile vascular system. Patients who respond with a rigid erection require no further vascular evaluation.Additional testing is indicated in select patients who either do not achieve an erection after penile injection and who are candidates for complex reconstructive surgery. Duplex Doppler ultrasound can help assess penile vascular function and characterize normal and abnormal penile structural anatomy, including fibrosis or calcification from Peyronie disease. Penile cavernosography and pudendal arteriography are rarely performed but can distinguish arterial from venous erectile dysfunction and help predict which patients may benefit from vascular surgery.

cushing disease

PPP 413, esp. for treatment. also 449 corticotroph adenoma causes: benign ACTH-secreting pituitary adenoma located in the anterior pituitary (94%); however, about 6% are ectopic in locations such as cavernous sinus, sphenoid sinus, ethmoid sinus, or posterior pituitary. Cushing disease is at least 3x more frequent in women than men. S/S: vary. Early: complain of nonspecific symptoms, such as fatigue or reduced endurance but may have few, if any, physical Sx. Central obesity w/ moon face, buffalo hump, supraclavicular fat pads, protuberant abdomen & thin extremities eventually develop in most patients w/ Cushing syndrome. Muscle atrophy causes weakness. backache, HA, HTN, osteoporosis, avascular necrosis of bone, acne, superficial skin infections. oligomenorrhea or amenorrhea in women or ED in men. thirst +polyuria, renal calculi, glaucoma, purple striae especially around the thighs, breasts, and abdomen, and easy bruisability. Unusual bacterial or fungal infections are common. Wound healing is impaired. Mental sx may range from diminished ability to concentrate to increased lability of mood to frank psychosis. Hyperpigmentation is common with ectopic ACTH-secreting neoplasms that tend to produce very high plasma ACTH levels; hyperpigmentation is uncommon with pituitary Cushing disease. Labs: glucose tolerance is impaired d.t insulin resistance. polyuria is present as result of increased water clearance; DM w/ glycosuria may worsen it. leukocytosis w/ relative granulocytosis and lymphopenia. Hypokalemia especially if ectopic ACTH secretion. late night salivary cortisol determinations should be 150 or less; if consistently greater than 250, abnormal. midnight serum cortisol >200 indicative of cushing syndrome. If high late night cortisol or abnormal dex suppresion test, do 24 hour urinary free cortisol and creatinine. If hi 24 hour free cortisol (>140nmol/d) or free cortisol:creatinine ratio of >95=hypercortisolims.Once hypercortisolism confirmed, plasma ACTH and DHEAs. plasma ACTH <6pg/mL and low serum DHEAs indicated a propable adrenal tumor whereas higher levels are produced by pituitary or ectopic ACTH secreting tumors. Treatment: Patients must receive treatment for cortisol-dependent comorbidities, including osteoporosis, psychiatric disorders, diabetes mellitus, hypertension, hypokalemia, muscle weakness, and infections. Bone densitometry is recommended for all patients and treatment is commenced for patients with osteoporosis. surgical Tx for pituitary cushing disease w/ transsphenoidal selective resection of adenoma even if pituitary MRI is normal or inconclusive. remission 90%; post-op hyponatremia frequently so monitor serum Na x2weeks. 1-2 weeks post op screen for secondary hypothyroidism w/ serum T4. empiric hydrocortisone post op cuz pituitary corticotrophs remain suppressed. Continue replacement therapy until cosyntropin test is normal. MRI 3 mo. post-op. Eval for recurrent Cushing disease. May repeat transsphenoidal surgery OR may just go ahead and do a BL laparoscopic adrenalectomy. if ectopic ACTH-secreting tumors, surgical resection, if cannot be resected d/t poor localization/metastatic, lap BL adrenalectomy. Medical Tx w/ mitotane, ketoconazole, and metyrapon often suppresses the hypercortisolism. If metastatic and visible w/ Octreoscan, they have somatic receptors so treat with somatostatin analogs pasireotide or octreotide to slow progression of malignancy. for patients who decline surgery or unsuccessful, Tx mineralocorticoid HTN w/ spirinolactone, eplerenon, and dihydropyridine CCBs.

multiple sclerosis

Patho/etiology: AA, inflammatory demyelinating disease of the CNS of idiopathic origin. Associated w/ axon degeneration of white matter (brain & spinal cord). Most common in women & YA 20-40y/o, colder climates, HLA-DR2. types of MS relapsing-remitting disease: most common. episodic exacerbations. progressive disease: progressive decline without acute exacerbations. secondary progressive: relapsing-remitting pattern that BECOMES progressive. S/S: sensory disturbances (pain paresthesias) followed by weakness (fatigue, gait and balance problems) and visual disturbances (diplopia, optic neuritis) are most common presenting symptoms. Trigeminal neuralgia. Uhthoff's phenomenon is worsening of Sx w/ heat (exercise, fever, hot tubs, weather etc.). Spinal cord symptoms (bowel/bladder dysfunction). PE: UMN signs (spasticity, upward babinski, hyperreflexia, muscle rigidity). Lhermittes sign (neck flexion causes lightning shock type pain). Marcus-Gunn pupil w/ optic neuritis (pupils dilate in light). Internuclear opthalmoplegia is the inability to adduct eye on side of lesion with nystagmus in other eye. cerebellar Charcot's neurologic triad (nystagmus, staccato speech, and international tremor), ataxia. Spinal cord Sx bowel/bladder dysfunction. Dx: clinical (at least 2 distinct episodes of CNS deficits). MRI w/ gadolinium best initial & most accurate test; showing hyperintense white matter plagues. proof at least 2 areas of white matter involvement before Dx is made. LP indicated if negative MRI, showing increased IgG & oligoclonal bands. small discrete bands in the gamma globulin region seen on electrophoresis, which reflects inflammatory cells penetrating the BBB. Tx: acute exacerbation- hi dose IV glucocorticoids 1st line. Plasmapheresis if not responsive to glucocorticoids. prevention of relapse and progression- Treatment of progressive MS Relapse prevention, 1st line tx Interferon Beta 1a (Rebif) 44mcg subq three times a week Interferon Beta 1b (Aconex) 30 mcg IM q week Interferon Beta 1b (Betaseron, Extavia) 0.25 mg subq on alternate days Glatiramer acetate (Copaxone) 20 mcg sub q daily If still not ok and 1st line is already in use, Natalizumab, Fingolimod, Teriflunomide Glatiramer acetate, an interferon, or dimethyl fumarate often used initially d/t favorable s/e profiles and availability, although the efficacy of early treatment with higher intensity therapy is being explored. In general, the medications most effective in reducing relapses have stronger immunomodulatory effects and more, albeit rare, serious adverse effects. Prescription of these agents should be managed by a specialist. Ocrelizumab is the only medication effective in slowing disability progression in primary progressive MS and is approved for this indication by the FDA. For patients w/ active secondary progressive disease, cladribine, ocrelizumab, and siponimod can be used. For patients with severe disease, limited evidence supports immunosuppressive therapy with rituximab, cyclophosphamide, azathioprine, methotrexate, or mitoxantrone. Plasmapheresis is sometimes helpful in patients with severe relapses unresponsive to corticosteroids. Symptomatic therapy for spasticity, neurogenic bladder, or fatigue may be required. Fatigue is especially common in multiple sclerosis, and modafinil (200 mg orally every morning) is an effective and FDA-approved therapy for this indication. Dalfampridine (an extended-release formulation of 4-aminopyridine administered as 10 mg orally twice daily) is efficacious at improving timed gait in multiple sclerosis. Depression and even suicidality can occur in multiple sclerosis and may worsen with interferon beta-1a therapy; screening and conventional treatment of such symptoms are appropriate. residual Sx of MS even when in remission weakness, numbness, tingling, or unsteadiness in a limb; spastic paraparesis; retrobulbar optic neuritis; diplopia; disequilibrium; or a sphincter disturbance such as urinary urgency or hesitancy. What may cause an acute exacerbation of MS? A number of factors (eg, infection) may precipitate or trigger exacerbations. Relapses are reduced in pregnancy but are more likely during the 2 or 3 months following pregnancy, possibly because of the increased demands and stresses that occur in the postpartum period.

syphilis

Patho/etiology: spirochete Treponema pallidum and has increased in incidence over the last 10 years; associated w/ risk-taking behavior such as drug use. The disease has 3 phases, w/ an incubation period of about three weeks: Primary syphilis: presents as a painless ulcer (chance) in the genital or groin region x3-6 weeks Secondary syphilis: presents as an erythematous rash involving the palms and soles or a condyloma lata, which is similar to the lesions of primary syphilis in its infectivity but differs in appearance. Tertiary syphilis (latent): Affects about 30% and is a representation of widespread systemic involvement and can present with major vessel changes, such as in the aorta, permanent CNS changes (neurosyphilis), or even benign mucosal growths called gummas. Dx: RPR/VDRL and confirmed by the treponemal antibody-absorption test (FTA-ABS). Lyme disease can cause a false positive. Tx: Benzathine PCN G, 2.4 million units IM × one dose for primary and secondary disease. Additional doses if the infection has been for >1 year or if the patient is pregnant. If the patient is penicillin-allergic, treat with doxycycline. for Gummas and congenital/late dz, IV PCN G . Jerisch-Herxheimer reaction: fever, HA, myalgias within 1st 24h of Tx

Gastroesophageal reflux disease

Patho/etiology: Lower esophageal sphincter (LES) incompetence. Hiatal hernias, abnormal clearance (during sleep, Sjogren's, anticholinergic meds, oral radiation therapy), delayed gastric emptying (gastric paresis w/ DM, partial gastric outlet obstruction). Risk factors: alcohol/caffeine use, smoking. S/S: typical= heartburn aka pyrosis, often retrosternal and postprandial. increased with supine position and may be relieved w antacids. water brash, sour taste, cough, sore throat. atypical hoarseness, aspiration pneumonia, wheezing, chest pain. Alarm symptoms dysphagia, odynophagia, weight loss, bleeding. Testing: If patient has complicated disease refractory to empiric Tx and alarm features (troublesome dysphagia, odynophagia, weight loss, iron deficiency anemia), do endoscopy. Esophageal pH monitoring. Treatment: MILD—lifestyle changes (weight loss, avoid EtOH caffeine chocolate large meals, quit smoking, avoid citrus juice or tomato based foods, elevate head of bed, wait 3 hours after eating to recline), antacids. Can try Gaviscon or H2 blockers if Sx persist. MODERATE—Sx several times per week or daily but still uncomplicated, PPI x 4-8 weeks, assess. If good response, can continue for 8-12 weeks then d/c. Continuous therapy only in intermittent 2-4 week courses. SEVERE + EROSIVE—endoscopy. May not have GERD—may have other DDx. Ablation indicated if Barret's, poorly controlled symptoms, or extraesophageal manifestations (chronic cough, wheeze, dental, laryngeal). LINX device is a minimally invasive magnetic artificial sphincter for Tx of GERD. Patient education for GERD lifestyle changes (weight loss, avoid EtOH caffeine chocolate large meals, quit smoking, avoid citrus juice or tomato based foods, elevate head of bed, wait 3 hours after eating to recline), antacids. Warning signs of GERD that require further work-up troublesome dysphagia, odynophagia, weight loss, iron deficiency anemia

Parkinson's disease

Patho/etiology: Movement disorder d/t idiopathic loss of dopaminergic neurons in the substantia nigra --> failure of ACh inhibition in the basal ganglia (dopamine is inhibitory whereas ACh is excitatory). Affects dopamine's ability to initiate movement. Onset of Sx at 45-65 y/o. S/S: Triad: resting tremor, bradykinesia, muscle rigidity. Normal DTR, relatively immobile face. dementia is a late finding. Resting tremor often first finding; pill-rolling tremor of the hand. worse at rest and with emotional stress but improves with voluntary activity and sleep. usually confined to one limb or side for years before it becomes generalized. Bradykinesia manifests in lack of swinging arms when walking and shuffling gait. Rigidity is increased resistance to passive movement (cogwheel, fixed posture, festination). myersons sign tapping the bridge of nose repetitively causes a sustained blink. decreased blinking, seborrhea of skin common. Dx: Clinical. Post-mortem histology has shown cytoplasmic inclusions (Lewy bodies) and loss of pigment cells seen in the substantia nigra. Tx: Levodopa-carbidopa is most effective treatment. dopamine agonists (bromocriptine, pramipexole, ropinirole) may be used as initial treatment. Anticholinergics. Amantadine increases dopamine. MAO-B inhibitors selegiline, rasagiline. COMT inhibitors entacapone, tolcapone. Deep brain stimulation is extremely effective for rigidity and tremors in select patients. when you select a particular med, side effects of meds: Levodopa most effective but S/E of N/V, orthostatic hypotension, somnolence, headache. Psychosis/hallucinations upon initiation of therapy. Dyskinesia and akinesia. Long term use associated with decreased efficacy (use at lowest minimal dose to reduce this). if stopped abruptly, syndrome similar to neuroleptic malignant syndrome can occur. dont give within 2w of MAOi, or in AACG, or if psychotic illness. Dopamine agonists (bromocriptine, pramipexole, ropinirole) used 1st line in younger patients (<65) to delay use of Levodopa. S/E similar to Levodopa with less motor adverse effects but more frequent non-motor s/e like sleep disturbances, dizziness, impulse control, hyper-sexuality. anticholinergics (trihexyphenidyl, benztropine). Most useful as monotherapy in younger patients (<70) whose primary symptom is tremors w/o significant bradykinesia or gait disturbance as it does not improve bradykinesia. Adjunctive treatment if severe tremor despite L-dopa or dopamine agonist Tx. Adverse effects include anticholinergic (cant see cant spit cant pee cant shit, tachycardia). May worsen glaucoma and BPH. amantadine is low potency and can help early on with mild symptoms only. improves long term L-DOPA induced dyskinesia. Adverse effects include livedo reticularis and ankle edema. avoid in epileptic pts. Rare=confusion and hallucinations (elderly) Selective MAO-B inhibitors (selegiline, rasagiline) can be used as early therapy in patients with very mild S/S, may have neuroprotective properties. Adverse effects include nausea, headache, confusion, hallucinations. COMT inhibitors (entacapone, tolcapone) good for adjunctive Tx with L-Dopa as it prolongs the therapeutic dose in patients experiencing "wearing off" periods. NOT used as monotherapy. Adverse effects include nausea, orthostatic hypotension, hallucination, GI Sx, brown discoloration of the urine. talcapone associated with hepatotoxicity. seroquel if nighttime SX, sleep disturbances/sundowning. Deep brain stim helpful

Epidydimitis

Patho: based on patient's age and RF. men < 35 chlamydia and gonorrhea men > 35 E.coli S/s: dysuria, unilateral scrotal pain, and swelling. + Prehn's sign = relief with elevation is a classic sign Tx: Over 35-Levofloxacin (Levaquin) 500 mg/day PO for 10 days OR Ofloxacin 300 mg PO BID for 10 days Under 35 - doxy 100mg PO BID for 10 days PLUS ceftriaxone 250 mg IM × 1 Refer sexual partner(s) for evaluation and treatment if contact within 60 days of the onset of symptoms

acute respiratory distress/failure

Patho: diffuse alveolar damage and surfactant leads to increased permeability of the capillary-alveolar barrier, leads to noncardiogenic pulmonary edema (protein rich), shunting, and hypoxemia without hypercarbia ARDS can occur in those who are critically ill or who have significant injuries ⇒ sepsis (most common), severe trauma, aspiration of gastric contents, near-drowning S/S: acute dyspnea and hypoxemia. multi-organ failure if severe. Rapid onset of profound dyspnea occurring 12-24 hours after the precipitating event Tachypnea, pink frothy sputum, crackles Testing: Severe hypoxemia despite supplemental O2. CXR shows air bronchograms, bilateral diffuse pulmonary infiltrates without cardiogenic pulmonary edema. Normal BNP, pulmonary wedge pressure, left ventricle function and echocardiogram Tx: noninvasive or mechanical ventilation + tx the underlying cause. CPAP with full face mask, PEEP, and low tidal volume. identifying and managing underlying precipitation and secondary conditions Tracheal intubation with the lowest level PEEP to maintain PaO2 >60 mmHg or SaO2 >90 ARDS is often fatal, the risk increases with age and severity of illness

pericardial effusion

Pericardial effusion is excess fluid between the heart and pericardium Abnormal accumulation of inflammatory fluid, immune cells → diffuse into interstitium → fluid pools in pericardial space → pericardial dilation → pressure on heart, vena cava → decreased cardiac filling → cardiac tamponade → decreased cardiac output Causes: Aortic dissection, heart failure, hypoalbuminemia, lymphatic obstruction, malignancy, radiation, renal failure, trauma, autoimmune disease, acute pericarditis (viral, bacterial, tuberculous, idiopathic in origin), myxedema, some drugs, iatrogenic, idiopathic Same symptoms as acute pericarditis except patient will now have signs of fluid buildup around the heart which include low voltage QRS complexes, electrical alternans, distant heart sounds and an echocardiogram showing a collection of pericardial fluid EKG showing low voltage QRS along with electrical alternans Echocardiogram with increased pericardial fluid Radiograph: Water bottle heart Treatment: Underlying cause, pericardiocentesis if the effusion is large Electrical alternans as seen by changing QRS amplitudes best seen in lead II

HTN

Primary hypertension is defined as a resting systolic BP ≥ 130 or diastolic BP ≥ 80 on at least two readings on at least two separate visits with no identifiable cause ACC/AHA classification of BP Normal: < 120/80 mmHg and < 80 mmHg Elevated: 120-129 mmHg and < 80 mmHg Stage 1: 130-139 mmHg or 80-89 mm Hg Stage 2: ≥ 140 mm Hg or ≥ 90 mm Hg For children between 1 and 13 years of age: Normal BP: Both systolic BP (SBP) and diastolic BP (DBP) <90th percentile Elevated BP: SBP and/or DBP ≥90th percentile but <95th percentile, or 120/80 mmHg to <95th percentile (whichever is lower) Stage 1 hypertension: SBP and/or DBP ≥95th percentile to <95th percentile + 12 mmHg, or 130/80 to 139/89 mmHg (whichever is lower) Stage 2 hypertension: SBP and/or DBP ≥95th percentile + 12 mmHg, or ≥ 140/90 mmHg (whichever is lower) Treatment goals: Normal: evaluate yearly and encourage healthy lifestyle changes Elevated: Recommend healthy lifestyle changes and reassess in 3-6 months Stage 1: Assess ten-year risk using the ASCVD risk calculator If risk < 10% start healthy lifestyle management and reassess in 3-6 months If risk > 10% or CVD, DM, CKD - lifestyle mod + 1 medication - reassess in 1 month If goal met after 1 month - reassess in 3-6 months If goal not met after 1 month, consider different med or titrate Continue monthly follow-up until goal achieved Stage 2: Health lifestyle + 2 BP-lowering medications If goal met after 1 month - reassess in 3-6 months If goal not met after 1 month, consider different med or titrate Continue monthly follow-up until goal achieved Medications For NON-BLACK patients, including those with diabetes: Initial treatment should be with either: ACE inhibitor or ARB Long-acting CCBs (most often a dihydropyridine such as amlodipine) or a thiazide-like diuretic (chlorthalidone or indapamide) For stage 2 HTN: the recommendation is: 2 BP-lowering medications of different classes For BLACK adults 2+ meds are recommended to achieve a target of <130/80 mm Hg Thiazide-type diuretics and/or CCBs are more effective in black adults at lowering BP alone or in multidrug regimens Some antihypertensives are contraindicated or indicated in certain disorders: CCB's for angina pectoris ACEi or ARB for DM w/ proteinuria ACEi are associated with cough, angioedema and can cause hyperkalemia. They are C/I in pregnancy Spironolactone can cause hyperkalemia BB C/I in asthma and may cause impotence CCB cause leg edema Verapamil and diltiazem are rate control CCBs α-blockers treat HTN and BPH Hydralazine may cause lupus-like syndrome and can cause pericarditis Hypertensive urgency/emergency: URGENCY: BP usually > 180/120 WITHOUT signs of end-organ damage. partial reduction of BP w/ relief of symptoms is the goal. use clonidine, captopril, slow release nifedipine. Parenteral drug therapy is usually not required. clonidine preferred. EMERGENCY: BP usually >180/120 WITH impending or progressing end-organ damag. Parenteral therapy especially if encephalopathy present. initial goal is to reduce pressure by no more than 25% (within minutes to 1-2 hours) then toward a level of 160/100 (within 2-6 hrs). XS reductions in pressure may precipitate ischemia (so avoid oral or sublingual fast acting nifedipine). sodium nitroprusside preferred. MALIGNANT HTN: Diastolic reading > 140 associated with papilledema and either encephalopathy or nephropathy. Therapeutic approach is identical to that used in other hypertensive emergencies. hydralazine preferred.

peptic ulcer disease

RF: H. pylori infection > NSAIDs > "other"; ZE syndrome, chronic medical conditions causing hypersecretion, EtOH, smoking, stress, being male, being elderly, steroids. S/S: dyspepsia, GNAWING, dull, hunger-like abdominal pain that could be partially relieved by food or antacids. Nausea, pain after eating, anorexia. Abrupt change or worsening in pain may indicate penetration or perforation. PE usually benign unless perf or penetration; still vague. Testing: Labs may show anemia if bleeding ulcers, leukocytosis in perforation, elevated amylase if pancreas extension, fasting serum gastrin may be obtained if ZE suspected. Upper endoscopy can ID gastric or duodenal ulcers; both should be biopsied for H. pylori and cancer (cancer more likely in gastric than duodenal). Non-invasive breath test or fecal antigen assay can ID H. pylori; fecal looks at antigens, breath looks at presence of urea. PPIs can cause false negatives and should be held for 15 days before testing. Treatment: Quadruple therapy with PPI BID (anti-secretory), bismuth subsalicylate, tetracycline QID, Metronidazole TID. STOP NSAIDs, smoking. H2 blockers second line to PPI. Risk factors for perf: 5% of ulcer patients have a perf, usually those on the anterior surface of stomach or duodenum. S/S: sudden, severe abdominal pain 2ary to chemical peritonitis. atypical Sx in elderly or debilitated patients or those receiving long-term corticosteroid therapy; they may have minimal initial Sx and present LATE with bacterial peritonitis, sepsis, and shock. PE: ill-appearing w/ a rigid, quiet abdomen and rebound tenderness. Hypotension develops later after bacterial peritonitis has developed. (If hypotension is EARLY w/ onset of pain, other abdominal emergencies should be considered like ruptured aortic aneurysm, mesenteric infarction, or acute pancreatitis) Testing: labs will show leukocytosis, +/- a mildly elevated serum amylase. abdominal CT usually diagnostic. Treatment: laparoscopic closure of perforations.

prostatitis

S/s: Sudden onset of fever, chills, and low back pain combined w/ urinary frequency, urgency, and dysuria. Dx: Care should be taken to perform a gentle rectal examination, since vigorous manipulations may result in septicemia. Prostatic massage is contraindicated. Labs: CBC shows leukocytosis and a left shift. UA shows pyuria, bacteriuria, and varying degrees of hematuria. Urine or expressed prostatic secretions cultures will demonstrate the offending pathogen. Imaging: bc can progress to prostatic abscess, a pelvic CT or transrectal ultrasound is indicated in patients who do not respond to abx in 24-48 hours. Tx: Men < 35: Chlamydia and Gonorrhea - ceftriaxone and azithromycin (or Doxycycline) E coli in men > 35 - treat with fluoroquinolones or Bactrim x 1 month Chronic prostatitis - treat with fluoroquinolones or Bactrim x 6-12 weeks

thalassemia

SMARTYPANCE: Family history of blood cell disorder, Microcytic hypochromic, Elevated iron Beta thalassemia major Most severe, Mediterranean descent, failure to thrive Hemoglobin electrophoresis: Hemoglobin A2 and F Treatment: transfusion dependent. iron chelation (deferoxamine) Beta thalassemia trait Mild anemia, often misdiagnosed as iron deficient Hemoglobin electrophoresis: Hemoglobin A2 Alpha thalassemia Chinese and Southeast Asians Hemoglobin electrophoresis: Hemoglobin H (H disease), Hemoglobin Bart's (hydrops fetalis), Hemoglobin A (trait) HEM/ONC/ENDO CARD: S/S: alpha if minor (2/4 abnormal alleles) or silent carrier state (1/4 abnormal alleles) clinically normal, maybe mild microcytic anemia. no Tx needed. If alpha thal intermedia, there's 3/4 abnormal. Patients symptomatic at birth (neonatal jaundice & anemia). hepatosplenomegaly, pigmented gallstones/ increased bone marrow hematopoiesis (frontal bossing, maxilla overgrowth). beta trait/minor only 1/2 abnormal alleles so may be asymptomatic or have mild to moderate anemia. intermedia is mild homozygous so anemia, hepatosplenomegaly, bony disease. Major (Cooley's anemia) is 2/2 abnormal alleles and deficient beta chains will lead to XS alpha chains that cannot form tetramers, leading to ineffective erythropoiesis and shortened RBC life span. after 6 mo of life, when fetal Hgb diminishes, anemia (severe, chronic, pallor, irritability, dyspnea, mental delays. if hemolytic, jaundice and hepatosplenomegaly). extramedullary hematopoiesis bony abnormalities, abnormal and delayed skeletal dev., extramedullary expansion (frontal bossing, hair on end appearance of hte skull, abnormal ribs), osteoporosis bc by age 10 red marrow is replaced by inactive yellow marrow leading to OP compression fractures, cord compression, scoliosis, and disc degeneration. endo abnormalities d/t iron overload (hypogonadism, DM, growth failure, hypothyroidism). Enlarged kidneys, cardiac dysfunction (HF, arrhythmias) Labs: alpha CBC shows microcytosis, hemolytic anemia with schistocytes, tear drop cells, increased reticulocytes, target cells, basophilic stippling, increased RBCs, decreased hemoglobin. Positive heinz bodies. hemolysis so increased indirect bilirubin, decreased haptoglobin. Normal or increased iron. hemoglobin electrophoresis shows HbH (beta chain tetramer). beta CBC shows hypochromic microcytic anemia, normal or increased RBC count, normal or increased serum iron. HgB about 6. Peripheral semar shows target cells, teardrop cells, basophilic stippling, nucleated RBCs. Skull X-rays show bossing with hair on end appearance d/t extramedullary hematopoiesis. Treatment: Mild Thalassemia (alpha trait or Beta minor) No Treatment Hemoglobin/alpha intermedia Folate supplementation; avoid medicinal iron and oxidative drugs(sulfonamides) Severe Thalassemia Regular transfusions, Folate supplementation, Splenectomy, Iron chelation (subq infusion of deferoxamine) Allogenic bone transplantation (for Beta thalassemia Major; only curative tx) Risk factors & causes for alpha and beta thalassemia ALPHA gene deletion; reduced alpha chain synthesis. Since all adult hemoglobin has alpha chains, there is no change in percent distribution of hgb A, A2 and FExcess Beta chains may form a Beta4 tetramer called hemoglobin HUnstable and precipitate leading to damage of red blood cell membranes; leads to bone marrow and peripheral hemolysisdecreased alpha-globin chain production; 4 genes DELETIONS determine it. Most common in SE Asians, Africans, Mediterraneans. BETAGenetic hemoglobinopathy characterized by decreased production of beta-globin chains, leading to XS alpha chains. RF= most common in mediterranean (Greek, Italian), Africans, and Indians.Point mutation rather than deletionAbsent globin chain expression is termed Beta0Reduced synthesis are termed Beta+The reduced Beta chains lead to a different distribution of Hgb A, A2 and Fbeta thalassemia trait (minor) has 1/2 abnormal alleles and can range from asymptomatic (usually) to mild-moderate anemia. beta thalassemia intermedia is the mild homozygous form, presenting with anemia, hepatosplenomegaly, bony disease. beta thalassemia major or Cooley's anemia has both beta genes mutated. Deficient beta chain production leads to XS alpha chains that are not able to form tetramers. this lads to ineffective erythropoiesis and shortened RBC life span.

MI

STEMI: myocardial necrosis with acute STE or q waves; coronary artery completely blocked; full thickness of myocardial wall involved; elevated troponin I, troponin T, CK, CK-MB (serial troponins - 3 in 24 hours) Location: Anterior wall - STE in leads I, AVL, V2-V6 Inferior wall: II, III, AFV Lateral wall: lateral leads - I, AVL, V4-6 and reciprocal STD in inferior leads Posterior wall: ST depression in V1-3 Tx: (while waiting for revascularization) Supplemental oxygen 2-4 L/min for patients w/ oxygen saturation <90% or respiratory distress Nitroglycerin (NTG) sublingual 0.4 mg q5min for a total of 3 doses, followed by IV if ongoing pain and/or HTN and/or management of pulmonary congestion if no C/I exist such as systolic <90 mm Hg or >30 mm Hg below baseline, right ventricle (RV) infarct, use of sildenafil or vardenafil within 24 hours or within 48 hours of tadalafil Morphine sulfate 4-8 mg IV w/ 2 to 8 mg IV repeated at 5-15 min intervals to relieve pain, anxiety, or pulmonary congestion Antiplatelet agents: Aspirin (ASA), non-enteric-coated, initial dose 162 to 325 mg chewed A loading dose of a P2Y12 inhibitor is recommended for patients with STEMI for whom PCI is planned. Prasugrel or ticagrelor is preferred (better than clopidogrel). Prasugrel 60 mg loading dose should be given as soon as possible for primary PCI. Prasugrel is C/I in patients w/ previous cva/tia. Do not recommend in patients aged >75 years or lower body weight (<60 kg). Ticagrelor 180 mg loading dose. Ticagrelor may cause transient dyspnea. Clopidogrel 600 mg loading dose should be given if neither prasugrel nor ticagrelor is available. Duration of DAPT is controversial. Standard recommendation is 6-12 months after PCI, depending on bleeding and ischemia risks, but newer generation stents may not require DAPT longer than 1 month. Anticoagulation therapy: Unfractionated heparin (UFH) 70- to 100-U/kg IV bolus Enoxaparin 0.5-mg/kg IV bolus Bivalirudin 0.75-mg/kg IV bolus and then 1.75-mg/kg/hr infusion for up to 4 hours after procedure (Revascularization) PCI versus fibrinolysis: Goal is to keep total ischemic time within 120 minutes. Door to needle time should be within 30 minutes or door to balloon time within 90 minutes. Coronary reperfusion therapy Primary PCI (balloon angioplasty, coronary stents) in the following: Symptom onset of ≤12 hours Symptom onset of ≤12 hours and C/I to fibrinolytic therapy irrespective of time delay Cardiogenic shock or acute severe heart failure (HF) irrespective of time delay from onset of MI Evidence of ongoing ischemia 12 to 24 hours after symptom onset Radial access > femoral access. Fibrinolysis If presenting to a hospital w/o PCI capability and cannot be transferred to a PCI-capable facility to undergo PCI within 120 minutes of first medical contact If no c/i, administer within 12 to 24 hours of symptom onset, if there is evidence of ongoing ischemia. Alteplase (tPA): 15-mg IV bolus, followed by 0.75 mg/kg (up to 50 mg) IV over 30 minutes and then 0.5 mg/kg (up to 35 mg) over 60 minutes; maximum 100 mg over 90 minutes or rpA or TNK-tPA. Adjunctive antiplatelet therapy with fibrinolysis Adjunctive anticoagulation therapy with fibrinolysis NSTEMI: myocardial necrosis but coronary artery not completely blocked - rise in cardiac markers without STE or q wave Labs: Troponin at 2-4 hours, peaks 12-24 hours, lasts 7-10 days CK/CK-MB: appears at 4-6 hours, peaks 12-24, returns normal 48-72 hours Myoglobin: appears at 1-4 hours, peak is 12 hours, returns to baseline within 24 hours Tx: BB + NTG + aspirin and Plavix + heparin + ACE-I + stain + reperfusion (less time-sensitive than STEMI

tetanus

Tetanus results from a toxin produced by the anaerobic bacteria Clostridium tetani. The toxin makes muscles become rigid and contract involuntarily (spasm) Clostridium tetani spores are ubiquitous in soil. The spores germinate in wounds where the bacteria produce a neurotoxin (tetanospasmin), which interferes with neurotransmission at spinal synapses of inhibitory neurons. The result is uncontrolled spasm and exaggerated reflexes Puncture wounds are most susceptible. The elderly, migrant workers, newborns, and injection drug users are at particular risk The first symptom is pain and tingling at the site of inoculation. Later muscle spasms, respiratory muscle tetany, and lockjaw Gram-positive organism neurotoxin Transmission: Rusty nail TX: Treatment includes wound debridement, airway protection, benzodiazepines for muscle spasm, tetanus immune globulin immediately, and three doses of tetanus toxoid given by the standard schedule Metronidazole or penicillin is also administered to destroy the organism and prevent toxin production Prognosis: High mortality Vaccination: DTaP is usually given at 2, 4, 6, and 12 to 15 months, with an additional dose at 4 to 6 years Tdap adolescent preparation is recommended at age 11 to 12 years for those who have completed the recommended childhood DTP/ DTaP vaccination series and have not received tetanus and diphtheria toxoid (Td) booster dose Subsequent boosters of Tdap are recommended every 10 years

hypercoagulable state

The differential diagnosis can be remembered with the mnemonic PVCS: Platelets: too many (usually more than 1 million/μL) or overactive (TTP, Heparin-induced thrombocytopenia (HIT), HUS, and HELLP). Vascular injury: from plaques, trauma, or burns. Clotting factors: anti-clotting factors protein C, protein S, or antithrombin III deficient or not working. Stasis and Surgery. Virchow triad is blood stasis, hypercoagulable state, and vascular injury. Genetic causes include antithrombin III deficiency, factor V Leiden (activated protein C resistance), protein C deficiency, protein S deficiency, dysfibrinogenemia, and abnormal plasminogen. Acquired hypercoagulable states are associated with malignancy (Trousseau's syndrome), pregnancy, nephrotic syndrome, ingestion of certain medications (especially estrogen), immobilization, myeloproliferative disease, ulcerative colitis and Crohn disease, Behçet syndrome, polycythemia vera, intravascular devices, DIC, hyperlipidemia (particularly familial type II hyperbetalipoproteinemia), PNH, TTP-HUS, hyperviscosity syndrome, anticardiolipin antibodies, HIT, and antiphospholipid syndrome. Heparin therapy (unfractionated heparin [UFH] or low-molecular-weight heparin [LMWH]) can cause HIT, causing a decrease in platelets (usually in half), followed by platelet activation causing clotting and infarction. Lupus anticoagulant. An IgM or IgG immunoglobulin is seen in 5% to 10% of patients with SLE but is more common in persons without lupus or in those taking phenothiazines. Factor V Leiden (MC): procoagulant clotting factor - amplifies the production of thrombin → clot formation Mutated factor V resistant to breakdown by activated Protein C - results in hypercoagulability Symptoms/physical exam - Increased DVT and PE, especially in young patients Diagnosis with activated protein C resistance assay (factor V Leiden specific functional assay) - if positive, confirm with DNA testing. Normal PT/PTT Tx: LMWH bridge to warfarin; long term antithrombotic therapy not recommended Protein C Deficiency: vitamin K dependent anticoagulant liver protein that stimulates fibrinolysis and clot lysis (inactivates factor V and VIII) - potentiated by protein S Protein C deficiency causes an increased risk of recurrent DVT and PE. May have a family history Dx: protein C/S functional assay: decreased protein C / S activity levels At risk for skin necrosis on warfarin Tx: heparin and oral anticoagulation for life Protein S Deficiency: Protein S is a vitamin K-dependent glycoprotein. It serves as a cofactor for activated protein C, which inactivates procoagulant factors Va and VIIa, reducing thrombin generation Venous thromboembolism (VTE; including deep vein thrombosis and pulmonary embolism) is the major clinical manifestation of protein S deficiency Diagnose with Protein C or S functional assay (preferred) - ↓ protein C or S activity levels Tx: heparin / oral anticoagulation for life Antithrombin III Deficiency: recurrent venous thrombosis and PE, repetitive intrauterine fetal death (IUFD) Antithrombin III = natural anticoagulant; inhibits thrombin (IIa), Xa and other proteases; potentiated by Heparin Associated with VTE; first episode 20-30 y/o TX: Asymptomatic pt requires anticoagulation only before surgical proceduresPt with thrombotic events require high dose IV heparin then oral anticoagulation indefinitely Antiphospholipid Antibody Syndrome: autoimmune; often associated with SLE; characterized by thromboses and recurrent spontaneous abortions Autoantibodies react against platelet membranes, activating endothelial cells and platelets → complement-mediated thrombosis Dx: lupus anticoagulant, anticardiolipin, DRVVT test, prolonged PTTTx: high dose IV heparin with thrombotic events then oral anticoagulation indefinitely

diptheria

caused by corynebacterium diptheriae (gram + bacillus) exotoxin after inhalation of resp. secretions. Rare in the US due to routine vaccination at 2, 4, 6 and 15-18 months with a booster at 4-6 years of age S/s: neck swelling d/t enlarged cervical lymphadenopathy (bull neck). tonsillopharyngitis or laryngitis. myocarditis. fever. malaise. may be asymptomatic carrier. pseudomembrane- gray membrane friable pn the pharynx that bleeds if scraped. Dx: clinical. culture confirmation (using loffler medium or tellurite agar). Treat with antitoxin (horse serum) and antibiotic (penicillin or erythromycin) x2w. abx prevent the spread, antitoxin reduce sequelae and increase recovery time. respiratory droplet isolation until 2 consec cultures 24h apart are negative. serial ecgs and cardiac enzymes to assess for myocarditis. if endocarditis, pencillin +AG. close contact ppx w/ erythromycin x7-10d or penicillin G x1dose. Prevention: DTaP schedule- 5 doses 2,4,6 mo. and 15-18mo, 4-6y. Tdap booster- 11-12y/o, pregnant mothers and those around them, 10 year intervals after 11-22years OR after injury if last booster was 5+years ago.

cholecystitis

causes-- infl of gallbladder almost always gallstones; when a stone becomes impacted in cystic duct and inflammation develops behind obstruction. could be caused by infectious agents (CMV, cryptosporidiosis, microsporidiosis) in patients w/ AIDS, or by vasculitis (I.e. polyarteritis nodosa, Henoch-Schonlein purpura). ACUTE Sx include rapid onset of intermittent cramping abdominal pain in the RUQ, gradually becomes worse and lasts several hours; fever, nausea, and vomiting may be present in some cases. PE: RUQ pain, guarding, and a +Murphy's sign (significant tenderness w/ palpation in the RUQ w/ inspiration). CHRONIC follows a more indolent course w/ less severe Sx that are shorter in duration and are recurrent. women>men. The incidence increases w/ age + Murphy's sign = acute RUQ pain/inspiratory arrest with GB palpation Precipitated by fatty foods or large meals Classic Patient is: Fertile + Fat + Forty + Boas sign = referred pain to right subscapular area due to phrenic nerve irritation Chronic cholecystitis may lead to porcelain GB (premalignant condition) Dx: high WBC (12-15K), total serum bilirubin may be elevated w/o BD obstruction, serum AST and alk phos often elevated. serum amylase may be moderately elevated. Imaging RUQ USN is usually first test and may show gallstones but is not specific for acute cholecystitis (signs may be gallbladder wall thickening, pericholecystic fluid, and a sonographic Murphy sign). plain abdomen films may show gallstones in 15% of cases. HIDA scan most specific for acute, can show an obstructed cystic duct if bilirubin is < 5mg/dL, when clinical suspicion is high w/ an equivocal ultrasound or when acalculous cholecystitis is suspected. Specificity can be improved by IV morphine which induces spasm of sphincter of Oddi. CT may show complications of acute cholecystitis such as *perforation or gangrene*. QUICK FACTS: Serum bilirubin and AST levels are usually normal EXCEPT @ the time of an attack. Patients w/ chronic cholecystitis rarely have abnormal laboratory studies. A plain abdominal film will detect only 10% to 15% of cases of cholelithiasis Tx: Laparoscopic cholecystectomy is procedure of choice for uncomplicated acute and chronic cholecystitis. Stones can be composed of cholesterol (most common), pigment, or mixed. Early cholecystectomy is generally preferred, best done during the first 24 to 48 h in the following situations. Prophylactic cholecystectomy for asymptomatic cholelithiasis is generally not recommended. SURGICAL RECALL when will alk phos be elevated? In bile duct obstruction; alk phos is made in the bile duct epithelium. What serum total bilirubin-> jaundice? 2.5 what leads to itching w/ jaundice? bile salts in dermis How does HIDA work? radioisotope study where isotope is concentrated in liver and secreted into bile. will demonstrate cholecystitis (d/t nonopacification of gallbladder from obstruction of CD), bile leak, or CBD obstruction IOC? intraoperative cholangiogram to r/o choledocholelithiasis, gallstone in CBD.

