MASTER RECURRENT

What structures are anchored to the perineal body? (4) What muscle is cut during mediolateral episiotomy? *recurrent*

"BELT" 1. Bulbospongiosus muscle 2. external anal sphincter muscle 3. Levator ani, external uretheral sphincter, and muscular coat of rectum (fibers from all of these) 4. Transverse perineal muscles (deep and superficial) *transverse perineal muscle* is cut during mediolateral episiotomy

what lobes of lungs are most commonly affected in pts laying down? (like if they get aspiration pneumonia for example)

*posterior segments* of upper lobes & *superior segments* of lower lobes

What are 3 important causes of rectal prolapse?

1. pregnancy 2. constipation 3. CF pts, esp children

What substances would you expect to be high in a baby w *neural tube defects*? (2) *recurrent*

Alpha fetoprotein (AFP) Acetylcholinesterase (AChE) these leak from the spinal canal into amniotic cavity

Pts that have apo E4 proteins are at increased risk for what? what about E2?

E4: increased *late onset familial alzheimer dementia risk* E2: decreased alzheimer dementia risk

What are the encapsulated organism?

ESPN Kardashians Have Sexy Bodies E coli Strep pneumo Pseudomonas N meningitidis Klebsiella H flu Salmonella group B strep (agalactiae)

Niacin def classic triad? *recurring card*

Niacin aka B3 = 3 D's of pellagra Dementia Dermatitis Diarrhia

Where do internal hemorrhoid drain to? external? what vein does inferior epigastric drain into? *recurrent*

internal hemorrhoids: part of hindgut --> drain to portal system (eventually to IVC of course). drain to *superior rectal vein* which is a part of the *inferior mesenteric vein* external hemorrhoids: drain into inferior rectal vein --> internal pudendal vein --> internal iliac veins aka they drain into *caval* system (i.e. IVC directly) **inferior epigastrics drain into EXTERNAL iliacs**

Buzzword: cavernous, blood filled vascular spaces in liver lined by a single epithelial layer biopsy? *recurrent*

this is *cavernous hemangioma* the most common benign liver tumor. usually present in 30-50 y/os enlarge via ectasia (ductal dilation) not hyperplasia or hypertrohpy

Buzzword: muscle biopsy showing very low carnitine content. what is dx and what is pathophys? what is a common ketone bodies that can be used in peripheral tissues? (2) *recurrent*

this is primary carnitine insufficiency. Carnitine is used in the oxidation of fatty acids, specifically it can bring fatty acids into liver mitochondria. this is important for when we are low in sugar so we can create energy otherwise we end up w hypoketotic hypoglycemia (i.e. low glucose and absence of ketones in urine) sx include muscle weakness and cardiomyopathy (S3 or other murmur) common FA that can be used by muscle is *acetoacetate* and also *beta hydroxybutyrate*

aside from opioids, blood transfusions, and hydroxyurea was a cool/unique way we can prevent sickle cell pts from getting cellular dehydration and thus a sickle cell attack?

Blocking Gardos channels these are Ca2+ dependent K+ channels that regualte transport of K+ and H2O thru RBCs.. if blocked, K+ and H2O EFFLUX is prevented --> prevents dehydration of erythrocytes --> reduces polymerization of Hb S

Bosentan MOA and use?

Bosentan (boss man stan) competitively inhibits endothelin use in tx of pulmonary arterial HTN. note this isn't pulmonary HTN which is by definition secondary to other dzs like left HF or chronic pulm dz Pulmonary arterial HTN usually presents in women 20-40 y/o w dyspnea and exercise intolerance. also family hx so mom will have died around 40 or 50 from this etc (BMPR2 gene)

what is the MAIN fxn and secretion site of the following: 1. gastrin 2. somatostatin 3. CCK 4. Secretin 5. GIP 6. Motilin

1. *gastrin*: Action: increased gastric H+ secretion Site: G cells in gastric antrum and duodenum 2. *somatostatin*: Action: lowers secretion of most GI hormones Site: D cells (pancreatic islets & gut mucosa) 3. *CCK*: Action: increases pancreatic ENZYMES and HCO3- secretion Site: I cells (small intestine) 4. *Secretin*: Action: increases pancreatic HCO3- and *lowers acid* secretion Site: S cells (small intestine) 5. *GIP*: Action: increases insulin release (this is why oral glucose leads to higher insulin spike) and also decreases acid prodxn Site: K cells (small intestine) 6. *Motilin* Action: increases GI motility Site: M cells (small intestine)

What are 3 sx classic of primary hyperparathyroidism? What is the MOA of hypercalcemia in PTH pts? What specific bone findings would you see in pts w excess PTH? *recurrent*

"Bones, stones, and psychiatric overtones" bone pain Ca2+ stones Psychiatric sx MOA: 3 ways 1. increased osteoclast --> bone resorption 2. increased renal tubular Ca2+ reabsorption (altho most pts still have net hypercalciuria leading to stones b/t increased filtered Ca2+ load) 3. increased prodxn of 1, 25 dihydroxyvitamin D which causes GI Ca2+ abs PTH excess = *subperiosteal resorption w cortical thinning* the increased bone resorption leads to osteoporosis, but unlike the typical osteoporosis of aging which is mostly in trabecular bone osteoporosis in PHPT is mostly seen in *cortical (compact) bone*. the tricky thing is that this appears as *subperiosteal* erosions radiologically

What are the sx of Kawasaki dz? *recurrent*

"CRASH & Burn" Conjunctivitis Rash on palms & soles Adenopathy (usually cervical) Strawberry tongue Hand/foot edema w desquamation (peeling) Burn = fever x 5 days vasculitis of medium arteries that classically affects young children vasculitis most commonly associated w MI! thus this is the ONLY TIME IN KIDS you give aspirin!!

Action card: draw the tree/differential thing for aphasias

"GET MY BUTT "TO MIAMI" WHEN "THE SNOW" COMES AROUND -Global aphasia -Mixed transcortical aphasia -Broca's aphasia -Transcortical motor aphasia -Wernicke's aphasia -Transcortical sensory aphasia -Conduction aphasia -Anomic aphasia Start w fluent? comprehends? repeats? *Gabby NSF wk 5 guide for answers if need be*

What are the spermatic cord layers and their corresponding normal adult layers?

"ICE TIE" Internal spermatic fascia --> Transversalis fascia Cremasteric muscle & fascia --> internal oblique External spermatic fascia --> external oblique

Whats the mnemonic for knowing blotting procedures and what they ID?

"SNoW DRoP" *Southern = DNA* (specific sequences in an unknown sample) *Northern = mRNA* (specific RNA sequences) *Western = Protein* (w the use of a labeled/marked antibody)

what classic sx do you see in stroke of: ACA MCA PCA

ACA: -contralateral paralysis & sensory loss of *lower limb & urinary incontinence* MCA: -contralateral paralysis & sensory loss of *face & upper limb* -APHASIA!! IF DOMINANT side (usually left) PCA: -contralateral hemianopia w macular sparing -alexia w/o agraphia if dominant hemisphere

in what brain region is brocas area? what about wernickes?

Brocas: frontal lobe near the outer edge of the glove mitten thing (M region). specifically *inferior frontal gyrus* of the *dominant [usually left] hemisphere* Wernickes: temporal lobe near the inner part of the glove mitten thing

The CFTR protein defective in CF pts is a _______ gated chloride channel

ATP gated!! (opens after it binds 2 ATP molecules) not voltage gated!

what is a non speech association w Broca's and wernicke's?

Brocas: right hemiparesis (face and upper limb) d/t proximity of frontal gyrus to primary motor cortex Wernicke: right superior visual field defect

Rapidly growing tumor mass in facial bone, jaw, or abdomen

Burkitt lymphoma. esp seen w chronic epstein barr virus

Buzzword: bug that produces "double zone" of beta hemolysis

C perfringens! remember the double zone fine at the market place

what 2 vaccinations are toxoid vaccines?

C tetani and corynebacterium dioptheria stimulates body to create antibodies w/o causing the dz!

What E Coli strain does NOT produce glucuronidase or ferment sorbitol? virulence of this e coli?

EHEC O157:H7 produces shiga like toxin which *inactivates* the 60s ribosomal subunit

what bug is most commonly responsible for UTIs after genitourinary procedures?

Enterococcus!! gram positive cocci in chains bc its part of strep family but it is *gamma hemolysis* i.e. reveals no hemolysis they're also *pyrrolidonyl arylamidase* (PYR) positive and able to grow in bile and in 6.5% sodium chloride (sketch w raise wages to 6.5%!)