DKA

causes: may be the initial manifestation of type 1 diabetes or may result from increased insulin requirements in type 1 diabetes patients during the course of infection, trauma, myocardial infarction, or surgery. may develop in patients with type 2 diabetes when severe stress such as sepsis or trauma is present. one of the more common serious complications of insulin pump therapy. Poor compliance is one of the most common causes of recurrent DKA. S/S: preceded by 1+ days of polyuria & polydipsia associated w/ marked fatigue, N/V. If unTx, mental stupor ensues that can progress to coma. Drowsiness is fairly common, frank coma only occurs in about 10% of patients. On PE, dehydration in a stuporous patient w/ rapid deep breathing and a "fruity" breath odor of acetone strongly suggests the Dx. Hypotension w/ tachycardia indicates profound fluid & electrolyte depletion, and mild hypothermia. Abdominal pain/tenderness may be present in absence of abdominal disease. cholecystitis or pancreatitis may occur w/ minimal S/S. Labs: plasma glucose of 350-900 mg/dL, serum ketones at a dilution of 1:8 or greater, hyperkalemia, slight hyponatremia, hyperphosphatemia, elevated BUN & serum creatinine levels, Acidosis may be severe (pH ranging 6.9-7.2 & serum bicarb ranging from 5-15); PCO2 is low (15-20 mm Hg) d/t compensatory hyperventilation. euglycemic DKA patient can have severe acidosis & fluid depletion but plasma glucose is only modestly elevated; usually <250 mg/day (13.9 mmol/L). This is seen in patients in whom DKA develops while receiving treatment w/SGLT2 inhibitors. DKA w/ lower glucose levels also occur in pregnancy and may reflect the expanded plasma volume & the increased glomerular filtration rate. Treatment: If mild (alert, 7.25-7.30) Tx in ED. If moderate (alert but 7.0-7.24) or severe (stuporose, <7), treat in ICU or step-down unit. Restore plasma volume & tissue perfusion, reduce blood glucose and osmolality, correct acidosis, replenish electrolyte losses, and ID/Tx precipitating factors. Gastric intubation if comatose to prevent aspiration. fluid replacement .9 NS (unless serum sodium >150, then .45%) start in ED ASAP 1L/hr then after 2L, 300-400mL/h. Once blood glucose is 250, change to 5% glucose to maintain glucose 250-300 and prevent hypoglycemia and cerebral edema. Insulin replacement after initiation of fluid replacement, give insulin IV .1unit/kg bolus. then IV dose of insulin .1unit/kg continuously infused or hourly IM injection. Potassium loss can be hi d/t polyuria & vomiting but serum will be hi b4 initiating Tx. As acidosis is corrected, hypokalemia may dev. if replacement isn't instituted with potassium chloride 10-30meq/h as long as patient is not uremic and has adequate urinary output. Dont start insulin until K+ is resolved if prevent hypokalemic. sodium bicarb is controversial but should be administered if arterial blood pH is 7 or less with careful monitoring.Add 1-2 ampules of NaCO3 to 1L of /45% saline with 20 mEq KCl and infused over 1-2 hours. repeat until arterial pH is 7.1. phosphate seldom required but if severe (less than 1mg/dL) develops during insulin therapy, give this per hour as K salt. Treat associated infection. transition to subQ insulin once DKA is controlled and patient is awake, able to eat. What can happen to a patient with DKA if you correct the electrolytes too rapidly? How do you prevent this complication? (1) development of hypokalemia from rapid shift of potassium into cells if the acidosis is overcorrected; (2) tissue anoxia from reduced dissociation of oxygen from hemoglobin when acidosis is rapidly reversed (leftward shift of the oxygen dissociation curve); and (3) cerebral acidosis resulting from lowering of cerebrospinal fluid pH.When blood glucose falls to approximately 250 mg/dL (13.9 mmol/L), the fluids should be changed to a 5% glucose-containing solution to maintain serum glucose in the range of 250-300 mg/dL (13.9-16.7 mmol/L). This will prevent the development of hypoglycemia and will also reduce the likelihood of cerebral edema, which could result from too rapid decline of blood glucose.

Complex regional pain syndrome

definition: formerly known as reflex sympathetic dystrophy (RSD). patho/etiology: autonomic dysfunction following bone or soft tissue injuries (eg. wrist or post-surgery). 30% have no Hx of injury demographics: MC effects upper extremities, women, >30y/o S/s: 4 main symptoms after an initiating event- 1. sensory: pain, hyperalgesia out of proportion to initial injury. 2. motor/trophic changes: decreased ROM and motor dysfunction with trophic changes (increased hair and nail growth initially then decreased growth) 3. edema or sweating changes 4. vasomotor: temp and skin color asymmetry with autonomic dysfunction Dx: mainly a clinical diagnosis. Radiographs may show patchy osteoporosis. Bone scintigraphy can show decreased uptake/activity. Diagnostic criteria: initiating event or immobilization persistent pain, allodynia, hyeralgesia Sx of edema, changes in skin BF, abnormal sudomotor activity No other obvious Dx Tx: NSAIDs. Physical and occupational therapy. anesthetic blocks, oral corticosteroids, TCAs, transcutaneous electric nerve stimulation. Vitamin C prophylaxis after fractures may reduce the incidence of CRPS.

hyperthyroidism

definition: production of too much thyroxine hormone. It can increase metabolism and accelerate the body's metabolism. Etiology: Grave's disease (autoimmune). Toxic adenoma, thyroiditis, pregnancy, amiodarone Presentation: Heat intolerance, palpitations, sweating, weight loss, tremor, anxiety, tachycardia Graves - Diffuse goiter with a bruit, exophthalmos, pretibial myxedema Thyroid storm - Fever, tachycardia, delirium Diagnosis: TSH (best test): Decreased in primary disease (↓ TSH and ↑ Free T4), elevated in secondary disease (↑ TSH and ↑ Free T4) T4: Elevated although may be normal Thyroid radioactive iodine uptake: Graves: Diffusely high uptake Toxic multinodular: Discrete areas of high uptake Antibodies: Graves: Anti-thyrotropin antibodies Treatment: BB (symptomatic), methimazole/propylthiouracil, radioactive iodine, thyroidectomy Thyroid storm- prompt beta-blockers, hydrocortisone, methimazole/PTU, iodine Thyroidectomy- most likely complication is injury to the recurrent laryngeal nerve (hoarseness) Antithyroid drugs during pregnancy and nursing PTU used to be the drug of choice during pregnancy because it causes less severe birth defects than methimazole. Experts now recommend that PTU be given during 1st trimester only. This is because there have been rare cases of liver damage in people taking it. After 1st trimester, women should switch to methimazole for the rest of the pregnancy. For women who are nursing, methimazole is probably a better choice than propylthiouracil (to avoid liver side effects) Thyroiditis Thyroiditis is a general term that refers to "inflammation of the thyroid gland". Thyroiditis includes a group of individual disorders causing thyroidal inflammation but presenting in different ways. Painful vs. Painless may be hypo or hyperthyroid Hashimoto's thyroiditis: Diffusely enlarged, painless, nodular goiter Subacute thyroiditis: Young women, after a viral infection Painful enlarged thyroid with dysphagia, mild fever Aspirin Postpartum thyroiditis: 1-2 months of hyperthyroidism after delivery Completely resolves, give propranolol for cardiac symptoms Suppurative thyroiditis: Fever, pain, redness, fluctuant mass. ↑ WBC Antibiotic/surgical drainage

cholangitis

infection of biliary tract. causes include choledocholithiasis (#1), stricture (post op), neoplasm (ampullary carcinoma), extrinsic compression (pancreatitis, pseudocyst)< ERCP, biliary stent. charcot's triad: classic picture of acute cholangitis 1. Fever 2. RUQ Pain 3. Jaundice Reynold's pentad: the above + mental status changes, shock/hypotension (if pus in biliary ducts) Dx: Charcot triad ORRR 2 elements and lab evidence of an inflammatory response (elevated WBC, CRP) elevated liver biochemical tests and imaging evidence of biliary dilation or cause of obstruction. leukocytosis, elevated bilirubin, elevated serum aminotransferase. If positive labs, IMAGING= USN/CT may show dilated bile ducts. EUS, Helical CT, and MRCP are accurate in showing bile duct stones and may be used in patients thought to be an intermediate risk for dev. bile stones (>55y/o, cholecystitis, bile duct diameter >6mm on US, serum bilirubin 1.8-4, elevated serum liver enzymes, pancreatitis). GENERAL Tx: abx for acute cholangitis. Biliary drainage with ERCP. Antibiotics in mild disease for 5 to 7 days; if blood culture positive, treat for 10 to 14 days. Once biliary drainage is achieved and patients are improved clinically, switch to oral antibiotics. Potential broad-spectrum regimens: Monotherapy with a β-lactam/β-lactamase inhibitor, such as ampicillin and sulbactam (3 g q6h) OR piperacillin/tazobactam (4.5 g q6h) OR ticarcillin/clavulanate (3.1 g q4h) PRIMARY SCLEROSING: multiple inflammatory fibrous thickenings of bile duct walls-> biliary strictures. RF: men aged 20-50. associated w/ IBD (UC>Crohn's) S/S: progressive jaundice, fatigue, pruritus, anorexia, and indigestion. May be Dx in presymptomatic phase d/t elevated alk phos level or a subclinical phase based on abnormalities on MRCP despite normal liver enzyme levels. Late in course may be osteoporosis, malabsorption of fat-soluble vitamins, and malnutrition. Testing: labs may show elevated alk phos, elevated or normal LFTs. MRCP shows segmental fibrosis of the bile ducts with saccular dilations b/w strictures. ERCP shows beads on a string. test patients for cholangiocarcinoma w/ CA 19-9 levels as 10% of pts --> cholangiocarcinoma. Tx: Intermediate doses of ursodeoxycholic acid 17-23 mg/kg/day have been reported to be beneficial for pruritis; NOT standard doses. stricture dilation for symptom relief. PRIMARY BILIARY: RF: middle-aged women, sjogrens, AA thyroid dz, Raynaud, scleroderma, hypothyroidism, celiac dz. S/S: asymptomatic for years; insidious onset of fatigue and pruritis. W/ progression, PE reveals hepatosplenomegaly. xanthomatous lesions on skin, tendons and around eyelids. Jaundice, steatorrhea, and portal HTN are late findings. Testing: labs show elevated alk phos, cholesterol (especially HDLs and lipoprotein X) and, in later stages, bilirubin. anti-mitochondrial abys are present in most at a ratio > 1:40, and Serum IgM elevated. Treatment: PBS TX= ursodeoxycholic acid 13-15mg/kg/day preferred; slows progression of dz and stabilizes. If incomplete response or intolerance, try obeticholic acid 5 mg QD PO increased to 10 mg @ 6 months. PRURITIS TX= cholestyramine 4g in water or juice TID for pruritis. the 5-HT3 serotonin receptor antagonist, ondansetron 4mg PO TID PRN as an alternative. If refractory, plasmapheresis or extracorporeal albumin dialysis may be needed. definitive tx is liver transplant.

Vitamin B12/folate deficiency

macrocytic anemia causes: vitamin B12 deficiency (decreased intake or decreased absorption bc of pernicious anemia or other malabsorbtive disorders, PPIS/H2 blockers, metformin, alcohol use) or folate deficiency (inadequate intake #1 cause w/ EtOH abuse or bad diet, increased requirements like preg/infant/hemolytic anemia/malignancy/psoriasis, impaired absorption, impaired metabolism, or loss thru dialysis). S/S: B12 only neuro Sx, increased methylmalonic acid. folate only no neuro Sx, normal methylmalonic. BOTH anemia, macrocytosis, macro-ovalocytes, decreased reticulocytes, hypersegmented neutrophils, increased homocysteine. Labs: BOTH increased LDH, increased homocysteine, increased MCV (macrocytic anemia), megaloblastic anemia (hypersegmented neutrophils, macro-ovalocytes, milk leukopenia and/or thrombocytopenia), low reticulocytes. B12 low serum B12, increased methylmalonic acid. Folate decreased serum folate, NORMAL methylmalonic acid. Treatment B12 Parenteral therapy w/ M/subq doses of 100mcg-1000mcg q day x 1 week; q week x 1 month and then monthly for lifeOnce correction of Sx, oral cobalamin may be used since 1% of dose is absorbed 1mg/day indefinitely If neuro Sx: long term parenteral therapy; folic acid therapy as well since may have concomitant deficiency, Immediate improvement in their sense of well being Hypokalemia may complicate first several days of therapy Reticulocytosis in first 5-7 days; clinical picture normalizes in 2 months CNS symptoms resolve if < 6 months in duration but become permanent if not treated promptly Folate Folic Acid replacement of 1mg/dResponse similar to what is see in Vitamin B12 deficiency Rapid improvement and sense of well being within 5-7 days Correction of hematologic abnormalities in 2 months Large doses may correct symptoms of B12 deficiency except for the neurologic damage How would you differentiate between folic acid deficiency anemia and B12 deficiency anemia? B12 deficiency will have elevated methylmalonic acid whereas it is normal in folate. This is bc B12 usually interacts with methylmalonic acid to make CoA in the body, so if we are deficient in it, it will just be running around free! not to mention, serum folate will be decreased if folate and b12 if b12.

glomerulonephritis

nephritic syndrome; E.O.D. is hematuria (RBC casts) with subnephrotic proteinuria. dependent edema, HTN. AKI (intrinsic)Patho/etiology: 5 possible causes; use serology to ID. 1. immune complex deposition moderate overproduction of antigen compared to antibody production. Complexes formed w/ marked antigen excess tend to remain in the circulation. IgA nephropathy, infection-related glomerulonephritis, lupus nephritis, and cryoglobulinemic glomerulonephritis (often associated w/ HCV). 2. Anti-GBM injury is related to autoantibodies against type IV collagen in the GBM rather than to immune complex deposition. either confined to the kidney or associated with pulmonary hemorrhage. The latter is Goodpasture syndrome. Pauci-immune small-vessel vasculitis associated w/ ANCAs, causing kidney diseases w/o direct immune complex deposition or antibody binding. injury is believed to be due to cell-mediated immune processes. i.e. granulomatosis w/ polyangiitis, a systemic necrotizing vasculitis of small arteries & veins associated w/ intravascular &extravascular granuloma formation. ANCA. 3. monoclonal IG-mediated deposition of a monoclonal immunoglobulin in glomeruli or tubular basement membrane or both. It is detected on immunofluorescent or immunohistochemical staining of kidney biopsies as monotypic immunoglobulin deposits. 4. C3 glomerulopathy results from predominant C3 deposition in the glomeruli w/ or w/o minimal deposition of immunoglobulins. It is also identified by immunofluorescence or immunohistochemistry. The pathogenesis of C3 glomerulonephropathy stems from abnormalities in regulation of the alternative pathway of complement. While checking the serum C3 level may be helpful, normal levels do not rule out C3 glomerulopathy. 5. Other hypertensive emergencies and the thrombotic microangiopathies such as hemolytic-uremic syndrome and thrombotic thrombocytopenic purpura S/S: hypertensive and edematous with an abnormal urinary sediment. The edema is found first in body parts with low tissue tension, such as the periorbital and scrotal regions. Labs: Serum creatinine can rise over days to months, depending on the rapidity of the underlying process. Dipstick and microscopic evaluation will reveal evidence of hematuria and typically subnephrotic proteinuria; there may be cellular elements such as dysmorphic red cells, red cell casts, and white cells. Red cell casts are specific for glomerulonephritis. spot urinary protein-creatinine ratios or 24-hour urine collections can quantify protein excretion; the latter can quantify creatinine clearance when renal function is stable.Additional tests include serum complement levels (C3, C4, CH50) that may be low in immune complex glomerulonephritis (except for IgA nephropathy) or C3 glomerulopathy and normal in pauci-immune, anti-GBM-related, and monoclonal immunoglobulin-mediated glomerulonephritides. Other tests include ASO titers, anti-GBM antibody levels, ANCAs. With few exceptions, a kidney biopsy is ultimately necessary to confirm the diagnosis, irrespective of laboratory data.

acute interstitial nephritis

patho/etiology: AIN= always involving NSAIDs, always involving neutrophils. Drugs - 5 Ps. Pee (diuretics, especially sulfa ones) Pain-free (NSAIDs) Penicillins and cephalosporins Proton pump inhibitors rifamPin Immunologic and infectious disease: strep, SLE, CMV, Sjogren's, Sarcoidosis inflammatory or allergic response in the interstitium with sparing of the glomeruli. S/S include fever, eosinophilia, maculopapular rash and arthralgia. WBC CASTS and eosinophiluria on UA. modest proteinuria (esp if NSAID induced) increased serum IgE and eosinophils. Diagnose with renal biopsy - will see interstitial inflammatory cell infiltrates Treat by discontinuing the offending drug, corticosteroids, Dialysis if needed, usually self-limiting if caught early

myasthenia gravis

patho/etiology: autoimmune peripheral nerve disorder d/t autoantibodies against the acetylcholine (nicotinic) postsynaptic receptor on the muscles, leading to weakness. MC in young women <40 and older men >50. strong association w/ an abnormal thymus gland (75%). S/S: 2 main clinical manifestations: ocular weakness and generalized weakness. weakness worse w/ repeated use and throughout the day. 1st ocular sx diplopia and ptosis; pupils are spared. generalized weakness includes bulbar/oropharyngeal weakness with prolonged chewing, dysphagia, dysphonia, dysarthria and respiratory muscle weakness, which may lead to respiratory failure (myasthenic crisis) Dx: (outpatient) ACR ABYs first choice. If ACR ABYs negative, do MuSK ABYs. EMG. Chest imaging (CXR, CT, MRI) in all patients to detect thymus gland abnormalities. (emergent setting) edrophonium/tensilon test will show brief improvement of Sx after administration. Ice pack test; application of ice x10 min improve ocular Sx. Tx: if myasthenic crisis or severe, plasmapheresis or IVIG. Long term treatment includes acetylcholinesterase inhibitors (neostigmine or pyridostigmine) 1st line. glucocorticoid, or azathioprine, cyclosporine. If no improvement with medical management, thymectomy even if thymus gland is normal because it can improve Sx and remove source of ABYs. AVOID fluroroquinolones, aminoglycosides, beta blockers as they all exacerbate MG. Cholinergic crisis definition and treatment. Definition: condition that develops as a result of overstimulation of nicotinic and muscarinic receptors at the NM junctions and synapses usually d/t the inactivation or inhibition of acetylcholinesterase (AChE), the enzyme responsible for the degradation of acetylcholine (ACh). Excessive accumulation of acetylcholine (ACh) --> sx of both muscarinic and nicotinic toxicity. These include cramps, increased salivation, lacrimation, muscular weakness, paralysis, muscular fasciculation, diarrhea, and blurry vision Treatment: stabilization of the patient and the removal of the offending toxic agent. ABCs! indications for advanced airway management and intubation in cholinergic crisis are: -Copious oral and nasal secretions compromising the patency of the airway -AMS w/ GCS <8 -Evidence of hemodynamic instability -Profound weakness of the respiratory muscles Vascular access should be established immediately with 2 large-bore peripheral IV access. Fluid should be started to maintain adequate circulation with continuous pulse oximetry and monitoring of vital signs. In the case of hemodynamic instability, central venous access should be established for infusion of vasoactive medications. Two types of antidotes are used for a cholinergic crisis: atropine and oximes. Atropine is an effective agent for the muscarinic effect of acetylcholine. It competitively binds to the postsynaptic muscarinic receptor thereby preventing further action of ACh. give atropine until signs of atropinization is present: Tachycardia,Warm, dry, flushed skin, Mydriasis oximes For the nicotinic effect in cholinergic crisis, the antidote is a class of drugs called the "oximes." Examples of oximes are pralidoxime and obidoxime. "molecular crowbar" that separates the bonded nerve gas or organophosphate from acetylcholinesterase. The separated AChE can then continue the process of chemical breakdown of ACh. other: seizure medication if seizing. When should patients be considered for a thymectomy in MG? in all patients under 65 y/o UNLESS weakness is restricted to extraocular muscles only. also ALL patients with thymoma

encephalitis

patho/etiology: infection of the brain parenchyma; HSV #1 cause. VZV, EBV, measles, mumps, rubella, HIV, St. Louis virus S/s: meningeal Sx include HA, neck stiffness, photosensitivity, fever, chills, N/V, seizures. The presence of AMS changes in personality, speech, and movement distinguishes encephalitis from aseptic meningitis (tho bacterial meningitis can have this stuff sometimes too, but cultures would be +). PE: focal neuro deficits. Dx: CT head to r/o space occupying lesions. LP after CT will show normal glucose, increased lymphocytes (similar to aseptic meningitis). MRI preferred for encephalitis; temporal involvement characteristic for HSV. PCR testing of CSF fluid is most accurate test for herpes encephalitis. Tx: IV acyclovir; early empiric treatment for HSV encephalitis should be initiated ASAP if encephalitis with no obvious cause. supportive Tx.

cardiac tamponade

patho/etiology: pericardial effusion causing significant pressure on the heart, impeding cardiac filling leading to decreased cardiac output and eventually shock (medical emergency). complication of acute pericarditis or trauma. Malignancy is the most common nontraumatic cause of tamponade. S/S: Beck's triad (distant or muffled heart sounds + increased JVP + systemic hypotension). pulsus paradoxus (exaggerated >10 mmHg decrease in systolic BP with inspiration). dyspnea, fatigue, peripheral edema, shock, reflex tachy, cool extremities. Testing: Echocardiogram pericardial effusion + diastolic collapse of cardiac chambers. ECG signs of pericardial effusion (low voltage QRS, electrical alternans). CXR may show enlarged cardiac silhouette "water bottle heart" Treatment: immediate pericardiocentesis to relieve pressure. volume resuscitation and pressor support if needed. pericardial window drainage if recurrent.

fibromyalgia

patho: central sensitization to pain; increased nociceptive signals, decreased anti-pain signals. may be a genetic component. may be primed by previous traumatic events (adverse childhood events, trauma, rape, war). Poor sleep contributes. S/S: chronic widespread pain (arthralgia, myalgia), fatigue, brain fog, various somatic complaints. overlap with regional functional disorders (IBS, HAs, vulvodynia). Females > males. Sx onset in adolescence or young adulthood. Workup: Hx, PE. Basic labs (CBC, thyroid, chem, +/- CRP). Avoid diagnostic fishing and testing for auto-immune conditions. 2011 ACR fibromyalgia criteria with 2016 revision is a survey based Dx tool. Score combines # of patient reported pain sites and somatic symptoms; easy to administer. Treatment: Cymbalta/duloxetine, Lyrica/pregabalin (acts on Ca++ channel), Savella/milnacipran (SNRI). Some off-label treatments as well. Adjunctive treatments include exercise (pool>land based), sleep optimization, treat underlying mood disorder, mindfulness, alternative medicine.

HIV

retrovirus that changes viral RNA --> DNA using reverse transcriptase. HIV1>HIV2 Acute seroconversion: 10-60% of pts do NOT have symptoms those that do--> flu like or mono like illness within 2-4w of infection (fever, fatigue, myalgias, generalized LAD, sore throat, weight loss). during this phase they are HIGHLY INFECTIOUS. Opportunistic infections: oral and esophageal candidiasis MC. CMV, PCP pneumonia, cryptosporidiosis. AIDS CD4 <200. recurrent severe and potentially life threatening infections or opportunistic malignancies. AIDS associated dementia/encephalopathy, HIV wasting syndrome. Labs associated with early HIV infections viral RNA usually high >100,000 often in millions and CD4+ count can drop transiently. leuks and lymphs vary during acute illness. CD4 count tend to be lower than CD8 count. elevated LFTs, mild anemia, thrombocytopenia. Dx of suspected early infections: combo antigen/ab immunoassay + HIV viral load testing via RT-PCR. If both are negative with high suspicion, repeat both tests within 1-2w. negative screening + positive virologic tests suggest early HIV. Positive screening with positive virologic tests suggest early or established infection. confirm with second test (repeat HIV RNA or serologic test) several weeks later--> + screening immunoassay should prompt a second antibody-only immunoassay. HIV RNA viral load can be + in window period and is also used to monitor infectivity and treatment effectiveness. routine screening for HIV infection 4th gen antigen/ab combo HIV1-2 immunoassay. It detects both HIV1 and HIV2 antibodies as well as HIV P24 antigen (viral core protein that appears in blood as the viral rna level rises following infection). if 4th gen assay is negative --> theyre not infected. if positive --> confirmatory HIV1/HIV2 ab differentiation immunoassay performed. if confirmatory test is positive, a plasma HIV RNA should be obtained to eval for acute infection. if confirmatory is negative or indeterminate, plasma HIV RNA should be performed. HIV RNA also performed in patients with concern for acute HIV infection. Management: ART for all HIV+ patients including asymptomatic regardless of CD4. test resistance before initiation. for treatment naive--> 2 diff NRTIs + INSTI (I.e. dolutegravir plus tenofovir/alafenamide-emtricitabine or bictegravir-emtricitabine-tenofovir) Abacavir C/I if HLAB*5701+ bc increased risk of HS RXN. If unable to take tenofovir or abacavir, do dolutegravir + lamivudine plus a boosted PI plus an NSTI or a boosted PI plus lamvudine. NNRTI= non nucleotide reverse transcriptase inhibitor NRTI=nucleotide reverse transcriptase inhibitor PI= protease inhibitor INSTI= integrase strand transfer inhibitor POST EXPOSURE PROPHYLAXIS PEP should be started within 72 hours of exposure The chances of contracting HIV from a needlestick injury involving a patient with known HIV is < 0.3% Testing should be done on the worker and the patient - resting at 6 weeks, 3 months and 6 months Can take antiretrovirals - combo therapy with drugs from different classes should be continued for at least 4 weeks, full course PEP reduces the chance of HIV transmission by up to 70%

Bronchiectasis

Definition: Permanent and irreversible dilation of the bronchial airways Patho: dilation of the airways and impairment of the mucociliary escalator --> repeat infections, airway obstruction, and peribronchial fibrosis. H. flu cause if no CF, P. aeruginosa cause if CF. S/S: persistent productive cough w/ thick sputum, dyspnea, pleuritic pain. hemoptysis possible d/t bronchial artery erosion. PE will show rales, wheezing, rhonchi. Testing: You're prob gonna do CXR first, which is usually abnml but nonspecific; findings include linear atelectasis, tram track appearance, and increased bronchial markings. High-resolution CT scan preferred imaging and shows thickened bronchial walls, airway dilatation, and lack of tapering of the airway (tram-tracks), signet ring sign (increased airway diameter > adjacent vessel diameter). PFTs are the gold standard and show an obstructive pattern that is NOT fully reversible (unlike asthma): decreased FEV1, decreased FEV1/FVC <70% predicted, decreased FVC. Hyperinflation so will show increased volumes (RV, TLC, RV/TLC, FRC). Tx: Conservative Tx includes chest physiotherapy for mucus clearance, mucolytics, bronchodilators. Empiric oral ABX therapy x10-14 days (Amoxicillin or Augmentin; ampicillin or tetracycline; TMP/SMX; Cipro) Prevention: 6-12 months macrolides OR inhaled aminoglycosides in CF patients w/ copious purulent sputum.

hypocalcemia

Definition: serum total calcium < 8.4 mg/dL ionized fraction of calcium < 4.4 mg/dL Presentation: QT prolongation, Trousseau's sign, Chvostek's sign Labs: ↓ Ca+ ↓ PTH ↑ phosphate EKG = Prolonged QT Treatment: IV calcium gluconate or calcium chloride

hypercalcemia

Definition: serum total calcium > 10.5 mg/dL ionized fraction of calcium > 5.6 mg/dL Presentation: "Stones, Bones, abdominal groans, psychiatric moans". EKG: shortened QT interval. Associated with malignancy and hyperparathyroidism Treatment: IV normal saline and furosemide

Hypothyroidism

Etiology: Hashimoto's (chronic lymphocytic/autoimmune), previous thyroidectomy/iodine ablation, congenital Presentation: Cold intolerance, fatigue, constipation, depression, weight gain, bradycardia Congenital: round face, large tongue, hernia, delayed milestones, poor feeding ("cretinism") Labs: TSH- elevated in primary disease. Low T4 (↑ TSH and ↓ Free T4) Hashimoto's: Antithyroid peroxidase, antithyroglobulin antibodies Treatment: Levothyroxine. Follow up with serial TSH monitoring

gout, pseudogout

GOUT Patho/etiology: inflammatory arthritis caused by monosodium urate (MSU). Caused by bodily mishandling of uric acid, a byproduct of purine metabolism. Over production or under excretion. Idiopathic (more common) or secondary (renal transplant, lead, inherited enzyme defects). S/S: Sudden onset of very painful monoarthritis (classically effects 1st MTP joint first, then midfoot, ankle, knee, elbow, wrist, finger). May be accompanied by prodromal features (fever, chills, extremity discomfort/paresthesia). Will resolve spontaneously in days to weeks even without treatment. Will have asymptomatic, intercritical periods but chronic gout can lead to destructive arthritis. Can be exacerbated by events such as surgery or illness. Crystals coalesce into tophaceous deposits that collect in joints and organs. Diagnostics: testing serum uric acid plays limited role; better for monitoring than Dx. Gold standard is synovial fluid aspiration for cell count and crystal analysis, look under polarized light microscopy which will show needle-shaped, negatively birefringent. Commonly diagnosed with clinical criteria. X-Rays limited role until gout has progressed. Labs during flare may show elevated WBC, high CRP/ESR. Treatment: acute treatment includes colchicine (1.2mg for first dose then follow with .6 mg an hour later; taken ASAP), PO NSAIDs, corticosteroids (prednisone 30mg daily x 2 days, decrease by 5 mg every 2 days), supportive (off-loading, ice). Chronic treatment includes urate lowering therapy allopurinol, febuxostat, probenecid. Add prophylactic therapy daily to prevent flares (colchicine, naproxen, or prednisone 5mg or less if CKD at least 3-6 months). Monitoring: check serum uric acid at baseline and monitor; keep it less than 6 mg/dL or less than 5 if patient has severe, tophaceous arthritis. Check SUA, CBC, liver and kidney function 1-2 weeks with ULT dose change, decrease monitoring frequency once SUA is stable and patient is asymptomatic. PSEUDOGOUT AKA calcium pyrophosphate deposition disease Patho/etiology: caused by calcium pyrophosphate crystal deposition; much less understood as opposed to gout. Commonly affects medium to large joints (knee, wrist, ankle). worse during illness or surgery. chondrocalcinosis commonly present in knee and wrist radiographs in asymptomatic patients. S/S: acute onset of monoarthritis usually in knee, wrist, or ankle. may be milder than a true gout flare but sometimes more severe. rarely can deposit in areas like the odontoid process causing a meningitis-like picture (crowned dens syndrome). chronic forms of CPPD can mimic osteoarthritis and even RA. Diagnosis: joint aspiration looking for rhomboid-shaped positively birefringent crystals. inflammatory pattern=increased WBCs. Plain films can be supportive sometimes to look for chondrocalcinosis at the joint. Treatment: Tx acute flares with steroids (PO or joint injection). Prophylactic care includes colchicine or NSAIDs.

hiatal hernia

Herniation of structures from the abd cavity thru the esophageal hiatus of the diaphragm. Sliding/Type I: GE junction slides into the mediastinum increasing reflux. MC type. Paraesophageal/Type II: Rolling hernia; fundus protrudes thru diaphragm with the GE junction remaining in its anatomic location. S/s: usually asymptomatic, incidental finding. May develop intermittent epigastric or substernal pain, postprandial fullness, retching or nausea. Tx: Sliding/type 1- manage GERD (PPIs, weight loss). Paraesophageal/rolling/type 2- surgical repair if complications (volvulus, obstruction, strangulation, bleeding, perforation).

Hypoventilation syndrome

Hypoventilation syndrome may be secondary to several mechanisms, including central respiratory drive depression (drugs -narcotics, benzodiazepines, neurologic disorders - multiple sclerosis, etc.), neuromuscular disorders (ALS, myasthenia gravis, etc.), chest wall abnormalities, obesity hypoventilation, and COPD Obesity hypoventilation syndrome (OHS), also known as Pickwickian syndrome, is a condition in which severely overweight people fail to breathe rapidly or deeply enough, resulting in low oxygen levels and high blood carbon dioxide (CO2) levels. S/s: sluggish/sleepy during day Sequelae: pulmonary HTN, cor pulmonale, secondary erythrocytosis DX: PFTs, sleep studies, CXR, arterial blood gas, serum bicarb TX: lifestyle, healthy weight, physical activity, CPAP, tracheostomy Sleep apnea falls into this category BUT Pickwickian will have hypoventilation while awake.

esophagitis

INFECTIOUS RF: common in immunocompromised patients. Most common causes are candida albicans (especially DM, steroid users), Herpes simplex, CMV (especially AIDS). S/S: odynophagia, dysphagia, substernal chest pain, candida esophagitis will have thrush, CMV may be present in colon and retina as well.Testing: endoscopy biopsy and brushings. Candida esophagitis will show diffuse, linear, yellow-white plaques adherent to mucosa. CMV esophagitis will have one to few large, shallow, superficial ulcerations. Herpes simplex will show multiple small, deep ulcerations. Treatment: candida esophagitis can be treated even without endoscopy; treat with fluconazole 400 mg qd PO x 14-21 days. CMV if HIV+ (which they usually are), treat with HAART + ganciclovir. Herpes (usually immunosuppressed) treat with oral acyclovir 400 mg x5 daily x14-21 days. EOSINOPHILIC RF: Patients generally have a history of atopy or other allergies. S/S: chronic dysphagia, food impaction. Testing: Serum testing demonstrates eosinophilia or IgE. Endoscopy with Bx required to establish Dx. Results vary; normal in some, others have rings, exudates, or strictures. Treatment: Trial of PPI BID x 2 months. Further Tx, refer to allergist.

polymyositis

Patho: Inflammatory myopathy d/t CD8+ lymphocyte infiltration of the endomysium. idiopathic autoimmune disorder leading to muscle inflammation, primarily involving the proximal limbs, neck, and pharynx. May effect heart, lungs, GI tract. Women 30-50. S/S: Progressive symmetric proximal muscle weakness (shoulders, hips). difficulty walking up stairs, squatting, raising arms up. No ocular or facial muscle involvement (unlike MG). Workup: increased muscle enzymes CPK, aldolase, myoglobin. Increased AST/ALT on LFT. Myositis-specific ABYs like Anti-Jo-1. ANA testing. Muscle Bx shows endomysial inflammation. Increased ESR, CRP, RF. EMG. Chest imaging to look for ILD. Consider co-existing cancer in adults; malignancy associated DM or PM. Treatment: High dose steroids, ACTH gel. immunomodulators (methotrexate, CeliCept, azathioprine), rituximab, IVIG.

Pneumonia in HIV/AIDs patients

PCP pneumonia Patho: pneumocystis jirovecii is a yeast-like fungus that does not respond to normal anti-fungals. common in immunocompromised (HIV, malignancy) especially if CD4 < 200. S/s: dyspnea on exertion, fever, nonproductive cough. Testing: labs will show increased LDH (>200), increased beta-d-glucan (β-d-Glucan is an attractive antigen in that it is found in a broad range of fungal agents). Direct fluorescent ABY stain. CXR will show diffuse bilateral interstitial infiltrates. Treatment: trimethoprim-sulfamethoxazole x 21 days. If HIV+, add prednisone if hypoxic (PaP2 <70 mmHg). Sulfa allergy, do dapsone-trimethaprim. HISTOPLASMOSIS Histoplasma capsulatum is a dimorphic oval yeast (not encapsulated despite its name). Transmission via inhalation of soil containing bird and bat droppings in the Mississippi and Ohio river valleys. also seen with demolition, people who explore caves, or excavators in those areas. RF- immunocompromised states (AIDs defining illness esp. if CD4 <150). S/s- most patienst asymptomatic. flu like Sx if symptomatic. Pneumonia is atypical presenting. Fever, nonproductive cough, myalgias. Dissemination in immunocompromised--> hepatosplenomegaly, fever, oropharyngeal ulcers, bloody diarrhea, adrenal insufficiency. can mimic TB. Dx- labs show increased alk phos and LDH. Pancytopenia. CXR shows pulm infiltrates, hilar or mediastinal LAD. Antigen testing via sputum (pCR) or urine is highly specific. Cultures of sputum are MOST specific test; blood cultures + only if disseminated/HIV. Tx- asymptomatic or mild pulm Sx <4w, no treatment. Mild-moderate disease treat with Itraconazole 1st line. Severe disease Tx w/ amphotericin B (or if itraconazole is ineffective).