Bite cells on peripheral smear?

G6PD deficiency

"infiltration of lamina propria of intestine w atypical lymphocytes"

GI MALT lymphoma (mucosa associated lymphoid tissue) this is associated w chronic H pylori infxn of the stomach

what tissues use insulin mediated glucose transporters? what tissues use insulin independent transporters?

GLUT4 = insulin mediated. only *adipocytes and muscle cells* use insulin mediated. GLUT1, 2, 3, and 5 are insulin independent transporters. all other tissues *brain, kidney, intestine, RBCs, liver* use independent. so really your "main" or "vital" organs need to get their sugar REGARDLESS of what goes on around in terms of insulin. they will find the way or by way to get their sugar. they're *vital* BONUS (idk how important this is :/ i hope Lord you can lemme know if i get more questions on it. i didn't get question on it but it was in the explanation :( feels like too much to memorize. Help Father) -GLUT 1: RBCs and BBB -GLUT2: hepatocytes, pancreatic *B* cells, renal tubules, small intestinal mucosa. major role in dietary glucose, reabs of glucose from kidney tubules, hepatic glucose reg, sensitivity of B cells to circulating glucose -GLUT3: placental & neuronal -GLU5: *fructose* . found in spermatocytes & GI

signet-ring cells - diagnosis?

Gastric carcinoma of the inflammatory type but if in ovaries --> KRUKENBERG TUMOR!! (i.e. gastric cancer that has metastasized to ovary)

What is the blood/gas partition coefficient?

It tells how *Soluble* these gases are. Remember, highly soluble gases have slow onset. if its highly soluble in blood that means it will dissolve easily in blood so we need a lot MORE of it to fill up the gas enough to saturate it and allow the gas to make it to the brain

"patches of demyelination" in brain of an HIV pt?

JC polyoma virus --> progressive multifocal leukoencephalopathy prefers oligodendrocytes hence patches of demyelination

Action card: look at some of the tumor promotors and suppressors on your phone in pics

Just for a little bit, don't stay there too long :) Maybe something to try and memorize the day before the exam

if the question stem says 47 chromosomes and intellectual disability what should you be thinking?

Klinefelters. aka 47 XXY. for this question they didn't give many other clues. they just said 47 chromosomes and mentioned intellectual disability... downs would also work but that wasn't an option

at what level in a CT would you expect to stop seeing the IVC?

L5!! that's the level at which the common iliac veins merge if youre above L5 you should see the IVC to the right of the aorta!! other markers are the that duodenum usually looks black bc it has air and it is found horizontally at the L2 level

What complications might you see ~5 days post MI? *recurrent*

LEAST COMMON v papillary muscle rupture --> acute severe pulm edema bc build up of blood back thru lungs IV septum rupture --> new holosystolic murmur 5-14 days pot MI: free wall rupture --> pericardial tamponade, severe hypotension & shock MOST COMMON ^

what is budd chiari syndrome?

LIVER infarction secondary to hepatic VEIN obstruction presents with painful hepatomegaly and ascites **hepatocellular carcinoma gives an increased risk for Budd Chiari syndrome also increased risk in *polycythemia vera pts*

Good immune response to leprosy leads to tuberculoid leprosy which is mild. what cell mediates this? poor immune response to leprosy leads to lepromatous leprosy which is pretty severe. what cell mediates this?

Leprosy is taken care of by *cell mediated immunity* 1. Th1 mediated. remember Th1 activates CD8+ t cells (cell mediated immunity). intact CMI. 2. Th2 mediated. Th2 activates B cells (humoral immunity). weak CMI

Sertoli vs leydig cell fxn in terms of sexual development?

Sertoli STOPS female insides from forming by secreting *anti mullerian hormone* (also produce androgen binding protein --> concentrate testosterone in the seminiferous tubules to enable spermatogenesis Leydig cells --> secrete testosterone --> stimulate wolffian ducts to develop into *internal male* repro organs. also turns into DHT to make external male repro organs if a pt had NON fxning sertoli cells but normal leydig cells they would have male AND female internals, but male externals bc leydig cells produce DHT which does external genitals

What are some of the cytokines involved in wound healing? (5) commonly, defect in which of these is realted to hypertrophic or disfiguring scars?

-TGF beta (also inhibits inflammation) -TGF alpha -platelet derived GF -fibroblast GF -vascular endothelial GF (VEGF) *TGF beta excess* --> fibroblast prolif to the point of hypertrophic or disfiguring scars of the lung, liver, kidney, and skin

What are some deficiencies seen in temporal lobe lesions? (5)

-aphasia (if dominant hemisphere lesion) -memory probs -seizures (complex partial and tonic clonic) -hallucinations (auditory, olfactory, visual) -meyers loop pie in the sky on contralateral eye injury

What are 4 common aging heart features?

-increased collagen content w/i ventricular wall -brownish perinuclear cytoplasmic inclusions (aka lipofuscin which is result of indigestible byproducts of subcellular membrane lipid oxidation) -sigmoid shaped ventricular septum -decreased left ventricular chamber size (particularly apex to base dimension)

what other findings might you see in a pt w psoriasis?

-pitting of the nails (but also yellow-brown discoloration, thickening, crumbling) -uveitis in the eye -PSORIATIC ARTHRITIS OMG JEN (PAIR!!) you chose celiacs...

Buzzphrases: "nonseptate hyphae" "sporangia"

1. "nonseptate hyphae" --> mucor and rhizopus. nonseptate hyphae that branch at wide angles like 90 degrees 2. "sporangia" is code for spores so mold fungi like rhizopus for example.

When there's a hemothorax, to which side does the trachea deviate?

TOWARD the AFFECTED side... think of the lung falling down and the trachea going w it affected side will look entirely white on CXR (kinda looks like pulm HTN but one side will be totally normal and 'see thru' like usual)

what are the V/Q ratios like at the lowest area of base vs highest area at apex

V/Q is lowest at base V/Q is highest at apex ventilation is generally the same in both altho somewhat low in apex somewhat high in base the real changes are in perfusion d/t gravity so it'll be really low in apex and really high in bases APEX: V low but Q is lower --> big V/Q BASE: V high but Q is really high --> low V/Q

How is Ascaris lumbricoides dx'ed? What about ancylostoma duodenale and necator americanus? what about strongyloides sterocoralis? what about trichinella spiralis?

Ascaris lumbricoides is w *eggs* in stool (groot lumber guy w little eggs in water around him) same w ancylostoma duodenale and necator americanus (eggs near puddles around these 2 swinging super heros) Strongyloides sterocoralis is w *larvae worms* in stool (strong superhere w worms going out of the intestinal wall) trichinella spiralis is w *cysts w/i striated muscle* (evil pig w striated muscle wall behind him that has cysts on it)

renal cell carcinoma + mutation on chromosome 3p (deletion) is d/t what gene being abn?

VHL! aka von hippel lindau caused by inactivated mutation in the tumor suppressor gene VHL.

what is the MOA of VIPomas?

VIP = vasoactive intestinal peptide it comes from pancreatic islet cells that *hypersecrete* VIP and causes increase HCO3- and *Cl-* loss into intestinal lumen. MOA: -binds to intestinal epithelial cells and activates *adenylate cyclase* activation --> cAMP prodxn --> Na+, Cl-, and water actively get SECRETED into bowel

"Azurophilic needle shaped granules" what translocation?

Auer rods!! --> acute promyelocytic leukemia (APL) which is a subset of *acute myelogenous leukemia* This is is a t(15;17) translocation! The Auer rods are fused lysosomal granules inside immature myeloid cells called "promyelocytes"

What nucleus of the brain does ACh come from?

Basal nucleus of Meynert "A choice (ACh) May not (meynert) be salient (basal nucleus of)

in a 14;18 translocation what is overexpressed?

Bcl2 --> prevention of apoptosis --> cells live longer this is seen in pts w non hodgkin follicular lymphoma

What is the specific MOA of beta blockers on aqueous humor i.e. what is their target and how could they help a pt w open angle glaucoma?

Beta 2 *increases aqueous PRODXN* which is from the *epithelial cells of the ciliary body* (boy in bugle 2 camp pouring water into eye shaped hat. he's PRODUCING more water) so the specific MOA of beta blockers on eyes is: blocks epithelial cells of the ciliary body from producing aqueous humor pts w open angle glaucoma have a blockage up aqueous humor uptake so it would be helpful to produce less. BONUS: -open angle glaucoma is seen in *african americans* more often -chronic loss of vision -enlarged cup to disc ratio (> 0.6 d/t loss of *ganglion cell axons*) -disc itself is pale d/t optic nerve atrophy (from the increased intraocular pressure)

buzzword: dark urine + pale stools + excess bilirubin (direct and total)

Biliary atresia!! dark urine: excessive renal excretion of biliruin pale stools: lack of intestinal bile excess bilirubin: liver is fine!! it's just that the vessels/tubes wtvr to transport the bile aren't working!! so the instestine isn't seeing thte bile!!

what are the TORCHS infxns?

Toxoplasmosis Other (Vzv, parvovirus, syphilis) Rubella (blueberry muffin rash, cataracts, heart probz) CMV HSV

what GI hormone inhibits gastric acid secretion aside from somatostatin?

Vasoactive intestinal peptide aka VIP! that can be a clue if pt presents w watery diarrhea that isn't getting better and you think it might be VIPoma check acid secretion levels in stomach

What sequences guides/direct the addition of the poly A tail?

consensus sequence "AAUAAA" bc poly A tail isn't transcribed from the DNA template. the DNA template doesn't have poly A tail, but that "AAUAAA" sequence near the 3' lets the ribosomes know where to add the poly A tail this tail is important bc it protects the mRNA from degradation w/i cytoplasm after it exits the nucleus

How does constrictive pericarditis show up on JVP wave? what about hypertrophic cardiomyopathy?

constrictive pericarditis: rapid y descent Hypertrophic cardiomyopathy: prominent a wave (bc have to contract extra hard to get all the blood in)

what part is in the core of CN3? parasympath fibers or motor fibers? what does this mean clinically?

core = motor!! this means pts suffering from compression --> more likely to have sx of parasympath so dilated eye that won't constrict whereas *ischemia* pts will have motor sx ('down and out')

What is a feared complication of Kawasakis?

coronary artery aneurysms

Buzzword: cystic solid mass from brain that has brownish yellow fluid rich in cholesterol?

craniopharyngioma --> suprasella tumor that comes from *rathkes pouch* --> embryonic precursor of anterior pituitary

suprasellar mass w 3 components (solid, cystic, and calcified) is what?

craniopharyngioma until proven otherwise!!

what is something that's importantly reabs at the terminal ileum? what pts are at risk for def?

crohns dz commonly affects the *terminal ileum* we reabs *bile acids* here which are important for abs of fat and fat soluble vitamins...damaged terminal ileum = no bile acid reabs --> A, D, E, K def --> coagulation factor deficiencies --> easy bruising!

What does cryoprecipitate contain and how is it diff from FFP?

cryoprecipitate only has factors 8, 12, vWF, and fibrinogen FFP has all the coag factors and this is what we give in warfarin OD cases you would NOT give FFP in heparin OD bc it contains antithrombin 3 which heparin speeds up. you give protamine sulfate for heparin OD

"exposure to pigeon droppings"

cryptococcus neoformans!! (pigeons in that egyptian type sketch)

pt w rapid onset SOB, palpitations, flushed skin after accidental exposure. dx?

cyanide toxicity classic is the "reddish skin discoloration" cyanide will bind Fe3+ w high affinity --> inhibit cytochrome c oxidase in mitochondria --> impaired oxidative phosphorylation --> severe lactic acidosis and death from anaerobic metabolism

elevated levels of methionine would mean what amino acid is essential in affected pts?

cysteine!! remember we learned this!! homocysteine gets converted to methionine OR cysteine. if there is a cystathionine synthase deficiency, you can't convert homocysteine into cysteine and thus it all gets shunted to the methionine side

what is the cause behind septic shock in the setting of a gram negative bacterial infxn?

d/t ENDOTOXINS in blood stream. regardless of gram negative bacteria, they all have *lipopolysaccharide* (LPS) LPS is released during destruction of bacterial cell wall. it has 3 regions: -O antigen -Core polysaccharide -lipid A *LIPID A IS RESPONSIBLE FOR TOXIC PROPERTIES OF LPS THAT LEADS TO GRAM NEG SEPSIS AND ENDOTOXIC SEPTIC SHOCK* it is lipid A!! it causes release of IL-1 and TNF alpha --> septic shock... fever, hypotension, diarrhea, oliguria, DIC, e tc Also important: LPS is *not actively* secreted by bacteria. it's a result of bacteriolysis OR during division. Lipid A is the toxic component of LPS

Buzzword: tartrate resistant acid phosphatase

aka TRAP Hairy cell luekemia!! cells are positive for TRAP THINK: TRAP for hairy -TRAP positive -Cells get TRAPPED in bone marrow --> dry tap (not rly what happens but just think of it that way) -cells get TRAPPED in spleen *red pulp* and can't go to lymph node --> no lymphadenopathy despite being a neoplastic proliferation of mature B cells

what findings would you see on histology of a biopsy of urticaria?

aka hives. hives are d/t increased permeability of microvasculature --> edema of the *superficial dermis* if the deep dermis and/or subQ tissue is involved we call it *angioedema*

Buzzword: tyrosinase def?

albinism!! melanocytes synthesize melanin from tyrosine via tyrosinase

vomiting & hypoglycemia after consumption of fruit or juice. dx?

aldolase B deficiency aka hereditary fructose intolerance

how does hyperglycemia lead to cataracts?

aldose reductase converts glucose to sorbitol using NADPH. it converts it at a faster rate than sorbitol can be metabolized to fructose by sorbitol DH. sorbitol accumulates in certain cells like *lens cells* --> influx of water --> *osmotic cellular injury* also, depletion of NADPH by aldose reductase increases oxidative stress which only makes it worse

GDP is bound to what subunit in an inactive G protein?

alpha subunit! when ligand binds to extracellular domain --> GDP switches to GTP and GTP will cause alpha subunit to dissociate from beta and gamma. this will then activate phospholipase C (Gq) or adenylate cyclase (Gs)

What is the rate limiting step of heme synthesis?

aminolevulinate synthase (ALA synthase) if a pt has a porphyria you wanna tx them by giving heme. heme has Fe2+ and protophyrin so you'll down regulate the protophyrin creation by stopping the rate limiting enzyme which is ALA synthase

damage to what area of the brain leads to inability to carry out calculations, read, or write?

angular gyrus of dominant parietal lobe!! this area is supplied by the *MCA* Gerstmann syndrome: presents w 1. finger agnosia, 2. agraphia, 3. left-right disorientation, 4. acalculia the reading and writing sx are d/t involvement of angular gyrus which is also involved in reading and speech

Where does the ACL attach?

anterior intercondylar area (fossa)

STEMI in leads V2-V5 indicate MI where..? *recurrent*

anterior wall of heart! d/t LAD* or LCX

What shows up first? anti HBc IgM or anti HBs IgM?

anti HBc IgM!! even during window period!! signifies ACUTE hep B. present even before anti HBs IgM! anti HBc Ig*G* always look for it to signify resolution/cure of hepatitis in pts. anti HBsAg IgG signifies successful HBV vaccination or clearance of HBsAg and remains detectable for life think: vaccination only? youve fought against the SURFACE. infection? youve fought against the SURFACE *and* the CORE

buzzword: flaccid bullae that spread laterally when pressure is applied on top. found in mouth. ab against?

antibodies again *desmosomes* --> specifically *desmogleins 1 and 3* pemphigus vulgaris. more common in oral mucosa. bullous pemphigoid is rare in mucosa and will have tense bullae that remain intact

what consequences would you see in a pt w Kartagener syndrome aside from infertility, chronic sinusitis, and situs inversus?

bronchiectasis!! aka persistent bronchial dilation!! bronchiectasis is d/t persistent chronic inflammation. these pts are at high risk for upper and lower resp tracts d/t impaired mucociliary clearance so they'll develop bronchiectasis! pathoma talked about this :)

what virus has an icosahedral nucleocapside and a + single stranded RNA genome?

cages in the sun w parot and david statue. sunny/orange so warm colors = RNA sun w + sign so + sense coxsackie virus. part of picornaviridae (pico parrot)

what is calcitonin and where does it come from?

calcitonin comes from parafollicular cells (C cells) of the THYROID it opposes the actions of PTH ... not important NORMAL for Ca2+ homeostasis but if PTH gets out of whack then yes, it will bring Ca2+ down from serum and keep it in bones

How can cancer cell blunt the cytotoxic T cell response ? (CD8+)

cancer cells will express programmed death ligand 1 (PD-L1) which binds to PD-1 receptor on CD8+ cells and *inhibits their ability to induce apoptosis* Tx w monoclonal ab against PD-1 or PD-L1 results in T cell disinhibition and ability to induce apoptosis in cancer cells :)

pts receiving parenteral nutrition thru a central venous catheter are at high risk for what bug infxn?

candidemia aka "pseudohyphae w blastoconidia" lipid emulsion in the parenteral nutrition soln is thought to promote growth of some Candida species

what is first line tx for trigeminal neuralgia?

carbamazepine!! MOA: inhibits neuronal high frequency firing by reducing the ability of Na+ channel to recover from inactivation

Wheezing + diarrhea + facial flushing + mass lesions on liver lobe & ileum?

carcinoid syndrome!! tx is surgery, but you should give octreotide (somatostatin analog) to tx sx until then

Where is the most common site of berry aneurysms?

circle of willis, specifically the anterior communicating artery BONUS: berry aneurysms are associated w Ehlers Danlos syndrome and AD PKD

"Microglial nodules and multinucleated giant cells"

classic for *viral infxns of CNS* esp HIV associated encephalopathy microglial nodules form when cells of microglia surround the neuron and phagocytize it.