CHF

PPP 54 RIGHT heart failure Patho: usually RV failure is secondary to LV failure. Primarily a disease of aging (75% 65+). 75% have antecedent HTN. S/S: fluid retention - patient exhibiting edema, hepatic congestion/ascites, sometimes loss of appetite and nausea d/t edema of the gut or impaired perfusion/ascites. Peripheral pitting edema, increased jugular pressure. LEFT heart failure Patho/Etiology: MCC is CAD and HTN. Also valvular disease and cardiomyopathies. S/S: increased pulmonary venous pressure/HTN/edema from fluid backing up into lungs (rales, rhonchi, wheezing, tachypnea). pink, frothy sputum. Cheyne-Stokes breathing. S3 gallop with systolic, S4 gallop with diastolic. cool, dusky pale extremities. BOTHHHHH: Differentiate between systolic HF and diastolic HF. Systolic--> problem with ejection. EF will be reduced, likely a weak DILATED ventricle (S3). Diastolic--> problem w/ filling; EF can often be preserved (though sometimes patients present with a combo of both S and D). Problem w/ filling due to big chunky ventricle; likely hypertrophic (S4). Do not use digoxin for diastolic. Really not loop diuretics required. New York Heart failure classification Class I (< 5%) without any limitation of physical activity Class II (10-15%): Patients with slight limitation of physical activity, they are comfortable at rest Class III (20-25%): Patients with marked limitation of physical activity they are comfortable at rest Class IV (35 - 40 %): Patients who are not only unable to carry on any physical activity without discomfort but who also have symptoms of heart failure or the anginal syndrome even at rest Testing: Echo SHF decreased EF, thin ventricular walls, dilated LV chamber. DHF preserved ejection fraction, thick ventricular walls, small LV chamber. CXR shows pulmonary edema, cephalization of flow followed by kerley B lines, bat wing appearance followed by cardiomegaly, pleural effusions. BNP if >1000 shows CHF is likely. cardiac enzymes to r/o MI. Tx: if decreased EF- first treat any reversible causes. then... 1) diuretic therapy. mild fluid retention? thiazides are good! (HCTZ, metolazone, etc.). More severe? use loop diuretic (furosemide, bumetanide, torsemide, etc.) if risk for hypokalemia, u can add spironolactone etc. 2) ACE inhibitors in conjunction with the above. within 2 days-several weeks, ask about hypotension. also monitor kidney and potassium levels. 3) BB; increase EF and decrease LV size and mass. Lifestyle: Patients should monitor their weight as an indication of fluid retention. could also use digitalis or nitrates/hydralazine. ICDs should be considered in patients with arryhthmias and chronic heart failure/LV systolic dysfunction. if NORMAL EF- diuretics/ACE inhibitors. ICDs and resynchronization devices dont really help.

endocarditis

Patho/etiology: mitral valve is most commonly involved (M-A-T-P) UNLESS IV drug use--then its the tricuspid valve. RF: increased age, rheumatic heart disease, IVDU, immunosuppression, prosthetic heart valves, congenital heart disease. S/S: persistent fever, malaise, fatigue, anorexia, weight loss, night sweats, new onset murmur or worsening of known murmur. Osler nodes are painFUL (Osler=Ow) or tender raised purple nodules on pads of digits and palms. Janeway lesions are painLESS erythematous macules on the palms and soles. Splinter hemorrhages (linear red-brown lesions under nail bed), petechiae of skin or mm. Roth spots are retinal hemorrhages with central clearing. Splenomegaly, septic arterial or pulm emboli, glomerulonephritis. Remember FROM JANE- Fever Roth spots Osler nodes Murmur Janeway lesions Anemia Nail bed hemorrhages Emboli Testing: blood cultures before abx initiation; 3 sets at least 1 hr apart if pt is stable. ECG at regular intervals to assess for new conduction abnormalities (prone to arrhythmias). echo TTE. consider TEE if TTE is not diagnostic; hi risk pt go straight to TEE says prof lyon. labs CBC, leukocytosis, anemia, increased ESR/RF. Duke Criteria for Dx-- 2 major criteria OR 1 major, 3 minor OR 5 minor. Major criteria: 1. 2 positive blood cultures drawn 12 hours apart (S. aureus, S. viridans, S. bovis x2 12h apart) 2. endocardial involvement (either + echo or clearly established new valv regurg) Minor criteria: 1. Predisposing factor 2. Fever 3. Vascular/embolic phenomena (Janeway lesions, septic arterial or pulm emboli, ICH). 4. immunologic phenomena (Osler's nodes, Roth spots, + RF, acute glomerulonephritis) 5. + blood culture not meeting major criteria 6. + echo not meeting major criteria Treatment: Depends on if valve is native or prosthetic. native valve anti-staph penicillin (nafcillin, oxacillin) + ceftriaxone or gentamicin. vanco substituted if penicillin allergy or MRSA suspected. prosthetic valve vanco+gentamicin+rifampin. fungal amphotericin B x 6-8 weeks. Often will need surgical innervation. PROPHYLAXIS (amoxicillin 2g 30-60min pre-procedure) AHA recommends this for patients WITH... predisposing congenital or valvular anomalies (prosthetic cardiac valve, previous infective endo, CHD, cardiac transplantation recipients in whom cardiac valvulopathy develops) WHO ARE...undergoing select dental procedures (any that involve manipulation of gingiva, the periapical region of the teeth or perforation of the oral mucosa INCLUDING routine cleaning), operations involving the respiratory tract, or operations of infected skin, skin structure, or musculoskeletal tissue.

Rheumatoid arthritis

Patho: infiltration of synovium with macrophages, plasma cells, T/B cells (create auto-reactive ABYs rheumatoid factor RF and anti-cyclic citrullinated peptide anti-CCP), neutrophils. Synovial angiogenesis and thickening, release of cytokines (TNF, IL-1, IL-6) and leukotrienes. Chronic inflammation leads to PANNUS formation. Cells of rheumatoid synovium express destruction enzymes. Erosion of joint architecture. Osteopenia leads to bone destruction. Epidemiology: Women > men 3:1. Bimodal onset (peaks in 20s-30s, then again in elderly women and men). Lower rates in Asia and Africa than ME and Europe. Select NA tribes (Pima, Yakima, Chippewa high). Risk factors: smoking, occupational exposure to silica or mineral oil, obesity, microbial insult (just a theory, viral trigger). Genetics w/ HLA-DR4, heritability 60%. S/S: Symmetric distribution of arthritis in small joints > large joints. MCPs and PIPs, but spares DIPs. Feet, wrists, ankles, knees, shoulders, hips, TMJ pain/swelling, sternoclavicular, acromioclavicular, articulations in cervical spine (could lead to C1/C2 subluxation leading to acute cord compression, neuro emergency. Be careful when intubating these patients cuz can lead to subluxation). lumbar spine, SI joints spared. Presence of synovitis (joint capsule feels squishy or boggy; loss of normal contour or valleys) and joint stiffness (upon walking and with prolonged sitting; at least 30-60min but usually many hours). Better w/ activity/exercise so worse when stationary and in early AM hours. constitutional Sx like low grade fever, fatigue and malaise. there are also some joint and tendon deformities (see other slide) and extra-articular manifestations: Rheumatoid nodules in high-pressure areas or even sclerae, lung parenchyma, pericardium. Vasculitis leading to purpuric rash, nail hemorrhages, aseptic cutaneous ulcers, mononeuritis multiplex (painful sensorimotor neuropathy d/t nerve infarction) rarely aortitis and intestinal infarction. Keratoconjunctivitis Sicca (dry eyes), episcleritis (superficial eye pain/redness, self-limited). Scleritis (diffuse or nodular, deep and may lead to scleral perforation so more severe), and corneal melt syndrome (most severe ophthalmic complication). Pleural effusions (exudate, low glucose), RA-ILD (progressive, fibrosing), diffuse alveolar hemorrhage (rare). Pericarditis (chronic, asymptomatic but found on routine EKG, autopsy), increased risk of CAD. Felty's syndrome (splenomegaly, neutropenia usually accompanied by vasculitis and ulceration). Anemia of chronic inflammation/disease, reactive thrombocytosis, LAD and increased risk of non-Hodgkin's lymphoma. Sjogren's. Significantly increased morbidity and mortality. Testing: clinical Dx, confirm w/ serology (CBC, CMP, ESR/CRP, auto-antibodies RF and anti-CCP). 2010 ACR/EULAR RA Classification criteria; 6+ is definite RA. Imaging includes plain films, may show juxta-articular osteopenia (ends of joints are more black than white d/t mineralization of bone), erosions, symmetric joint space narrowing. May be normal in early disease; correlates with disease activity and progression. Arthrocentesis (synovial fluid aspiration) helpful. Fluid analysis in RA will show WBC 2-50K, PMNs 75-80%, yellowish fluid, cloudy turbidity, negative culture, no string sign. Treatment: refer to rheumatology. Start conventional DMARD therapy (disease modifying anti rheumatic therapy) ASAP +/- prednisone bridge (or Medrol dose pack) short term. Treat-to-target; monitor response q1-3months, if no response escalate therapy. Adjunctive PO NSAIDs, local intra-articular steroids, PT, surgery (joint replacement, fusion, tendon reconstruction). Methotrexate 1st line DMARD; oral or subQ injection once weekly 15-25mg. takes 4-6 weeks to achieve initial responds. Other conventional synthetic DMARDs include sulfasalazine/SSZ which is oral and has S/E of diarrhea and cytopenia but is safe in pregnancy. Also leflunomide/LEF that is oral, inhibits dihydrorotate dehydrogenase and interferes with production of DNA/RNA, NOT SAFE in pregnancy. Hydroxychloroquine used in lupus more often but can be used orally in combo with MTX and SSZ triple therapy. Biologics not 1st line but used if MTX has been inadequate; usually ADD and do combo therapy. Major classes are TNFi subQ every 1-2 weeks or IV 4-8 weeks; etanercept, infliximab, adalimumab; all work well just expensive. IL-6i Toxilizumab, anti-B cell Rituximab, T-cell costimulatory inhibitor Orencia/Abatacept, IL-1i Anakinra/Kineret daily injection so rarely used. JAK inhibitors.

SLE

Patho: loss of immune tolerance to one's own body resulting in systemic immune dysregulation. stepwise multisystem phenomena (skin/mucocutaneous, kidney, neuropsych, pleura/lungs, heart, joints, hematologic) S/S: skin classic photosensitive rash; facial malar (cheek) erythema that spares the nasolabial folds. Discoid rash is hyperpigmented plaques or patches on face, ears, scalp. Oral ulcers. biopsy PRN. kidney if there is renal involvement (lupus nephritis) this is a poorer outcome. onset may be sudden w/ cola-colored urine, peripheral edema or insidious w/ polyuria, HTN, puffy eyes and feet. 2+ protein on urine dipstick or >500mg/24hr. urine sediment findings include RBC clasts. pleura/lungs pleurisy (inflammation of superficial CT layer of lungs), exudative effusion, pneumonitis, alveolar hemorrhage, pulmonary HTN. Heart pericarditis is most common heart manifestation. Libman-Sacks endocarditis (non-bacterial valvular vegetations), accelerated atherosclerosis and higher rates of MI (x10). Neuropsych seizures, acute psychosis, various other manifestations like CN palsies, aseptic meningitis, non-specific HAs, cognitive dysfunction. Joints non-destructive inflammatory polyarthritis small>large joints. Hem leukopenia, absolute lymphopenia, hemolytic anemia, thrombocytopenia, antiphospholipid antibodies and lupus anticoagulant leads to higher risk of blood clots. Workup: ANA testing (lots of false +), ANA subserologies (anti-dsDNA, anti-Smith, SSA, SSB, RNP). CBC, metabolic panel, UA w/ microscopy. Complement proteins C3 and C4. Treatment: non-pharm Tx includes sun protection, smoking cessation, family planning (conceive in low activity state). pharm includes hydroxychloroquine/Plaquenil decreases mortality and flares, patients need annual opthalm exam. corticosteroids for controlling flares. Benlysta/belimumab acts on B-cells; subQ or IV biologic. Newest. Immunosuppressants PO mycophenolate mofetil, IV cyclophosphamide.

Asthma meds (quick relief v. chronic control)

QUICK RELIEF SABAs (short acting beta agonists) Albuterol, levalbuterol, terbutaline, epinephrine Indications: 1st line treatment for acute exacerbation (most effective and fastest) MOA: bronchodilator (especially peripherally), decreases bronchospasm, inhibits release of bronchospastic mediators, increases ciliary mvmt, decreases airway edema and resistance. Administration: MDI, nebulizer (latter is commonly used in ED) q20min x3 doses and reevaluation after 3 doses. S/E include B1 cross RXN--> tachycardia, arrhythmias, muscle tremors, CNS stim, hypokalemia. Anticholinergics (antimuscarinics) ipratropium MOA: central bronchodilator (inhibits vagal mediated bronchoconstriction) and inhibits nasal mucosal secretions. Synergy between b2 agonists and anticholinergics (can add to SABA for acute). Most useful in the 1st hour. S/E: thirst, blurred vision, dry mouth, urinary retention, dysphagia, acute glaucoma, BPH. Corticosteroids Prednisone, methylprednisolone, prednisolone MOA: anti-inflammatory. All but the mildest exacerbations should be discharged on a short course of oral corticosteroids (3-5d) unless C/I. Steroids decrease relapse and reverse the late pathophysiology. Short courses don't need tapering unless on chronic steroids or recent treatment with repeated short courses in a short period. Onset of action 4-8 hours for both oral and IV. S/E: immunosuppression, catabolic, hyperglycemia, fluid retention, osteoporosis, growth delays. LONG TERM CONTROL Inhaled corticosteroids (ICS) beclomethasone, flunisolide, triamcinolone Indications: 1st line long term, persistent (chronic maintenance). effective long term control with very low incidence of systemic side effects. MOA: cytokine & inflammation inhibition S/E: oral candidiasis (using spacer and rinsing mouth after inhaler use decreases risk), dysphonia. Long-acting B2 agonists (LABA) Salmeterol. ICS/LABA combo budesonide/formoterol, fluticasone/salmeterol. MOA: bronchodilator prevents Sx (esp. nocturnal Sx) Indications: long-acting B2 agonists added to steroids (or other long term asthma medications) ONLY if persistent asthma is not controlled with ICS alone (increasing ICS dose or adding laba is = efficacy). Once asthma controlled x3mo., step down off LABA is recommended. C/I: NOT used as a rescue drug in acute exacerbations or as mono-therapy for long term asthma. Mast cell modifiers cromolyn, nedocromil MOA: inhibits mast cell and leukotriene mediated degranulation. Used as prophylaxis only. Indications: improved lung function, decreased airway reactivity (inhibits acute response to cold air, exercise, sulfites), minimal side effects (throat irritation). effective prophylaxis may take several weeks. Leukotriene modifiers/receptor antagonists (LTRA) montelukast, zafirlukast, zileuton MOA: blocks leukotriene-mediated neutrophil migration, capillary permeability, smooth muscle contraction via leukotriene receptor inhibition. zileuton does so via 5-lipooxygenase inhibition. Indications: useful in asthmatics with allergic rhinitis / aspirin induced asthma. prophylaxis only. S/E: minimal side effects (increased LFTs, HA, GI, myalgias). Zafirlukast has been associated with churg-strauss syndrome (Churg-Strauss syndrome is a disorder marked by blood vessel inflammation. This inflammation can restrict blood flow to organs and tissues, sometimes permanently damaging them. This condition is also known as eosinophilic granulomatosis with polyangiitis (EGPA)) THEOPHYLLINE MOA: methylxanthine (like caffeine) bronchodilator that improves respiratory muscle endurance, PD inhibitor that inhibits leukotriene synthesis and inflammation, not used often d/t narrow therapeutic index. Smoking decreases theophylline levels so higher doses of theophylline are needed in smokers. it is a nonselective adenosine receptor antagonist. Indications: long term asthma PPX in selected patients; NOT used in asthma exacerbations. A/E: nervousness, N/V, anorexia, HEADACHE, CNS/respiratory stimulant, diuresis, tachycardia. many drug interactions. Narrow TI--> toxicity causes ARRHYTHMIAS AND SEIZURES. OMALIZUMAB (Xolair) anti-IgE antibody used in severe uncontrolled asthma.

mallory-weiss tear

Risk factors include Hx of EtOH abuse with heavy retching. S/S: patients present with hematemesis; 50% have recent Hx of vomiting or straining. Testing: stabilize patient then undergo upper endoscopy, which reveals small mucosal tears (as opposed to esophageal rupture in which the tears are transmural). Treatment: most patients will spontaneously stop bleeding w/o treatment, but refractory patients can be treated with Epi injections or endoscopic hemostatic therapies (coagulation, banding, clipping).

cirrhosis

Risk factors: causes include chronic viral hepatitis, alcohol, drug toxicity, autoimmune and metabolic liver diseases. Mexican/African Americans have higher frequency than whites bc of higher rates of risk factors. Higher coffee and tea consumption is protective for those at increased risk of liver injury S/S: asymptomatic for long period, onset of Sx may be insidious or less often abrupt. Fatigue, disturbed sleep, muscle cramps, weight loss. If advanced, anorexia, N/V, reduced muscle strength, reduced exercise capacity. Hematemesis, abdominal pain, amenorrhea, ED. skin manifestations spider veins, palmar erythema, dupuytren contractures. Evidence of vitamin deficiencies glossitis and cheilosis. Weight loss and wasting due to sarcopenia. Appearance of chronic illness, jaundice (mild at first then increasing in severity). PE: liver is enlarged and firm if not hard and has a sharp or nodular edge. Splenomegaly present in 35-50%, associated w/ increased risk of complications. Superficial veins on abdomen/thorax are dilated. Ascites, pleural effusions, peripheral edema and ecchymoses are late findings. Encephalopathy late in course. Fever in 35% (mostly associated EtOH hepatitis, spontaneous bacterial peritonitis or another intercurrent infection) Testing: LABS= Lab findings absent or minimal in early or compensated cirrhosis. Macrocytic anemia, low WBC due to hypersplenism or high WBC due to infection. Thrombocytopenia is most common cytopenia in cirrhosis patients d/t alcoholic marrow suppression, sepsis, folate deficiency splenic sequestration. Prolongation of PT d/t reduced clotting factors; bleeding risk correlates poorly. Modest elevations of AST and alk phos; progressive elevation of bilirubin. serum albumin decreases. gamma globulin increased levels. Risk of DM increased in those with Hep C, alcoholism, hemochromatosis or NAFLD. Vitamin D deficiency in 91% of patients. IMAGING= Ultrasound helpful for assessing liver size and detecting ascites or hepatic nodules including small hepatocellular carcinomas. doppler may establish patency of splenic, portal, and hepatic veins. CT/MRI good for further characterizing hepatic nodules. Nodules suspicious for malignancy may be biopsied under US or CT guidance. Treatment: Abstain from EtOH. If fluid retention, Na restriction. Diet palatable with adequate calories. Protein 1-1.5g/kg/day in compensated cirrhosis and 1.5g/kg/day if malnutrition. If hepatic encephalopathy, protein reduced to 60-80g/day. Muscle cramps tx w/ L-carnitine 300mg PO QID. vitamin supplementation desirable. HAV, HBV, pneumococcal, yearly flu vaccines. liver transplantation in appropriate candidates is curative.

Paget disease of the bone

patho: nonmetabolic bone disorder of unknown origin leading to XS bone destruction and attempts at repair just lead to weakened, hypertrophic bone. Secondary OA may result. RF for osteosarcoma in adults. S/S: males 2x more than females, after age 40. may be asymptomatic. skull enlargement, bone pain, bowing of long bones, pathologic fractures, shunting to bones leads to warmth and high output HF. Dx: X-Rays show dense, expanded bones with radiolucency and opacity (lytic lesions). bone scan is diagnostic. elevated alk phos. Treat: treat symptomatic patients with NSAIDs and bisphosphonates (which reduce bone resorption and may improve pain and quality of life), and occasionally, calcitonin Surgery can help correct bone deformities, decompress an impinged nerve, and reduce fractures.

viral hepatitis

TRANSMISSION Hep A fecal-oral Hep B sexual, parenteral, perinatal hep C parenteral most common (IVDU, needle stick injuries, blood transfusion prior to 1992), sex and perinatal not common. Hep D requires hep B as envelope protein to get it; parenteral. Hep E fecal-oral the channel A & E's shows are THE SHIT (or shitty, depending on your opinion) S/s: Most are asymptomatic but if they become symptomatic its stuff like malaise, anorexia, N/V, fever, abd pain, decreased urge to smoke. specifics below- Hep B- asymptomatic usually but theres phases u should know. subclinical/anicteric phase includes constitutional Sx, decreased desire to smoke. Icteric phase jaundice (only 30% of peeps). fulminant phase (see fulminant hepatitis slide). Hep E- increased risk of fulminant hepatitis in pregnant women, malnourished, or patients with preexisting liver dz. Dx: All gonna have elevated transaminases, bilirubin. hep A- IgM anti-HAV if acute. IgG past exposure w/ negative IgM. hep B- step 1: look at HBsAg. if negative, you'll have to do step 3. if positive, you dont. step 2: look at core antibody. If IgM, acute infection. If IgG, chronic. step 3: surface Ag was negative, so look at HBsAb! if positive, this indicates immunity bc vaccination or past infection/recovery. If the only thing positive was HBsAb, there was a vaccination. If core IgG aby was + along with HBsAb, there was a recovery. hep C- HCV Abs + within 2-6 weeks. HCV RNA confirmatory and will be + within 1-2w of infection; may be + in pts with - Ab testing. Best way to determine viral replication activity. If RNA negative, but Ab +, resolved infection. Genotype to determine effective Tx options. Hep D- total anti-HDV confirmed by immunochemical staining of liver Bx for for HDAg or RT-PCR assays for HDV RNA in serum. Hep B serologies also performed. Hep E- IgM anti-HEV Tx- hep A- usually self limited so no Tx needed; doesn't go to chronic usually and doesn't become fulminant usually. Post-exposure prophylaxis for healthy ppl 40 or less, HAV vaccine > IG within 2w of exposure. For healthy ppl >40, HAV vaxx +/- IG rather than IG alone within 2w of exposure. For immunocompromised or chronic liver disease >1 y/o, HAV vaxx + IG within 2w of exposure. hep B- supportive for acute as most will not --> chronic. if chronic, antiviral therapy w/ entecavir, tenofovir if persistent severe Sx, stop after confirmation that pt has cleared HbSag (2 tests 4w apart) hep C- lots --> chronic, cirrhosis, HCC so we treat with ledipasivir-sofosbuvir, elbasvir-grazoprevir, or others. Monitor PCR-RNA viral load 12 and 24w post-therapy. these new Tx can reactivate hep B so always do HBV testing prior to Tx. Older regimen was w/ pegylated interferon alpha-2b + ribavirin but this could --> psychosis, depression, thrombocytopenia, leukopenia, arthralgias, anemia. hep D- no FDA approved Tx; interferon alpha for chronic HDV. Liver transplant definitive. Hep E- no Tx needed as self limited and not associated with chronic BUTTT our pregnant patients can --> fulminant hepatitis especially during 3rd trimester so monitor them. Prevention- Hep A- preexposure PPx with vaxx 2 DOSES; 1st dose at 12-24 months, 2nd dose given at least 6 months after the first dose. Make sure high risk patients (MSM, day care workers, international travel, homeless) have their vaxx. Hep B- vaxx given to infants at birth, 1-2mo., 6-18 mo. In adults w/o prior vaxx, 3 doses at 0 mo., 1 mo., 6 mo. vaxx C/I if allergic to baker's yeast. Hep C- no vaxx Hep D- vaxx for hep B! (see above) Hep E- nothin from Dr. Nunu--> both hep B and hep C can --> HCC, but hep C you will prob have cirrhosis first unlike hep b

scleroderma

aka systemic sclerosis Patho: multisystem inflammatory, autoimmune disease. Progressive fibrosis of skin, small vessels and organs (GIT, lung, kidneys). Female>male. Onset between 15-40. S/S: Spectrum of severity anywhere from limited cutaneous to diffuse cutaneous. Limited cutaneous (AKA CREST syndrome) leads to calcinosis cutis, Raynaud's, esophageal dysmotility, sclerodactyly, telangiectasia. Diffuse cutaneous more skin involvement, interstitial lung disease, pulmonary HTN, scleroderma-renal crisis, digital ischemia. Work-up: ANA (majority are +), ANA subserology (anti-centromere, anti-Scl-70; present in more serious disease). CBC, CMP, UA, assess for cardiopulmonary involvement (chest x-ray, cardiac echo, high-res chest CT). Treatment: No disease modifying agents. Symptomatic treatment. For Raynauds, CCBs, PDE-5 inhibitors (sildenafil), topical nitroglycerine for active skin ulcers. Treat GERD w/ PPIs. immunomodulators for severe systemic disease. Scleroderma-renal crisis is an emergency to be treated with ACEi. avoid steroids and BB.

hypoparathyroidism

causes: often seen after thyroidectomy; in this case, usually transient but may be permanent. Could be s/p parathyroid adenoma removal. Transiently after the surgical removal of a single parathyroid adenoma for primary hyperparathyroidism leads to suppression of remaining glands and accelerated remineralization of the skeleton (hungry bone syndrome; hypocalcemia can be severe). Other causes ADHH is a genetic mutation w/ autosomal dominant hypocalcemia with hypercalciuria (no PTH). DiGeorge's syndrome presents in infancy with seizures and congenital cardiac and facial abnormalities. Wilson's disease damage from copper. Hemochromatosis (iron). Functional deficiency of PTH from magnesium deficiency can be Tx if correcting Mg problem (alcoholics, diuretics, intestinal malabsorption and PPIs). Pseudohypoparathyroidism is if there is a renal resistance to PTH d/t genetic mutations. Hypermagnesemia also suppresses PTH secretion (kidney dz and those taking mg-containing laxatives, antacids). Congenital hypoparathyroidism. S/S: Dependent on severity and rate of development of hypocalcemia as well as individual factors. If acute after parathyroidectomy, severe Sx even with mildly low or even low-normal serum calcium levels. If chronic, may have few Sx. tetany, carpopedal spasms, tingling of lips and hands, muscle and abdominal cramps, psychological changes. NM irritability perioral numbness, feet/hand paresthesia, myalgias, muscle cramps, spasms w/ tetany, hyperactive reflexes, laryngospasm that can cause respiratory stridor. cardiovascular bradycardia, ventricular arrhythmias, and impaired ventricular EF. CNS seizures, psychiatric changes, irritability, fatigue and cognitive impairment, parkinsonian and EPS Sx. ophthalmic papilledema, cataracts. renal occur d/t hypercalciuria: nephrolithiasis, nephrocalcinosis and kidney dz. dermatologic dry, rough skin, dry hair, scalp and eyebrow hair loss, brittle fingernails w/ transverse grooves. Chronic with hyperphosphatemia, calcification in soft tissues such as joints skin and arteries. PE: + Chvostek's sign (facial nerve irritability/spasms elicited by tapping the nerve). + Trousseau's sign (carpal spasm induced by arterial occlusion of the arm with a blood pressure cuff). Defective nails and teeth. Cataracts. Slit lamp shows posterior lenticular cataract formation. ECG shows heart block, prolonged QTc interval and ST-T changes suggestive of MI. Labs: Serum calcium low, serum phosphate high, serum magnesium may be low, urine calcium excretion reduced, alk phos normal. serum PTH low or not elevated in presence of hypocalcemia. brain calcifications are visible on CT of basal ganglia in 50% of patients with chronic hypocalcemia. Bones may appear denser than normal and BMD is usually increased particularly in the L spine. Cutaneous calcification may occur. Tx: vit. D and Calcium Tetany- secure airway, IV calcium gluconate

pneumoconioses

pneumoconioses AKA environmental lung diseases; chronic fibrotic lung diseases secondary to inhalation of mineral dust. rule of thumb from podcast... if the mineral comes from the ground (coal worker's, silicosis) the radiologic findings will be in the UPPER lobes (opposite of where the disease came from). if the mineral comes from the ceiling like asbestosis, the findings tend to be in the LOWER lobes. SILICOSIS Occupational dz caused by inhalation of silicon dioxide. Greatly increases the risk for TB and non TB mycobacterium infections. Patho- silica deposits activate alveolar macrophages --> fibrogenesis. RF- silica dust inhalation like in quarry work w/ granite, slate, quartz, pottery makers, sandblasting, glass and cement manufacturing, coal mining, masonry, hydraulic fracturing. S/s- chronic cases are often asymptomatic, dyspnea on exertion, nonproductive cough, crackles. more acute cases present with dyspnea, cough, weight loss, fatigue. Dx- CXR shows multiple small (<10mm) round nodular opacities (miliary pattern) primarily in the UPPER LOBES. Eggshell calcifications of hilar and mediastinal nodes (only seen in 5-20%). bilateral nodular densities progress from periphery to the hilum. Lung Bx. Tx- removal from exposure mainstay of Tx. nonspecific supportive management w/ corticosteroid, oxygen. COAL WORKER'S PNEUMOCONIOSIS (black lung dz) Lung dz from inhalation and deposition of coal dust particles. S/s- dyspnea, cough. fine crackles (rales) often heard. Caplan syndrome is coal worker pneumoconiosis with RA (serologic positive). Dx- small nodules predominantly in the UPPER LUNG with hyperinflation of lower lobes in an obstructive pattern (looks like emphysema). PFT shows obstructive pattern. Lung Bx shows dark black lungs (not needed for Dx) Tx- supportive BERYLLIOSIS Patho- granulomatous pulmonary disease caused by beryllium exposure. beryllium is often alloyed with nickel, aluminum, and copper so people who work in those industries are at increased exposure. RF- aerospace, electronics, ceramics, tool and dye manufacturing, jewelry making, fluorescent light bulbs. S/s- dyspnea, cough, joint pain, fever, weight loss. Dx- CXR normal in 50%, in others hilar lymphadenopathy and increased interstitial lung markings (similar to sarcoidosis). Beryllium lymphocyte proliferation test to assess lymphocyte uptake of thymidine. PFT: restrictive lung pattern. Bx shows noncaseating granulomas. Tx- corticosteroids, oxygen. MTX if corticosteroids fail. Complications- Associated with increased risk of lung, stomach, and colon Ca. BYSSINOSIS Patho- lung disease d/t cotton exposure in the textile industry (may be caused by flax or hemp dust exposure). S/s: dyspnea, wheezing, cough, chest tightness. Sx get worse at the beginning fo the work week then improve later in the week or on the weekend ("Monday fever") ASBESTOSIS patho- slow, progressive, diffuse pulmonary fibrosis as a result of inhalation of asbestos fibers. seen 15-20 years after lengthy exposure to it. RF- destruction, repair, or renovation of old buildings, insulation and fire-resistant products, ship building. Asbestos was commonly used d/t its fire-resistant, thermal, and electrical insulation attributes. S/s- dyspnea on exertion and cough. bibasilar crackles. Dx- CXR shows pleural plaques (pleural thickening or calcification of the parietal pleura) esp. Involving the LOWER LOBES. Interstitial fibrosis (honeycomb lung) irregular linear opacities esp. on the lower lobes. Shaggy heart sign- indistinct heart border, ground glass appearance of the lung fields. PFTs show a restrictive lung pattern with normal or increased FEV1/FVC, normal or decreased FVC, decreased lung volumes. Bx may show linear asbestos bodies in the lung tissue "ferruginous bodies". Tx- no specific therapy. bronchodilators, O2, corticosteroids, +/- lung transplant. Complications- bronchogenic carcinoma MC, malignant mesothelioma of the pleura is most specific.

fulminant hepatitis

acute hepatic failure in patients w/ hepatitis etiologies: acetaminophen MCC in US. viral hepatitis, autoimmune hepatitis, drug RXNs (tolcapone, the dopamine promoter), sepsis. Reye syndrome (fulminant hepatitis in kids post-ASA after a viral infection esp. chickenpox) S/s: encephalopathy (vomiting, coma, AMS, seizures, asterixis, hyperreflexia, cerebral edema, increased ICP) coagulopathy (increased PT, INR >or equal to 1.5, and eventually increased PTT d/t decreased hepatic production of coag factors), hepatomegaly and jaundice, reye syndrome (hands and feet rash, intractable vomiting, liver damage, encephalopathy, dilated pupils w/ minimal response to light, multi organ failure) Dx: Sx + hepatic encephalopathy + abnml LFTs + increased INR >1.4 hypoglycemia common d/t hepatic gluconeogenesis, increased ammonia (encephalopathy), labs to ID cause (acetaminophen levels, viral serologies) Tx: supportive. IVF, mannitol for ICP, PPI stress ulcer PPX. Blood products of platelets or cryoprecipitate for active bleeding coagulopathy. Liver transplant definitive.

acute hepatitis

acute viral hepatitis clinical manifestations: prodromal phase- malaise, arthralgia, fatigue, URI Sx, anorexia, decreased desire to smoke (!!!), N/V, abd pain, loss of appetite, acholic stools. hep A is associated with spiking fever. icteric phase- jaundice (most don't develop this phase, but if present, jaundice happens once the fever subsides) labs: increased ALT and AST (usually both >500 if acute, <500 if chronic). may have hyperbilirubinemia. outcomes: clinical recovery within 3-16w. 10% HBV and 80% HCV become chronic chronic defined as >6 mo. duration; ONLY HBV, HCV, HDV associated with chronicity. can ---> ESLD, hepatocellular carcinoma. can become fulminant-encephalopathy, coagulopathy, hepatomegaly, jaundice, edema, ascites, asterixis, hyperreflexia

pancreatitis (acute and chronic)

acute pancreatitis RF: gallstones, EtOH, hypercalcemia, hyperlipidemia, meds, infections, ERCP, CF, celiac disease, abdominal trauma, smoking, obesity. S/S: abrupt epigastric abdominal pain that is steady and severe. Pain worse with walking and lying down, and better with leaning forward and sitting. Pain radiates to back, N/V, recent alcohol abuse, epigastric tenderness with possible distention and decreased bowel sounds. Fever, tachycardia, possible hypotension, pallor, cool clammy skin. Testing: elevated amylase and lipase >3x normal (Lipase best). Leukocytosis, proteinuria, elevated serum bilirubin, blood EtOH levels, elevated BUN and Cr, triglycerides, calcium, LDH, ALT>150 suggests biliary pancreatitis, AST/ALT ratio 2:1 think alcohol. abdominal x-ray may show gallstones or a sentinel loop (a segment of air-filled small intestine in the LUQ). abdominal USN to r/o gallstones. CT abdomen/pelvis w/o contrast if AKI. ERCP only if pancreatitis is from cholangitis or bile duct stone (if hi suspicion d/t EtOH, risks outweigh benefits) Treatment: Mild disease "pancreatic rest"; NPO then advance diet to clear liquids, then soft, then low fat regular. Bed rest, IVF, NG tube if ileus, meperidine for pain control (or morphine). Severe disease, large amounts of IVF 500-1000mL/hr for several hours, then 250-350mL/hr. NPO, then advance diet; may need TPN. ICU monitoring, calcium gluconate if hypocalcemia. Correct any coagulopathies. Possible IV abx if pancreatic necrosis (imipenem and possible cefuroxime). General surgery consult (only if d/t stones)I infectious disease consult. Eventual cholecystectomy if due to gallstones. Pancreatic abscess requires percutaneous or surgical drainage. Ranson criteria: 3+ of the following predict a severe course complicated by pancreatic necrosis w/ sensitivity of 60-80% Age >55 WBC >16K glucose >200 mg/dL LDH >350 AST >250 development of the following within the first 48 hours indicates a worsening prognosis hematocrit drop of >10%. BUN rise >5mg/dl Arterial PO2 of <60 mmHg Serum calcium of <8 mg/dl base deficit over 4mEq/L estimated fluid sequestration of >6L. mortality rates based on # of criteria present 0-2=1% 3-4=16% 5-6=40% 7-8=100% CHRONIC PACNREATITIS RF: occurs most often in patients w/ alcoholism. risk increases w/ duration & amount of alcohol consumed. Tobacco smoking accelerates the progression of alcoholic chronic pancreatitis. Genetic risk factors, can be part of different AA disorders. S/S: persistent or recurrent episodes of epigastric and LUQ pain, anorexia, N/V, constipation, flatulence, weight loss, steatorrhea. Labs show elevated serum amylase and lipase during an attack, but likely will be low-normal on a day to day basis. Elevated serum alkaline phosphatase and bilirubin (d/t compression of bile duct), glycosuria, XS fecal fat. Imaging plain abdominal x-rays may show calcifications d/t pancreaticolithiasis (30%). CT abdomen/pelvis may show calcifications with possible atrophy. ERCP is the most sensitive test for chronic pancreatitis. Treatment: low fat diet. Avoid EtOH. Pain control though avoid opioids bc addiction is common. Pancreatic enzyme supplements especially for people w/ steatorrhea. Tx DM or hyperlipidemia. Monitor for pancreatic cancer.