What do metalloproteases do?

cleaves and inactivates endogenous peptides including natriuretic peptides, glucagon, oxytocin, bradykinin

Thick walled spherules packed w endospores in pt w pneumonia... what bug?

coccidioides immitis think about the san juaquin sketch w the bushes that have endospores in them and are round looking

buzzword: muddy brown casts. what is this and what part of the kidney is most commonly affected?

code for "acute tubular necrosis" straight portion of PCT is most commonly affected!! and thick ascending loop of Henle bc these are the most *metabolically active* segments of the nephron and are w/i the medulla both of these are found in the *renal medulla* which is the area of kidney most prone to ischemic injury bc it has low blood supply even during normal conditions so imagine when they're in ischemia

What is the MOA behind T cell mediating autoimmune dzs?

commonly d/t TNF receptor mutations such as mutation in Fas ligand or fas receptor. Fas R is expressed on T cells. once activated (i.e. they've detected something bad/foreign) T cells begin to express FasL which can bind to Fas R on the same cell or adjacent lymphocytes. constant presence of stimulating self antigens --> activated T lymphocytes --> tons of apoptosis!! which would be fine if these T cells die but mutations involving the Fas R or Fas L can *prevent* apoptosis of autoreactive lymphocytes THIS IS WHY TNF ALPHA IS A TARGET FOR IBD PTS!! bc Fas Ligand and Receptor are part of the TNF family.

large anterior fontanelle + large tongue + umbilical hernia + floppiness + poor feeding

congenital hypothyroidism at risk for severe and irreversible intellectual disability --> levothyroxine by age 2 can normalize cognitive & physical development

excess vitamin D prodxn can be seen in what lung disorder?

sarcoidosis! or other granulomatous dz's like TB bc they have a PTH independent conversioin of 25 hydroxyvit D to active 1,25 hydroxy vit D by *1 alpha hydroxylase* bc granulomatous dz's have activated macrophages which have the 1 alpha hydroxylase :o

intensely pruritic rash worse at night? ("difficulty sleeping")

sarcoptes scabiei mite and eggs!! i.e. scabies!! commonly affects flexors of wrist, lateral surfaces of fingers, and the finger webs this is a type 4 hypersensitivity

The cutaneous neurofibromas of NF1 is from what type of cell?

schwann cells!! :O aka come from neural crest

action card: label the pressure volume loop. where do valves open and close?

see your phone for pic

pt w recurrent pneumonia + celiac dz + anaphylactic rxn during blood transfusion. dx?

selective IgA def pts w severe IgA def can form IgE antibodies against IgA! so when they get blood products they can develop potentially fatal anaphylaxis. even if its the right match bc there might still be small amounts of IgA! ABO incompatibility does NOT present w anaphylaxis bc this is IgE mediated. ABO incompatibility is d/t preexisting IgM or IgG antibodies that cross react w antigens from the transfused blood --> fever, chills, severe hemolysis, circulatory collapse

Buzzword: psamomma bodies on ovarian tumor

serous cystadenocarcinoma most common ovarian cancer

Buzzword: psammoma bodies on ovarian mass

serous cystadenocarcinoma (epithelial ovarian neoplasm) most common ovarian cancer

most common ovarian cancer?

serous cystadenocarcinoma. will see *psammoma bodies* !!

ovarian tumor + signs of virilization like sx in female. what type of tumor?

sertoli leydig!! they come from sex cord stroma and secrete testosterone --> signs of virilization

Who has the lower ID 50? shigella or salmonella?

shigella!! requires 500 sometimes even just 10 bacteria!! salmonella requires like 10^7 other low ID50s are campy, entamoeba histolytica, and giardia lamblia

what benzos are short acting? intermediate? long?

short: triazolam, midazolam Intermediate: oxazepam, alprazolam, lorazepam, clonazepam long: diazepam, chlordiazepoxide, flurazepam -olam = short/intermediate. Oxazepam (ox in sketchy pancake restaurant) benzos can sometimes be used when pt is barely starting on SSRI for anxiety bc it takes a while for SSRIs to work

Buzzword: lung histopath showing central areas of whorled collagen fibers *recurrent*

silicosis (mining, sand blasting, foundries) the SILLY EGG SANDwish i FOUND is MINE! "Eggshell" calcifications of hilar lymph nodes on CXR

Buzzword: anti SSA (Ro) or anti SSB (La) *recurring*

sjogrens syndrome! commonly seen in females ... causes large salivary glands and dental caries d/t dry mouth from lack of normal saliva

What layers does a cricothyrotomy go thru?

skin superficial cervical fascia (including subQ fat and plastyma muscle!!) investing & pretracheal layers of deep cervical fascia cricothyroid membrane

what is the #1 thing you can advice your pts to decrease mortality? esp in DM pts?

smoking cessation!! :o this is by far the most effective preventive intervention for almost all pts esp those w DM (greatly increase risk of MI & decreases immediately upon smoking cessation tho not back to baseline)

Major risk factor for developing bladder cancer?

smoking!! also > 60 y/o and occupational exposure to rubber, plastics, or aromatic amine containing dyes also cyclophosphamide

Multiple sclerosis pt w new demyelinating lesion in the mid thoracic spinal cord. What might you find in urodynamic studies?

spastic bladder aka bladder hypertonia d/t UMN lesion this would present as uncontrolable urge to urinate aka urge incontinence d/t overactive detrusor

what muscle can get injured during a posterior triangle of the neck procedure?

spinal accessory nerve --> trapezius or SCM!! sx: impaired abduction of arm *above horizontal*, drooping shoulder, scapula winging deltoid injury would cause impaired abduction at angles BELOW the horizontal plane

lung tumor in pt that also has hypercalcemia?

squamous cell carcinoma! can secrete PTH related protein (PTH will be low) --> hypercalcemia

Buzzword: hilar mass in lung in pt w heavy smoking hx

squamous cell carcinoma!! 2nd most common lung cancer. smoking is highest risk for these!! histology : keratin pearl (think: squamous skin)

Buzzword: crumpled tissue paper cells in bone marrow. d/t what def? classic triad of sx?

these are Gaucher cells seen in AR Gaucher dz d/t beta glucocerebrosidase def --> excess glucocerebroside --> lipid laden macrophages that look like "wrinkled tissue paper" or "crumpled newspaper" or "wrinkled silk" TRIAD: pancytopenia (or just thrombocytopenia or just anemia) + hepatosplenomegaly so ab distension + bone pain d/t invasion/inflammation of these macrophages bottom line: if they show you a macrophage or white cell looking thing that has crumply looking cytoplasm --> Gauchers

Cavitary lesions in the context of TB means what?

the infxn has healed d/t the release of proteases, nitric oxide, and reactive O2 species from macrophages when they created the caseating granuloma but caused damage. basically signifies your body had an appropriate immune response but had collateral damage

what drugs are these: glycopyrrolate, hyoscyamine, propantheline

these are *selective muscarinic antagonists* (not in sketchy) but they're given to pts w myasthenia gravis that are experiences excess ACh. they selectively block muscarinic receptors everywhere except on skeletal muscle so pts that are experiencing diarrhea, urination, miosis, bronchospasm, emesis, lacrimation (DUMBBELLSS) will stop those sx but ACh will still work on skeletal muscle!

"fibrous bands are seen extending from the cecum and right colon to the retroperitoneum causing extrinsic compression of the duodenum"

these are Ladd's (fibrous) bands that are seen in "failure of midgut rotation around the SMA" aka midgut malrotation this causes intestinal obstruction and will see *bilious emesis* in the first few days of life

rash that started on face and rapidly spread down body. tender lymphadenopathy blitateral behind ears

togavirus specifically rubella!! if it starts in face and spreads down could also be rubeola (measles) but this doesn't have postauricular lymphadenopathy

how do you tx pubic lice?

topical *permethrin* i totally guessed on uworld and got it right so make sure you learn it! works by blocking parasite Na+ ion conduction in nerve cell membrane channels --> louse paralysis andn death

Expected excretion rate formula? how would they ask this in a question

total filtration rate -- total tubular reabsorption rate. they would give you inulin clearance, PAH clearance, plasma concentration and tubular reabsorption inulin clearance is another way of saying *GFR* so to get total filtration rate you would multiply (Plasma concentration i.e. how much is in the blood)*(inulin clearance i.e. how much got filtered) this gets you the total filtration rate then subtract the tubular reabs of substance A

HOX genes encode for what type of proteins?

transcription regulation factors that play an important role in segmental organization of the embryo

What enzyme takes ribulose 5 phosphate to fructose 6 phosphate?

transketolase this is important for formation of nucleic acid synthesis

Buzzword: "aorta lying anterior, inferior, and to the right of pulm artery"

transposition of the great arteries d/t failure of fetal aorticopulm septum to spiral can see elevated lactate d/t anaerobic metabolism d/t poor oxygenation of blood

injections given where increase risk of trendelenburg gait?

trendelenburg gait is also called gluteus medius gait. injections in the *superomedial* part of butt risk injury to the *superior gluteal nerve* and thus trendelenburg gait BONUS: -superomedial, inferomedial, and inferolateral risk injury to sciatic nerve -anterolateral gluteal region is the safest :)

What nerve exits the brainstem at the middle cerebellar peduncle level?

trigeminal!! this is a key neuroanatomic landmark for locating the nerve! can show MRI and if you see the cerebellum attach to something near the middle part of the brain you're at the level of the middle cerebellar peduncle and the only nerve exiting in the medial portion there is the CN5!

thin membrane on pts scalp + sac w loop of bowel protrudes + cleft lip and palate

trisomy 13 aka patau syndrome the mentioned are all midline defects d/t defective prechordal mesoderm fusion . could also see holoprosencephaly as a midline defect also see w polydactyly and cutis aplasia (aka thin membrane on scalp)

Buzzword: prominant occiput and small mandible in newborn + rocker bottom feet + clenched hands w overlapping fingers (hypertonia) what about a new born w cleft lip/palate + polydactyly + omphalocele or umbilical hernia

trisomy 18!! edwards syndrome!! trisomy 13!! not associated w overlapping fingers like trisomy 18

What does a fungus ball look like on CT and what is it d/t?

d/t aspergillus fumigatus seen in pts w hx of some lung cavity like "recovered from TB years ago" or "emphysema x 20 yrs" or "hx of sarcoidosis" aspergillus likes to invade those tissues and form fungus balls. this is called *colonizing* and is sometimes described as "radiopaque structure that *SHIFTS* when the pt changes position"

"stacked brick" intestinal adhesion is likely d/t what organism?

enteroaggregative E coli (EAEC) this is seen in persistent diarrhea in infants in developing countries and in those w advanced immunosuppression like AIDS

what does oxaloacetate require in order to form back into phosphoenolpyruvate (PEP) and go up gluconeogenesis?

enzyme PEP carboxykinase AND GTP this GTP can be gotten from the conversion of succinyl CoA to Succinate by succinyl CoA synthetase which releases GTP

Buzzwrod: charcot leyden crystals

eosinonphil derived crystals seen in asthma

what type of casts are seen in the kidneys of pts a multiple myeloma?

eosinophilic casts composed of Bence Jones proteins. bence jones proteins are just another name for free light chains

quick quick: what do tyrosine kinase receptors code for in general?

growth factors!! so "accelerate cell proliferation" insulin, IGF-1, FGF, PDGF, EGF HER2 oncogene is also a growth factor! in fact, its an epidermal growth factor w tyrosine kinase activity

"segmental demyelination and endoneurial inflammatory infiltrate composed of lymphocytes & macrophages"

guillain barre syndrome thought to be d/t molecular mimicry after immune response to campy ascending symmetric muscle weakness is seen. rapidly progressive

What bugs produce urease? what do they increase the risk for?

increased risk for struvite!! (ammonium magnesium phosphate) stones! this is esp true for proteus, but there are others. "Pee CHUNKSS" Proteus Cryptococcus H pylori Ureaplasma Nocardia Klebsiella S epidermidis S saprophyticus

All antidepressants carry risk of inducing _____________ in susceptible pts

inducing mania!! susceptible pts are pts that have a family hx so like if pt given anti depressant and then has a manic episode and mom were to say 'oh yeah ive had some of those before' then the reason behind the mania would be the sertraline or whatever antidepressant was given

what is the pathophys behind giant cell arteritis?

inflammatory infiltrate in temporal artery d/t cell mediated immunity, specifically CD4+ T cells *recruited by IL 6!!!* IL6 normally increases acute phase proteins and stimulates fever. but apparently also involved in giant cell arteritis. don't feel bad about missing it jen :) it wasn't even on pathoma!

what is metyrapone?

inhbits the last step of cortisol synthesis (i.e. 11 beta hydroxylase) which would cause upregulation of HPA axis to increase cortisol again you'd see increase in ACTH, *urinary 17 hydroxycorticosteroid*, and 11 deoxycortisol

what are 3 ways the long thoracic nerve is commonly injured?

injury to long thoracic nerve would lead to winged scapula d/t serratus anterior being paralyzed 1. penetrating trauma 2. axillary lymph node dissection 3. chest tube insertion

what does a positive Candida antigen reaction signifiy?

intact T lymphocyte fxn bc this is a type 4 hypersensitivity test usually given in question stem to tell you T cells are fine and its another cell problem (commonly B cells)

Where is the AV node located?

interatrial septum near the opening of coronary sinus (i.e. w/i RA) if you wanna get more specific it's near the insertion of the *septal leaflet of tricuspid valve* & *orifice of the coronary sinus*

What cytokine increases expression of MHC 1 and MHC 2? *recurrent*

interferon gamma! it's responsible for increasing expression of MHC 1 and 2 thus improving antigen presentation in all cells!

what is the relationship b/w pancreatitis and hypertriglyceridemia?

it's a vicious cycle small quantities of pancreatic lipase *normally* leaks into pancreatic capillaries where they metabolize TG into free fatty acids high levels of TG can get metabolized into free fatty acids which have toxic and inflammatory effects on the pancreas

what blood type can cause fetal hemolysis?

type O!! type A and B have IgM antibodies. type O usually has IgG and thus can cross placenta!! happens in about 3% of pregnancies but more importantly is the idea that it can happen *in the first pregnancy* (unlike Rh) bc antibodies against the A or B antigens happen commonly as these antigens can be present in foods, bacteria, viruses

Buzzword: spindle cells positive for cytokeratin and/or calretinin *recurrent*

mesothelioma pts will present w *pleural thickening* this is esp seen in asbestos pts (ALTHO REMEMBER ASBESTOS PTS ARE AT INCREASED RISK FOR BRONCHIAL CARCINOMA more than mesothelioma. but if you see mesothelioma it's d/t asbestos)

findings of reverse transcription PCR in a pt w CML?