acromegaly

aka somatotroph adenoma causes: nearly always caused by a pituitary adenoma (<1% are malignant). Usually sporadic but may rarely be familial (MEN types 1 or 4). McCune-Albright syndrome and Carney complex (more rare). Very occasionally caused by ectopic secretion of GHRH or GH by a lymphoma, hypothalamic tumor, bronchial carcinoid, or pancreatic tumor. S/S: XS GH leads to tall stature and gigantism if in youth (before closure of epiphyses). Afterward, acromegaly (hands enlarge and doughy, moist handshake is characteristic). Fingers widen, CTS is common. Feet grow (width). Facial features coarsen because bones and sinuses of skull enlarge. Mandible more prominent. Macroglossia and hypertrophy of pharyngal and laryngeal tissue (deep voice, difficult intubation, maybe OSA). HTN, cardiomegaly. Insulin resistance leads to DM in 30%. Arthralgia and degenerative arthritis. Spinal stenosis. Colon polyps. GH-secreting pituitary tumors usually lead to hypogonadism by cosecretion of PRL increase or by direct pressure upon normal pituitary tissue. ED/decreased libido, irregular menses in women. Hi risk of gestational diabetes and HTN. Labs: random serum IGF-1 for screening. Fast x8hr, not acutely ill, no exercise on day of testing for assay including: serum GH, IGF-1 (increased by 5x in acromegaly), PRL (d/t cosecreting in GH secreting tumor), glucose, liver enzymes and serum creatinine or BUN bc liver failure or kidney dz can misleadingly elevate GH. serum Ca to exclude hyperparathyroid, serum inorganic phosphorus frequently elevated, serum TSH/T4 as secondary hypothyroidism is common in acromegaly. EXCLUDE ACROMEGALY IF serum GH < 1 mcg/L. If >1mcg/L do glucose suppression test: glucose syrup PO and serum GH measured 60 min later. Acromegaly excluded if serum GH is below .4 w/ ultrasensitive GH assay. Treatment: pituitary transsphenoidal microsurgery tx of choice. Apparent surgical cure and remission in all clinical Sx but mildly elevated serum GH or IGF-1 post-op. Corticosteroids perioperatively and tapered to replacement doses over 1 week; hydrocortisone is d/c and cosyntropin stim test is performed 6 weeks after surgery. At that time, patient is screened for secondary hypothyroidism and secondary hypogonadism. if incomplete remission post-Sx, dopamine agonist cabergoline monotherapy for patients with IGF-1 levels above normal but <2.5x normal. Will shrink 1/3 of acromegaly associated pituitary tumors by more than 50%. somatostatin analogs ocreotide and lanreotide monthly subQ injection. tamoxifen, or pegvisomant (GH receptor antagonist, daily subQ injection. monitor carefully for growth of pituitary tumor and hi s/e and extremely expensive). if refractory to both transsphenoidal surgery and medical therapy, stereotactic radiosurgery followed by life long ASA 81mg.

anal fissures and fistulas

fissures RF: usually d/t trauma from straining, constipation (hard stools) or from Crohn's. Linear or rocket-shaped ulcers that are usually <5mm in length. MC site is posterior midline. S/S: severe tearing pain during defecation followed by throbbing discomfort, hematochezia. Dx made by history and visual inspection w/ anoscopy. Sentinel pile (thickened mucosa) is found below the fissure. Unless findings suggest a specific cause or the appearance and/or location is unusual, further studies are not required Tx: First line treatment includes increasing dietary fluid and fiber. Stool softeners. Protective ointments, sitz baths. Nitroglycerin ointment, topical Ca channel blocker, or botulinum toxin type A injection. fistulas RF: associated w/ anal fissures/abscesses/Crohn's. def: Anorectal fistula is an open tract bw 2 epithelium-lined areas and is associated w/ deeper anorectal abscesses. Communication between rectum and perianal skin. Generally located within 3 cm of the anal margin. Fistulae will produce anal discharge and pain when the tract becomes occluded. Dx can be made via PE, proctoscope. must be treated surgically (fistulotomy)

CVA types /Sx

cerebellar stroke vertigo, nausea, vomiting, nystagmus, ipsilateral limb ataxia. contralateral spinothalamic sensory loss in the limbs may also be present. deafness due to cochlear infarction may follow occlusion of the anterior cerebellar artery, which may also cause ipsilateral facial spinothalamic sensory loss and weakness. massive cerebellar infarction may lead to obstructive hydrocephalus, coma, tonsillar herniation, and death. MCA stroke Most common type. Contralateral sensory and motor deficits greater in face and arm; then leg>foot. only lower half of face involved (can raise forehead). visual: contralateral homonymous hemianopsia and gaze preference toward the side of the lesion initially. Dominant (90% left) hemisphere: aphasia (superior/expressive/broca OR inferior/receptive/wernickes), math comprehension deficits, and agraphia. Nondominant (usually right) hemisphere: spatial deficits, dysarthria, neglect of other side, anosognosia, apraxia, flat affect, impaired judgement, impulsivity. ACA stroke contralateral sensory and motor deficits greater in leg, foot, > arm. face usually spared. urinary incontinence. contralateral homonymous hemianopsia, gaze preference towards the side of the lesion. Personality/cognitive deficits like confusion, flat affect, impaired judgement. PCA stroke the Vs for vertebral: vertigo/nystagmus, vomiting, visual changes (diplopia). post. cerebral artery: homonymous hemianopsia that may spare the macula, alexia without agraphia, visual hallucinations, sensory loss, coma, limb ataxia, nystagmus, cerebellar signs, nausea, vomiting, drop attacks. Vertebrobasilar artery involvement causes "crossed Sx"; ipsilateral CN deficits w/ contralateral motor or sensory deficits. diplopia, dizziness, nausea, vomiting, limb/gait ataxia, coma, cerebellar dysfunction. Asymmetric but bilateral deficits are the rule in basilar infarcts (hemiparesis on one side, motor or reflex abnormalities on the other side). Lacunar stroke S/s and prognosis 5 different presentations. 1. Pure motor most common. hemiparesis or hemiplegia in absence of sensory or "cortical signs" (aphasia, agnosia, neglect, apraxia, or hemianopsia). 2. ataxic hemiparesis ipsilateral weakness and clumsiness in the leg > arm. 3. Pure sensory deficits numbness, paresthesias of the arm, face, and leg on one side of the body in the absence of motor or cortical signs. 4. Sensorimotor weakness and numbness of the face, arm, and leg on one side of the body in the absence of the aforementioned cortical signs. 5. dysarthria (clumsy hand syndrome). Dysarthria, facial weakness, dysphagia and slight weakness and clumsiness of one hand in the absence of cortical signs. Prognosis: good! partial or complete deficit resolution ranging from hours up to 6 weeks.

angina pectoris

class 1: only with very strenuous activity class 2: w/ prolonged or rigorous activity (slight limitation of activity) class 3: w/ daily activity (marked limitation of activity) class 4: at rest (no activity) can be divided into STABLE and UNSTABLE (there's also vasospastic down below) stable--> short in duration (<30min, usually 5min), relieved w/ rest or NTG. unstable--> longer duration (can be >30min), pain at rest, not relieved w/ NTG/resting. if pain at rest, usually 90% occlusion. STABLE ANGINA Patho/etiology: complication of CAD. Inadequate tissue perfusion d/t imbalance between increased demand and decreased coronary artery blood supply. usually symptomatic w/ occlusion of 70%+ S/S: chest pain that is classically substernal, poorly localized, exertional, short in duration (<30 min but often resolves within 5 min of cessation activity). relieved with rest or NTG. may radiate to arm teeth lower jaw back epigastrium or shoulders. PE normally normal. Testing: ECG will show ST depression, T wave inversions, poor R wave progression, T wave pseudonormalization. stress testing most important noninvasive test; exercise for those that can tolerate exercise, if not, pharmacologic stress testing. coronary angiograpy definitive test; defines location and extent of CAD. Treatment: medical typical outpatient regimen includes 1. daily aspirin 2. daily beta blockers 3. sublingual nitroglycerin PRN 4. daily statin. (CCB can be used in lieu of BB if BB contraindication or in vasospastic disorder like prinzmetal angina). reduction of risk factors HTN and DM control, exercise, diet, smoke cessation. revascularization is definitive. Percutaneous transluminal coronary angioplasty is indicated in 1 or 2 vessel disease in non-DM pts not involving the left main coronary artery with normal or near normal EF. Coronary artery bypass graft is indicated if left main coronary artery stenosis, 3 vessel disease (or 2 in DM), or decreased left ventricular EF < 40% ASA? --> low dose for primary prevention in select pts 40-70 not at increased risk of bleeding. UNSTABLE ANGINA patho/etiology: usually 2ary to acute plaque rupture and varying degrees of coronary artery thrombosis. atherosclerosis is the number one cause but coronary artery vasospasm maybe also. S/S: chest pain retrosternally not relieved with rest or nitroglycerin, pain at rest lasting >30 min. Pain at rest usually indicates 90%+ occlusion. PE may be normal. Testing: 12 lead ECG showing subtotal occlusion; ST depressions +/- T wave inversions. cardiac enzymes will be NEGATIVE (diff from STEMI, NSTEMI) Treatment: MONA, beta blockers, heparin. No emergent reperfusion. VASOSPASTIC ANGINA Prinzmetal/Variant Angina: patho: ischemia that results from coronary vasoconstriction; tends to involve the right coronary artery and there may be no fixed stenoses. S/S: chest pain occurs w/o the precipitating factors and is associated w/ ST segment ELEVATION (not depression). pain most often in the AM, women <50. Testing: transient ST elevations that resolve w/ Sx resolution (CCBs, NTG). May have ST depressions. Angiography to r/o atherosclerotic dz and may show coronary vasospasm w/ the use of ergonovine, hyperventilation, or acetylcholine. Dx is made AFTERRR angiography. Treatment: CCBs 1st line qhs. NTG 2nd line. Acute episode, give ASA and heparin until atherosclerosis is r/o. BB avoided cuz they can lead to more unopposed vasospasm. Cocaine induced MI/vasospasm ❄️ ❄️ Patho: cocaine --> myocardial ischemia & infarction by causing coronary artery vasospasm or by increasing myocardial energy requirements. may also contribute to accelerated atherosclerosis and thrombosis. angiographic demonstration of NO significant obstruction of major coronary vessels and coronary spasms that responds to intracoronary nitroglycerin or CCB. Testing: ECG evidence of ischemia during pain sometimes w/ ST segment elevation. May be diagnosed with challenge via ergonovine but this is risky and nonspecific. Treatment: CCBs and nitrates 1st line. ASA, heparin, benzos until atherosclerotic dz r/o. Avoid BBs.

Fungal pneumonia (in general, not just HIV/AIDs)

common in immunocompromised pt (AIDs, steroid use, organ transplant) Coccidioides (valley fever) Patho- Coccidioides immitis grows in soil in arid desert regions in southwestern US (new mexico, southern california), mexico, Central and south america. When soil is disrupted--> spore inhalation. S/s- in the primary pulm dz, 60-65% are asymptomatic. mild flu-like illness w/ fever, chills, nasopharyngitis, HA, cough, pleuritic chest pain. non-remitting cough/bronchitis non-responsive to conventional tx. In full blown Valley fever, you get fever, arthralgia (pain and swelling of the knees and ankles), skin involvement (erythema nodosum, erythema multiforme, or maculopapular rash). In disseminated or persistent, CNS involvement (meningitis) in 50%. Can affect any organ esp. the lungs, skin, soft tissue, lymph nodes, and joints.. Dx- EIA for IgM and IgG. Cultures most definitive. PCR, skin testing. Histology shows spherules (thick walled spherical structure containing endospores) seen in tissues. Can get CSF complement fixing antibodies, fungal CSF pattern if meningitis. CXR will show persistent cavitations, miliary pneumonia, abscesses, nodules. Tx: fluconazole or itraconazole. amphotericin B for severe disease or pregnancy in the 1st trimester. Pulmonary aspergillosis: The majority of cases occur in people with underlying illnesses such as tuberculosis or chronic obstructive pulmonary disease (COPD), but with otherwise healthy immune systems Patho- Aspergillus fumigatus is a fungus that MC effects the lungs, sinuses, CNS. Transmitted via inhalation; commonly found in garden and houseplant soil and compost. Types- Allergic bronchopulmonary aspergillosis- Type I HS reaction occurring almost exclusively in patients with asthma, bronchiectasis, or CF. Classically presents with refractory asthma, fever, malaise, and intermittent expectoration of brownish mucus plugs in the sputum. Dx w/ increased IgE, Aspergillus skin test positivity. CXR shows changes of bronchiectasis, prenchymal opacities, or atelectasis. Tx w/ tapered oral steroids + chest physiotherapy. Itraconazole in some cases. Aspergilloma- fungus colonizes a preexisting pulm cavitary lesion. can be asymptomatic incidental finding on the CXR or patient may complain of cough or hemoptysis. CXR shows air crescent sign (radiopaque structure "fungal ball" that moves when the patient changes position) If asymptomatic, observation. If symptomatic, surgical resection. Acute invasive aspergillosis- fever, HA, toothache, epistaxis, invasive chronic sinusitis. hemoptysis, pleuritic CP, dyspnea. Increased LDH. Often fatal. Usually occurs in severely immunocompromised patients. Dx w/ galactomannan levels, beta-d glucan assay, PCR, culture. CXR shows single or multiple nodules with a halo sign (rim of ground glass opacity) with or without cavitation, patchy or segmental consolidation, peribronchial infiltrates. Voriconazole drug of choice. isavuconazole or caspofungin alternatives. amphotericin B may be adjunctive to voriconazole. surgical debridement if refractory. Cryptococcus: etiology- cryptococcus neoformans or C. gatti (an encapsulating budding round yeast) Transmission- inhalation of pigeon and bird droppings RF- immunocompromised (HIV w/ CD4 count <100) S/s- meningoencephalitis MCC of fungal meningitis. presents with headache and meningeal signs (neck stiffness, nausea, vomiting, photophobia). meningeal signs uncommon in patients with HIV. Pulmonary Sx include pneumonia (cough, pleuritic CP, dyspnea), nodules, abscess, or pleural effusions. Skin lesions if disseminated. Dx- LP shows fungal CSF pattern (increased WBC lymphs mostly, decreased glucose, increased protein). LP performed even if pulm or derm Sx. CSF eval shows cryptococcal antigen via latex agglutination or ELISA OR use india ink to show encapsulated yeast. May have + blood cultures in patients with HIV. Tx- amphotericin B + flucytosine x2w followed by oral fluconazole x10w. If immunocompetent pneumonia, fluconazole or itraconazole x3-6 mo. Histoplasma capsulatum: SEE PNEUMONIA IN AIDS PTS SLIDE Histoplasma capsulatum is a dimorphic oval yeast (not encapsulated despite its name). Transmission via inhalation of soil containing bird and bat droppings in the Mississippi and Ohio river valleys. also seen with demolition, people who explore caves, or excavators in those areas. RF- immunocompromised states (AIDs defining illness esp. if CD4 <150). S/s- most patienst asymptomatic. flu like Sx if symptomatic. Pneumonia is atypical presenting. Fever, nonproductive cough, myalgias. Dissemination in immunocompromised--> hepatosplenomegaly, fever, oropharyngeal ulcers, bloody diarrhea, adrenal insufficiency. can mimic TB. Dx- labs show increased alk phos and LDH. Pancytopenia. CXR shows pulm infiltrates, hilar or mediastinal LAD. Antigen testing via sputum (pCR) or urine is highly specific. Cultures of sputum are MOST specific test; blood cultures + only if disseminated/HIV. Tx- asymptomatic or mild pulm Sx <4w, no treatment. Mild-moderate disease treat with Itraconazole 1st line. Severe disease Tx w/ amphotericin B (or if itraconazole is ineffective).

cardiomyopathies

couple things to remember S3- 3 looks like a big balloon. heard in DILATED. S4- 4 looks sharp and hard, heard in HYPERTROPHIC HOCM and MVP murmurs increase with decreased venous return (standing, valsalva) unlike other murmurs. DILATED MC type. Patho/Etiology: 20-35% have family Hx. Largely idiopathic. MI. Viral infections (enteroviruses/coxsackievirus B), alcohol/cocaine abuse, autoimmune, thyroid disorders, B1/thiamine deficiency. S/S: gradual Sx of heart failure. PE shows rales, elevated JVP, cardiomegaly, S3 gallop rhythm, murmurs of mitral or triscupid regurgitation, peripheral edema, ascites. If severe, Cheyne-stokes breathing, pulsus alternans, pallor/cyanosis. Testing: ECG and CXR. ECG shows left ventricular dilation, decreased ejection fraction, thin ventricular walls, ventricular hypokinesis. CXR shows cardiomegaly, pulmonary edema, pleural effusion. Tx: BASH. Beta blockers, ACE inhibitors>ARBS, Spironolactone, Hydralazine/NTG (these are the LIFE SAVING mortality reducing meds). For Sx, furosemide, digoxin/other inotropes. D/c EtOH if this is the root cause. RESTRICTIVE Patho/Etiologies: non-dilated ventricle which impedes ventricular filling (basically just a HARD ventricle that is not necessarily hypertrophic tho); commonly caused by infiltrative disease (amyloidosis, sarcoidosis, hemochromatosis). Chemo, radiation. S/S: RHF>LHF (peripheral edema, JVD, hepatomegaly, ascites, GI Sx (LHF= dyspnea, fatigue lung sx). Kussmaul's sign (increase in JVP w/ inspiration). S3 may be heard, pulm HTN. Testing: echo shows non-dilated ventricles w/ normal or slightly thick ventricles. diastolic dysfunction, market dilation of both atria. In amyloidosis, bright speckled myocardium. CXR shows normal ventricular chamber size, enlarged atria. Pulm congestion. ECG shows low voltage QRS, arrythmias. LABS shows increased BNP. endomyocardial biopsy shows amyloidosis associated with apple-green birefringence w/ Congo red staining. Treatment: chemo, bone marrow transplantation may help. otherwise Tx underlying cause (chelation for hemochromatosis, glucocorticoids for sarcoidosis). Diuretics can help in acute stage but XS diuresis can be bad for kidneys. Tafamidis for amyloidosis related cardiomyopathy pending approval in US. HYPERTROPHIC Patho/etiology: LVH (>1.5cm thick on echo) unrelated to any pressure or volume overload. Inherited autosomal dominant trait; patients usually present in childhood. S/S: dyspnea, chest pain, syncope, dizziness, arrhythmias. Sudden cardiac death in adolescent or preadolescent children especially during times of exertion bc V fib. PE: harsh systolic murmur at LSV. Murmur intensity increases with decreased venous return (Valsalva, standing) and decreased murmur with increased venous return (squatting, supine, leg raise). Loud S4, mitral regurg, pulsus bisferiens. Testing: echo shows asymmetrical ventricular wall thickness 15 mm +. Systolic anterior motion of mitral valve Treatment: BB/CCB first line. Myomectomy (surg) used in young patients refractory to meds; alcohol septal ablation other option. patients should avoid dehydration, extreme exertion, and exercise. Cautious use of digoxin (increases contraction), nitrates, and diuretics (decrease LV volume). 💔Honorable mention TAKOTSUBO 💔 Patho: follows a high catecholamine surge (usually following very stressful/emotional event). 15% of patients will have coexisting CAD. Usually postmenopausal women. S/S: Angina and dyspnea present. Rare syncope; arrhythmias not uncommon. Testing: ECG ST elevation, deep anterior T wave inversion (which usually resolves over time). CXR either normal or shows pulmonary congestion. echo LV apical dyskinesia not consistent with any particular coronary distribution. Urgent cardiac cath shows LV apical ballooning in association with normal coronaries. cardiac enzymes initially positive but often taper quickly. Treatment: immediate tx like any acute MI. Aspirin, beta-blockers, and ace inhibitors until LV fully recovers.

pulmonary HTN

definition: elevated mean pulmonary arterial pressure >20mmHg w/ pulm vascular resistance >3 Wood units. patho: increased pulm vascular resistance --> RVH --> increased RV pressure --> RHF PRIMARY= most common in middle aged or young women (mean age = 50 y/o). BMPR2 gene defect, which normally inhibits pulm vessel growth/constriction. SECONDARY= pulm HTN d/t pulm dz, sleep apnea, PE, cardiac, metabolic, or systemic disease. categories: Group 1: PRIMARY. "Pulmonary arterial hypertension"; idiopathic, inherited, drug/toxin induced, connective tissue disease, HIV, schistosomiasis (worms). DIRECTLY affecting pulmonary arteries. Group 2: Most common; pulmonary HTN d/t left heart disease. Systemic issue. Group 3: Pulmonary HTN d/t lung disease and/or hypoxemia. Group 4: Pulmonary HTN d/t chronic thromboembolism S/s: dyspnea, fatigue, CP, weakness, cyanosis, edema, exertion syncope if severe, PE: accentuated S2 d/t prominent P2. may have a fixed or paradoxically split P2. Signs of RHF Include JVP, peripheral edema, ascites. Pulm regurg, RV heave, systolic ejection click. Dx: CXR shows enlarged pulm arteries, interstitial or alveolar edema, signs of RHF. ECG may show cor pulmonale (RVH, R axis deviation, R atrial enlargement, right BBB). Right heart cath is DEFINITIVE Dx and gold standard; shows elevated pulm artery pressure, RV pressure, and increased pulm vascular resistance, CBC shows polycythemia with increased Hct. Tx: Correct underlying disease if identified. Primary Tx is going to be a vasoreactivity trial with inhaled nitric oxide, IV adenosine, or CCB +Vasoreactive--> CCBs first line. Prostacyclins, PD5 inhibitors, endothelin receptor antagonists. O2 therapy especially if associated with COPD. Long term anticoagulation in some. Heart-lung transplant definitive.

sjögren syndrome

definition: relatively common chronic, autoimmune, systemic, inflammatory disorder of unknown cause attacking the exocrine glands It is characterized by dryness of the mouth, eyes, and other mucous membranes due to lymphocytic infiltration of the exocrine gland and secondary gland dysfunction Salivary glands - xerostomia (dry mouth) Lacrimal glands - dry eyes (keratoconjunctivitis sicca) Parotid enlargement diagnosis: ANA (especially anti-SS-A (R0) and anti-SS-B (La) (+) Rheumatoid Factor (RF) (+) Schirmer Test (<5mm lacrimation in 5 min) Treat: artificial tears, pilocarpine (cholinergic) for xerostomia Pilocarpine: a cholinergic drug that increased lacrimation and salivation (side effects include diaphoresis, flushing, sweating, bradycardia, diarrhea, N/V, incontinence and blurred vision) Cevimeline: stimulates muscarinic cholinergic receptors

COPD

definition: chronic inflammatory lung disease that causes obstructed airflow from lungs d/t loss of elastic recoil & increasing airways resistance Includes emphysema and chronic bronchitis ⇒ both usually coexist with one being more dominant Damage to the lungs from COPD can't be reversed Risk factors: Cigarette smoking/exposure is the most important risk. Alpha 1 antitrypsin deficiency = genetic and linked to COPD in patients < 40y/o (protects elastin in lungs from damage by WBCs) EMPHYSEMA panacinar/diffuse= seen in alpha-1 antitrypsin def. Centralobular= smokers Exposure to irritants (e.g. cigarette smoke) → degrades elastin in alveoli, airways → lose elasticity → low pressure during expiration pulls walls of alveoli inward → collapse → air-trapping distal to collapse → septa breaks down → neighboring alveoli coalesce into larger air spaces → decreased surface area available for gas exchange Loss of elastin → lungs more compliant (lungs expand, hold air) Alveolar air sacs permanently enlarge, lose elasticity → exhaling is difficult DOE = hallmark symptom Hyperinflation of lungs + hyperresonance to percussion decreased/absent breath sounds, decreased fremitus, barrel chest (increased AP diameter), quiet chest, pursed-lip breathing Individuals are able to oxygenate blood (pink) but they have to purse their lips to do so (puffers) = Pink Puffers! Pursing lips increases pressure in the airway → keeps the airway from collapsing → weight loss Barrel chest due to air trapping and hyperinflation of lungs CXR reveals loss of lung markings, hyperinflation, increased AP diameter PFTs show FVC decreased (esp. FEV1) + increased TLC (due to air trapping) ABG/ labs: respiratory alkalosis, mild hypoxemia, normal CO2 CHRONIC BRONCHITIS Defined as a chronic cough that is productive of phlegm occurring on most days for 3 months of the year for 2 or more consecutive years without an otherwise-defined acute cause Exposure to irritants (e.g. cigarette smoke) → hypertrophy/hyperplasia of bronchial mucous glands, goblet cells in bronchioles, cilia less mobile → increased mucus production, less movement → mucus plugs → obstruction in bronchioles → air-trapping → productive cough Rales (crackles), rhonchi, wheezing, signs of cor pulmonale (peripheral edema, cyanosis) ABGs: Respiratory acidosis (arterial PCO2> 45 mmHg, bicarbonate > 30 mEq/L) PFT's: FEV1/FVC ratio of less than 0.7 Increased TLC (air trapping) Chest radiograph: peribronchial and perivascular markings ↑ HGB and HCT are common because of the chronic hypoxic state Pulmonary HTN with RVH, distended neck veins, hepatomegaly Obese and cyanotic = blue bloaters Dx: PFTs/spirometry = gold standard diagnosis COPD FEV1 = important factor of prognosis and mortality (< 1 L = increased mortality) Obstruction: decreased FEV1, decreased FVC, decreased FEV1/FVC; Hyperinflation: increased lung volumes: increased RV, TLC, RV/TLC, increased FRC (functional residual capacity) CXR/CT scan Emphysema: hyperinflation: flat diaphragm, increased AP diameter, decreased vascular markings; bullae Chronic bronchitis: increased AP diameter, increased vascular markings, enlarged right heart border ECG: cor pulmonale: RVH, RAE, RAD, R-sided heart failure (due to longstanding pulmonary hypertension), MAT, hypertension General Management: Regular physical activity, supplemental O2 for patients with resting hypoxemia (pao2 <56 or sat <88% or cor pulmonale). Long term use of oxygen reduces mortality and improves QOL in severe COPD as hypoxic vasoconstriction takes place --> pulm HTN --> cor pulmonale. Oxygen can reduce R atrial pressure. Minimally symptomatic, low risk of exacerbation (category A): SAMA>sSABAs; Current says "Some clinicians prefer ipratropium as a first-line agent because of its longer duration of action and absence of sympathomimetic side effects. Some studies have suggested that ipratropium achieves superior bronchodilation in COPD patients. Other clinicians prefer SABAs because they are less expensive and have a more rapid onset of action, commonly leading to greater patient satisfaction. At maximal doses, beta-2-agonists have bronchodilator action equivalent to that of ipratropium but may cause tachycardia, tremor, or hypokalemia."- its rly up to you. More symptomatic, low risk of exacerbation (category B): ADD a LAMA>LABA to the above. Minimally symptomatic on day-to-day basis (category C): LAMA OR LAMA+LABA OR LABA + inhaled glucocorticoid. Higher symptom burden (category D): LAMA + LABA (preferred) or LABA + inhaled glucocorticoid. If persistent, triple inhaler therapy recommended (LAMA + LABA + glucocorticoid). *could also do replacement of a-1 antitrypsin* Surgical options: (1) lung reduction surgery (resection of 20-30% of volume in patients with ADVANCED lung hyperinflation and diffuse emphysema) (2) lung transplantation (for patients w/ decreased life expectancy otherwise, exhaustion of other care, otherwise functioning body systems, support system) (3) bullectomy (for severe bullous emphysema. pursued when a single bulla occupies at least 30-50% of hemithorax).

asthma

i made a separate slide for asthma drugs S/s: Most often young patients present w/ wheezing and dyspnea often associated with illness, exercise, and allergic triggers Airway inflammation, hyperresponsiveness, and reversible airflow obstruction Dx and monitor with peak flow: PFT's >12% increase in FEV1 after bronchodilator therapy FEV1 to FVC ratio < 80% (You would expect the amount of air exhaled during the first second (FEV1) to be the greatest amount In asthma, since there is an obstruction (inflammation) you will have a decreased FEV1 and therefore a reduced FEV1 to FVC ratio Treatment guidelines: Mild Intermittent: <2x /week or 3-night Sx per month Step 1: SABA PRN Mild Persistent: >2x /week or 3-4 night Sx per month Step 2: Low-Dose inhaled corticosteroids (ICS) daily Moderate Persistent: Daily symptoms or more than 1 nightly episode per week Step 3: Low-Dose ICS + Long-acting beta2 agonist (LABA) daily Step 4: Medium-Dose ICS +LABA daily Severe Persistent: Symptoms several times per day and nightly Step 5: High-Dose ICS +LABA daily Step 6: High-Dose ICS +LABA +oral steroids daily Acute treatment: Oxygen, nebulized SABA, ipratropium bromide, and oral corticosteroids Making Sense of Forced Vital Capacity Forced expiratory volume (FEV) measures how much air a person can exhale during a forced breath. The amount of air exhaled may be measured during the first (FEV1), second (FEV2), and/or third seconds (FEV3) of the forced breath. Forced vital capacity (FVC) is the total amount of air exhaled during the FEV test You would expect the amount of air exhaled during the first second to be the greatest amount. In asthma, since there is an obstruction (inflammation) you will have a decreased FEV1 and therefore a reduced FEV1 to FVC ratio. Asthma+ nasal polyps+ ASA sensitivity= Samter's triad

autoimmune hepatitis

not even sure if this counts, topic list said "acute and chronic hepatitis" so dont take this card too seriously idk Risk factors: young to middle aged women (though it can happen in any gender at any age), having first degree relatives that are affected patients. S/S: 34% (especially elderly) are asymptomatic. if symptomatic, insidious onset; usually present with acute hepatitis, following a viral illness, or exposure to drug or toxin. Amenorrhea. multiple spider telangiectasias, cutaneous striae, acne, hirsutism, and hepatomegaly. extrahepatic features include arthritis, Sjogren's, thyroiditis, nephritis, UC, hemolytic anemia. Testing: LABS serum aminotransferase levels >1000 U/L. total bilirubin usually increased. If type I (classic), ANA and/or smooth muscle ABYs are found in serum. Serum gamma globulin levels are elevated. If type 2 (more common in girls <14 in Europe) is more common to have circulating antibodies to liver-kidney microsome type 1 (anti-LKM1) w/o smooth muscle ABYs or ANA. Treatment: Prednisone 30mg +/-azathioprine 50mg (immunosuppressive medication). Taper down prednisone over course of few weeks to 10mg prednisone. Candidates for therapy are symptomatic patients with aminotransferase levels elevated 10-fold or asymptomatic patients with modest enzyme elevations depending on the clinical circumstances and histologic severity. Asymptomatic patients usually have a good long term prognosis without therapy.

DVT

patho/etiology: Most DVTs originate in the calf. risk factors virchows triad= intimal damage, stasis, hypercoagulability. S/S: unilateral swelling and edema of the lower extremity > 3cm. Calf pain & tenderness; may be warm to palpation. Homan sign. Testing: D-dimer. if positive follow with ultrasound. contrast venography is gold standard but rarely used. Treatment: anticoagulation first line. LMWH + warfarin, LMWH+ either dabigatran or edoxaban, or monotherapy with apixaban or rivaroxaban. IVC filter if 1. recurrent DVT/PE despite adequate anticoagulation OR 2. stable patients in whom anticoagulation is contraindicated OR 3. right ventricular dysfunction with an enlarged RV on echocardiogram. thrombolysis or thrombectomy reserved for massive DVT/severe cases in hemodynamically unstable.

hydrocele

A hydrocele is a fluid-filled sac around a testicle, often first noticed as swelling of the scrotum Common in newborns and usually disappears without treatment within the first year. Older men can develop hydroceles, sometimes due to inflammation or injury Hydroceles are usually painless but may become large and inconvenient. An ultrasound may be needed for diagnosis On physical exam mass will transilluminate Treatment usually involves watchful waiting. In rare circumstances, surgery is needed

varicocele

A varicocele is an enlargement of the veins within the scrotum (dilation of the pampiniform plexus) A varicocele may develop as a result of poorly functioning valves that are normally found in veins. In other cases, it may occur from compression of a vein by a nearby structure Varicoceles often produce no symptoms but can cause low sperm production and decreased sperm quality, leading to infertility Bag of worms in the scrotum (made worse when patient is upright and improves when patient is supine) More common on left Varicoceles that cause no symptoms typically require no treatment. Cases in which symptoms occur can be repaired surgically

acute/chronic bronchitis

ACUTE BRONCHITIS Patho: usually caused by viruses (adenovirus, parainfluenza, influenza, corona, coxsackie, rhinovirus, RSV). COULD BE (rarely) bacterial via S. pneumoniae, H. flu, M. cat, mycoplasma. S/S: cough x 5 days - 3 weeks (may be productive), malaise, dyspnea, wheeze, URI Sx, hemoptysis, maybe wheezing and rhonchi. Dx: clinical Dx, CXR unremarkable only used if pneumonia expected. Cough, hemoptysis, malaise, dyspnea, wheezing, URI Sx, wheezing/rhonchi or normal upon PE. Tx: Systemic (fluids, antitussives, antipyretics, analgesics) CHRONIC BRONCHITIS Patho: Chronic inflammation leads to mucus gland hyperplasia, goblet cell mucus production, dysfunctional cilia, and infiltration of neutrophils and CD8+ cells. This increases susceptibility to infections. Dx: PFT!! Increased volumes, FEV1/FVC <70%, and DLCO normal. CXR shows pulmonary HTNTx: Category A= SABA or SAMA PRN Category B= SABA + LAMA Category C= LAMA or LAMA + LABA Category D= LABA + LAMA or LABA + inhaled glucocorticoid (fluticasone)

reactive arthritis

AKA Reiter's syndrome Patho: post-infectious immune response to GU or GI infections (Shigella, salmonella, yersinia, campylobacter, chlamydia). Associated with HLA-B27 S/S: Triad of conjunctivitis, urethritis, and asymmetric oligoarticular arthritis. (can't see, can't pee, can't climb a tree). Acute or subacute oligoarthritis of the lower extremities following GI or GU infection. May be associated with skin lesion of feet (keratoderma blenorrhagicum) or genitals (circinate balanitis). Dx: UA and STI-specific assays. Consider stool studies for active GI infection, synovial aspiration PRN. Imaging. Tx: only treat with abx if infection is active; otherwise no indication. 1st line is NSAIDs. refractory cases treat with steroids, csDMARDs, biologics.

guillan barre syndrome

AKA acquired autoimmune demyelinating polyradiculopathy of the PNS patho/etiology: Autoantibody attacks the myeline sheath of the peripheral nerves after an infection. increased incidence with campylobacter jejuni (most common) or other antecedent GI or respiratory infections, CMV, EBV, HIV, mycoplasma, immunizations, and postsurgical. S/S: symmetric, ascending weakness and sensory changes beginning in the distal lower extremities. May also develop weakness of the respiratory muscles and bulbar muscles (swallowing issues). PE: LMN signs (decreased deep tendon reflexes, flaccid paralysis, weakness). sensory deficits, CN palsies CN VII. autonomic dysfunction (tachy, arrhythmias, hypotension or HTN, breathing difficulties) Dx: EMG shows decreased motor nerve conduction velocities and amplitude. CSF analysis shows high protein but normal WBC count (1-3 weeks post onset). PFT to assess peak inspiratory pressure and FVC bc both decrease with this. can determine need for intubation. Tx: Plasmapheresis or IVIG 1st line for ABY removal and neutralization. Mechanical vent if respiratory failure or decreased FVC on PFTs. NO PREDNISONE (whereas steroids are sometimes indicated in MG Tx, they dont help in gbs and some studies even show they may worsen outcomes... tho this is limited) Px: 60% full recovery in one year, 10-20% have permanent disability.

acute / chronic leukemia

AML: hallmark of acute leukemia is the combination of pancytopenia with circulating blasts. However, blasts may be absent from the peripheral smear in as many as 10% of cases ("aleukemic leukemia"). The bone marrow is usually hypercellular and dominated by blasts (greater than 20%). Hyperuricemia may be seen. If DIC, fibrinogen level will be reduced, the prothrombin time prolonged, and fibrin degradation products or fibrin D-dimers present. Meningeal leukemia will have blasts present in the spinal fluid. Auer rod, an eosinophilic needle-like inclusion in the cytoplasm, is pathognomonic of AML and, if seen, secures the diagnosis. Tx: patients </=60 treated with the objective of cure. Most patients w/ AML are treated w/ a combination of an anthracycline (doxorubicin or daunorubicin or idarubicin) plus cytarabine, either alone or in combination with other agents. Older patients with AML who are not candidates for intensive chemotherapy may be given 5-azacitidine or decitabine, in combination with the bcl2 inhibitor venetoclax. Once a patient has entered remission, post-remission therapy should be given with curative intent whenever possible. Options include continuation of chemotherapy and allogeneic stem cell transplantation. Patients >60, stem cell replacement>chemo. Once leukemia has recurred after initial chemotherapy, the prognosis is poor. For patients in second remission, transplantation offers a 20-30% chance of cure. Targeted therapies directed at recurrent genetic mutations (FLT3, IDH1/IDH2) are available for these patients. CML: elevated WBC; the median WBC at Dx is 150,000/mcL. myeloid series is left shifted, with mature forms dominating and with cells usually present in proportion to their degree of maturation. Blasts are usually <5%. Basophilia and eosinophilia may be present. At presentation, the patient is usually not anemic. RBC morphology is normal, and nucleated red blood cells are rarely seen. The platelet count may be normal or elevated. bone marrow is hypercellular, with left-shifted myelopoiesis. hallmark of the disease is the bcr/abl gene (Philadelphia chromosome 22) that is detected by PCR. W/ progression to the accelerated & blast phases, progressive anemia & thrombocytopenia occur, & the % of blasts in the blood & bone marrow increases. Blast-phase CML is diagnosed when blasts comprise >20% of bone marrow cells. Tx usually not emergent even w/ white blood counts over 200,000/mcL. goal of therapy is normalization of the hematologic abnormalities & suppression of the malignant bcr/abl-expressing clone. Tx of choice consists of a tyrosine kinase inhibitor (eg, imatinib>>, nilotinib, dasatinib) targeting the aberrantly active abl kinase. Second, a major cytogenetic response should be achieved, ideally within 3 months but certainly within 6 months. A major cytogenetic response = when <35% of metaphases contain the Philadelphia chromosome as measured by PCR. patients have a worse prognosis if these targets are not achieved. Patients with advanced-stage disease (accelerated phase or myeloid/lymphoid blast crisis) should be treated with a tyrosine kinase inhibitor alone or in combination with myelosuppressive chemotherapy. ALL: usually children 2-5. Many patients are asymptomatic when the diagnosis is made bc of the finding of abnormal blood counts. Fatigue, infection, or bleeding related to bone marrow failure are usually the presenting S/S. Course may be indolent, and the dz may present as a wasting illness with fever, weight loss, and general debility. On examination, splenomegaly may be present in combination with pallor, bleeding, and various signs of infection. Myelodysplastic syndromes can also be accompanied by a variety of paraneoplastic syndromes prior to or following this diagnosis. Labs: Anemia may be marked w/ MCV normal or increased. On peripheral blood smear, macro-ovalocytes may be seen. WBC count is usually normal or reduced, and neutropenia is common. The neutrophils may exhibit morphologic abnormalities, including deficient numbers of granules or deficient segmentation of the nucleus, especially a bilobed nucleus (Pelger-Huet abnormality). The myeloid series may be left shifted & small numbers of promyelocytes or blasts may be seen. The platelet count is normal or reduced, and hypogranular platelets may be present. bone marrow is characteristically hypercellular but occasionally may be hypocellular. Erythroid hyperplasia is common, and signs of abnormal erythropoiesis include megaloblastic features, nuclear budding, or multinucleated erythroid precursors. The Prussian blue stain may demonstrate ringed sideroblasts. In the marrow, too, the myeloid series is often left shifted, with variable increases in blasts. Deficient or abnormal granules may be seen. A characteristic abnormality is the presence of dwarf megakaryocytes with a unilobed nucleus. Genetic abnormalities define MDS; there are frequent cytogenetic abnormalities involving the long arm of chromosome 5 as well as deletions of chromosomes 5 and 7. Some patients w/ an indolent form of the disease have an isolated partial deletion of chromosome 5 Tx: combo chemotherapy, including daunorubicin, vincristine, prednisone, and asparaginase. patients w/ Philadelphia chromosome-positive ALL (or bcr-abl-positive ALL) should have a tyrosine kinase inhibitor, such as dasatinib or ponatinib, added to their initial chemo. Patients should also receive CNS prophylaxis so that meningeal sequestration of leukemic cells does not develop. After achieving complete remission, patients may be treated w/ either additional cycles of chemotherapy or high-dose chemotherapy and stem cell transplantation. relapsed disease, the bispecific antibody blinatumomab targeting CD19 and the antibody-drug conjugate inotuzumab ozogamicin targeting CD22 have shown remarkable activity and are considered superior to traditional chemotherapy options. CLL: clonal malignancy of B lymphocytes. The disease is usually indolent, with slowly progressive accumulation of long-lived small lymphocytes. disease of older patients, with 90% >50 years and a median age at presentation of 70 years. Many patients will be incidentally discovered to have lymphocytosis. Others present with fatigue or lymphadenopathy. On exam, 80% of patients will have diffuse lymphadenopathy and 50% will have enlargement of the liver or spleen labs: isolated lymphocytosis. WBC count is usually > 20,000/mcL & may be markedly elevated to several hundred thousand. Usually 75-98% of circulating cells are lymphocytes. Lymphocytes appear small & mature, w/ condensed nuclear chromatin, & are morphologically indistinguishable from normal small lymphocytes, but smaller numbers of larger and activated lymphocytes may be seen. The hematocrit and platelet count are usually normal at presentation. bone marrow is variably infiltrated with small lymphocytes. immunophenotype of CLL demonstrates coexpression of the B lymphocyte lineage marker CD19 with the T lymphocyte marker CD5. Hypogammaglobulinemia is present in 50% of patients & becomes more common w/ advanced dz. In some, a small amount of IgM paraprotein is present in the serum. Tx: Most cases of early indolent CLL require no specific therapy, and the standard of care for early-stage disease has been observation. Indications for treatment include progressive fatigue, symptomatic lymphadenopathy, anemia, or thrombocytopenia. These patients have either symptomatic & progressive Rai stage II disease or stage III/IV disease. Initial tx consists of targeted biologic therapy: ibrutinib (a Bruton tyrosine kinase inhibitor targeting B-cell receptor signaling; well tolerated but serious bleeding in warfarin) OR venetoclax (a bcl2 inhibitor resulting in apoptosis but associated w/ tumor lysis syndrome) in combo w/ anti-CD20 aby therapy (obinutuzumab, infusion RXNs). Choice b/w these agents is based on toxicity & preference. Relapsed or refractory: both venetoclax and ibrutinib or another BTK inhibitor, acalabrutinib, are good. Allogeneic transplant offers potentially curative tx for patients w/ CLL, but it should be used only in patients whose disease cant be controlled by the available therapies

Heart murmurs

ARMS rest HOCM and MVP increase with decreased venous return Aortic Stenosis: harsh systolic ejection crescendo-decrescendo at the right upper sternal border with radiation to neck and apex Dyspnea, angina, syncope with exertion; squatting increases intensity; split S2 Increased BNP, helmet cells (schistocytes); cardiomegaly Aortic Regurgitation: soft high pitched, blowing, crescendo-decrescendo along left sternal border; loud leaning forward/squatting Leaflets of aorta don't close during diastole → blood regurgitates from the aorta into left ventricle → volume overload left ventricle S3 or S4 with severe; water-hammer pulse (arterial pulse large and bounding) Mitral Stenosis: diastolic low pitched decrescendo rumbling with an opening snap heart best at the apex with pt. lying lateral decubitus position Leaflets of the mitral valve thicken, stiffen from rheumatic fever → valve doesn't open well in diastolic; cause = rheumatic heart Left atrial hypertrophy, may also have mitral regurge Mitral Regurgitation: blowing holosystolic murmur at the apex with split S2 radiating to the left axilla Mitral valve doesn't close fully in systole → blood regurge from LV to LA → murmur Caused by: CAD, HTN, MVP, rheumatic, heart valve infection; apical S3 = volume overload on the ventricle Mitral Valve Prolapse: midsystolic ejection click heard best at the apex Abnormal systolic ballooning in part of the mitral valve into the left atrium Tricuspid Stenosis: mid-diastolic rumbling murmur at LLSB with opening snap RARE! Leaflets of tricuspid valve = stiff/immobile → impaired RV filling from decreased tricuspid valve orifice = increased RA pressure → right and left heart failure Tricuspid Regurgitation: high pitched holosystolic murmur at LLSB radiates to the sternum and increases with inspiration Tricuspid fails to close fully in systole, blood regurgitates from RV → RA = murmur Pulmonary Stenosis: harsh, loud, medium pitched systolic murmur heard best at 2nd/3rd left intercostal space that may increase with inspiration Stenosis of pulmonic valve impairs flow across the valve; increases afterload on the ventricle widely split S2; early pulmonic ejection sound; RVH Pulmonary Regurgitation: high pitched early diastolic decrescendo murmur at LUSB that increases with inspiration Blood leaks abnormally backward from pulmonary artery though pulmonic valve → RV (RHF)

pneumonia (bacterial v. viral)

ATYPICAL V. TYPICAL ORGANISMS "TYPICAL" S. pneumonia H. influenzae Klebsiella pneumoniae Staph aureus (Taylor Swift Has Kanye SEETHING) CXR shows LOBAR pneumonia S/s- sudden onset of fever, productive cough and purulent sputum, pleuritic chest pain, rigors (esp. strep pneumo), tachycardia, tachypnea. PE shows signs of consolidation like bronchial breath sounds, dullness on percussion, increased tactile fremitus and egophony, inspiratory rales. "ATYPICAL" Viruses chlamydophila pneumoniae Mycoplasma pneumonia legionella pneumophila (Velvet Crabs Live Around Maine) CXR shows diffuse, patchy intersitial or reticulonodular infiltrates (same w/ viruses) S/s- low grade fever, dry nonproductive cough. extrapulmonary Sx common like myalgias, malaise, sore throat, HA, N/V/D, bullous myringitis. PE is often NORMAL and signs of consolidation are normally absent. HAP definition: pneumonia occurring > 48 hours after hospital admission. Often caused by pseudomonas, MRSA, klebsiella pneumoniae, and other organisms found on hospital. CAP most commonly strep pneumoniae OR (#2 most common) H. flu Strep pneumoniae: most common cause of CAP; typical presentation is rusty blood tinged sputum with chills/RIGORS. gram + diplococci. H. influenzae: 2nd most common cause of CAP; more often seen in extremes of age, immunocomp, underlying resp disease, alcoholism. gram - rod. staph aureus: common POST viral infection, also seen in HAP (MRSA). CXR will have bilateral multilobar infiltrates or even cavitations. gram + cocci in clusters. K. pneumoniae: chronic alchoholism, patients with chronic illness (DM). PURPLE colored currant jelly sputum. CXR shows cavitary lesions. gram - rods. Mycoplasma: young and healthy people in late summer/early fall. dry/nonproductive cough. URI prodrome. Bullous myringitis. cold autoimmune hemolytic anemia (IgM). Tx w/ azithromycin or doxy. Legionella: water-related. immunosuppressed, smokers, elderly. Diarrhea. Hyponatremia. Increased LFTs. Headache, confusion. Urine antigen or PCR for ID. Tx w/ macrolides. ASPIRATION PNEUMONIA MCC anaerobes (peptostreptococcus, bacteroides). increased incidence w/ periodontal dz. in chronically ill, gram- rods and staph aureus may also be a cause. Patho- inhalation of oropharyngeal and gastric microbes. RF- reduced consciousness, protracted vomiting. MC in RLL d/t vertical angle of right mainstem bronchus. Associated with foul smelling sputum (rotten eggs ), pulmonary abscesses, and empyema. CURB-65 criteria: admission if score of 2+ Confusion Uremia (>30 mg/dl or BUN >7mmol/L) RR > or equal to 30 BP low (S <90, D <60) Age > 65. Tx: OUTPATIENT CAP: macrolide or dozy. fluroquinolones only 1st line IF comorbid conditions/recent abx use. INPATIENT CAP: b-lactam (ceftriaxone) + either macrolide (clarithro/azithro) or doxy OR broad spectrum fluoroquinolone (levo, moxi) HAP: anti-pseudomonal B lactam (pip-tazo, ceftazidime, cefipime)+ either anti-pseudomonal AG or FQ. Add vanco if MRSA suspected. Add Bactrim and steroids if PCP suspected. Add levofloxacin or azithro if legionella is suspected. If documented b-lactam allergy, FQ +/- clinda. ASPIRATION cover for anaerobes. Unasyn (ampicillin-sulbactam) 1st line (IV) or Augmentin (PO) based on if they're admitted or not. If hospital acquired aspiration (????), do imipenem, meropenem, pipericillin-tazo.

cholera

An acute infectious disease of the small bowel caused by Vibrio cholerae a gram-negative bacteria which secretes a toxin that causes a life-threatening, rice water diarrhea Typically through contaminated water or seafood Characteristics include severe "rice water" diarrhea with extreme fluid and electrolyte depletion, vomiting, muscle cramps, prostration, and potential death without replacement of fluids and electrolytes Diagnosis is confirmed by stool culture Endemic areas: India, Southeast Asia, Africa, Middle East, Southern Europe, Oceania, South, and Central America Treat with oral rehydration + antibiotics (macrolides, fluoroquinolones, and tetracyclines)

UTI

An infection in any part of the urinary system, the kidneys, bladder, or urethra E. coli (most common) Dysuria without urethral discharge, urgency, frequency, hematuria, new-onset incontinence (in toilet-trained children). Abdominal or suprapubic pain Absence of fever, chills, or flank pain. Change in urine color/odor Urine dipstick: nitrite, leukocyte esterase Urinalysis: pyuria, bacteriuria +/− hematuria +/− nitrites Urine culture (gold standard)> 100 k CFU/mL (women)> 1000 CFU/mL men or cath patients→ takes 24 h to obtain results Treat with Nitrofurantoin (not over age 65), Bactrim, Fosfomycin Ciprofloxacin - reserved for complicated cases Postcoital UTI: single-dose TMP-SMX or cephalexin may reduce the frequency of UTI in sexually active women Lower UTI in pregnancy Nitrofurantoin (Macrobid): 100 mg PO BID × 7 days Cephalexin (Keflex): 500 mg PO BID × 7 days Interstitial cystitis: Symptoms relieved with voiding. Diagnosis of exclusion. "Hunner's ulcer" on cystoscopy

acid base disturbance

Average values "24/7 40/40" 24 (HCO3, base) / 7.40 (pH) / 40 (CO2, acid) Three-Step Approach to Acid-Base Disorders Look at your PH (7.35-7.45 is normal) < 7.35 = acidosis > 7.45 = alkalosis Next look at your PCO2 is it normal low or high (35-45 normal) ↑ CO2 and ↓PH = respiratory acidosis ↓ CO2 and ↑ PH = respiratory alkalosis If you don't see a change in the CO2 in relation to the PH then take a look at the HCO3 Finally, look at the HCO3 is it normal low or high (20-26 normal) ↓ HCO3 and ↓PH = metabolic acidosis ↑ HCO3 and ↑ PH =metabolic alkalosis compensation: metabolic acidosis A simple rule for deciding whether the fall in Pco2 is appropriate for the degree of metabolic acidosis is that the Pco2 should be equal to the last two digits of the pH. For example, compensation is adequate if the Pco2 decreases to 28 when the pH is 7.28. Alternatively, the Pco2 can be predicted by adding 15 to the observed(down to a value of 12).

cardiac arrest

Cardiac arrest is a sudden loss of blood flow resulting from the failure of the heart to pump effectively Signs include loss of consciousness and abnormal or absent breathing Some individuals may experience chest pain, shortness of breath, or nausea before cardiac arrest V-tach or V-fib causes 75% of episodes of cardiac arrest 5 Hs: Hypoxia, hypovolemia, hyperkalemia/hypokalemia, H+ (acidosis), hypothermia 5 Ts: Tamponade, tension pneumothorax, toxins, thromboembolism (PE), thrombosis (MI) TX: Treatment for cardiac arrest includes immediate cardiopulmonary resuscitation (CPR) and, if a shockable rhythm is present, defibrillation Among those who survive, targeted temperature management may improve outcomes An implantable cardiac defibrillator may be placed to reduce the chance of death from recurrence

rocky mountain spotted fever

Caused by Rickettsia rickettsii a species of bacterium that is spread to humans by the American dog tick (Dermacentor variabilis) from rosh: A 14-year-old boy presents to the Emergency Department for a rash. He reports the abrupt onset of fever, headache, and myalgias three days ago. This morning, he developed a blanching, red, macular rash on his wrists and palms that now involves his extremities and trunk. What is the most likely cause of his symptoms? 2-14 days after tick bite will develop flu-like symptoms: fevers and chills, myalgias, and headache Red maculopapular rash first on wrists and ankles (palms and soles) then spreading centrally over 2-3 days. The face is usually spared Indirect fluorescent antibody (IFA) test remains the standard method of diagnosis of RMSF Treat with doxycycline or chloramphenicol second line

renal calculi

Colicky flank pain radiating to the groin, hematuria, CVA tenderness, and nausea and vomiting CT scan (spiral CT) without contrast of the abdomen and pelvis is the gold standard for diagnosis Urinalysis will often show microscopic hematuria BUN and Cr levels (for evaluation of renal function) and also calcium, uric acid, and phosphate levels Four types: Calcium oxalate (80%): Most common, excess oxalate, hyperparathyroidism, radiopaque - avoid grapefruit juice (makes calcium oxalate stones worse) Struvite (10%): Associated with chronic UTI with Klebsiella and Proteus species, radiopaque Uric Acid (7%): Form in individuals with persistently acidic urine - Excess meat/alcohol, gout, radiolucent Cystine (1%): Rare genetic, radiolucent (young boy with kidney stones) General measures (for all types of stones) Analgesia: IV morphine, parenteral NSAIDs (ketorolac) Vigorous fluid hydration—beneficial in all forms of nephrolithiasis Antibiotics—if UTI is present Alpha-blocker therapy (Flomax) for patients with symptomatic ureteral stones >5 mm and ≤10 mm to facilitate ureteral stone passage (usually given to most patients independent of size) Outpatient management is appropriate for most patients. Indications for hospital admission include: Pain not controlled with oral medications Anuria (usually in patients with one kidney) Renal colic plus UTI and/or fever Stones < 5 mm will have an 80% chance of spontaneous passage Stones > 5 - 10 mm have a 20% chance of passage and may require elective lithotripsy - patients should be considered for early elective intervention Stones > 10 mm are not likely to pass spontaneously. Ureteral stent or percutaneous nephrostomy (gold standard) should be used if renal function is jeopardized. Urgent treatment with extracorporeal shock wave lithotripsy can be used for renal stones of less than 2 cm or for ureteral stones of less than 10 mm

hyperkalemia

Definition: serum potassium of > 5-5.5 mEq/L Causes: Seen in the late stages of kidney failure stage 5 Can be seen in spironolactone and ACEI use and acute renal failure Presentation: Peaked T waves prolonged QRS, muscle fatigue Treatment: CBIGKDROP calcium gluconate (antagonize the effect of K on the heart), beta agonists (salbutamol) or bicarb, Insulin, glucose (drive potassium back into cell). Pearls: hyperkalemia w/ EKG changes must be treated immediately the next progression is sine waves, V-tach and V-Fib to actually remove excess K, you need GI cation exchangers: Veltassa- patiromer calcium 8.4g PO daily. Requires 7-24h to lower K Kayexalate- sodium polystyrene sulfonate 15mg PO or rectally. This requires 1-4h to lower K. This may be repeated q6h.

tension headaches

Definition: recurrent episodes of headache lasting minutes to days. S/S: Widespread, dull pain lasting hours. Pressing or tightening pain of mild to moderate intensity. Bilateral in location and does not worsen with routine physical activity. +/- Photophobia or phonophobia. No nausea. Chronic average frequency of more than 15 days per month for greater than 6 months. At least two of these pain characteristics: pressing (non-pulsating) quality, mild or moderate intensity (may inhibit but not prohibit activities). Bilateral location. No aggravation by walking stairs or similar routine activity. Treatment Non-pharmacologic therapies same as migraine (eliminate triggers, biofeedback, relaxation, exercise, CBT, quite smoking, acupuncture, maintain regular eat/sleep pattern.) Preventative Tx w/ TCA amitriptyline or SSRI. Abortive care includes NSAIDs.

hypernatremia

Definition: serum sodium of > 145 mmol/L Etiology: Diarrhea, burns, diuretics, hyperglycemia, diabetes insipidus, a deficit of thirst S/s: Poor skin turgor, dry mucous membranes, flat neck veins, hypotension, increased BUN/CR ratio > 20:1 Decrease circulating volume = decrease of flow to kidneys means more bound urea in the blood which means ↑ BUN Dx: assess urine volume, osmolality, and the osmole excretion rate (multiply urine osmolality X urine volume). urine volume <.5mL/min = oliguric can be d/t reduced water intake, nonrenal water loss (GI, fever), shift of water into cells d/t rhabdo or seizures. >.5mL/min=nonoliguric; THEN look at urine osmolality. can be d/t diabetes insipidus if <250mOsm/kg. If >300mOsm/kg, osmotic diuresis. Both glucose and urea in the urine can cause this. Tx: infusion of 5% dextrose in water; once corrected, switch to 1/2 NS to prevent hyponatremia, cerebral edema. If concurrently volume depleted, priority should be to restore euvolemia via the administration of isotonic fluids.correct free water deficit (the amount of water calculated to restore the sodium concentration to normal, 140). water deficit=TBW X serum Na-140/140. TBW is 40-60% of current body weight.underlying cause should be identified and addressed. If central DI, vasopressin deficiency should be replaced by administration of DDAVP. from Syed if hypernatremia+HYPOvolemia, isotonic NS until volume resuscitation, then switch to .45% saline or 5% dextrose. if EUvolemia, water ingestion or 5% IV dextrose. If GFRif HYPERvolemic, loop diuretics+5% dextrose.

valvular heart disease

Diastolic Murmur: almost always mean heart disease Early = regurgitative flow through an incompetent valve (usually aortic) Rumbling = mid/late diastole suggests stenosis of AV valve (usually mitral) Aortic regurgitation: soft, high pitched, blowing diastolic along LSB with pt sitting, leaning forward after exhaling Mitral stenosis: diastolic low pitched decrescendo and rumbling with opening snap at apex Pulmonary regurgitation: high pitch, decrescendo murmur at LUSB, increases with inspiration Tricuspid stenosis: mid-diastolic rumbling at LLSB with opening snap Midsystolic Murmurs: aka ejection murmurs; MC kind of heart murmur; peak near mid systole and stop before S2; gap between murmur and S2 pathologic - secondary to structural cardiovascular abnormalities physiologic - secondary to physiologic alteration in body innocent - not associated with detectible physiologic/structural abnormality Aortic stenosis: systolic ejection crescendo-decrescendo RUSB Pulmonic stenosis: hard midsystolic ejection crescendo-decrescendo murmur with widely split S2 at LSB that radiates to left shoulder and neck HCOM: medium-pitched, mid-systolic murmur that decreases with squatting and increases with straining S4 gallop and apical lift with a thick, stiff left ventricle Mitral valve prolapse: midsystolic ejection click at the apex Pansystolic (holosystolic) murmurs - pathologic; heard when blood flows from high to low-pressure chamber; begins immediately with S1 and continues up to S2 Mitral regurgitation: blowing holosystolic murmur at the apex with a split S2 Tricuspid regurgitation: high pitched holosystolic murmur at mid-LSB Ventricular septal defect: harsh holosystolic murmur heard at LSB with wide radiation and fixed, split S2

Diverticular disease

Diverticulosis is defined as large outpouchings of the mucosa at the vasa recta of the colon. RF include low fiber diet, constipation, obesity. S/s: painless rectal bleeding, particularly in an elderly patient. Dx: colonoscopy is the test of choice once upper GI bleed r/o. Radionuclide imaging (technetium99 tagged RBC scan) followed by arteriography if bleeding not visualized on colonoscopy. Tx: bleeding usually stops spontaneously; resuscitation (2 large bore IVs, fluids and/or blood products PRN, correct coagulopathies). Endoscopic therapy to control bleeding if active (epinephrine). Asymptomatic diverticulosis can be followed on a high fiber diet, use of bran, or psyllium. Diverticulitis is defined as inflammation of the diverticula caused by obstructing matter (fecalith) d/t infection and macroperforation. Presents with LLQ pain, low grade Fever, ↑ WBC, N/V, bloating and generally don't bleed. PE often normal; may have tender mass present if inflammation, abscess. Dx: CT w/ contrast test of choice; colonoscopy and barium enema NOT USED d/t perf risk. Labs show leukocytosis. Tx: if uncomplicated, treat with outpatient ABX (flagyl and cipro or levo) x7-10days and clear liquid diet or diet as tolerated. Surgery if refractory to medical therapy, frequent recurrences, perforation, or strictures. Admit if perf, abscess, osbtruction, fistula. CT guided percutaneous drainage may be needed in acute diverticulitis with abscesses >3cm for resolution AND Uncomplicated with high risk (high fever, sepsis, immunosuppressed, increased age, or inability to tolerate PO intake). -lo fiber diet til 6w no sx SURGICAL RECALL: Describe the patho? weakness in bowel wall develops at points where nutrient blood vessels enter between antimesenteric and mensenteric teniae, increase intraluminal pressures then cause herniation thru these areas. What is the most common site? sigmoid colon. Is colonoscopy safe in acute diverticulitis? no MC fistula in diverticulitis? colovesical (to bladder)

Diabetes mellitus type 1 Dx and drugs

Dx with random plasma glucose of 200 mg/dL or plasma glucose of 126 mg/dL+ after overnight fast on MORE THAN ONE occasion. Ketonemia, ketonuria or both. diabetes mellitus autoantibody panel: islet cell autoantibodies (ICAs), antibodies to insulin (IAAs), antibodies to glutamic acid decarboxylase (GAD65), antibodies to zinc transporter (ZnT8). Tx: Insulinssss rapid acting: things are rapid in LA and the women are "fast"- Lispro and Aspart. They have their lips and ass done. -given at same time as meal short-acting: Regular. Given 30-60min prior ot meal and often used WITH intermediate or long acting insulin. Intermediate: NPH, Lente. Covers insulin for half a day or overnight (Night Light). Often combined w/ rapid or short acting. Often given at bedtime (esp. NPH). Long acting: Detemir, glargine. Covers insulin for one full day 6-24h aka basal insulin. Glargine causes fewer hypoglycemic episodes than nPH. Long acting should NOT be mixed with other types of insulin in the same syringe. Pre-mixed formulas- Humulin 70/30 (NPH/reg), Novolin 70/30, novolog 70/30, humulin 50/50. generally given BID before midtime. How would you switch a patient who is on a twice daily insulin premix schedule to a basal/bolus insulin dosing schedule? you take 75% of that, then make 50% basal and 50% bolus (bolus divided into 3 premeal doses) How does sliding scale dosing differ from basal/bolus dosing with correction factor? sliding scale is based on blood glucose level and type of insulin (mild rapid acting, moderate, aggressive). basal/bolus allows for establishment of a basal profile tailored to the patient allowing for better overnight and between meals glucose control. patient is reminded of this when he or she attempts to give additional correction bolus before the effect of the previous bolus has worn off ("insulin on board" feature). This feature reduces the risk of overcorrecting and subsequent hypoglycemia.From blackboard:Sliding Scale: progressive increase in the pre-prandial or hs dosing of insulin based on blood glucose ranges. sliding scale.pdf This is an example of the directions to initiate a sliding scale regarding the type of insulin being used. Correction factor is based on an individuals sensitivity to insulin and how much insulin is required to lower the BS by 50mg/dl.For example: if in general, 1 unit of insulin is required for 15 mg carbohydrates and 1 unit of insulin is required to lower BS by 50 mg/dlSo, if the patient has a meal containing 60g of carbohydrates, they will need 4 units of insulin. But, if their BS is high prior to the meal, they will need to add insulin based on the correction factor in order to be in the target range post-prandial. IE: if the targeted BS is 120 and their pre-prandial BS is 170 (and 1 unit of insulin lowers BS by 50 mg/dl), they will need an additional 1 unit of insulin to meet their target (4 units for the carbohydrates, 1 unit for the correction factor) Somoygi v. Dawn and Tx: Somogyi effect nocturnal hypoglycemia leads to a surge of counter-regulatory hormones to produce high blood glucose levels by 7 AM. can be treated by lowering the basal insulin dose at bedtime or by eating a snack at bedtime. Dawn effect Early morning hyperglycemia ( b/w 5-9am) d/t circadian rhythm. reduced tissue sensitivity to insulin between 5 AM and 8 AM. Increase basal rate of insulin from .7 to .8 unit per hour from 3 to 8AM. PPP says the 11pm dose is usually normal and 8am preprandial is usually high-- the key is to look at 3am dose. if it rises with the sun its dawn.

diabetes mellitus type 2 Dx, meds

Dx: Plasma glucose of 126 mg/dL + after overnight fast on MORE THAN ONE occasion. 2 hours after 75g oral glucose, diagnostic value is 200 mg/dL or more. HbA1c 6.5%+ (preferred bc 8-12 weeks picture). HTN, dyslipidemia, and atherosclerosis are often associated. Tx: @ time of Dx, Initiate weight loss + exercise + Metformin If HbA1c not at target after 3 months Metformin + another agent If HbA1c not at target after 3 months Metformin + two agents If HbA1c not at target after 3 months Metformin + insulin +/- other noninsulin agent Drug MOAs- secretagogues, stimulate insulin secretion: Sulfonylureas, meglitinide analogs, D-Phenylalanine derivatives. lower glucose by effects on liver, muscle, adipose tissue: biguanides, TZDs affect carb absorption: alpha-glucosidase inhibitors. incretins, stimulate insulin release and inhibit glucagon: GLP-1 receptor agonists, DPP-4 inhibitors. SGLT2 inhibitors: block glucose reabsorption causing glycosuria in patients with DM. reduces the threshold for glycosuria from a plasma glucose threshold of about 180 mg/dL to about 40. Drug S/E- sulfonylureas: hypoglycemia (esp. in patients with renal/liver dz), weight gain. 1st gen tolbutamide/orinase can cause flushing w/ EtOH. 2nd gen glycburide/DiaBeta/Micronase hypotension, caution in CVD/eldery, C/I in kidney and liver dz. Glipizide C/I in kidney and liver dz but ok in elderly. Meglitinide analogues: hypoglycemia and weight gain. D-phenylalanine derivatives: cause hypoglycemia and weight gain. biguanides: caution in patients w/ renal dz; C/I in patients with Cr>1.4 in women, 1.5 in men. No weight gain (loss if anything). GI upset (anorexia, N/V, diarrhea), lactic acidosis (rare). TZDs: Avandia increases cholesterol (LDL>HDL) but Actos does not raise LDL, just lowers trigs and increases HDL. Weight gain. Can help NAFLD. Edema (worse w/ combo therapy in insulin) can lead to HF. C/I in NYHA class III and IV. increase in fracture risk in women. macular edema. If liver dz or elevated ALT x2.5, C/I. Anemia, weight gain, and possible increase in bladder cancer w/ pioglitazone. a-glucosidase inhibitors flatulence d/t undigested carbs in bowel, diarrhea. hypoglycemia risk w/ insulin or sulfonylureas. dont use miglitol in end stage kidney dz. caution in liver and renal dz.GLP-1 receptor agonists GI N/V, diarrhea, increased risk of severe pancreatitis, possible kidney injury. C/I in MEN. DPP-4 inhibitors: hypersensitivity RXNs (anaphylaxis, angioedema, and exfoliative skin conditions). Increased URI risk, small increased risk of pancreatitis, diffuse joint pain (resolves with d/c). Saxaglipin & alogliptin may increase risk of HF. SGLT2 inhibitor: major... increased UTIs and genital candidiasis, pyelonephritis and septicemia. hypotension. increased risk of amputations and decreased bone density, increased breast and bladder cancer. increased risk of DKA in type 1 so not used. WEIGHT GAIN sulfonylureas, meglitinide analogs, D-phenylalanine derivatives, TZDs, insulins NEUTRAL (may even cause weight loss) biguanides, DDP-4 WEIGHT LOSS GLP-1 agonists, SGLT2 inhibitors.

prostate cancer

E.O.D.: Prostatic induration on digital rectal examination (DRE) or elevation of PSA. Most often asymptomatic. Rarely: systemic symptoms (weight loss, bone pain). S/S: may manifest as discrete nodules or areas of induration within the prostate on a DRE. However, most prostate cancers are currently detected because of elevations in serum PSA (not DRE findings). Patients rarely present with signs of urinary retention or neurologic symptoms from epidural metastases and cord compression. Obstructive voiding symptoms are most often due to BPH, which occurs in the same age group. Nevertheless, large or locally extensive prostatic cancers can cause obstructive voiding symptoms. Lymph node mets can lead to lower extremity lymphedema. Bc the axial skeleton is the most common site of metastases, patients may present w/ back pain or pathologic fractures. Labs: serum PSA useful in detecting & staging prostate cancer, monitoring response to treatment, and identifying recurrence before it becomes clinically evident. As a screening test, PSA is elevated (>4.0 ng/mL) in 10-15% of men. Prostate cancer will be diagnosed in approximately 18-30% of men with PSA 4.1-10 ng/mL and 50-70% of men with PSA greater than 10 ng/mL. However, no PSA threshold excludes the diagnosis of prostate cancer. Patients w/ urinary retention or with ureteral obstruction due to loco-regionally advanced prostate cancers may present with elevations in BUN or serum creatinine. Transrectal ultrasound-guided biopsy is the standard method for detection of prostate cancer. Annual prostate cancer screening White male with average risk screen at 50 years old Black male, positive family history, or + BRCA mutations - screen at 40 years old Prostate-specific Antigen, Digital Rectal Examination, and Transrectal Ultrasonography If PSA level >10 ng/mL, TRUS with biopsy is indicated, regardless of DRE findings. If DRE is abnormal, TRUS with biopsy is indicated, regardless of PSA level. If PSA is <4.0 ng/mL and DRE is negative, annual follow-up is indicated If PSA is 4.1 to 10.0 and DRE is negative, a biopsy is usually recommended Some types of prostate cancer grow slowly. In some of these cases, monitoring is recommended Other types are aggressive and require radiation, surgery, hormone therapy, chemotherapy, or other treatments.

diapetes insipidus

E.O.D: ADH deficiency w/ polyuria (2-20 L/day) & polydipsia. Hypernatremia if fluid intake is inadequate. Types: central- no production of ADH (MC). idiopathic, destruction of posterior pituitary, head trauma, CNS tumor, sarcoid granuloma. nephrogrenic- partial or complete renal insensitivity to ADH. Meds like Lithium, amphotericin B, demeclocycline can cause this. Hypokalemia or hypercalcemia. ATN. hyperparathyroidism. S/S: intense thirst, especially with a craving for ice water, w/ vol. of ingested fluid varying from 2L-20L daily, and polyuria w/ large urine volumes and low urine specific gravity (usually <1.006 with adequate fluid intake). The urine is otherwise normal. Partial diabetes insipidus presents w/ less intense Sx & should be suspected in patients w/ enuresis. Most patients w/ DI are able to maintain fluid balance by continuing to ingest large volumes of water. However, in patients w/o free access to water or with a damaged hypothalamic thirst center and altered thirst sensation, DI may present w/ hypernatremia and dehydration. DI is aggravated by administration of high-dose corticosteroids, which increases renal free water clearance. Lab: 24 hour urine volume >2L. urine osmolality low. Plasma osmolality of 300mOsm/kg or more implies DI. Hyperuricemia. Plasma AVP levels are usually low(<1 pg/mL) w/ central DI but normal or elevated (>2.5 pg/mL) with nephrogenic DI. VASOPRESSIN CHALLENGE: administer desmopressin acetate 5-10mcg intranasally. Measure urine volume, serum sodium 12 h before and after. If central DI, there will be a reduction in thirst and urine volume. If nephrogenic, there will be no response. From 5MinuteConsult: Blood chemistries (hypernatremia, hyperglycemia) Kidney function tests Plasma osmolality Urine osmolality Urine specific gravity Radioimmunoassay of plasma or urinary vasopressin, following adequate osmotic hypovolemic stimulus (see above), is confirmatory and may aid in distinguishing mixed and partial defects. Low urine specific gravity and osmolality alone are not diagnostic of DI. However, a urine osmolality >600 mOsm/L rules out DI. Urine-to-plasma osmolality ratio may be difficult to interpret; low ratios may be found in patients with primary polydipsia. However, plasma osmolality >300 mOsm/L, urine osmolality <300 mOsm/L, or urine-to-plasma osmolality ratio <1 in a patient with polyuria are suggestive and indicative of need for definitive testing Water deprivation test (Miller-Moses test) evaluates the ability to concentrate urine in response to conditions expected to maximally stimulate ADH secretion (reduction in volume of ≥3% and/or serum sodium level ≥145). Response to exogenous ADH aids in differentiating between CDI and NDI; tests include: Water is withheld, and urine and plasma osmolality are measured at hourly intervals (<7 hours total is generally sufficient). A rise in urine osmolality indicates an intact ADH response. A rise in plasma osmolality or failure of urine osmolality to rise indicates poor ADH response. Performing the test during the day, not overnight, minimizes risk of serious volume depletion/hyponatremia; patients with DI will continue to urinate even when dehydrated. If the results support the diagnosis of DI, desmopressin should be administered to determine ability of collecting tubule to respond to hormone (CDI vs. NDI) If the diagnosis of DI is made, further workup should be aimed at identifying etiology. In case of CDI, this might include cerebral MRI Tx: CDI- DDAVP/desmopressin 1st line intranasal or oral. Carbamazepine 2nd line. chlorpropamide. NDI- correct underlying cause. sodium and protein restriction. HCTZ, indomethacin, or amiloride If Sx persist. Amiloride for lithium-induces as well.

polymyalgia rheumatica

E.O.D: Age >50. Markedly elevated ESR and CRP. definition: pain and stiffness in shoulders and hips lasting for several weeks without other explanation. Patho: polymyalgia rheumatica + giant cell arteritis usually coexist and have preference for the same HLA haplotypes, and show similar patterns of cytokines in blood and arteries. S/S: clinical Dx based on pain & stiffness of the shoulder & pelvic girdle areas, frequently associated w/ fever, malaise, and weight loss. In ~2/3 of cases, polymyalgia occurs in the absence of giant cell arteritis. Because of the stiffness and pain in the shoulders, hips, and lower back, patients have trouble combing their hair, putting on a coat, or rising from a chair. no muscle weakness. Testing: Anemia and elevated acute-phase reactants (generally ESR higher than 30 mm/h and CRP more than 0.5 mg/dL) are present in most cases. Treatment: isolated polymyalgia rheumatica (not having "above the neck" symptoms of headache, jaw claudication, scalp tenderness, or visual symptoms) are treated w/ PO prednisone 10-20 mg/d x2-4 weeks then attempt slow taper. If patient does not experience dramatic improvement within 72 hours, the diagnosis should be revisited. Flares common (50%+) as prednisone is tapered, which may necessitate increasing prednisone, sometimes up to 2y. Tapering of prednisone should be based on Sx & not solely on labs bc ESR can fluctuate. The addition of weekly methotrexate may increase the chance of successfully tapering prednisone in some patients.

G6PD deficiency

E.O.D: X-linked recessive disorder seen commonly in American black men (10-15%). Episodic hemolysis in response to oxidant drugs or infection. Bite cells & blister cells on peripheral blood smear. Reduced levels of glucose-6-phosphate dehydrogenase bw hemolytic episodes. S/S: usually healthy, w/o chronic hemolytic anemia or splenomegaly. Hemolysis occurs episodically as a result of oxidative stress on the RBCs, generated either by infection or exposure to certain medications. Meds initiating hemolysis that should be avoided include dapsone, methylene blue, phenazopyridine, primaquine, rasburicase, toluidine blue, nitrofurantoin, trimethoprim/sulfamethoxazole, sulfadiazine, pegloticase, and quinolones (remember BDMN P3 QRST) Other meds, such as chloroquine, quinine, high-dose aspirin, and isoniazid, have been implicated but are less certain as offenders since they are often given during infections. hemolytic episode is self-limited because older RBCs (w/ low enzyme activity) are removed & replaced w/ a population of young RBCs (reticulocytes) w/ adequate functional levels of G6PD. Severe G6PD deficiency (as in Mediterranean variants) may produce a chronic hemolytic anemia. Labs: Between hemolytic episodes, the blood is normal. During episodes of hemolysis, the hemoglobin rarely < 8 g/dL (80 g/L), and there is reticulocytosis and increased serum indirect bilirubin. Peripheral blood cell smear often reveals a small number of "bite" cells—cells that appear to have had a bite taken out of their periphery, or "blister" cells. Heinz bodies may be demonstrated by staining a peripheral blood smear with cresyl violet. enzyme assays for G6PD reveal a low level but may be falsely normal if they are performed during or shortly after a hemolytic episode during the period of reticulocytosis. In these cases, the enzyme assays should be repeated weeks after hemolysis has resolved. In severe cases of G6PD deficiency, enzyme levels are always low. Treatment: No treatment is necessary except to avoid known oxidant medications.