messenger RNA transcript containing BCR and ABL exons this is bc reverse PCR does from mRNA --> cDNA (i.e. reversal of nl DNA --> RNA) cDNA = "mRNA transcript" in answer choices bc theyre complementary also bc reverse transcription PCR uses mRNA to go back to cDNA it wouldn't have stuff like promoters and enhancer regions which are cut out in the post translational process! by definition reverse transcription PCR is used to detect mRNA (kinda like how southern = DNA; northern = mRNA; western = proteins)

what is methylene tetrahydrofolate reductase involved in? draw the reaction until you know it Jen. God has your back. biochem is hard but He'll help you thru

methylene tetrahydrofolate is (THF-CH3) aka folate we always think about!! :) Homocysteine can go 1 of 2 ways: 1. methionine 2. cystathionine 1. if it wants to go down the methionine path it needs to pick up a couple of friends. it needs *methionine synthase* which gives it a methyl group. ok great but where does it get this methyl group from? *methyl-tetrahydrofolate* to go down this path you also need vitamin B12 as a cofactor. so bottom line: w/o *methyltetrahydrofolate* you can't use methionine synthase properly and thus can't go down the methionine pathway and you'll have deficiency of methionine BONUS: *methylene tetrahydrofolate reductase* regenerates methyl tetrahydrofolate to have it ready every time :) it uses FAD as a cofactor 2. if it wants to become cystathionine it needs help from 3 things: a. cystathionine synthase b. serine c. B6 its okay if this is confusing jen. God has spoken and He will get you thru this. not by your own doing. its okay. pg 84 in FA has this. try to draw it until you know it <3 even if it seems like its taking a long time. this is the thing pathoma described as: folate comes into the cell and becomes THF. THF can't exist by itself it gets methylated immediately THF-methyl but it doesn't want it so it gives it to B12 so then its THF + B12-methyl. this can now power the reaction of homocysteine to methionine last bonus: elevated levels of plasma homocysteine are an independent risk factor for thrombotic events

what cells does shigella primarily infect?

microfold (M) cells in Peyer patches of the ileal mucosa thru endocytosis!! can't bind to all intestinal cells thus they exhibit specificity for M cells so it would be wrong to say intestinal cells. it might in some cases, but not the major MOA. big she gorilla jumping into M trampoline pad

"mid diastolic rumble" what is the dx and what is a common complication?

mid diastolic rumble = mitral stenosis!! common complication is for the left atrium to dilate bc not able to get all blood out all the time --> left atrium dilation compresses esophagus and nearby structures including the *left recurrent laryngeal* --> hoarseness!

what comes out of the foramen spinosum?

middle meningeal artery & vein!!

what artery is found at the jxn of the frontal, parietal, temporal, and sphenoid bones i.e. the "pterion H thing"?

middle meningeal!! which is a branch of the maxillary artery!!

pts w Kallmann syndrome have absence of GnRH secretory neurons in hypothalamus d/t failure of what?

migration from the olfactory placode!! they'll present w anosmia! BONUS: -commonly d/t mutation in the KAL-1 gene or the fibroblast growth factor receptor-1 gene which code for proteins required in this migration -pubic hair is normal bc adrenarche occurs normally

what is the most common valve affected by infective endocarditis?

mitral valve!! (same as rheumatic heart dz. recall M > A > T. regurg > stenosis) however infective endocarditis is commonly seen in *mitral valve prolapse* esp w regurg. so mitral valve prolapse w regurg is the most common *predisposing condition* for native valve infective endocarditis in developed nations in developing nations a frequent cause of infective endocarditis would be rheumatic heart dz

Use of anti seizure medication during pregnancy should make you think of what defect?

neural tube defects! commonly caudal neural tube but CAN ALSO BE ANENCEPHALY!! which would present as polyhydramnios!!

"generalized paralysis" commonly d/t?

neurosyphilis progressive dementia & generalized paralysis

what cell on CBC would you expect to increase as a result of prednisone?

neutrophils! steroids cause the adhesion of neutrophils to the blood vessels to weaken so instead of hanging like bats theyre let loose in the blood! (neutrophil demargination) glucocorticoids decrease all other WBCs tho and are used to tx autoimmune/inflammation bc of this (lower basophils, eosinphils, lymphocytes, monocytes)

pt w pupils that are dilated, new ab pain, diarrhea, and lacrimation. dx?

opioid withdrawal cocaine would be kinda similar you'd see dilated pupils but the key give away is *lacrimation* that's something only seen w opioid withdrawal. also *yawning* is also pretty specific to opioid withdrawal also the diarrhea is NOT seen in cocaine or amphetamine OD so another clue toward opioids

where does the efferent limb of the eye light reflex pathway originate? where does it synapse?

originates in the *edinger westphal nuclei* aka preganglionic. then it will continue to the celiac ganglion where it will synapse and the postganglionic will innervate the iris sphincter to constrict this is where the afferent post gang will synapse (afferent pregang synapsed at pretectal nucleus)

3 y/o boy that has a fever and is refraining from using his right leg. passive ROM does NOT elicit pain and no joint effusion is seen but he refuses to bear weight on it. what is going on and what part of the bone is most likely affected?

osteomyelitis! our only clue was that he was a little boy. hematogenous osteomyelitis affects kids, particularly boys. didn't give any more explanation as to how we should know it was osteomyelitis :o osteomyelitis most commonly affects the *metaphysis of long bones* !! this is bc the region has slow flowing sinusoidal vasculature that is conductive to microbial passage BONUS: *vertebral body* is the most common location for hematogenous osteomyelitis in ADULTS.

what is avascular necrosis and what are common causes?

osteonecrosis or avascular necrosis is d/t impaired blood supply to a segment of bone. femoral head is most common location common causes include *sickle cell dz* (d/t thrombotic occlusions of arteries), glucocorticoid therapy (MOA not known), vasculitis, alcoholism (MOA not known) commonly presents as chronic, progressive groin and hip pain that is worse by weight bearing bc femoral head is most common bone affected. there will be no swelling, erythema, or warmth.

Owl eyes is diagnostic of what cancer?

owl eyes = reed sternberg cells on lymph node biopsy. described as "abundant cytoplasm, bilobed or double nuclei and inclusion like eosinophilic nucleoli" diagnostic of classic hodgkin lymphoma sx are usually nontender lymphadenopathy or lymphadenopathy that's accidentally detected on routine chest xray. associated w B sx (fevers, night sweats, weight loss) has bimodal age of distribution w a peak in the 20s and another in 60s CBC unremarkable. lymph node biopsy is how you definitely dx malignancy. you'll see these reed sternberg cells.

what type of molecule is oxaloacetate? why is this relevant?

oxaloacetate is an example of an *alpha keto acid* when it reacts w an amino acid to form a new amino acid we call that *transamination rxns* these require vitamin B6 cofactor aka pyridoxine example: glutamate (AA) + oxaloacetate (alpha keto acid) --> aspartate (AA) + alpha-ketoglutarate (alpha keto acid)

what is the first enzyme that sets off the whole zymogen chain in GI tract? what protective mechanism does the pancreas have? (2)

pancreas makes all the zymogens and does so in an inactive form. the first one to start the chain is *trypsin* which gets activated in the DUODENUM by duodenal enterokinase... if it gets activated before in the pancreas --> pancreatitis PROTECTION: 1. Pancreas has a trypsin inhibitor (*SPINK1*) which comes from pancreatic acinar cells and inhibits trypsin formation 2. trypsin can *cleave itself* at a secondary site and turn itself off. most common hereditary pancreatitis mutations leads to abn trypsin that can't turn itself off

pregnant pt w arthritis gives birth to baby w pleural effusion, pulm hypoplasia, ascites. what virus is responsible?

parvovirus naked. ssDNA virus. in adults presents as arthralgia/arthritis but causes hydrops fatalis in babies (presents as severe anemia, heart failure, pleural effusions, pericardial effusions, ascites)

"snowstorm on US"

pathognemonic for *COMPLETE* mole can also describe as "multiple cystic edematous hydropic villi" or "multiple bilateral ovarian cysts" (these aren't the actual complete mole but rather in complete moles you get super high levels of Beta hCG which can cause theca lutein cysts i.e. cysts in the ovaries) or "bunch of grapes" appearance BONUS SNACK: -complete moles are p57 negative d/t absence of a maternal genome

Buzzword: endocardial thickening and fibrosis of tricuspid and pulmonary valves how do we dx?

pathognomonic/CHARACTERISTIC of *carcinoid heart dz* aka *carcinoid syndrome* that most commonly start in GI and metastasize to liver. these tumors secrete lots of things, but especially histamine, serotonin, and vasoactive intestinal peptide. these hormones can be released directly into systemic circulation if the cancer has metastasized to the liver (if it hasn't metastasized the liver will catch these and metabolize them) From there, carcinoid heart dz is caused by *excessive serotonin* --> fibroblast growth and fribrogenesis. this happens in the *right side* of the heart (i.e. tricuspid and pulm valves) bc in the lungs we have monoamine oxidase which inactivates serotonin so it doesn't damage left side of heart We dx this by checking *5 hydroxyindoleacetic acid aka 5 HIAA* which is the end product of serotonin metabolism

What are 3 consequences of polyhydramnios i.e. increased abdominal circumference out of proportion for gestational in pregnancy?