EBV

EBV AKA HHV-4 infectious mononucleosis characterized by fever, LAD, tonsillar pharyngitis (80% of adults are +). Patho: EBV infects B cells. transmitted by saliva (kissing disease 😘😘😘😘) esp 15-25! S/s: fever, LAD (POSTERIOR CERVICAL), tonsillar pharyngitis that may be exudative, petechiae on hard palate. fatigue, HA, malaise, splenomegaly, hepatomegaly. maculopapular rash in 80% Tx with ampicillin Dx w/ + heterophile antibody screen (Monospot) - may not appear early in the illness (positive within 4 weeks). elevated LFTs. rapid viral capsid antigen test. on peripheral smear, Atypical lymphocytes with enlarged nuclei and prominent nucleoli LUQ pain 2/2 splenomegaly and are at risk for splenic rupture - athletes should avoid vigorous sports for at least the first 3-4 weeks of the illness Treatment is supportive. steroids only if airway obstruction, hemolytic anemia, or severe thrombocytopenia. strep and ebv can coexist. symptoms may last for months. COMPLICATIONS hodgkin lymphoma, burkitt lymphoma, cns lymphoma, nasopharyngeal carcinoma, gastric carcinoma.

bacterial meningitis

Epidemiology: both gram+ and gram- aerobic bacteria cause meningitis in children, elderly, and immunosuppressed. S. pneumoniae is the most common bacteria affecting all ages except infants then N. meningitidis and H. influenzae. Patho: interactions bw meningeal bacteria and the host --> meningeal inflammation, vascular injury, disruption of blood-brain barrier, vasogenic, interstitial and cytotoxic edema, disruption of normal CSF flow. S/S: fever, headache, sensorial disturbances, neck and back stiffness, Kernig (pain w/ passive leg extension) and Brudzinski (legs flex when flex neck). Testing: Do a gram stain smear or <<<culture of the CSF. WBC will be elevated, low glucose, increased protein, MARKEDLY increased opening/tap pressure. Treatment: Give everyone vancomycin to cover strep pneumo. 18-50, vanco and ceftriaxone (for strep pneumo and n. meningitides). 50+, vanco plus ampicillin plus ceftriaxone (for s. pneumo, n. meningitides, listeria, gram negative). Impaired cellular immunity, vanco plus ampicillin plus cefepime Post-surgical or post traumatic, vanco plus cefepime. START ABX ASAP, THEN order LP emergently. If >ICP, common in bacterial meningitis. Rarely a risk of brain herniation that would prevent LP. If patient is high ICP and is elderly, immunocompromised, presents with a coma, focal neuro signs, or papilledema, you need CT first. IV dexamethasone for patients with increased ICP for 2-4 days. ONLY give to a patient who probably has bacterial meningitis, who is immunocompetent, and has no steroid C/I. Sequela: neurological injury d/t meningeal inflammation plus cerebral vasculitis, cerebral edema, cerebral necrosis and hydrocephalus. Meningeal bacteria don't easily penetrate the pia mater and invade the brain. Complications: Even with proper treatment, these may develop. Seizures (1/3) early in meningitis. Focal neuro signs (25%) VIII deafness, VI and III, diplopia. In children, 15% have language disorders or delayed language development, 10% cognitive impairment. Mortality in 5-25% depending on strain of infecting bacteria and any predisposing illness. When do we need to prophylactically treat family/close contacts with bacterial meningitis? Family has increased risk of developing meningitis. If N. meningitides, treat all close contacts w/ rifampin 600mg PO BID x2d or ciprofloxacin, single oral dose of 500 mg. If patient has H. influenzae type B meningitis, chemoprophylaxis in kids <4 y/o in close contact with no vaccine.

hyperparathyroidism

Excess PTH; MCC is parathyroid adenoma; parathyroid hyperplasia or enlargement. Lithium. Men I and IIa. Malignancy is rare. Men 1- hyperPTH, pituitary tumors, pancreatic tumors. Men 2- hyperPTH, PCC, medullary thyroid carcinoma. S/s: most are asymptomatic. Signs of hypercalcemia "stones, bones, abdominal groans, psychic moans" AKA nephrolithiasis, painful bones, fractures, ileus, constipation, N/V, weakness, decreased DTRs, depression, anorexia, anxiety. Dx: Triad of hypercalcemia + intact increased PTH + decreased phosphate. Increased 24hr urine calcium excretion, increased vitamin D. Ancillary- may have osteopenia on bone scan. imaging studies to detect parathyroid adenoma (USN, nuclear scanning). Tx: parathyroidectomy is definitive. Vitamin D and calcium supplementation post parathyroidectomy to prevent hypocalcemia. Cinacalcet inhibits release of PTH in patients that are not surgical candidates. Observation in mild cases. If severe hypercalcemia --> IVF; may need furosemide if severe. SURGICAL RECALL: Secondary hyperPTH? Increased serum PTH resulting from calcium wasting caused by renal failure or decreased GI calcium absorption, rickets or osteomalacia; calcium levels are usually low What plain XRay findings are classic? Subperiosteal bone resorption (usually in hand digits; said to be "pathognomonic" for HPTH!) DDx for hypercalcemia? CHIMPANZEES Calcium overdose Hyperparathyroidism (1 /2 /3 ) Hyperthyroidism, Hypocalciuric Hypercalcemia (familial) Immobility/Iatrogenic (thiazide diuretics) Metastasis/Milk alkali syndrome (rare) Paget's disease (bone) Addison's disease/acromegaly Neoplasm (colon, lung, breast, prostate, multiple myeloma) Zollinger-Ellison syndrome Excessive vitamin D Excessive vitamin A Sarcoid

transient ischemic attacks

Focal neurological deficit of acute onset. Clinical deficit resolves completely within 24 hours. Risk factors for vascular disease often pregnant. Patho/etiology embolization, BV abnormalities (carotid / aortic stenosis etc.), hematologic causes (polycythemia, sickle cell, hyper-viscosity, antiphospholipid antibody syndrome, severe anemia with preexisting cerebral artery disease), subclavian steal syndrome. S/S vary markedly among patients. Sx are abrupt and without warning. Recovery is rapid often within a few minutes. Specific Sx depend on the arterial distribution effected. Rare LOC or acute confusion but is often erroneously blamed for such symptoms. DX CT or MRI within 24h of Sx to exclude small cerebral hemorrhage or cerebral tumor. Reveal acute or subacute infarction which is seen up to 1/3 of cases despite resolution of symptoms. noninvasive imaging of cervical vasculature includes carotid duplex US, MR or CT angiography.ID any HTN, heart disease, hematologic disorders, DM, hyperlipidemia, PAD, CBC/FBS/lipids/HIV/syph.ECG, echo, agitated saline contrast if believed cardiac source.blood cultures if endocarditis. Holter monitor for a fib. Treatment Hospitalization if seen within a week because there is a risk for early recurrence; ABCD2 score to assess recurrence risk (4+ need for hospitalization). If a fib, anti-coagulate with warfarin; dont need to bridge with heparin but could bridge with ASA. Long term with a fib; not usually started in the acute setting. antiplatelet therapy for everyone; could be combo ASA+Plavix

seizure disorders

Focal seizures with retained awareness (consciousness maintained) This type of focal seizure was previously known as a simple partial seizure No alteration in consciousness. Abnormal movements or sensations Focal seizures with a loss of awareness (consciousness impaired) This type of focal seizure may also be called a focal dyscognitive seizure (previously known as complex partial seizures) Altered consciousness, automatisms (ie. Lip-smacking) Present with a postictal state (confusion and loss of memory) which differentiate them from absence seizures Treatment - phenytoin, and carbamazepine are drugs of choice Generalized seizures occur when there is widespread seizure activity in the left and right hemispheres of the brain. Start midbrain or brainstem and spreads to both cortices The different types of generalized seizures are: Absence seizures (formerly known as petit mal) Characterized by a brief impairment of consciousness with an abrupt beginning and ending. At times involuntary movements may occur, but they are uncommon and the patient has no recollection and witnesses commonly miss them Tonic-clonic or convulsive seizures (formerly known as grand mal) Bilaterally symmetric and without focal onset Begins with a sudden loss of consciousness—a fall to the ground Tonic phase: very stiff and rigid 10-60 seconds. Clonic phase: generalized convulsions and limb jerking Postictal phase: a confused state Atonic seizures (also known as drop attacks) Looks like syncope, sudden loss of muscle tone Clonic seizures During a clonic seizure, a person may lose control of bodily functions and begin jerking in various parts of the body. He/She may temporarily lose consciousness, followed by confusion. Tonic seizures Extreme rigidity then immediate LOC, but not followed by a clonic phase Myoclonic seizures Muscle jerking, but not the tonic phase, occurs in the morning Additional seizure types: Febrile Seizure Convulsion associated with an elevated temperature greater than 38°, > 6 mos < 5 years, absence of central nervous system infection or inflammation Infantile Spasms Infantile spasms are a type of epilepsy seizure but they do not fit into the category of focal or generalized seizures Psychogenic Non-epileptic Seizures (PNES) Psychogenic non-epileptic seizures are not due to epilepsy but may look very similar to an epilepsy seizure Status epilepticus Status epilepticus (SE) is a single epileptic seizure lasting more than five minutes or two or more seizures within a five-minute period without the person returning to normal between them Two forms: convulsive and nonconvulsive Convulsive status epilepticus presents with a regular pattern of contraction and extension of the arms and legs Nonconvulsive status epilepticus includes complex partial status epilepticus and absence status epilepticus Benzodiazepines (lorazepam) are the preferred initial treatment after which typically phenytoin is given

parasitic infections

Helminth infestations all intestinal infections Helminths are worm-like parasites that infect several species. Those that infect humans include the following: Nematodes: roundworm (Ascaris), hookworm, pinworm - Cause GI symptoms and cough! Treat with mebendazole Pinworm: anal pruritus in a child in the morning, scotch tape test - the parent will go in early in the morning before the child wakes and apply scotch tape on the rectum and present for exam, also with pinworm paddles Ascaris lumbricoides (roundworm) - most common intestinal helminth worldwide found in contaminated soil - small worm load will be asymptomatic. Larger load may cause vague abdominal symptoms, a high load may migrate to the pancreatic duct, bile duct, appendix, diverticula and cause symptoms at the site Cestodes: Tapeworms - Cause GI symptoms and weight loss! Treat with praziquantel Trematodes: flukes, including Schistosoma, avian and mammal schistosomes (cercarial dermatitis or swimmer's itch) In any parasitic infection, eosinophilia may be present Treatment: Pinworm and most other roundworms with mebendazole Tapeworms and flukes with praziquantel Malaria Presents with periods chills, fever and sweats (fever every 3 days). Caused by Plasmodium vivax, p. malaria, p. ovale, p. falciparum (most virulent) Transmitted by Anopheles mosquito Splenomegaly typically after > 4 days of symptoms Diagnose with Giemsa stain peripheral smear (thin and thick) - parasites in RBCs, thrombocytopenia, increased LDH Treat with chloroquine or mefloquine for chloroquine-resistant p. falciparum Pinworms Pinworm infection, also known as enterobiasis vermicularis, is a human parasitic disease caused by the pinworm (a type of roundworm). mc sx is itching in the anal area. Perianal itching esp at night (eggs are laid at night) Eggs cling to the fingers while itching and are transmitted to other people either directly or through food or surfaces The eggs can thrive for 2-3 weeks on an inanimate object Diagnosis is with a "scotch tape test' done in the early morning. Can see the eggs under microscopy Treatment is with albendazole or mebendazole Toxoplasmosis Toxoplasma gondii is a parasitic protozoan that causes the disease toxoplasmosis Triad of encephalitis + chorioretinitis + intracranial calcifications in AIDS patients with a CD4 < 100 Pregnant female with exposure to cat feces: Toxoplasmosis is the reason we tell pregnant mothers not to change cat litter CT of the brain shows ring-enhancing lesions. Toxo IgG and IgM Congenital toxoplasmosis is part of ToRCH syndrome Treatment: Prophylaxis for all HIV patients with CD4 count < 100 with Bactrim

hypovolemia

Inadequate fluid intake/excess water loss: no thirst, fluid loss, urinary loss, GI loss, burns, diuretics, osmotic diuresis (hyperglycemia), sodium excess, diabetes insipidus tachycardia, orthostatic/regular hypotension, low urine output, dry mucous membranes, poor skin turgor, altered mental status, diaphoresis.if d/t hemorrhage, might be trauma, melena, hematemesis, hematochezia, pulsatile abdominal mass. Signs: Tachycardia, postural hypotension JVD not visibleDry mucous membranes (tongue) and decreased skin turgorHypothermia, pale extremitiesOliguria DX: Measure serum Na+, K+, Cl−, HCO3− High Na+ > 145 Increased hematocrit (3% for each liter lost) Metabolic alkalosis BUN: Cr >20:1 FeNa: <1% (prerenal azotemia) Pulmonary artery catheter (Swan-Ganz) to measure CVP (definitive): decreased CVP, PCWP, pulse pressure ⇒ DI: Neurogenic (central) - caused by deficient secretion of vasopressin (ADH = anti-pee hormone) from the posterior pituitary Nephrogenic: kidneys unresponsive to normal vasopressin levels à inherited x-linked or from lithium / renal disease Low urine sodium and polyuria Urine osmolality of less than 250 despite hypernatremia, indicated diabetes insipidus TX: Correct volume deficit Bolus to achieve euvolemia, begin with an isotonic solution (NS or lactated ringers) Monitor HR, BP, UOP, and weight Maintain UOP at 0.5-1.0 mL/kg/h Replace blood loss with crystalloid at 3:1 ratio Maintenance fluid D5/NS solution with 20 mEq KCl/L (most common) Beware with rapid fluid correction --> pulmonary edema See fluid and electrolyte disorders

influenza

Influenza is a viral resp infection caused by orthomyxovirus -->fever, coryza, cough, headache, and malaise 3 strains: A, B, and C vaccination: Everyone > 6 mo should receive an annual influenza vaccine. Avoid vaccination: severe egg allergy, previous reaction, GBS within 6 weeks of previous vaccination, GBS in the past 6 weeks, <6 mo old. Avoid FluMist in pt with asthma Dx: clinical. rapid flu test isolated from the throat or nasal mucosa in clinic; most accurate during the first few days of illness Gold standard = RT-PCR or viral culture take 3-7 days to return. CXR in primary influenza pneumonia will show bilateral diffuse infiltrates. false-negative results occur more commonly than false-positive results. Tx: symptomatic (for most) or w/ antivirals ⇒ ideally < 48 hours - Tamiflu (oseltamivir), inhaled Relenza (zanamivir), IV Rapivab (peramivir), and oral baloxavir (Xofluza)Zanamivir and Oseltamivir both treat influenza A and B ⇒ (think Dr. "OZ" treats the flu) Indications for antiviral treatment: hospitalized, outpatient with severe/progressive illness, an outpatient at high risk for complications (immunocompromised, pt with chronic medical conditions, >65 yo, pregnant women / 2 weeks postpartum)

CVA workup, treatment

Initial tests Most important EMERGENT NONCONTRAST HEAD CT within 20 minutes of arrival followed by subsequent multimodal CT (perfusion CT, CTA) or MRI to improve Dx of acute ischemic stroke if no hemorrhage present on CT w/o contrast. Do not let this delay tPA though! Serum glucose ECG CBC and lytes Coag studies Baseline trops Can also consider LFTs, tox screen, blood EtOH, ABGs, LP if suspected SAH, EEG HEMORRHAGIC -Goal is to decrease bleeding while maintaining circulation -Want to lower systolic BP to 140mmHg w/ IV labetalol or nicardipine especially if not d/t an AVM bc the likely cause is HTN -platelet transfusion for thrombocytopenia -reverse coagulopathies w/ FFP, prothrombin complex concentrates, vitamin K, or specific reversal agents (patient on heparin, give protamine. Dabigatran, idarucizumab. Apixaban, betrixaban, edoxaban, rivaroxaban, give andexanet. -Monitor ICP, give mannitol and/or hypertonic saline. ISCHEMIC -Different from hemorrhagic because you actually are relying on a higher blood pressure to maintain cerebral perfusion, so withhold antihypertensives unless systolic >220 or diastolic >120. BP must be <185/110 for tPA. -MCC is a thrombotic or embolic occlusion of major vessel, so breaking down that clot is mainstay of treatment. -Technically thrombolysis w/ tPA should be done within 3 hours of Sx onset- BUT off label can be up to 4.5 hours (if <80 + NIH <25 + not a DM w/ previous stroke). Shoot for door-to-needle time of <60min. -Exclusion criteria for thrombolysis: Any history of ICH or new Sx suggestive of ICH MI within 3 mo. Head trauma or prior stroke within 3 mo. GI malignancy or bleed within 21d Major surgery within 14d BP >185/110 Active bleeding/acute trauma If LMWH previous 24h or platelets <100K Glucose <50 Seizure w/ postictal neurologic impairment Multilobar infarction >1/3 cerebral hemisphere Arterial puncture at noncompressible site within 14d. -Manage elevated ICP w/ head elevation and mannitol. - Once hemorrhage has been excluded by CT, aspirin (325 mg orally daily) is started immediately unless the patient received thrombolysis, in which case aspirin is initiated after a follow-up CT has ruled out thrombolytic-associated hemorrhage at 24 hours. Dual antiplatelet therapy should be used for 21 days in patients with minor stroke -thrombectomy can be performed within 24hrs of Sx onset of large artery occlusion in the anterior circulation - If acute hydrocephalus, ventricular drainage (shunt). If cerebellar hemorrhage, Surgical evacuation. BOTH- PT/OT /speech therapy after acute care.

hepatic cancer

MC primary neoplasm of liver RF: chronic liver disease (chronic hepatitis, cirrhosis), hereditary hemochromatosis, aflatoxin B1 exposure (aspergillus spp.) S/s: asymptomatic. malaise, weight loss, jaundice, abd pain, hepatosplenomegaly. Dx: contrast enhanced CT scan or MRI tailored for liver lesion eval. Liver Bx. ↑ alpha-fetoprotein - A rise in serum AFP in a patient with cirrhosis or hepatitis B should raise concern that HCC has developed Tx: Surgical resection if confined to a lobe and not associated with cirrhosis. Screening- USN surveillance q6mo w/ or without alpha fetoprotein in high risk pts (I.e. active hep B with high AST and/or viral load). Px: typically diagnosed late in its course, and the median survival following diagnosis is approximately 6 to 20 months SURGICAL RECALL: AKA? hepatoma What % of pt with cirrhosis will develop HCC? 5% Sx? Dull RUQ pain, hepatomegaly (painful hepatomegaly classic) Indications for transplant? cirrhosis, no resection candidacy, no distant or LN mets, no vascular invasion, single tumor <5cm or 3 nodules with none >3cm. Which subtype has best Px? fibrolamellar hepatoma (young adults) Prognosis under following conditions: unresectable? almost none survive 1 yr. resectable? 35% alive at 5 years.

renal vascular disease

Narrowing of one or both of the renal arteries. Patho: caused by atherosclerotic occlusive disease (80-90%) or fibromuscular dysplasia (10-15%). 5% of americans w HTN have this; mostly those 45+ with Hx atherosclerotic disease. Other risk factors include CKD, DM, tobacco use, HTN. S/S: refractory HTN, new onset HTN in an older pt, pulmonary edema w/ poorly controlled HTN, AKI with ACE inhibitors, unexplained HTN in woman <40 y/o. PE may show abdominal bruit on affected side. Testing: LABS elevated BUN and serum creatinine if severe renal ischemia. If bilateral, may have hypokalemia (decreased blood flow, RAAS is activated). IMAGING 1. Doppler ultrasound is highly sensitive and specific but very operator and patient dependent. 2. CT angiography (spiral CT w/ IV contrast). 3. MRA very effective but expensive. 4. Renal angiography is the gold standard BUT more invasive than others so it is performed after a positive screening test (above). Treatment: Treat the cause. atherosclerotic ischemic renal disease medical management, angioplasty +/- stenting, and surgical bypass. fibromuscular dysplasia better Px; percutaneous transluminal angioplasty is often curative.

gonococcal infections

Neisseria gonorrhoeae gram - diplococci S/s: urethritis and cervicitis --> discharge (anal, vaginal, penile, pharyngeal), PID, epididymitis, prostatitis. disseminated--> triad of dermatitis (maculopapular, petechial rash), polyarthralgia, and tenosynovitis (tenderness along the tendon sheath). often associated with fever, chills, malaise. also purulent septic arthritis esp. the knee--> occurs more frequently during menses Dx: NAAT most sensitive and specific. first void or first catch if urethritis. if disseminated, multiple sites (urethral, rectal, pharyngeal, cervical). UA or dipstick- +leukocyte esterase on dipstick or 10+wbc/hpf on microscopy. synovial fluid- NAAT or culture on chocolate agar. Tx: arthritis--> iv ceftriaxone urethritis and cervicitis--> ceftriaxone 500mg IM + doxy or azithro

nephritis

Nephritis is inflammation of the kidneys and may involve the glomeruli, tubules, or interstitial tissue surrounding the glomeruli and tubules Types: Glomerulonephritis is inflammation of the glomeruli. Glomerulonephritis is often implied when using the term "nephritis" without qualification. Interstitial nephritis (or tubulointerstitial nephritis) is inflammation of the spaces between renal tubules. Nephritis is often caused by infections, and toxins, but is most commonly caused by autoimmune disorders that affect the major organs like kidneys Pyelonephritis is an inflammation that results from a urinary tract infection that reaches the renal pelvis of the kidney Lupus nephritis is inflammation of the kidney caused by systemic lupus erythematosus (SLE) Athletic nephritis is nephritis resulting from strenuous exercise DX: Nephritis can produce glomerular injury - blood tests, X-rays and an ultrasound can help ascertain if the individual has the condition This can lead to reduced glomerular blood flow, leading to reduced urine output (oliguria) and retention of waste products (uremia) As a result, red blood cells may leak out of damaged glomeruli, causing blood to appear in the urine (hematuria) TX: Treatment of nephritis depends on what has provoked the inflammation of the kidney(s). In the case of lupus nephritis, hydroxychloroquine could be used

pituitary adenoma

Noncancerous tumors in the pituitary gland that don't spread beyond the skull Most common tumors are microadenomas that are functional (hypersecretion of pituitary hormones), nonfunctional or compressive <1 cm in diameter, whereas adenomas that are >/=1 cm are commonly referred to as macroadenomas S/S: diminished temporal vision, or bitemporal hemianopsia d/t location of the mass at the sella turcica ⇒ tumor applies pressure on the optic chiasm of the optic nerve resulting in loss of vision in the temporal visual fields Lactotroph adenomas (prolactinomas MC) are pituitary masses ⇒ hypersecretion of prolactin S/s: amenorrhea, galactorrhea, and headaches Growth hormone tumor: gigantism, acromegaly Corticotroph adenoma: Secrete ACTH ⇒ present with Cushings syndrome Thyrotroph adenoma: Secrete TSH ⇒ presents with hyperthyroidism DX: MRI is the study of choice to look for sellar lesions/tumors Endocrine studies: Prolactin, GH, ACTH, TSH, FSH, LH TX: dopamine agonists cabergoline and bromocriptine; if dopamine agonists are unsuccessful, transsphenoidal resection of the pituitary tumor should be considered In women, estrogen therapy can also be used due to the associated hypogonadism

tuberculosis

Organism: Mycobacterium tuberculosis Presentation: Cough, night sweats, weight loss, post-tussive rales, endemic area, immunocompromised. Xray: cavitary lesions, infiltrates, ghon complexes in the apex of lungs Acid-fast bacilli stain Biopsy: Caseating granulomas Mantoux Skin Test is positive if: > 5 mm: Patients at high risk of developing active TB if infected, such as those who have chest x-ray evidence of past TB, who are immunosuppressed because of HIV infection or drugs (eg, TNF-α inhibitors, corticosteroid use equivalent to prednisone 15 mg/day for > 1 mo), or who are close contacts of patients with infectious TB > 10 mm: Patients with some risk factors, such as injection drug users, recent immigrants from high-prevalence areas, residents of high-risk settings (eg, prisons, homeless shelters), patients with certain disorders (eg, silicosis, renal insufficiency, diabetes, head or neck cancer), and those who have had gastrectomy or jejunoileal bypass surgery > 15 mm: Patients with no risk factors (who typically should not be tested) Treatment: Latent treatment: Rifampin (RIF) daily for four months (regimen abbreviation: 4R). Isoniazid (INH) and RIF daily for three months (regimen abbreviation: 3HR) Isoniazid 5 mg/kg (300 mg maximum) orally daily for 9 months Isoniazid 5 mg/kg (300 mg maximum) orally daily for 6 monthsIsoniazid 15 mg/kg (900 mg maximum) orally twice weekly◊ for 9 or 6 months Active treatment: quad therapy - Isoniazid, Rifampin, Ethambutol, Pyrazinamide for 8 weeks Isoniazid- peripheral neuropathy (give with B6) Rifampin - Orange body fluids, hepatitis Ethambutol - Optic neuritis, red-green blindness Pyrazinamide - Hyperuricemia Prophylaxis for household members: Isoniazid for 1 year

Bell palsy

Patho/etiology: CNVII palsy leading to hemifacial weakness/paralysis d/t inflammation or compression. LMN disorder. Idiopathic but could be related to HSV rxn. RF: DM, pregnancy (esp. 3rd trimester), post URI, dental nerve block. S/S: sudden onset of ipsilateral hyperacusis 24-48 hrs followed by unilateral facial weakness or paralysis involving the forehead, taste disturbance (anterior 2/3), biting inner cheek, eye irritation d/t decreased lacrimation & inability to fully close eyelid. Bell phenomenon: eye on effected side moves laterally and superiorly when eye closure is attempted. Dx: Dx of exclusion. you're prob gonna do full CVA workup. Tx: no tx required, 85%+ of cases resolve within 1 month. Supportive tx includes artificial tears or eye patches worn during sleep. prednisone, esp. if started within first 72 hrs of symptoms, reduces time to full recovery and increases likelihood of complete recuperation. Acyclovir in combination with glucocorticoids in severe cases has been shown to improve Sx and timing of recovery.

myocarditis

Patho/etiology: inflammation of heart muscle MC in young adults. myocellular damaging leading to myocardial necrosis and dysfunction, leading to HF. infectious viral most common (enteroviruses-coxsackivirus B) or bacterial. autoimmune SLE, RA. other uremia, medications (clozapine, methyldopa, antibiotics, isoniazid, cyclophosphamide, indomethacin, phenytoin, sulfonamides). S/S: viral prodrome for several days followed by symptoms of systolic dysfunction (dilated cardiomyopathy). palpitations, tachycardia. HF Sx dyspnea, fatigue, exercise intolerance, S3 gallop. Other megacolon, pericarditis (pericardial rub/effusion). Testing: CXR shows cardiomegaly. ECG shows sinus tachy, normal, or pericarditis (diffuse ST elevations and PR depressions in precordial leads). labs may have positive cardiac enzymes, increased ESR. echo ventricular systolic dysfunction. endomyocardial biopsy gold standard, shows infiltration of lymphocytes with myocardial tissue necrosis. usually reserved for severe or refractory cases. Treatment: supportive mainstay of treatment is standard systolic HF Tx (ACE inhibitors, diuretics, beta blockers). Immunosuppressants if chronic. IVIG if giant cell, eosinophilic.

essential tremor

Patho/etiology: uncertain, but it is sometimes inherited in an autosomal dominant manner. Responsible genes have been identified at 3q13, 2p22-p25, and 6p23. S/S: may begin at any age and is enhanced by emotional stress. The tremor usually involves one or both hands, the head, or the hands and head, while the legs tend to be spared. The tremor is not present at rest, but emerges with action. Examination reveals no other abnormalities. Ingestion of a small quantity of alcohol commonly provides remarkable but short-lived relief by an unknown mechanism. tremor typically becomes more conspicuous with time. Occasionally, it interferes with manual skills and leads to impairment of handwriting. Speech may also be affected if the laryngeal muscles are involved. Tx: often unnecessary. When it is required because of disability, propranolol may be helpful. Long-term therapy is typical; however, intermittent therapy is sometimes useful in patients whose tremor becomes exacerbated in specific predictable situations. Primidone (low dose) may be helpful when propranolol is ineffective parkinsons v. ET: The family history, the character of the tremor, and lack of other neurologic signs should distinguish essential tremor from Parkinsonism. Essential tremor doesn't cause associated health problems, while Parkinson's carries other symptoms, such as stooped posture and balance problems. Essential tremor may affect the voice box, but Parkinson's does not.

pulmonary embolism

Patho: Complication of underlying venous thrombosis. Microthrombi are normally lysed within the venous circulatory system, but under pathological conditions they escape to grow and propagate. These clots break loose and embolize to block pulmonary BV. S/S: Triad: hemoptysis 3%, chest pain 17%, dyspnea 60%. Although this is not always accurate. This is how patients actually tend to present: 96% will have tachypnea, 58% have rales, 53% have accentuated second heart sound, 44% have tachycardia, 43% have fever. Work up for patients with suspected PE Use Well's criteria PE unlikely (<4)? Rapid ELISA D-dimer. Comes back negative, follow OFF anticoagulation. Positive, helical CT. Normal, PE negative. Intermediate, USN or pulm angiography. Positive, treat for PE. PE likely? Go straight to helical CT, skip D-dimer! S1Q3T3 on ecg (rare) Treatment Decide b/w fibrinolytics and anticoagulants. ALWAYS anti-coagulate, fibrinolytics OK if hemodynamically UNSTABLE, no hx stroke or active internal bleeding. How long to anti-coagulate? First episode with a reversible risk factor: 3-6 months First episode w/ idiopathic etiology: 12 months Nonreversible risk factors/recurrent disease: 6-12 months to indefinitely Management of PE (or suspected PE) in pregnant patients DVT and PE are common during all trimesters of pregnancy and 6-12 weeks post-partum.· Diagnostic approach the SAME in pregnant patient as non-pregnant· Heparin, Fibrinolysis (alteplase), chest CT, nuclear perfusion lung scans all safe in pregnancy· Warfarin NOT safe in pregnancy

pheochromocytoma

Patho: RARE tumors of the sympathetic NS that arise from adrenal medulla and usually secrete epinephrine, norepinephrine, and dopamine. Fatal in 1/3 patients PRIOR to Dx. Triggers include surgery, exercise, pregnancy, medications (tricyclic antidepressents, opiates, metoclopramide, glucagon, histamine). S/S: HTN (temporary or sustained). PHE= Palpitations, Headache, Excessive Sweating. Chest/abdominal pain, weakness, fatigue, weight loss despite increased appetite. Testing: Best initial test will show increased plasma free metanephrines. Diagnosis is confirmed with 24-hour urine collection for metanephrine. Increased 24-hour urine level of vanillylmandelic acid (VMA) After lab testing, proceed with CT scan or MRI for imaging of adrenal glands. MIBG scanning is done to find the location of pheochromocytoma. It is also used to find metastasis that occurred from pheochromocytoma. Treatment: ultimately complete adrenalectomy after 1-2 weeks of medical therapy-- nonselective alpha blockade (phenoxybenzamine or phentolamine) 1-2 weeks followed by beta blockers or CCB to control BP prior to Sx. Do not initiate therapy with beta blockade to prevent unopposed alpha constriction during catecholamine release triggered by surgery or spontaneously. For patients actively in hypertensive crisis, phentolamine, nitroprusside, or nicardipine can be used to acutely lower the BP.

sarcoidosis

Patho: exaggerated t cell response to a variety of antigens or self-antigens, leading to central immune system activation, granuloma formation, and peripheral immune depression. S/S: 50% asymptomatic (found on imaging). PULM: dry cough, dyspnea, chest pain, rales. LYMPH: intrathoracic lymphadenopathy (hilar nodes, paratracheal). SKIN: erythema nodosum, lupus pernio, maculopapular rash, parotid gland enlargement. EYES: anterior uveitis CARDIAC: restrictive cardiomyopathy. RHEUMATOLOGIC: arthralgias, fever, malaise, weight loss, hepatosplenomegaly. NEURO: CN palsies especially CNVII, diabetes insipidus. LOFGREN SYNDROME: triad of erythema nodosum, bilateral hilar LAD, polyarthralgias with fever--> very specific, dont even need a Bx in this case Testing: based on compatible clinical/radiological findings, noncaseating granulomas. CXR best initial test, shows bilateral hilar LAD. Stage 1= BHL (no Sx / mild pulm Sx) Stage 2= BHL + ILD Stage 3= ILD only Stage 4= fibrosis (restrictive Dz) PFT may show restrictive pattern; primarily used to monitor response to Tx. Tissue biopsy MOST ACCURATE and reveals noncaseating granulomas. Labs will show increased ACE levels, hypercalcemia, increased vitamin D. Tx: asymptomatic; observation. Spontaneous remission in 2 years in most w/o treatment. Symptomatic; oral corticosteroids 1st line. Methotrexate, hydrochloroquine (for severe skin lesions). Remember= ACE Levels Super High ACE= African American C= dry cough E= erythema nodosum L= lupus pernio S= steroids H= bilateral Hilar LAD

rheumatic fever

Patho: most common between 5-15 y/o. Systemic immune process sequela of strep throat. Effects mitral and other valves acutely, rarely leading to heart failure. S/S: (MAJOR) carditis, arthritis, chorea, erythema marginatum, subQ nodules. JONES describes the major criteria- Joint involvement, Ouch my heart (a stretch), Nodules, Erythema marginatum, Sydenham chorea. (MINOR) fever, ESR > 60 mm/h OR CRP > 3 mg/dL. Dx: JONES criteria presence of 2 major criteria or one major and two minor criteria establishes diagnosis. Tx: bed rest until temperature returns to normal (w/o use of antipyretics), SED rate and resting pulse rate and ECG have returned to normal. Salicylates markedly reduce fever and relieve joint pain/swelling, though they do not effect disease process itself (adults require large doses whereas children can have lower). Penicillin or erythromycin is used to eradicate strep infection if present. short course of Corticosteroids if response to salicylates is inadequate, can improve joint symptoms rapidly.

carcinoid tumor

Patho: neuroendocrine tumors characterized by slow growth, low metastasis, well-differentiated. Lung 2nd most common site of carcinoid tumors (GI #1). May secrete serotonin, ACTH, ADH, or melanocyte stimulating hormone. S/S: <60 y/o. focal wheezing, cough, hemoptysis, SIADH, Cushing's, obstruction. Carcinoid syndrome: flushing, tachycardia, and bronchoconstriction (d/t histamine release), diarrhea (d/t serotonin release), hypotension (hemodynamic instability) Dx: bronchoscopy will show pink-purple well-vascularized centrally-located tumor. Biopsy is definitive. Tx: surgical excision as they are usually resistant to radiation and chemo. Ocreotide may be used to reduce Sx as it will decrease secretion of active hormones.

polyarteritis nodosa

Patient will present as → a 45-year-old male with generalized symptoms such as malaise, fever, sore throat, and joint and muscle aches and pains. He also complains of numbness, tingling, sensory disturbances, and weakness. On PE, you notice the presence of tender lumps under the skin, especially on the thighs and lower legs. Laboratory testing is notable for a newly elevated creatinine of 2.6 mg/dL, ESR, and CRP. He is also seropositive for hepatitis B virus, ANCA-negative, and guaiac positive. patho/etiology: blood vessel disease characterized by inflammation of small and medium-sized arteries (vasculitis), which can restrict blood flow and damage vital organs and tissues Most common in middle-aged men. Associated with Hepatitis B and C . Increased microaneurysms w/ aneurysmal rupture leading to hemorrhage and thrombosis as well as organ ischemia or infarction Damage to affected artery ⇒ HTN, aneurysm, thrombosis, necrosis S/s: Renal: HTN d/t increased renin production (may progress to renal failure) Constitutional: fevers, myalgias, arthritis CNS: neuropathy, amaurosis fugax, peripheral neuropathy Dermatologic: livedo reticularis, purpura, ulcers, gangrene Diagnosis requires confirmation with either a tissue biopsy or angiogram Biopsy of an affected artery (gold standard) demonstrates necrotizing arteritis ⇒ or arteriography showing the typical aneurysms in medium-sized arteries ↑ ESR. ANCA negative (P-ANCA positive in < 20% of cases) Renal or mesenteric angiography: microaneurysms with abrupt cut-offs of small arteries) TX: Steroids (prednisone) +/- cyclophosphamide if refractory Plasmapheresis in patients with Hepatitis B virus

idiopathic pulmonary fibrosis

Patient will present as → a 55-year-old female who is a current smoker presents with a 9-month history of respiratory symptoms, including dyspnea on exertion, thoracic pain, and dry cough, which were preceded by a pulmonary infection. On auscultation, you hear inspiratory crackles. Pulmonary function tests (PFTs) show only mild impairment of vital capacity with decreased lung volume and a normal to increased FEV1/FVC ratio. AKA idiopathic fibrosing interstitial pneumonia; MC ILD. Patho/etiology: progressive scarring of the lungs d/t an unknown cause. MC in men >40, smokers. In order to be considered "idiopathic", you must rule out other common causes such as drugs (amiodarone), and environmental or occupational exposures. non-idiopathic: viral infections, environmental (silica, hard metal dust), medication, genetics, XRT, GERD S/s: progressive dyspnea, nonproductive cough. PE shows fine, dry bibasilar inspiratory crackles. clubbing of the fingers may be seen. Dx: CXR shows basal predominant reticular opacities (honeycombing). CT is preferred, shows reticular honeycombing, focal ground glass opacification, traction bronchiectasis or bronchiolectasis. PFTs show a restrictive pattern (normal or increased FEV1/FVC, normal or decreased FVC, decreased lung volumes, decreased DLCO). Bx shows honeycombing (large cystic airspaces from cystic fibrotic alveolitis) Tx: no effective medical management; lung transplant only possible cure (Poor prognosis without transplant). Strategies include smoking cessation, oxygen. Pirfenidone and nintedanib are antifibrotic agents that may slow progression but does not significantly benefit mortality.

peripheral vascular disease (PAD, PVD)

Peripheral artery disease is atherosclerotic disease of the LE (and vessels outside the heart and brain) Sx: intermittent claudication = MC presentation; reproducible pain/discomfort in lower extremity brought on by exercise with exercise and relieved with rest; erectile dysfunction. Aortic bifurcation, common iliac = buttock, hip groin claudication--> Leriche syndrome refers to a buildup of plaque in the iliac arteries → claudication, impotence, decreased femoral pulses. Femoral artery: thigh/upper calf claudication (MC) Popliteal artery: lower calf claudication Signs: weak or absent distal pulses, arterial bruits, loss of hair, shiny atrophic skin, pallor with dependent rubor The 6 P's caused by acute arterial embolism: pain, pulselessness, pallor, paresthesias, poikilothermia (inability to regulate temperature), paralysis DX: arteriography is the gold standard (clinically only done if revascularization is planned); Doppler ultrasonography; ankle-brachial-index (ABI) < 0.9 (normal = 1-1.2) A falsely high index may indicate severely hardened, non-compressible leg vessels Tx: Risk factor modification: d/c tobacco, control diabetes, hypertension, hyperlipidemia Medications: B-blocker, ACE-I, statins Platelet inhibitors: cilostazol = mainstay of treatment (helpful for intermittent claudication), aspirin, clopidogrel (Plavix) Revascularization: Angioplasty → Fem-pop bypass → Endarterectomy Chronic Venous Insufficiency: Symptoms: progressive edema, itching, dull pain, ulcerations Signs: shiny, thin, atrophic skin Severe disease: ulceration (stasis ulcer, dermatitis) - PAINLESS Diagnostics: clinical; duplex ultrasonography Management: prevention, elevation, avoid extended standing or sitting, compression hose Interventions: wet compresses, compression boots or stockings, skin grafting

cardiac arrythmias/conduction disorders

Premature Beats PVC: Early wide bizarre QRS, no p wave seen PAC: abnormally shaped P wave PJC: Narrow QRS complex, no p wave or inverted p wave Paroxysmal supraventricular tachycardia narrow, complex tachycardia, no discernible P waves Atrial fibrillation/flutter A-fib: Irregularly irregular rhythm with disorganized and irregular atrial activations and an absence of P waves A-flutter: Regular, sawtooth pattern and narrow QRS complex Sick sinus syndrome Brady-tachy: Arrhythmia in which bradycardia alternates with tachycardia Sinus arrest: prolonged absence of sinus node activity (absent P waves) > 3 seconds Sinus arrhythmia Normal, minimal variations in the SA Node's pacing rate in association w/ the phases of respiration. Heart rate frequently increases with inspiration, decreases with expiration Ventricular arrhythmias: Premature ventricular contractions (PVCs) Early wide "bizarre" QRS, no p wave seen Ventricular tachycardia 3+ consecutive VPBs, displaying a broad QRS complex tachyarrhythmia Torsades de pointes Polymorphic ventricular tachycardia that appears to be twisting around a baseline Ventricular fibrillation Erratic rhythm with no discernable waves (P, QRS, or T waves) Atrioventricular block First Degree AV Block: The PR interval is longer than 0.2 seconds or one block on EKG. Type I Second Degree (Wenckebach): progressive lengthening of PR interval then missed QRS complex. Type II Second Degree (Mobitz): fixed PR interval with occasional dropped QRS complexes Third Degree AV Block: no association between P wave and QRS complex Bundle branch block Left: R and R' (upward bunny ears) in V4-V6 Right: R and R' (upward bunny ears) in V1-V3

multiple myeloma

Presentation: older adults (~65 y/o). BREAK your bones: Bone pain, Recurrent infections, Elevated Ca++, Anemia, Kidney injury. MC presenting complaints are those related to anemia, bone pain, kidney disease, and infection. Bone pain is most common in the back, hips, or ribs or may present as a pathologic fracture, especially of the femoral neck or vertebrae. Patients may also come to medical attention bc of spinal cord compression from a plasmacytoma or the hyperviscosity syndrome (mucosal bleeding, vertigo, nausea, visual disturbances, alterations in mental status, hypoxia). Many patients are diagnosed bc of lab findings of elevated total protein, hypercalcemia, proteinuria, elevated SED rate, or abnormalities on serum protein electrophoresis obtained for symptoms or in routine screening studies. Few patients come to medical attention because of organ dysfunction due to amyloidosis. Exam: pallor, bone tenderness, or soft tissue masses. Patients may have neurologic signs related to neuropathy or spinal cord compression. Fever occurs mainly with infection. Acute oliguric or nonoliguric kidney injury may be present d/t hypercalcemia, hyperuricemia, light chain cast injury, or primary amyloidosis. Labs: Anemia. RBC morphology is normal, but rouleaux formation is common and may be marked. Absence of rouleaux formation, however, excludes neither plasma cell myeloma nor the presence of a serum paraprotein. The neutrophil and platelet counts are usually normal at presentation. hallmark of myeloma is the finding of a paraprotein on serum or urine protein electrophoresis (PEP) or immunofixation electrophoresis (IFE). The majority of patients will have a monoclonal spike visible in the gamma- or beta-globulin region of the PEP . Bence Jones protein (IgG light chain) found on urine electrophoresis. Blood smear: Only rarely will plasma cells be visible on peripheral blood smear. Dx: CRAB HELPS! C= elevated Ca R= renal failure A= anemia B= bone lesions. Tx: bone marrow transplant = definitive Melphalan (alkylating agent, which inhibits DNA and RNA synthesis, causing the death of both dividing and non-dividing tumor cells), steroids, thalidomide, bortezomib

adrenal insufficiency

Primary (Addison's disease): autoimmune, infections, disease of adrenal gland ⇒ decrease in cortisol secretion Adrenal gland destruction causing lack of cortisol and aldosterone secretion Autoimmune (70%), infectious (tuberculosis), vascular (thrombosis/hemorrhage), metastatic, medications (rifampin, barbiturates, phenytoin, ketoconazole) Dx: increased ACTH, decreased cortisol, decreased aldosterone Secondary: pituitary adenoma or discontinuation of steroid - pituitary failure! Exogenous steroid use (most common); hypopituitarism Dx: decreased ACTH, decreased cortisol, normal aldosterone Adrenal crisis = acute adrenal insufficiency Dx: 8 AM serum cortisol and plasma ACTH alone with ACTH stimulation test High ACTH, low cortisol = primary Low ACTH, low cortisol = secondary CRH stimulation test: differentiates between causes of adrenal insufficiency Primary/Addison's (adrenal): high ACTH, low cortisol Secondary (pituitary): low ACTH, low cortisol Adrenal autoantibodies can be assessed; CXR for TB (CT of adrenals) Autoimmune: atrophied adrenals TB / granulomas: enlarged adrenals + calcification Bilateral adrenal hyperplasia = genetic enzyme defect Tx: Addison's: cortisol replacement therapy + androgen replacementGlucocorticoid + mineralocorticoid ⇒ hydrocortisone = 1st line, fludrocortisone for primary Addison's disease only Secondary: cause = focus of treatment (pituitary adenoma resection, wean steroid therapy slowly) Mark as complete

gastric cancer

RF: Chronic H. pylori infection most common (leads to an intestinal type gastric cancer which resembles intestinal cancers in forming glandular structures). Could also be acquired or hereditary mutations (less common, namely in the Asian population. Causes diffuse gastric cancer that is poorly differentiated, has signet ring cells and lacks glandular formation). S/S: Determined in part by the location of the tumor, but include dyspepsia, vague epigastric pain, anorexia, early satiety, weight loss. Signs of metastasis include a palpable supraclavicular lymph node (Virchow's node), an umbilical nodule (Sr. Mary Joseph), rigid rectal shelf, or ovarian mets. Testing: endoscopy. Treatment: Curative surgical resection (not always possible if late detection) w/ post-op chemo or chemoradiation. Palliative modalities.

coronary vascular disease

RF: DM is worst; considered a CAD equivalent. smoking (most important MODIFIABLE). hyperlipidemia. HTN. men >45 or women > 55. family Hx of CAD (especially father or brother before 55 and mother or sister before 65) Pathologic process affecting coronary arteries usually d/t atherosclerosis --> inadequate tissue perfusion as there is increased demand and decreased coronary artery blood supply. leads to angina MOA of atherosclerotic disease: Foam cells are macrophages that gobble up lipids in the wall; it then dies off and stays there and becomes a foam cell; when it dies it releases cytokines that attract more macrophages to the area ⇒ plaque clot Fibrous plaque forms over lipid core: Complete clot -> ST-elevation MI; Incomplete clot -> unstable angina/NSTEMI Vulnerable plaque is easy to rupture; thick plaque is stable Adhesion, activation, aggregation, propagation of clot, platelet adherence Stress testing Stress ECG Indications: only if baseline ECG is normal. + if ECG changes (ST depressions, T wave inversions, poor R wave progression) OR reproduction fo Sx. Limitations: does not locate area of ischemia Myocardial perfusion imaging uses thallium or technetium for imaging. Indications: if baseline ECG is ABnormal (unlike stress ECG). Gives info re: the location and extent of ischemia Can be performed with exercise OR a pharmacologic agent if pt cannot exercise like adenosine or dipyridamole (vasodilators) C/I include bronchospastic dz, hypotension, aV blocks. Theophylline and caffeine should be stopped at 48h and 12h before, respectively. Stress echocardiogram indications: if baseline ECG is ABnormal (unlike stress ECG). Gives info re: the location and extent of ischemia. Can be performed with exercise or pharmacologic if pt cannot exercise w/ positive inotropes (dopamine or dobutamine). C/I if severe LV outflow obstruction (aortic stenosis), ventricular arrythmias, recent MI (1-3d), or severe systemic HTN Other stress test considerations-- patients w/o Hx of CAD, antianginal meds should be withheld 48 hr prior to test (CCBs, BBs, NTG) If known Hx of CAD, d/c them prior to testing. Coronary angiography definitive Dx/gold standard. Cath outlines coronary artery anatomy and defines location, extent of CAD Indications: 1. confirm/exclude CAD in patients w/ Sx consistent with CAD 2. confirm/exclude CAD in patients with negative noninvasive testing for CAD. 3. Patients who may possibly need revascularization (PTCA or CABG).

celiac disease

RF: Typically presents bw 6 months-24 months old (when solid food is introduced). Most common (1/250) whites w/ European ancestry. S/S: depends on length of small intestine involved and age at presentation. Infants <2 years show typical Sx of malabsorption, diarrhea, weight loss, abdominal distention, weakness, muscle wasting, growth retardation. Stools are loose to soft, large, floating, oily or greasy, foul smelling. May be watery and frequent (up to 12 per day). Children and adults have Sx of chronic diarrhea, dyspepsia, flatulence secondary to colonic bacterial digestion of malabsorbed nutrients, weight loss variable. Atypical presentation in many adults; very few GI Sx but present are fatigue, short stature, amenorrhea, reduced fertility, osteoporosis, dental enamel hypoplasia, anemia. Dermatitis Herpetiformis cutaneous variant of celiac disease; a skin rash with itching papulovesicles over extensor surfaces of the extremities and over trunk, scalp, and neck; in <10% of patients with celiac disease. Testing: Qualitative (Sudan stain) or quantitative stool assessment for fecal fat. Serological tests include anti-glutens (anti-gliadin IgG and IgA) and anti-self (anti-endomysial IgA and anti-tissue transglutaminase IgA, AKA tTG). Check for IgA deficiency. Anti-self antibodies are undetectable after 6-12 month of GF diet. Mucosal Bx in patients w/ a + serologic test. Endoscopic bx of distal duodenum or proximal jejunum for confirmation of Dx. Normal biopsy excludes Dx, positive biopsy indicates need for repeat biopsy after a trial of GF diet. Treatment: remove all gluten from diet (wheat, rye, barley); work w/ dietician bc even some meds are made w gluten. Most also have lactose intolerance. Short-term dietary supplements need (A, B12, D, E).

renal cell carcinoma

RF: smoking. clear cell MC, then transitional cell. Sx: 60% of patients presented with gross or microscopic hematuria. Flank pain or an abdominal mass was detected in approximately 30% of cases. The triad of flank pain, hematuria, and mass was found in only 10% of patients, and often a sign of advanced disease. Fever can occur as a paraneoplastic symptom. Sx of metastatic disease (cough, bone pain) occur in 20-30% of patients at presentation. D/t widespread use of ultrasound and cross-sectional imaging, renal tumors are frequently detected incidentally in individuals with no urologic symptoms. labs: Contemporary studies suggest hematuria is present in less than 50% of patients. Erythrocytosis from increased erythropoietin production occurs in 5%, though anemia is more common; hypercalcemia may be present in up to 10% of patients. Stauffer syndrome is a reversible syndrome of hepatic dysfunction (with elevated liver tests) in the absence of metastatic disease.Imaging: Solid renal masses are often first identified by abdominal ultrasonography or CT. CT and MRI scanning are the most valuable imaging tests for renal cell carcinoma. These scans confirm the character of the mass and provide valuable staging information with respect to regional lymph nodes, renal vein or vena cava tumor thrombus, and adrenal or liver metastases. CT and MRI also provide valuable information regarding the contralateral kidney (function, bilaterality of neoplasm). Chest radiographs or CT exclude pulmonary metastases. Bone scans should be performed for large tumors and in patients with bone pain or elevated serum alkaline phosphatase levels. Brain imaging should be obtained in patients with high metastatic burden or in those with neurologic deficits. TX: surgery with radical nephrectomy = curative

rheumatic heart disease

Rheumatic heart disease is a consequence of rheumatic fever characterized by inflammation and scarring of the heart valves Most commonly affects the mitral valve > aortic valve > tricuspid valve Etiology → at least 1 episode of acute rheumatic fever from group A streptococci Patho: Cumulative inflammation and scarring of the heart valves resulting from an abnormal immune response to group A streptococci. Molecular mimicry between streptococcal M protein and cardiac proteins--> Cross-reaction of antibodies to streptococcal M protein with self-antigens Immune-mediated (type II) hypersensitivity The disease is characterized by valve regurgitation (early stage), most commonly of the mitral valve and valve stenosis (late-stage) The early-stage may last for years and may be asymptomatic The onset of symptoms usually occurs 10-20 years after acute rheumatic fever SX: palpitations, dyspnea, mitral regurgitation, mitral stenosis, aortic regurgitation, or aortic stenosis DX: based on clinical presentation and confirmed with echo. Echocardiography → valvular abnormalities, including regurgitation or stenosis Labs: ↑ anti-streptolysin O (ASO) titers Histology: Aschoff bodies (granulomas with giant cells) on heart valves TX: Prophylaxis to prevent recurrence or worsening of rheumatic heart disease. All patients w/ rheumatic heart disease should undergo prophylaxis with penicillin (or sulfadiazine if allergic) for the specified time period below: No evidence of carditis ⇒ 5 years or until age 21 (whichever is longer) Evidence of carditis w/o valvular abnormalities ⇒ 10 years or until age 21 (whichever is longer) Evidence of carditis and valvular abnormalities ⇒ 10 years or until age 40 (whichever is longer) Operative: valve repair or replacement depending on type and severity of valve pathology. Surgical repair vs. Percutaneous intervention

Cor pulmonale

Right ventricular enlargement & eventually failure secondary to lung disorder that causes pulmonary HTN (alot of vascular resistance in pulm--> harder for RV to push against--> hypertrophy) Etiology: COPD (most common), pulmonary embolism, vasculitis, asthma, ILD, acute respiratory distress syndrome PE: Lower extremity edema, neck vein distention, hepatomegaly, parasternal lift, tricuspid/pulmonic insufficiency, loud S2 DX: echocardiogram that shows evidence of increased pressure in the pulmonary arteries and right ventricle (RVH, R axis deviation, R atrial enlargement, R BBB) F/u tests can be done to ID the underlying cause, for example, spirometry can be done to look for chronic lung disease The gold standard diagnostic test to directly measure pulmonary pressures and assess for response to vasodilating medications is a right heart catheterization. CBC might show polycythemia with increased hematocrit. TX: Diagnose and treat the underlying condition before cardiac structure change becomes irreversible Diuretics not helpful! May be harmful

esophageal strictures

Risk factors: 5% of patients with esophagitis have stricture formation. Usually at gastroesophageal junction. S/s: gradual solid food dysphagia over course of months-years; often reduction in heartburn. Testing: endoscopy with biopsy to r/o cancer. Treatment: balloon dilation via flexible bougies 1 to several sessions. Long term PPIs to decrease recurrence. webs, rings: Esophageal web: thin membranes in the mid-upper esophagus. May be congenital or acquired Plummer-Vinson: esophageal webs + dysphagia + iron deficiency anemia Strictures often d/t scarring from the healing process of ulcerative esophagitis A Schatzki ring is a diaphragm-like mucosal ring that forms at the esophagogastric junction (the B ring). If the lumen of this ring becomes too small, Sx occur. The cause is not clear, but such rings are usually found in older individuals and have been observed in 6% to 15% of patients undergoing a barium swallow study; however, only 0.5% of those being examined have significant symptoms. Sx correlate w/ size of the lumen of the ring: a lumen of more than 20 mm in diameter provides few if any Sx; if it is less than 13 mm in diameter, chronic and more severe Sx occur. Most patients have intermittent, nonprogressive dysphagia for solid food that occurs while consuming a heavy meal with meat that was "wolfed down," hence the pseudonym the "steakhouse syndrome." Sometimes the meal is regurgitated, relieving the block, and eating can be resumed. Patients with a Schatzki ring are also at risk for GERD. A diagnosis is confirmed by radiographic barium swallow or endoscopic means, and if symptoms are sufficiently troublesome, the treatment of choice is rupture of the ring by dilation.

esophageal varices

Risk factors: Cirrhosis MCC in adults, portal vein thrombosis most common in children. Risk for rupture depends on size of varices, presence of red whale markings on endoscopy, severity of underlying liver disease, or ongoing active EtOH abuse. S/S: varices do not cause Sx but patient will present with acute upper GI bleeding after vomiting, retching, or withdrawal. Bleeding may be severe, causing hypovolemic shock. Underlying coagulopathy bc liver disease. Testing: upper endoscopy for diagnostics and therapeutics. Treatment Acute: stabilize patients volume status and address coagulopathy. Resuscitation with IV fluids, FFP, and vitamin K. Patients with cirrhosis should undergo abx prophylaxis with fluoroquinolones or 3rd gen cephalosporin. Lactulose given to help prevent encephalopathy. Tx with octreotide (vasoactive) reduces portal pressure and stops bleeding in about 80% of patients. Once stabilized, undergo emergent endoscopy; Tx any ID'd sources of bleeding with balloon tamponade or variceal banding. Chronic: can give transvenous intrahepatic portosystemic shunts (TIPS) for portal HTN, BB + band-ligation, or liver transplantation for severe cirrhosis/liver dz

hemorrhoid

Risk factors: increased venous pressure d/t straining, pregnancy, obesity, prolonged sitting, cirrhosis w/ portal HTN. S/S: BRBPR, streaks of blood on TP. If chronically prolapsed, may result in a sense of fullness or discomfort w/ mucoid perianal discharge. pain if inflamed internal hemorrhoid. Staging: grade i= confined to anal canal. grade ii= mucosal prolapse occurs during straining. grade iii= prolapsed hemorrhoids require manual reduction. grade iv= remain chronically protruding. Treatment: stage i and ii conservative tx; increase fluid intake, increase fiber. No straining, limit time on toilet. stage iv same as stage i+ii with addition of OTC topicals like Prep H, Anusol, Tucks. Suppositories (combo of emollients, anesthetics, vasoconstrictors, astringents, steroids). refractory hemorrhoids sclerotherapy, photoligation, band therapy. surgical excision for small subset of patients with chronic, severe bleeding.

chlamydia

The most common sexually transmitted infections Gram-negative rod. Intracellular Asymptomatic, dysuria Diagnosis: NAAT Gram stain reveals no organisms Treatment: doxycycline 100 mg PO two times per day for 7 days or (1) Azithromycin 1g PO x 1 + Ceftriaxone 500 mg IM x 1 to cover for gonorrhea Alternative: erythromycin 500 mg QID x 7 days levofloxacin 500 mg P daily x 7 days In pregnancy: Azithromycin 1 g PO single dose or Amoxicillin 500 mg PO tid x 7 days

irritable bowel syndrome

Risk factors: lower visceral pain threshold, underlying psychiatric issues (depression, anxiety, or somatization). 2/3 of patients are women. S/S: late teens, early 20's. Straining, urgency, bloating. May have other somatic or psychological components i.e. anxiety, depression, heartburn, fatigue, myalgias. Usually PE is normal, but may have lower abdominal tenderness. Could be IBS-D (diarrhea), IBS-C (constipation), IBS-M (mixed). Testing: Labs CBC, BMP, Mag, Phos, thyroid studies, ESR. Fecal calprotectin level can screen for IBD; levels >50 do endoscopy. Stool testing for parasitic infections. Colonoscopy reserved for older patients or those patients with alarm symptoms. Celiac testing. Treatment: reassurance; explain that the alterations in visceral motility and sensitivity may be exacerbated by environmental, social, or psychological factors like foods/meds/hormones/stress. Lifestyle Encourage patients to log Sx and any associating factors. Avoid fatty foods and caffeine. R/O lactose intolerance or celiac. Avoidance of FODMAPs (pretty much anything made w/ wheat/barley/rye). High fiber diet, increase water intake if constipation predominant. Diarrhea - diphenoxylate or loperamide (Imodium) Constipation - Colace, psyllium, cisapride Tegaserod maleate (Zelnorm) is a serotonin agonist introduced for the treatment of IBS Rifaximin (Xifaxan) - antibiotic approved for IBS-D Health maintenance: Avoid dairy products and excessive caffeine, high fiber diet, physical exercise, stress management, and relaxation techniques Comorbid: Depression, anxiety, somatization

colorectal Cancer

Risk factors: usually no risk factors. family Hx of neoplasia, >50y/o, poor diet, IBD. L.O.F of 1+ tumor suppressor genes, or activation of oncogenes. low dose ASA decreases the risk. S/S: as they grow slowly, it can take years to show Sx. asymptomatic tumors detected by fetal occult blood. right sided symptoms include chronic blood loss, Fe deficiency anemia, fatigue, weakness. Fecal material liquidy, obstruction uncommon. left sided apple core bowel circumferentially, solid fecal matter, obstruction, colicky abdominal pain and change in bowel habits, constipation alternates with increased frequency and loose stools. red-streaked stool, hematochezia, tenesmus, urgency. PE usually normal, may be able to palpate mass in abdomen. heck liver for hepatomegaly. labs CBC for anemia, high LFTs if metastases, CEA measured in proven colorectal CA. Levels increased in 70%, not correlating with CA stage. Post-surgery CEA levels normal. colonoscopy diagnostic procedure of choice; can do Bx. imaging CXR to look for metastatic lung cancer. abdominal and pelvic CT scans for staging (though intra-op palpation and USN more accurate for liver mets). for rectal CA, pelvic MRI needed to determine depth of CA thru rectal wall. staging: TNM 0=carcinoma in situ (no invasion) 1=tumor invades submucosa or muscularis propria. 2= invasion into subserosa or tissues around colon or rectum OR it invades visceral peritoneum OR other organs/structures. 3=bowel wall perforation w/ lymph node involvement. 4=distant metastasis. Treatment: if patient can tolerate anesthesia and have lesions that can be resected, do surgery (treatment of choice). regional lymph node dissection for staging. adjuvant therpay for stage III (post-op chemo w/ FOLFOX), stage IV (post-op chemo with FOLFOX 1st line).F/U post-Sx: evaluate q3-6mo x2-5 years w/ Hx, PE, fecal occult blood testing, LFTs, CEA levels. Colonoscopy w/in 6-12mo post-op THEN every 3-5 years to look for polyps or CA. If any + results, do CXR and abd CT to look for recurrent or metastatic dz.

thyroid cancer

S/S: Papillary 80% of all thyroid cancers; slow growing and excellent prognosis. Generally presents as a single thyroid nodule, but can be multinodular. Rarely metastasizes but if it does, regional lymph node. Can be asymptomatic, or present as painless, palpable nodule. Thyroid function tests are generally wnl. Patients 1st undergo a thyroid USN to identify the nodule(s) and then FNA of any suspicious nodules. Highly treatable with surgery Follicular More aggressive than papillary. Metastasize to neck nodes, bones, lung (follicular metastasizes Far). Metastatic sites can secrete hormone and produce thyrotoxicosis. Serum thyroglobulin levels elevated Medullary About 2-3% of all thyroid cancers. Some have familial (genetic) component. Metastasizes early to local nodes, muscle, trachea, mediastinum. Later to bones, lungs, adrenals, liver. Causes flushing and diarrhea. Elevated levels of serum calcitonin (can be used to monitor disease) Anaplastic About 2% of thyroid cancers. Older patients, rapidly enlarging mass. Aggressive cancer with early metastasis. 5 Year survival rate of 5% Treatment: Papillary + Follicular: thyroidectomy (total or near total) usually followed by post-op Levothyroxine to replace hormone production and suppress tumor regrowth. Post-surgery radioiodine in some patients who are high or sometimes intermediate risk. Monitor thyroglobulin levels, TSH, and neck US post-op. Medullary: total thyroidectomy that may include dissection of lymph nodes and surrounding fatty tissue on the ipsilateral side. MTC does not take up iodine. May order urinary metanephrine levels to rule out PCC. Calcitonin levels are used to monitor for recurrence or residual disease. Anaplastic: most are not amenable to surgical resection. External beam radiation or chemo. Palliative tracheostomy may be needed to maintain airway.

nephritic syndrome

S/S: Glomerular hematuria (and RBC casts if glomerular bleeding is heavy) Proteinuria of 1-3 g/day HTN Edema Rising creatinine over days to months S/s: oliguria, fever, abdominal/flank pain. azotemia. acute decrease in GFR leads to sodium retention. This is clinically manifested by edema (not as bad as nephrotic), first seen in regions of low tissue pressure such as the periorbital and scrotal areas, and by HTN. Heavy glomerular bleeding from inflammation may result in gross hematuria (smoky or cola-colored urine). rapidly progressive glomerulonephritides (RPGNs), with systemic symptoms, are at the "most severe" and clinically urgent end of the nephritic spectrum. Labs: elevated BUN/Cr. UA-- urine dipstick is positive for protein (subnephrotic) and blood. Urinary microscopy reveals red blood cells that are misshapen or dysmorphic from traversing a damaged glomerular filtration barrier. RBC casts are seen w/ heavy glomerular bleeding and tubular stasis.Bx-- Definitive diagnosis of the underlying glomerular disease cannot be made without a kidney biopsy. Candidates for biopsy are patients for whom test results would influence management; exceptions include those with advanced underlying CKD, those who cannot adhere to medical therapy or those for whom immunosuppressive therapy is not appropriate, or those for whom the presentation is "classic" for a particular disease. C/I include a bleeding diathesis, thrombocytopenia, and uncontrolled hypertension. Bx will show hypercellular (WBCs, mesangial cells), immune complex deposition. If crescent shape of glomerulus, RPGN! admit

HSV

S/S: burning and stinging. Neuralgia may precede or accompany attacks. The lesions consist of small, grouped vesicles on an erythematous base that can occur anywhere but that most often occur on the vermilion border of the lips and the penile shaft, the labia, the perianal skin, and the buttocks. Regional lymph nodes may be swollen and tender. The lesions usually crust and heal in 1 week. Immunosuppressed patients may have unusual variants, including verrucous or nodular herpes lesions at typical sites of involvement. Dx: Direct fluorescent antibody slide tests offer rapid, sensitive diagnosis. Viral culture or PCR may also be helpful. Herpes serology is not used in the diagnosis of an acute genital ulcer. However, specific HSV-2 serology by Western blot assay or enzyme-linked immunosorbent assay (ELISA) can determine who is HSV-infected and potentially infectious, but routine HSV-2 screening is not recommended by the United States Preventive Services Task Force. multinucleate giant cells on Tzanck smear. Tx: 1st clinical episode- acyclovir 400mg PO 5x/d. valacyclovir 1000mg PO BID. famciclovir 250 mg PO TID. all x7-10d. for recurrent episodes, valtrex 500mg PO BID x3d Prevention: Sunscreens are useful adjuncts in preventing sun-induced HSV-1 recurrences. A preventive antiviral medication should be started beginning 24 hours prior to ultraviolet light exposure, dental surgery, or orolabial cosmetic surgery. The use of latex condoms and patient education have proved effective in reducing genital herpes transmission in some studies but have not proved beneficial in others. No single or combination intervention absolutely prevents transmission.

BPH

S/S: obstructive and irritative complaints. Obstructive Sx include hesitancy, decreased force and caliber of the stream, sensation of incomplete bladder emptying, double voiding (urinating a second time within 2 hours), straining to urinate, and postvoid dribbling. Irritative symptoms include urgency, frequency, and nocturia. American Urological Association (AUA) symptom index is most important tool used in eval of pts PE: DRE shows smooth, firm, elastic enlargement of the prostate. Induration, if detected, must alert the clinician to the possibility of cancer, and further evaluation is needed (ie, PSA testing, transrectal ultrasound, and biopsy). Exam of the lower abdomen should be performed to assess for a distended bladder. Labs: UA to exclude infection or hematuria. PSA if life expectancy >10 y; increases the ability to detect prostate cancer over DRE alone; however, because there is much overlap between levels seen in benign prostatic hyperplasia and prostate cancer, its use remains controversial. usually >4 Imaging: Upper tract imaging (CT or renal ultrasound) is recommended only in the presence of concomitant urinary tract disease or complications from BPH (hematuria, UTI, CKD, Hx of stone disease). As included in the Choosing Wisely (ABIM Foundation) initiative, neither serum creatinine nor imaging (ultrasound, CT, MRI) should be routinely ordered for patients with benign prostatic hyperplasia. Cystoscopy is not recommended to determine the need for treatment but may assist in determining the surgical approach in patients opting for invasive therapy. Tx: Conservative measures; e.g. decrease fluid intake before bedtime/going out; avoid caffeine, alcohol (mild diuretic effects) Alpha-adrenergic receptor blockers (terazosin, tamsulosin) → decrease prostate, bladder, urethral muscle tone 5-alpha reductase inhibitors (finasteride) → decrease DHT synthesis → reduce prostate gland size Phosphodiesterase-5 enzyme inhibitors (e.g., tadalafil) → induce smooth muscle relaxation TURP (transurethral resection of the prostate) if refractory to meds → removes excess prostate tissue to relieve obstruction - sexual dysfunction and urinary incontinence

gastritis

S/s: Dyspepsia (belching, bloating, distension, and heartburn) and abdominal pain are common indicators of gastritis Three causes: 1. Infection - H. pylori (most common) Location: antrum and body Studies: urea breath test or fecal antigen 2. Inflammation of the stomach lining (NSAIDS and Alcohol) NSAIDs: cause gastric injury by diminishing local prostaglandin production in the stomach and duodenum Alcohol: a leading cause of gastritis 3. Autoimmune or hypersensitivity reaction (e.g. pernicious anemia) Location: Body of the fundus Pernicious anemia: + schilling test + ↓ intrinsic factor and parietal cell antibodies Treatment and diagnosis: stop NSAIDs, stop smoking. empiric therapy with acid suppression 4-8 wk of PPI If no response, consider upper GI endoscopy with biopsy and ultrasound Test for H. pylori infection → if H. pylori (+) treat with (CAP) - clarithromycin + amoxicillin +/- metronidazole + PPI (i.e. Omeprazole) Quadruple therapy (PPI, Pepto, and 2 antibiotics metro + tetracycline) for one week (From GI didactic) atrophic gastritis A form of auto immune Chronic gastritis associated with chronic information, gland atrophy, and epithelial metaplasia. Patients are at increased risk for developing gastric adenocarcinoma T cell mediated destruction and auto antibodies against intrinsic factor and parietal cells can lead to B 12 deficiency/pernicious anemia Lack of parietal cells can lead to hypochlorhydria and hyperGastrinemia. Iron deficiency can also occur because gastric acid normally enhances iron absorption.

pneumothorax

SPONTANEOUS pneumothorax primary= without underlying disease secondary= with underlying disease (COPD, asthma) cause: rupture of subpleural apical blebs in response to high negative intrapleural pressures risks: tall, thin boys and men 10-30 y/o S/S: chest pain on affected side and tachypnea/dyspnea. Sx usually begin during rest and usually resolve within 24 hours. Diagnostics: decreased tactile fremitus, unilateral lag, diminished breath sounds. lab findings will usually be normal CXR will demonstrate visceral pleural line/ deep sulcus in supine position. Tx: STABLE patient with small (<15%) pneumothorax, observation appropriate. Supplemental oxygen can facilitate reabsorption of the air. repeat imaging after 6 hours. if no progression, discharge. if progression, chest tube. LARGER pneumothorax, need aspiration of air (catheter or small bore chest tube). TENSION pneumothorax causes: check-valve mechanism allows air to ENTER upon inspiration but does not allow it to EXIT on expiration; increasing intrathoracic pressure. Risks: penetrating trauma, severe lung infection, or positive pressure inflation. could happen w/ medical procedures (iatrogenic) S/S: tachycardia, hypotension, mediastinal shift. Diagnostics: CXR will show large amount of air (darkness) on affected side, contralateral shift of mediastinum. Tx: Needs immediate decompression with large bore needle or immediate chest tube placement. POTENTIAL FOR RECURRENCE IN SPONTANEOUS : 30% of patients will have another spontaneous pneumothorax (50% if ur a smoker and dont quit!) With recurrence, referral for surgery (bleb resection, pleurodesis) is appropriate. No long-term complications in most patients. ALL patients should stop smoking, avoid high altitudes, scuba diving.

chronic renal failure

Stage 1: normal GFR (>90) Stage 2: Early GFR (60-89) Stage 3: Moderate GFR (3a 45-59) ( 3b 30-44) Stage 4: Severe GFR (15-29) Stage 5: Kidney failure (GFR < 15=dialysis) E.O.D: Decline in the GFR over months to years. Persistent proteinuria or abnormal renal morphology may be present. HTN in most cases. Symptoms and signs of uremia when nearing end-stage disease. Bilateral small or echogenic kidneys on ultrasound in advanced disease patho/etiology: Over 70% of cases of late-stage CKD are d/t DM or HTN/vascular disease. Glomerulonephritis, cystic diseases, chronic tubulointerstitial diseases, & other uro diseases account for the remainder. Genetic polymorphisms of the APOL-1 gene have been shown to be associated with an increased risk of the development of CKD in persons of African descent. CKD usually leads to a progressive decline in kidney function even if the inciting cause can be identified and treated or removed. Destruction of nephrons leads to compensatory hypertrophy and supranormal GFR of the remaining nephrons in order to maintain overall homeostasis. compensatory hyperfiltration leads to overwork injury in the remaining nephrons, which in turn causes progressive glomerular sclerosis and interstitial fibrosis. Angiotensin receptor blockers (ARBs) and ACE inhibitors can help reduce hyperfiltration injury and are helpful in slowing the progression of proteinuric CKD (highest risk). S/S: Stages 1-4 CKD are asymptomatic. Symptoms develop slowly with the progressive decline in GFR, are nonspecific, and do not manifest until kidney disease is far advanced (GFR less than 5-10 mL/min/1.73 m2), and at this time S/S will be related to uremic syndrome; sallow and ill appearance, halitosis (uremic fetor), and the uremic encepholopathic signs of decreased mental status, asterixis, myoclonus, and possibly seizures. fatigue, anorexia, nausea, and a metallic taste in the mouth. CNS Sx such as irritability, memory impairment, insomnia, restless legs, paresthesias, and twitching, Generalized pruritus without rash may occur, as may decreased libido and menstrual irregularities. Pericarditis (Rare). Medications that are cleared by the kidneys will accumulate as kidney function worsens and toxicity may ensue; an important example is insulin and an increasing risk of significant hypoglycemia if doses are not appropriately reduced. most common physical finding in CKD is hypertension; this is due in part to impaired sodium excretion. It is often present in early stages of CKD and tends to worsen with CKD progression. In later stages of CKD, sodium retention may lead to clinically apparent volume overload. S/S of uremia warrant immediate hospital admission & nephro consult for initiation of dialysis. uremic syndrome is ameliorated w/ dialytic therapy DDx: Urinary obstruction, hypovolemia, hypotension, nephrotoxins (such as NSAIDs, aminoglycosides, or proton pump inhibitors), severe or emergent hypertension, and heart failure exacerbation should be excluded. Labs: defined by an abnormal GFR persisting for at least 3 months. Persistent proteinuria or abnormalities on renal imaging (eg, polycystic kidneys or a single kidney) are also diagnostic of CKD, even when eGFR is normal. helpful to plot eGFR vs time; if multiple measurements are available, the rate of progression to ESRD can be roughly estimated . If the slope of the line acutely declines, potentially reversible renal insults should be excluded (see DDx). Anemia, hyperphosphatemia, hypocalcemia, hyperkalemia, and metabolic acidosis are common complications of advanced CKD. Proteinuria may be present; quantify it for cause and prognosis. Imaging: small, echogenic kidneys BL (<9-10 cm) by USN suggests the chronic scarring of advanced CKD. Large kidneys can be seen w/ adult polycystic kidney disease, diabetic nephropathy, HIV-associated nephropathy, plasma cell myeloma, amyloidosis, and obstructive uropathy. Tx: protein restriction (animal protein). salt and water restriction (2g/d). potassium restriction when GFR < 10-20. phosphorus restriction (limit processed food, cola beverages. limit eggs, products, nuts, beans, meat). Stage 4: GFR 15-29 Dialysis and kidney transplant Stage 5: GFR < 15 Kidney transplant Management includes BP control < 130/80, ACE or ARB, A1c 6.5-7.5%

syncope

Syncope refers to a transient loss of consciousness/postural tone secondary to an acute decrease in cerebral blood flow Characterized by a rapid recovery of consciousness without resuscitation Cardiac syncope - arrhythmias (e.g. AV block, sick sinus syndrome), obstruction of blood flow (e.g. aortic stenosis, hypertrophic cardiomyopathy), massive MI Vasovagal syncope (neurocardiogenic) most common cause Orthostatic hypotension - defect in vasomotor reflexes, common in elderly, diabetics, patients taking certain medications (e.g. diuretics, vasodilators) Cerebral vascular disease - a rare cause of syncope Other noncardiogenic causes include metabolic causes (e.g., hypoglycemia, hyperventilation), hypovolemia (e.g., hemorrhage), hypersensitivity (syncope precipitated by wearing a tight collar or turning the head), mechanical reduction of venous return (e.g., Valsalva maneuver, postmicturition), and various medications (e.g., β-blockers, nitrates, antiarrhythmic agents)

hyperlipidemia

USPSTF recommends screening for patients with NO evidence of CVD and NO other risk factors should begin at 35 years of age. NCEP recommends screening all adults at age 20 years regardless of risk factors FOUR GROUPS MOST LIKELY TO BENEFIT FROM STATIN THERAPY: 1. Patients w/ any form of clinical atherosclerotic cardiovascular disease (ASCVD) 2. Patients w/ primary LDL levels of 190+ 3. Patients WITH DM, 40 to 75 years of age, with LDL levels of 70-189 4. Patients WITHOUT diabetes, 40 to 75 years of age, with an estimated 10-year ASCVD risk ≥ 7.5% Risk assessment for 10-year and lifetime risk is recommended using an updated ASCVD risk calculator Sx: although most have no symptoms, >1000 mg/dL of VLDL/trigs result in eruptive xanthomas (red-yellow papules; especially on buttocks) High LDL result in tendinous xanthomas (Achilles, patella, back of hand); usually indicate genetic hyperlipidemias extremely high trigs (>2000 mg/dL) lipemia retinalis (cream colored blood vessels in the fundus) Persons who have LDL-C levels of 190+, or triglyceride levels of 500+ should be assessed for secondary causes of hyperlipidemia. Persons 21 years or older who have LDL-C levels of ≥ 190 mg per dL should be treated with hi intensity statin therapy unless contraindicated. If high-intensity statins are not tolerated, the maximum tolerated intensity should be used. In persons with untreated LDL-C levels of 190 mg per dL or greater, statin therapy may be intensified to achieve a minimum 50% LDL-C reduction. When the maximum intensity of statin therapy is reached, a non-statin may be added to further reduce LDL-C levels. Potential benefits, adverse events, drug-drug interactions, and patient preferences should be considered. Primary prevention in persons WITH diabetes and LDL-C of 70 - 189 Persons 40 to 75 years of age who have diabetes should start or continue moderate-intensity statin therapy In those with 7.5% or greater estimated 10-year ASCVD risk, high-intensity statin therapy is reasonable, unless contraindicated In persons younger than 40 years or older than 75 years, potential benefits, adverse events, drug-drug interactions, and patient preferences should be considered when deciding to initiate, continue, or intensify statin therapy. "High intensity therapy" lowers LDL by 50% or more on average. Includes atorvastatin/Lipitor 40-80mg, or rosuvastatin/Crestor 20-40mg. "Moderate intensity" lowers LDL by 30-50% on average. Atorvastatin 10-20mg. Rosuvastatin 5-10mg. simvastatin/Zocor 20-40mg. pravastatin/Pravachol 40-80mg. "Low intensity" daily dosage lowers LDL-C by <30%. Simstavastatin 10mg. Pravastatin 10-20mg. lovastatin 20mg. fluvastatin 20-40mg.