polyhydramnios (if severe) causes *uterine enlargement* complications: 1. preterm labor 2. placental abruption 3. uterine atony d/t uterine overdistension which makes giving vaginal birth or ejecting placenta impossible

antibodies against what part of N meningitidis would lead to immunity?

polysaccharide capsule!! we give a vaccine thats capsular polysaccharide antigens bound to diphteroid toxin which will allow for MHC presentation --> T cell stimulation & a stronger longer lasting immune response

what is the most common porphyria?

porphyria cutanea tarda whcih is d/t defect in *uroporphyrinogen decarboxylase* and it leads to *Photosensitivity and blistering* in areas of sun exposure and elevated levels of uroporphyrinogen in urine

what are sx of rhabdomyolysis?

positive blood on urine dipstick in the *absence of RBCs* suggests myoglobinuria this is commonly seen after a crush injury or prolonged muscle activity (like seizures!!!) or drug/rx use (statins, *amphetamines*, heroin) blood on dipstick detects *heme pigment* from hemoglobin AND myoglobin so its possible to get a positive dipstick for blood w/o any blood the heme pigment is release from myoglobin --> acute tubular necrosis by direct cytotoxicity & renal vasoconstriction --> hyperkalemia, hyperphosphatemia, hyperuricemia

What should be given to all pts that go thyroid removal post op?

post op and beyond they should take *oral calcium and vitamin D* d/t injury of parathyroid glands. active form of vitamin d is *calcitriol*

what are common vitamin E def sx? what presents similarly?

posterior column & spinocerebellar tract demyelination!! also motor weakness/DTR presents similarly to vitamin B12!! but won't have megaloblastic anemia, hypersegmented neutrophils, or high serum methylmalonic acid!

anal fissures most commonly occur along what part of the anus?

posterior midline!! likely bc this area has the least blood flow and thus makes it sensitive to trauma and slows healing times

most common cause of bilateral fetal hydronephrosis in boys?

posterior urethral valves (i.e. urethra obstructed w a membrane and can't pee out so urine will reflux back thru ureters and dilate them and cause hydronephrosis

what stimulates release of bicarb in the duodenum and pancreas?

presence of acid in the duodenum and jejunum causes release of *secretin* from S cells in mucosa --> stimulates bicarb from submucosal glands (i.e. brunner glands in duodenum) & pancreas

Buzzword: 45 y/o woman w intense pruritis that is very severe esp at night

primary biliary cirrhosis autoimmune destruction of intrahepatic bile ducts & cholestasis commonly associated w other autoimmune dz's like Sjogren's syndrome, raynaud's, scleroderma, thyroid dzs that are autoimmune, celiacs

if you hear HTN + very low plasma renin activity what should go thru ur head? what about high renin and HTN?

primary hyperaldosteronism aka excess secretion from zona glomerulosa of adrenals. why? Bc aldosterone works to hold on to Na+ and thus water. this increases blood volume --> increased BP and *decreases renin activity* since we aren't running out of fluid. to further confirm your suspicion, sometimes they'll say pts have *muscle weakness* bc aldosterone also wastes K+ which can lead to muscle weakness, cramps, rhabdomyolysis, cardiac arrythmias Remember: glomerulosa: aldosterone fasciculata: cortisol reticularis: DHEA/sex hormones ADDITIONAL READ: *the high volume* triggers *ANP* which will waste fluid and Na+ that's why you don't see these pts w edema or hypernatremia! this is called "aldosterone escape" High renin + HTN is likely *renal artery stenosis* d/t decrease renal blood flow causing activation of renin and thus HTN

In what part of the lung lobes do you see primary tb infxn? what about secondary?

primary tb infxn is in the middle or lower lobes. secondary is in the top lobes (right part of sketchy cactus has dots on the top part)

what is an important risk factor for a molar pregnancy?

prior miscarriage

MOA of mifepristone?

progesterone antagonist. results in apoptosis and necrosis of the uterine decidua --> prevents further development of a 1st trimester pregnancy terminates pregnancies. commonly used w misoprostol which is a PGE1 analog

"Cytoplasmic inclusions in oligodendrocytes"

progresive multileukoencephalopathy (PML)

what is the next best step for a pt coming in w months of loose stools and ab discomfort? no other risk factors or red flags?

pt probly has malabsorptive disorder d/t some etiology. but first we have to establish malabsorption. fats are the most sevrely affected macronutrient in generalized malabsorption so its a good place to start: stool microscopy w *sudan 3 stain* --> checks for *fat malabsorption* which is the most sensitive strategy for sreening for malabsorptive disorders

what is the diff b/w reassortment and recombination?

reassortment is the exchange of whole genome segments. this requires * segmented viruses* for example influenza virus recombination is exchange of *genes* b/w 2 diff viruses. this is what can be done by *dsDNA non segmented* viruses like HSV for example

What is the most *dangerous* complication of subarachnoid hemorrhage?

rebleeding. most common too (30% of pts) vasospasm is also common but not the most common. sx will be totally diff itll be like weakness of arm and leg whereas rebleeding would be severe HA

pts w portal HTN can develop splenomegaly d/t congestion what specific part of spleen?

red pulp! i think this is where blood is processed? idk for sure but think about it that way! back up of blood from liver --> celiac vein --> back up to splenic vein and into spleen's red pulp

What is Kehr sign?

referred pain (commonly to left shoulder) to shoulder region C3-C5 d/t PERITONEAL irritation (ruptured spleen, peritonitis, hemoperitoneum. blood is irritating to body)

diff b/w vasopressin and desmopressin? what does desmopressin cause and what can it tx?

vasopressin is ADH that vasoconstricts (acts on V2 in collecting duct for the increased H2O abs and V1 on vascular SM for the vasoactive effects) desmopressin is ADH that does not induce vasoconstriction (only binds V2 in collecting duct) desmopressin causes release of vWF and factor 8 and can be used in tx of von willbrand dz

High QRS voltage in precordial leads ?

ventricular hypertrophy!! usually d/t prolonged untreated HTN

"beat to beat variation in pulse amplitude"

very large pericardial effusion or cardiac tamponade d/t the swinging motion of the heart in pericardial fluid seen as beat to beat variation in QRS complex amplitude

buzzword: coiled (corkscrew) hairs

vitamin C def aka scurvy leads to impaired collagen hydroxylation which happens *within the rough ER*.

what virus has a bar shaped protein core w 2 +single stranded RNA molecules?

wizard scene w sunny/warm colors out the window w sun shining rays (+ sense). wizard is wearing a white robe (enveloped), wizard hat has 2 dragons (2 copies of single stranded RNA) also has reversus transcriptus book bc HIV has reverse transcriptase enzyme HIV.

where does cryptococcus neoformans normally live and how is it transmitted?

yeast that has thick polysaccharide capsule. normally lives in soil contaminated w bird droppings and it's inhaled into alveoli of the lungs first. if immunocomp it can disseminate by spreading from the lungs into circulation and penetrating endothelial cells of cerebral capillaries

What is CD28? what cells is it found in?

you always get this confused!! :) but you wont anymore <3 CD28 is found on T CELLS and it interacts w B7 found on antigen presenting cells!! this is a *costimulatory* signal necessary for T cell activation!!

Action card: look at FA pg 548 and try to learn a couple at a time *recurrent*

"Peace I leave w you; My perfect peace I give to you; not as the world gives do I give to you. DO NOT let your heart be troubled, nor let it be afraid. Let My perfect peace CALM YOU in *every* circumstance & give you courage & strength for every challenge John 14:27

Where is the defect in/sx: 1. Guillain Barre 2. Myasthenia gravis 3. Lambert-Eaton syndrome 4. Botulinum *recurrent*

1. Guillan-Barre (commonly seen after campy infxn d/t CD8+ infiltration AND AB formation.. segmental demyelination) is an *ascending paralysis* 2. Myasthenia gravis: autoimmune attack against *postsynaptic NICOTINIC receptors* will show *episodic* diplopia and ptosis but NO muscarinic block sx (like dry mouth or mydriasis) and it will NOT get better w rapid repetitive nerve stimulation. Fun fact: most MG pts also have a thymoma or other thymic abn, just bc they show you a CT doesn't mean you should get intimidated if the sx sound like MG (i.e. get tired easily, worse at end of day, eyes involved 3. Lambert-Eaton: auto antibodies against *presynaptic voltage gated CA2+ CHANNELS*: can have muscarinic block sx and improved w rapid nerve stimulation but initial weakness usually involves proximal legs so ascending again 4. Botulinum inhibits *acetylcholine release* from presynaptic cells so we'll see sx that are nicotinic but also muscarinic block sx (dry mouth, fixed pupillary dilation)! so similar to Lambert-eaton but is *descending* skeletal sx are the classic 3 D's: "diplopia, dysphagia, dysphonia" FINAL CONCLUSIONS lambert-eaton and botulinum are the most similar w LE being *ascending* paralysis and botulinum being *Descending* paralysis