acute GI bleed

Upper GI Bleed: bleeding that originates proximal to the ligament of Treitz Hematemesis: vomiting of blood or coffee-ground emesis Melena: black tarry stool Orthostatic hypotension, tachycardia, abdominal tenderness - causes include: Peptic ulcer: upper abdominal pain Esophageal ulcer: odynophagia, gastroesophageal reflux, dysphagia Mallory-Weiss tear: emesis, retching, or coughing prior to hematemesis Esophageal varices with hemorrhage or portal hypertension: jaundice, abdominal distention (ascites) Malignancy (gastric cancer and right-sided colon cancer): dysphagia, early satiety, involuntary weight loss, cachexia Severe erosive esophagitis: odynophagia (painful swallowing), dysphagia and retrosternal chest pain Treatment: Supportive care: NPO, IV access, oxygen, IV fluids of isotonic crystalloid Transfuse for hemodynamic instability despite fluids, Hgb < 9 in high-risk patients (elderly, CAD), Hgb < 7 in low-risk patients Treat with IV PPI until confirmation of the cause of bleeding - treat the underlying cause Surgery—duodenotomy or gastroduodenostomy, ligation of bleeding Lower GI bleed: Hematochezia (BRBPR): the passage of maroon or right red blood or clots per rectum Orthostatic hypotension or shock - causes include: Hemorrhoids: painless bleeding with wiping Anal fissures: severe rectal pain with defecation Proctitis: rectal bleeding and abdominal pain Polyps: painless rectal bleeding, no red flag signs Colorectal cancer: Painless rectal bleeding and a change in bowel habits in a patient 50-80 years of age Diverticulosis is generally an incidental finding since diverticular bleeding is usually of greater volume

candidiasis

Vaginal candidiasis vulvar itching, erythema and white curdy discharge KOH shows hyphae Tx with miconazole cream x 1-7 days or fluconazole 150 mg PO single dose Esophageal candidiasis Very common in AIDS patients May present with substernal dysphagia, GE reflux, or nausea with or without pain Diagnosis is by EGD with biopsy will demonstrate linear erosions on endoscopy Treat with fluconazole Oral Thrush Friable white plaques that bleed if scraped Treat with nystatin Intertrigo Moist macerated areas, pruritic rash BEEFY RED ERYTHEMA with distinct scalloped borders and satellite lesion Treat with clotrimazole, ketoconazole, miconazole, topical, keep the area dry

varicella zoster

Varicella (chickenpox): primary infections - clusters of vesicles on an erythematous base. Dewdrops on a rose petal in different stages It starts on the face and spreads down Acutely causes chickenpox - becomes latent in the dorsal root ganglion Symptomatic treatment may use acyclovir in special populations Herpes zoster (shingles): varicella reactivation causing a maculopapular rash along one dermatome Identified via tzanck smear with visualization of multinucleated giant cells Zoster Opthalmicus: shingles involving CCN V, dendritic lesions on slit lamp exam if keratoconjunctivitis is present Zoster Oticus (Ramsay-Hunt Syndrome): facial nerve (CN VII) otalgia, lesions on the ear, auditory canal and TM, facial palsy auditory symptoms Treat shingles with acyclovir, valacyclovir, and famciclovir - given within 72 hours to prevent post-herpetic neuralgia Postherpetic Neuralgia: pain > 3 months, paresthesias or decreased sensation. Treat with gabapentin or TCA, topical lidocaine gel, and capsaicin Herpes zoster vaccine is a live, attenuated virus vaccine - vaccination is recommended for immunocompetent adults > 60 years of age

clotting factor disorders

Von Willebrand Disease (vWD) - missing protein for platelet function The Hemophilias Hemophilia A ↓ clotting factor VIII Hemophilia B ↓ clotting factor IX Von Willebrand Disease (vWD) 30-year-old woman w/ Hx recurrent nosebleeds and heavy menses. She recently read that taking a baby ASA was good for the heart. However, ever since she started taking aspirin, she has been experiencing more and more nosebleeds. Her father and paternal uncle similarly have histories of prolonged nosebleeds. Labs show increased PTT, normal PT, and increased bleeding time. patho: von Willebrand factor is found in plasma, platelets, and the walls of blood vessels. When the factor is missing or defective, platelets cannot adhere to the vessel wall at the site of an injury. As a result, bleeding does not stop as quickly as it should. Most common genetic bleeding disorder, autosomal dominant ↓von Willebrand's factor (vWF) and ↓ Factor VIII (bc vWF is a carrying protein for VIII) You can differentiate this from hemophilia by lack of hemarthrosis, small amounts of superficial bleeding, common to have bleeding with minor injury and petechiae. Treat with DDAVP (desmopressin) or in cases of excessive bleeding a transfusion of concentrated blood clotting factors containing von Willebrand factor Hemophilia is a hereditary bleeding disorder caused by a deficiency in one of two blood clotting factors: factor VIII (A) or factor IX (B). X-linked recessive so will affect males (most of the time) Hemophilia patient will present as → a 3-year-old boy whose mom is concerned about his prolonged nosebleeds. Ever since he was about 2 years old, he has had multiple episodes of nosebleeds that stopped only after hours. On PE his right elbow is slightly swollen and tender to palpation. There is a family history of unexplained bleeding in the patient's maternal uncle. Lab results reveal increased PTT that corrects after mixing studies. Lateral radiograph of the knee shows swelling of the soft tissues from blood accumulation in the knee. There are two forms of hemophilia: Hemophilia A, which accounts for about 80% of all cases, is a deficiency in clotting factor VIII ("Aight") Hemophilia B is a deficiency in clotting factor IX (Christmas disease) Hemarthrosis, bruising and bleeding ↑ PTT, normal PT and platelets, with ↓ Factor VIII or ↓ Factor IX on assay Treatment involves the replacement of factor VIII or IX

ITP

causes: autoimmune; ABYs bind to platelets @GPIIb/IIIa & accelerate their clearance from circulation. Primary & idiopathic in most adults. Can be associated w/ CT disease, lymphoma, meds, & infections. S/S: Mucocutaneous bleeding, petechiae, purpura. Easy bruising. Mucosal bleeding. Clinically significant bleeding usually does not occur until the platelet count falls below 20,000 Labs: Isolated thrombocytopenia (bc autoimmunity against platelets only!). normal coag studies. May have anemia if significant bleeding has occurred. R/O HIV & Hep C. Bone marrow not necessary for diagnosis, but may be beneficial in certain cases (Unexplained additional cytopenias, new onset in patient > 40, no response to standard therapy). If lymphoma suspected, do a CT scan of C/A/P Treatment: refer to hematology. Admit to hospital if severe thrombocytopenia and/or high risk for bleeding. Mainstay of treatment is corticosteroids. Add IVIG (intravenous immunoglobulin). When both given, response is seen in 24-36 hrs. Avoid platelet transfusion unless active bleeding. Rituximab is used for corticosteroid-refractory ITP; Promacta (oral) and Nplate (SC) can also be used. Splenectomy has a response rate of over 50% and is used in refractory ITP

coma

a state of unarousable unresponsiveness; duration typically <2-4 weeks; rarely cases are longer and up to 12 months. Fails to respond normally to painful stimuli, light, or sound; lacks a normal wake-sleep cycle; and does not initiate voluntary actions Glasgow Coma Scale Best eye response If local injury, edema, or otherwise unable to be assessed, mark "Not testable (NT)" Spontaneously (+4) To verbal command (+3) To pain (+2) No eye opening (+1) Not testable (NT) Best verbal response If intubated or otherwise unable to be assessed, mark "Not testable (NT)" Oriented (+5) Confused (+4) Inappropriate words (+3) Incomprehensible sounds (+2) No verbal response (+1) Not testable/intubated (NT) Best motor response If on sedation/paralysis or unable to be assessed, mark "Not testable (NT)" Obeys commands (+6) Localizes pain (+5) Withdrawal from pain (+4) Flexion to pain (+3) Extension to pain (+2) No motor response (+1) Not testable (NT) Score of < 9 = coma! Score: 13-15 may indicate mild dysfunction, although 15 is the score a person with no neurologic disabilities would receive Score 9-12 may indicate moderate dysfunction Score 8 or less is severe dysfunction

delirium

acute cognitive dysfunction secondary to some underlying medical condition and is usually reversible. most common presentation of altered mental status in the inpatient setting Visual hallucinations are the most common type experienced by patients with delirium High-risk after surgery especially in those with heart disease or diabetes Fall precautions - patients with delirium are six more times likely to fall Alcohol abuse is the most common cause of delirium, specifically, delirium tremens Delirium is a side effect of acute hyperthyroidism known as thyroid storm Underlying organic cause: UTI, pneumonia, metabolic changes, CVA, MI, TBI, medications (anticholinergics, benzodiazepines, opioids) DX: Mental status examination (MMSE) Labs (chemistry, B12/folate) LP in a febrile, delirious patient (cerebral edema) Treat the cause of delirium (almost always reversible) and provide supportive care, including sedation when necessary Haloperidol for agitation/psychosis Supportive

esophageal cancer

adenocarcinoma and squamous cell carcinoma how they differ: ADENOCARCINOMA MCC in US; younger caucasian males with Barret's esophagus, smoking, high body mass index. EtOH Is NOTTT a risk factor (it is in squamous cell) Seen in the DISTAL ESOPHAGUS, esophagogastric junction. SQUAMOUS CELL MC worldwide 50-70 y/o, more common in african americans in the US Smoking and EtOH major risk factors. also poor nutritional status, low intake of fruits and veggies, drinking beverages at high temps (Thermal injury), HPV, N-nitroso compounds, atrophic gastritis, achalasia, tylosis. Seen in the mid-UPPER third of esophagus. how they're the same: protective factors: ASA, NSAIDs. S/s: usually extensive disease by the time they're symptomatic :( progressive dysphagia is hallmark Sx, odynophagia. weight loss, anorexia, IDA. CP, anorexia, cough, hematemesis, reflux, hoarseness (recurrent laryngeal nerve). Horner's syndrome, tracheal-esophageal fistula. hypercalcemia w/ squamous cell carcinoma. Dx: upper endoscopy with Bx diagnostic test of choice. early lesions may look like superficial plaques, nodules, or ulcerations. advanced lesions may appear as strictures, ulcerated masses, circumferential masses, or large ulcerations. Double contrast barium esophagram. Pretreatment staging w/ endoscopic US is preferred method. pre-op bronchoscopy with Bx and brush cytology for locally advanced lesions. CT neck, chest, abdomen. PET/CT scan. Tx: esophageal resection may be combined with chemo. radiation therapy, chemo (5-FU). Palliative stenting to improve dysphagia may be needed in advanced cases.

TTP

causes: (primary) autoantibodies vs. ADAMTS-13 (AKA vWFCP) leads to accumulation of ultra-large vWF multimers, which bridge and aggregate platelets in absence of hemostatic triggers leading to vessel obstruction and organ dysfunction. (secondary) pregnancy ABY, congenital decreased aDAMTS-13 d/t mutation, damage to endothelial cells in setting of cancer, stem cell transplant, or HIV. DITMA (drug induced). S/S: only 25% will have classic pentad: 1. thrombocytopenia 2. microangiopathic hemolytic anemia 3. fever 4. kidney dz 5. neuro abnormalities.Kidney dysfunction more common in HUS. Labs: hemolytic anemia (anemia, elevated LDH, decreased haptoglobin, elevated indirect bilirubin, reticulocytes, schistocytes on smear, negative direct antiglobulin test AKA Coombs). thrombocytopenia, reduced ADAMTS-13 activity w/ presence (acquired) or absence (Inherited) of ADAMTS-13 inhibitor. NORMAL coagulation studies (unlike DIC!). Tx.Immediate plasma exchange (NOT transfusion) is essential w/ the exception of Shiga-mediated HUS. Initiate treatment if TMA is strongly suspected. Done once daily until platelet count and LDH have returned to normal & maintained x2 days. Tx Is then tapered & counts monitored for relapse. FFP may be given if exchange will be delayed. DO NOT give platelet transfusion unless bleeding. All patients should be hospitalized. What is HUS, how is it related to TTP? HUS is hemolytic uremic syndrome & is also a thrombotic microangiopathy like TTP but is d/t platelet activation by exotoxins. Seen in kids w/ recent Hx of gastroenteritis usually but also seen in adults w/ HIV, SLE, antiphospholipid syndrome, or chemo. triad is thrombocytopenia, hemolytic anemia, and renal dysfunction (d/t uremia). do not do plasma exchange if shiga mediated.

concussion

definition: mild TBI --> AMS w/ or w/o LOC May result after blunt force or acceleration/deceleration head injury S/s: HA, dizziness, psychological Sx, and cognitive impairment. confusion (confused or blank expression, blunted affect). amnesia (pretraumatic/retrograde or posttraumatic/antegrade. duration of pretraumatic is usually brief). visual disturbances (blurred or double vision). Delayed responses and emotional changes. signs of ICP like persistent vomiting, worsening HA, increasing disorientation, changing levels of consciousness. Dx: CT w/o contrast study of choice. MRI fi prolonged Sx >7-14d with worsening of Sx. CTA if vascular injury suspected. Tx: cognitive and physical rest; some form of observation recommended x24h. Patients may resume strenuous activity after resolution of Sx and recovery of memory as well as cognitive functions. Stepwise approach Step 1: back to regular activities Step 2: light aerobic exercises - walking stationary cycling no resistance training Step 3: sports specific exercise - running or skating drills Step 4: non-contact training drills Step 5: Full contact practice Step 6: Return to sports - normal gameplay If symptoms return stop activities. After a minimum of 24 hours of no symptoms can start again at the previous step.

solitary pulmonary nodule

definition: single, small (30mm or less) usually well-circumscribed lesion surrounded entirely by pulm parenchyma. etiologies: infectious granulomas MC (>75%) esp. mycobacteria (TB) or fungi (histoplasmosis, coccidioidomycosis). May also be benign or malignant tumors; thymoma MC mediastinal tumor. risk of malignancy: increased risk if spiculated nodule (the pic attached to this card is spiculated), larger than 2cm, irregular borders, asymmetric calcification, upper lobe location, >40 y/o, smoker, enlarging lesions, abnml PET scan. decreased risk if well circumscribed smooth borders, <1cm, dense diffuse calcification, <30years old, nonsmoker, no change in size, normal CT. dx: CXR will reveal nodule, CT is best to determine likelihood of malignancy. PET scan best to determine metabolic functioning of nodule. Tx: low probability of malignancy=active surveillance w/ monitoring for changes. intermediate=bronchoscopy if central lesion. transthoracic needle aspiration for peripheral lesion. high=resection with biopsy.

cytomegalovirus

enveloped double-stranded linear DNA virus in the herpesvirus family (HHV5). spread by body fluids or vertical transmission. present in 70% of people but only symptomatic in immunocompromised patients. primary dz: usually asymptomatic but can cause a syndrome that is similar to mono but lacks severe pharyngitis, LAD reactivation: MC in immunocompromised. colitis MC--> diarrhea, fever, abd pain, bloody stools. increased risk in HIV CD4 <100 retinitis--> decreased visual acuity and floaters. fundoscopy shows hemorrhage with yellow white soft exudate. MC when CD4 <50. esophagitis--> odynophagia w/ large superficial ulcers on UE pneumonitis--> esp. post-transplant neuro--> encephalitis, GBS Dx: serologies (antigen tests, igm, igg titers), PCR. labs show lymphocytes with atypical lymphocytosis. Bx of tissues shows owls eye appearance (epithelial cells with enlarged nuclei surrounded by clear zone and cytoplasmic inclusions) Tx: for reactivation, ganciclovir. 2nd line is foscarnet, cidofovir, valacyclovir. for primary dz, supportive PPX in HIV w/ valganciclovir if cd4 <50 CONGENITAL CMV: can --> stillbirth., prematurity, and hydrops fetalis MC congenital viral infection; part of ToRCH syndrome. S/s: most are asymptomatic at birth but neonates may have petechiae, jaundice at birth, hepatosplenomegaly. Neuro Sx include sensorineural hearing loss MC, periventricular calcifications, cerebral palsy, vision impairment (including chorioretinitis) and seizures. Dx: urine or saliva viral titers. urine or saliva PCR most accurate test. Tx w/ ganciclovir

cerebral aneurysm

patho/etiology: berry / saccular aneurysms tend to occur at bifurcations, are frequently multiple, and usually asymptomatic. usually anterior C.O.W. especially at A or P communicating arteries, at bifurcation of MCA, and at the bifurcation of the internal carotid artery. RF include smoking, HTN, females. S/S: may cause focal neuro deficit by compressing adjacent structures. however, most are asymptomatic or produce only nonspecific Sx until they rupture; at which time subarachnoid hemorrhage results Dx: digital subtraction angiography (BL carotid and vertebral studies), which generally indicates the size and site of the lesion, sometimes reveals multiple aneurysms, and may show arterial spasm if rupture has occurred. CTA/MRA usually not adequate if for operation. Tx: prevent hemorrhage. symptomatic but unruptured aneurysms merit prompt treatment, either surgically or by endovascular techniques. the decision to treat or monitor asymptomatic aneurysms discovered incidentally is complicated and depends on aneurysm size, location, RF for rupture, and treatment related morbidity.

varicose veins

patho/etiology: dilation of superficial veins due to failure of the venous valves in the saphenous veins, leading to retrograde flow, venous stasis, and pooling of blood. risk factors include family Hx, female gender, increased age, standing for long periods, obesity, increased estrogen, chronic venous insufficiency. S/S: mostly asymptomatic but cosmetic issues. dull ache or pressure sensation. pain is worse with prolonged sitting or standing and is relieved with elevation. PE will show dilated visible veins, telangiectasias, swelling, discoloration, venous stasis ulcers. +/- mild ankle edema. Treatment: conservative compression stockings, leg elevation, pain control. ablation catheter based endovenous thermal ablation (laser or radiofrequency). ligation and stripping, sclerotherapy.

Aortic aneurysm

patho/etiology: focal aortic dilation > 3.0cm; infrarenal most common. proteolytic degeneration of aortic wall and CT inflammation. risk factors include smoking, >60 y/o, male caucasians, CT disorders. S/S: usually asymptomatic; found incidentally. symptomatic, unruptured abdominal/flank/back pain. abdominal bruit may be auscultated and pulsatile abdominal mass may be palpated. symptomatic, ruptured hypotension or syncope. flank ecchymosis. abdominal, flank, or back pain, abdominal bruit, pulsatile mass. Screening: -all men 65-75 who have ever smoked get an abdominal ultrasound. > or equal to 5.5cm OR >.5cm expansion in 6 months=immediate surgical repair even if asymptomatic >4.5cm=vascular surgeon referral 4-4.5cm= monitor by ultrasound every 6 months 3-4cm= monitor by US every year. Diagnosis: CT scan w/IV contrast best initial test in symptomatic hemodynamically stable patients to determine presence, size, extent. focused bedside ultrasound test of choice in hemodynamically unstable patients. abdominal ultrasound good for patients who are asymptomatic with suspected AAA to monitor progression. patients with known AAA w/ S/S of rupture can be taken directly to OR for surgical repair without preoperative imaging. Treatment: symptomatic or ruptured requires immediate surgical repair (endovascular stent graft or open repair). beta blockers reduce shearing forces, decreases expansion and rupture risk.

giant cell arteritis

patho/etiology: granulomatous vasculitis of the extracranial branches of the carotid (temporal, occipital, opthalmic, posterior ciliary). closely related w polymyalgia rheumatica. women 50+. S/S: localized abrupt headache, jaw claudication with mastication, visual changes (ant ischemic optic neuritis, monocular vision loss, amaurosis fugax). scalp tenderness, may be tender or pulseless temporal artery. Testing: mostly clinical diagnosis based on headache, jaw claudication, fever, and visual changes. labs increased ESR&CRP. normocytic normochromatic anemia. temporal biopsy is definitive. temporal artery ultrasound may show thickening (halo sign), stenosis, or occlusion. Treatment: high dose corticosteroids once GCA is expected to prevent blindness, the most common complication! don't wait for biopsy results. Steroid sparing agents or steroid refractory agents like methotrexate, azathioprine. Low dose aspirin.

phlebitis

patho/etiology: inflammation and/or thrombosis of a superficial vein. most commonly associated with IV cath, pregnancy, varicose veins. Trousseau sign migratory thrombophlebitis associated w/ malignancy i.e. pancreatic cancer. S/S: local phlebitis will have tenderness, pain, induration, edema, erythema along the course of the vein under the skin. may feel a palpable cord. Testing/Dx: clinical Dx usually. venous duplex ultrasound will sometimes show a noncompressible vein. hypercoagulbility workup wills how Factor V Leiden, a prothrombin gene mutation, etc. Migratory phlebitis do a malignancy workup, carcinoembryonic antigen (CEA), prostate specific antigen (PSA), colonoscopy, CT scan, etc. Treatment: support with NSAIDs, extremity elevation, warm compresses. vein ligation/excision (aka phlebectomy) if extensive varicose veins, septic phlebitis, or persistent symptoms despite supportive measures. if febrile assume septic; IV abx penicillin + aminoglycoside. if clot near saphenofemoral junction consider anticoagulation.

pericarditis

patho/etiology: most commonly idiopathic and viral (coxsackievirus and echovirus). Could be Dressler Syndrome (post MI pericarditis + fever + pleural effusion). autoimmune, uremia, bacterial, radiation, meds. fibrinous or serofibrinous usually post-MI, infectious. serous, related to autoimmunity I.e. SLE, RA S/S: sudden onset of pleuritis (sharp, worse w inspiration), persistent, postural chest pain (better w sitting forward, worse w supine). Pain may radiate to shoulder, back, neck, arm, epigastric area. PE shows pericardial friction rub best head at end expiration while upright and leaning forward. Testing: ECG diagnostic test of choice will show diffuse ST elevations in the precordial leads with associated PR depressions in those leads. may have cardiac enzyme positivity. echocardiogram useful to evaluate for an associated pericardial effusion and/or signs of cardiac tamponade. Treatment: anti-inflammatory meds NSAIDs or Aspirin x 7-14 days; symptoms will subside in 1-2 days. colchicine second line. if they have Dressler syndrome (post MI pericarditis + fever + pleural effusion) use aspirin or colchicine; other NSAIDs will interfere with myocardial scar formation.

Arterial embolism/thrombosis

patho/etiology: rapidly developing/sudden limb ischemia; vascular emergency. thrombotic occlusion most common cause (with preexisting PAD); most common in the superficial femoral or popliteal artery. S/S: parasthesias, pain, pallor, pulselessness, poikilothermia, eventually paralysis (worst prognosis). Sx usually DISTAL to the occlusion. decreased cap refill, decreased or absent pulses, cool temp. Testing: bedside arterial doppler to assess for pulses. CT angiography. if limb is immediately threatened, they can undergo further eval and tx in surgical suite. Treatment: reperfusion via surgical bypass. surgical or catheter based thromboembolectomy, endarterectomy. thrombolytic therapy or percutaneous angioplasty. supportive pain control, fluid resuscitation, unfractioned heparin.

aortic aneurysm dissection

patho/etiology: tear through innermost layer of aorta (intima) due to cystic medial necrosis. ascending >descending. associated w/ high mortality. risk factors include HTN, >50y/o, MARFAN, men, family Hx, Turners, Ehlers-Danlos, pregnancy. S/S: sudden onset of severe tearing chest. upper back pain; may radiate between scapulae. ascending will have anterior chest pain (especially type A). aortic arch will have neck/jaw pain. descending will have interscapular pain (especially type B). unequal BP in both arms (>20 diff between arms). decreased peripheral pulses. may be hyper or hypotensive. Classification: DeBakey Type 1= originates in ascending aorta, propagates at least to the aortic arch and often beyond it. Type 2=originates in and is confined to the ascending aorta. Type 3= originates in descending aorta, rarely extends proximally but will extend distally. Stanford A= involves ascending aorta and/or aortic arch and possible descending. (debakey 1 and 2, proximal) B= involves descending aorta distal to left subclavian artery w/o involvement of the ascending aorta or aortic arch. (debakey 3, distal) Testing: CT angiogram, MR angiogram, and TEE most common first line imaging. CXR shows widened mediastinum, but may be normal in 10% so this doesnt r/o anything. Treatment: surgical used in acute proximal (stanford A/DeBakey I and II) OR acute distal with complications (vital organ involvement, impending rupture etc.). Preoperative BP control. Medical used in descending/distal (Stanford B/Debakey III). Nonselective BB (labetalol) with sodium nitroprusside added PRN. systolic BP lowered to a goal of 100-120mmHg within 20 min.

lyme disease

patho/etiology: tick-borne bacterial infection and inflammatory arthritis caused by borrelia burgdorferi. epidemiology: Found a lot in northeast US S/S: early localized classic erythema migrans or "bulls eye rash" rash days after tick bite. Usually minimally symptomatic, slight burning or itching. May be accompanied by flu-like symptoms and LAD. early disseminated weeks to months after initial infection leads to rheumatic symptoms (migratory arthralgia, transient large joint effusions), cardiac (AV block, myocarditis), neurologic (Bell's palsy, meningitis, radiculoneuritis), skin (secondary annular lesions). late stage chronic oligoarticular arthritis, encephalopathy, chronic skin lesions, polyneuropathy. Diagnosis: Can Dx'd clinically in an endemic area with highly suggestive features. Serologic ABY testing: 1st do EIA or IFA; if negative, explore other Dx or obtain convalescent serum. If positive or equivocal, if Sx present for <=30 days, do IgM and IgG Western blot. If Sx present for > 30 days, IgG Western Blot only. Treatment: doxycycline 1st choice. short courses of doxy do nOT cause dental staining when given to children <8y/o. Some people have post-treatment Lyme disease syndrome (controversial); Sx such as fever, arthralgia, brain fog. Cash operation. Chronic antibiotics not recommended.

pyelonephritis

patho: infectious inflammatory disease involving the kidney parenchyma and renal pelvis. Gram-negative bacteria are the most common causative agents including E coli, Proteus, Klebsiella, Enterobacter, and Pseudomonas. Gram-positive bacteria are less commonly seen but include Enterococcus faecalis and Staphylococcus aureus. The infection usually ascends from the lower urinary tract—with the exception of S aureus, which usually is spread by a hematogenous route. S/S: fever, flank pain, shaking chills, and irritative voiding symptoms (urgency, frequency, dysuria). Associated nausea and vomiting and diarrhea are common. Signs include fever and tachycardia. CVA tenderness is usually pronounced. Labs: CBC shows leukocytosis and a left shift. UA shows pyuria, bacteriuria, and varying degrees of hematuria. White cell casts may be seen. Urine culture demonstrates growth of the offending organism, and blood culture may also be positive. Imaging: In complicated pyelonephritis, renal ultrasound may show hydronephrosis from a stone or other source of obstruction. CT scan may demonstrate decreased perfusion of the kidney or focal areas within the kidney and nonspecific perinephric fat stranding. Tx: Outpatient: FQ (Cipro/Levaquin)/Bactrim for 1-2 weeks (longer if immunocompromised) Inpatient: IV FQ, 3rd/4th gen cephalosporins, extended-spectrum penicillins, gentamicin Failure to respond ⇒ US/imaging F/up urine cultures not mandatory following tx in uncomplicated cases

acute abdomen

peritonitis- pain, tenderness, rigid abdominal muscles, fever, nausea, and vomiting. Renal CC: colicky right-sided flank pain, nausea, vomiting, hematuria, CVA tenderness Workup: UA, BUN/Cr, CT abdomen, renal US, KUB, blood cultures Ddx: nephrolithiasis, renal cell carcinoma, pyelonephritis, GI etiology, glomerulonephritis, splenic rupture Pancreas: CC: dull epigastric pain that radiates to the back Workup: CT abdomen, CBC, electrolytes, amylase, lipase, AST, ALT, bilirubin, alkaline phosphatase, U/S abdomen Ddx: pancreatitis, pancreatic cancer, peptic ulcer disease, cholecystitis/choledocholithiasis Gallbladder: CC: RUQ pain Workup: RUQUS, CBC, CMP, HIDA scan, MRCP/ERCP, amylase, lipase, alkaline phosphatase, bilirubin Ddx: cholecystitis, choledocholithiasis, hepatitis, ascending cholangitis, Fitz-Hugh-Curtis syndrome, acute subhepatic appendicitis Liver: CC: RUQ pain, fever, anorexia, nausea, vomiting, dark urine, clay stool Workup: CBC, amylase, lipase, liver enzymes, viral hepatitis serologies, UA, U/S abdomen, ERCP, MRCP Ddx: acute hepatitis, acute cholecystitis, ascending cholangitis, choledocholithiasis, pancreatitis, primary sclerosing cholangitis, primary biliary cirrhosis, glomerulonephritis Spleen: CC: severe LUQ pain that radiates to left scapula w hx of infectious mono Workup: CBC, CXR, CT/US of the abdomen Ddx: splenic rupture, splenic infarct, kidney stone, rib fracture, pneumonia, perforated peptic ulcer Stomach: CC: burning epigastric pain after meals Workup: rectal exam (occult blood in stool), amylase, lipase, lactate, AST, ALT, bilirubin, alkaline phosphatase , upper endoscopy (H.pylori biopsies), upper GI series Ddx: peptic ulcer disease, perforated peptic ulcer disease, gastritis, GERD, cholecystitis, mesenteric ischemia, chronic pancreatitis Pipes: CC: crampy abdominal pain, vomiting, abdominal distention, inability to pass flatus Workup: rectal exam, CBC, electrolytes, CT abdomen/pelvis, colonoscopy DDx: intestinal obstruction, small bowel/colon cancer, volvulus, gastroenteritis, food poisoning, ileus, hernia, mesenteric ischemia/infarction, diverticulitis, w/ alternating diarrhea/. Constipation: diverticulitis, Crohn's disease, ulcerative colitis, abscess, IBS, celiac disease, GI parasitic infection (amebiasis, giardiasis) Pelvis: CC: RLQ pain, nausea, vomiting, dysuria, hematuria Workup: pelvic exam, urine hCG, doppler U/S, rectal exam, UA, CBC, CT abdomen, laparoscopy, chlamydia, and gonorrhea testing Ddx: ovarian torsion, appendicitis, ectopic pregnancy, ruptured ovarian cyst, pelvic inflammatory disease, bowel infarction/perforation, endometriosis, vaginitis, cystitis, pyelonephritis

polycystic kidney disease

podcast-- Polly the parrot (polycystic KD) is the Most Violent Parrot (MVP) bc she sits on your shoulder and pecks at your Berry Aneurysms)EOD: Multiple cysts in both kidneys; number of cysts depends on patient age. Combination of hypertension and large palpable kidneys / flank mass suggestive of disease. Autosomal dominant chromosomal abnormalities present in some patients. patho: among the most common hereditary diseases in the United States, affecting 500,000 individuals, or 1 in 800 live births. develops by age 60 years in up to 50% of patients. 2 genes account for this disorder: ADPKD1 on the short arm of chromosome 16 (85-90% of patients) and ADPKD2 on chromosome 4 (10-15%). Patients w/ PKD2 mutation have slower progression of disease and longer life expectancy than those with PKD1. Other sporadic cases w/o these mutations are also recognized. S/S: Abdominal or flank pain & microscopic or gross hematuria are present in most patients. Hx of urinary tract infections and nephrolithiasis is common. A family history is present in 75% of cases, and >50% of patients have HTN that may precede clinical manifestations of the disease. large kidneys. 40-50% have concurrent hepatic cysts; pancreatic and splenic cysts may occur. Hemoglobin tends to be maintained as a result of erythropoietin production by the cysts. Urinalysis may show hematuria and subnephrotic Dx: patients w/ confirmed family Hx of PKD1, USN confirms the Dx; 2+ more cysts in patients < 30 years, 2+ more cysts in each kidney in patients aged 30-59 years, and 4+ more cysts in each kidney in patients aged 60+ are diagnostic for autosomal dominant polycystic kidney disease. these criteria do not apply to individuals w/o a known family Hx patients WITHOUT a known family history of polycystic kidney disease require additional diagnostic evaluation including CT scanning, which reveals innumerable cysts in cases of polycystic kidney disease. In some cases, genetic testing for ADPKD1 and ADPKD2 mutations may be required. Sequelae: pain, hematuria, renal infection, nephrolithiasis, HTN, cerebral aneurysms, other (mitral valve prolapse in up to 25% of patients, aortic aneurysms, and aortic valve abnormalities. Colonic diverticula are more common in patients with polycystic kidneys.) TX: no cure, treatment is supportive, BP control ACE-I/ARB for HTN, treat infections with antibiotics, dialysis/transplant with renal insufficiency

huntington's disease

watch osmosis https://www.osmosis.org/learn/Huntington_disease characterized by chorea and dementia. patho/etiology: autosomal dominant inheritance and occurs throughout the world, in all ethnic groups, with a prevalence rate of about 5 / 100,000. There is an expanded and unstable CAG trinucleotide repeat in the huntingtin gene at 4p16.3; longer repeat lengths correspond to an earlier age of onset and faster disease progression. caudate nucleus and putamen atrophy, decreased glucose metabolism. S/S: onset is usually between 30-50 years of age. The disease is progressive and usually leads to a fatal outcome within 15-20 years. The initial symptoms may consist of either abnormal movements or intellectual changes, but ultimately both occur. The earliest mental changes are often behavioral, with irritability, moodiness, antisocial behavior, or a psychiatric disturbance, but a more obvious dementia subsequently develops. The dyskinesia may initially be no more than an apparent fidgetiness or restlessness, but eventually choreiform movements and some dystonic posturing occur. A parkinsonian syndrome with progressive rigidity and akinesia (rather than chorea) sometimes occurs in association with dementia, especially in cases with childhood onset. Dx: established with a widely available genetic test, although such testing should be pursued under the guidance of a licensed genetic counselor. CT scanning or MRI usually demonstrates cerebral atrophy and atrophy of the caudate nucleus in established cases. Positron emission tomography (PET) has shown reduced striatal metabolic rate. DDx: Nongenetic causes of chorea include stroke, SLE and antiphospholipid antibody syndrome, paraneoplastic syndromes, infection with HIV, and various medications. In younger patients, self-limiting Sydenham chorea develops after GAS infections on rare occasions. If a patient presents solely with progressive intellectual failure, it may not be possible to distinguish Huntington disease from other causes of dementia unless there is a characteristic family history or a dyskinesia develops. Tx: purely symptomatic. Tetrabenazine for dyskinesia. reserpine as well but more peripheral effects and a worse s/e profile. Treatments that block dopamine receptors like haloperidol can help too. clozapine for behavioral disturbances. Offspring should be offered genetic counseling. Genetic testing permits presymptomatic detection and definitive diagnosis of the disease.

iron deficiency anemia

↓ MCV (microcytic), ↓ MCH (hypochromic), ↑ TIBC, ↓ Ferritin (best test, low iron stores), Target cells, pica, and nail spooning MC cause of anemia and usually from blood loss In men: chronic occult bleeding; women = menses Always consider GI bleed S/S: fatigue, palpitations, SOB, weakness, HA, tinnitus, (nail), atrophic glossitis (tongue), angular cheilitis. Associated with pica and nail spooning (koilonychia) Dx: Microcytic/hypochromic anemia CBC: low reticulocyte count, high RDW Iron studies: decreased serum iron, transferrin saturation; ↑ TIBC, ↓ Ferritin (best test, low iron stores) < 15 (diagnostic) H & H: <13.5 & 39 for men; < 12 & 37 for women Peripheral smear: poikilocytes; rarely bone marrow examination; hemoccult if indicated Tx: FeSO4 325 mg TID Ferrous sulfate 3 mg/kg once or twice daily between meals with juice (not milk) Ferrous fumarate 100-200 mg/day in 2-3 doses; ferrous gluconate 3-6 mg/kg/day in 3 doses s/e: gray staining/teeth (liquid preps); GI upset/constipation 6w to correct; 6mo. to replete iron stores; recheck blood counts every 3 months x 1 year Packed RBCs when Hgb <8 DDx: Other causes decreased MCV: lead poisoning, sideroblastic anemia, basophilic stippling, thalassemia Dysphagia from esophageal webs (Plummer-Vinson syndrome: unknown cause; thin tissue growths block esophagus)