What are 3 important mitochondrial syndromes? *recurrent*

1. Leber hereditary optic neuropathy --> bilateral vision loss 2. Myoclonic epilepsy w ragged red fibers: myoclonic seizures & myopathy associated w exercise. skeletal muscle bx shows irregularly shaped muscle fibers (ragged red fibers) 3. Mitochondrial encephalomypathy w lactic acidosis and stroke-like episodes (MELAS)

What are examples of signal transduction systems (i.e. translocation of signal to nucleus and gene transcription)? (5)

1. MAP kinase 2. PI3K (phosphoinositide 3 kinase)/Akt/mTOR pathway 3. Inoitol phospholipid pathway 4. cAMP pathway 5. JAK/STAT pathway

in what rxns is vitamin B1 involved in (4) this will be a repeating card jen. try to learn 2 for now

1. pyruvate DH (pyruvate --> acetyl CoA; aka glycolysis end product to TCA) 2. alpha ketoglutarate DH (TCA enzyme) 3. Branched chain alpha ketoacid DH (essential for catabolism of branched AA like leucine, isoleucine, valine) 4. Transketolase (used in PPP to convert ribulose 5P to glycolysis intermediates) THINK: ATP Alpha ketoglutarate DH Transketolase Pyruvate DH dx low thiamine or thiamine def by measuring transketolase activity before and after adding thiamine pyrophosphate. if it improves --> thiamine def

What do ACE inhibitors do to: Renal perfusion Intraglomerular pressure filtration fraction? *recurrent*

ACE inhibitors dilate efferent arteriole 1. DECREASE renal perfusion 2. Decrease intraglomerular pressure since blood is flowing faster/smoother 3. Decrease filtration factor bc since it decrease intraglomerular pressure aka GFR you're decreasing how much is getting filtered thus pts are at increased risk of acute kidney injury (tho ACE inhibitors are usually well tolerated) the reason they're at increased risk for kidney injury is bc the body normally constricts efferent arteriole to maintain GFR, but since ACE inhibitors inhibit prodxn of angiotensin 2 they inhibit the body's natural autoregulation response and thus GFR goes down the key thing to take away that you totally confused was that RBF decreases! (i think this might be true only for bilateral stenosis pts bc they can't over come it but im not too sure so for now im gonna assume decreased renal perfusion in both bilateral and unilateral unless God tells me otherwise)

What puts pts at increased risk for aspiration pneumonia?

AMS *impairing cough reflex* --> recall aspiration pneumonia is d/t oral secretions going down lungs (commonly peptostreptococcus, bacteriodes, prevotella, fusobacterium)

What is the differential for someone w an anion-gap metabolic acidosis? what is the formula for anion gap metabolic acidosis? *recurring card; it's ok if you don't get it the first time jen <3 :)*

Anion gap = Na - (Cl + HCO3-) normal is 10-14 ddx: MUDPILES Methanol Uremia DKA Propylene glycol/paraldehyde Isoniazide/iron Lactic acidosis Ethylene glycol (antifreeze) Salicylates (aspirin)

What sequence is found at the 3' end of a tRNA molecule? What does the 3' terminal hydroxyl group serve as? How can you know if a question is asking about tRNA? What enzyme loads the appropriate amino acid to the tRNA? recurrent

CCA!! you've had 2 questions on this and you keep getting it wrong. You'll get it right now tho :) 3' terminal hydroxyl group serves as an amino acid binding site thru aminoacylation They might mention the uniquely modified bases like dihydrouridine, ribothymidine, pseudouridine that are only found in the T loop of tRNAs. Aminoacyl tRNA synthetase loads the appropriate amino acid to the 3' terminal hydroxyl group

What are the CYP450 inhibitors? *RECURRENT*

CRACK AMIGOS Ciprofloxacin (UTI) Ritonavir (protease inhibitors) Amiodarone Cimetidine (H2 blocker so decreases stomacha cid) Ketoconazole (or other conazoles like itraconazole) Acute alcohol Macrolides (*except azithromycin*) Isoniazid (TB tx) Grapefruit juice Omeprazole (PPI) Sulfonamides

What is the most common cause of coronary sinus dilation? *recurrent*

CS communicates freely w the right atrium and will become dilated by any factor that causes dilation of right atrium. most common cause of coronary sinus dilation is *elevated right sided heart pressure* secondary to *pulmonary HTN*

What are the catalase positive organisms?

Cats Need PLACESS to Belch their Hairballs Catalase positive: Nocardia Pseudomonas Listeria Aspergillus Candida E coli Staphylococci (Staph aureus, Staph epidermidis, staph saprophyticus) Serratia Burkholderia cepacia H pylori

RA can manifest in the PIP and MCP, but spares the DIP. What other joint is commonly involved in RA? *recurrent*

Cervical spine!! Remember chris sent you that pic where he was reading about RA? it can lead to *subluxation* other joints are wrists, elbows, knees hips & lumbosacral joint are usually spared

When do you see Chvostek's sign? *recurrent*

Chovsteks & traousseous are seen in HYPOcalcemia --> tetany!! not hyper calcemia like you always think lol so it could be seen in pts that don't have parathyroids (low Ca2+) like digeorge pts

Buzzword: bilateral absence of vas deferens in male *recurrent*

Cystic fibrosis!!! don't get confused w primary ciliary dyskinesia aka kartageners syndrome! very very similar, but will infertility is d/t immotile sperm NOT absent vas deferens Pathophys behind CF: mutation in CFTR gene --> impaired ion transport Pathophys behind kartageners: dynein arm defect --> abn ciliary motion

Does valsalva increase or decrease pre load? what about standing up? *RECURRENT*

DECREASES PRELOAD You keep confusing this but you won't anymore. Increased pressure = less blood can return to the heart bc stopping IVC from dumping it all to RA when you stand blood goes down to feet a bit so can't return as much to heart these maneuvers decrease intensity of almost everything excess HOCM

What do high levels of fructose 2,6, bisphosphate mean in terms of glycolysis? and whats up w PFK2?

F2,6-BP regulates fructose 6 phosphate to fructose 1,6 BP (aka glycolysis) via PFK 1 F2,6BP regulates fructose 1,6 BP --> fructose 6 phosphate via F-1,6-BPase When F2,6-BP is *HIGH* that means we are in a *low* energy state so it's gonna activate PFK so increase glycolysis (& thus inhibits gluconeogenesis bc we're low energy; we don't have the energy to be making glucose. we have to break down glucose to get ATP) When F2,6 BP is *LOW* that means we have high energy and we can afford to make glucose so we create fructose 1,6 BPase to go back to fructose 6 phosphate and up to glucose PFK2 adds another layer of confusion bc PFK2 controls F2,6BP insulin *activates* PFK2 which will increase F2,6BP which will in turn say "LOW ENERGY" which makes us breakdown sugar. this is good bc the purpose of insulin is to lower your sugar so that includes breaking it down as well as hiding it via glycogenesis

Buzzword: anti glomerular basement membrane *recurrent*

Goodpasture syndrome. a subtype of rapidly progressive (crescentric) glomerulonephritis which is a nephritic syndrome. usually involves kidney & lungs

What are the CYP450 inducers? *RECURRENT*

Guiness, Corona, PBRS induce Chronic Alcoholism Griseofulvin Carbamazepine Phenytoin Barbiturates Rifampin (TB rx!) St John's wort (herp for depression) Chronic Alcoholism

What are MHC1 molecules made up of? 2 things apparently! What about MHC2?

MHC 1: 1. MCH class 1 heavy chain 2. beta 2 microglobulin MHC2: alpha and beta polypeptide chains

What heart murmurs/sounds are louder when laying on left lateral decubitis ? *recurrent*

MS MR S3 S4

Buzzword: Little girl with spontaneous *painless* lower GI bleeding. Why is she bleeding? what about little girl w spontaneous *painful* currant jelly stools?

Meckel diverticulum if painless. this is an outpouching of GI tract of all the layers. this is d/t *failed obliteration of omphalomesenteric (vitelline) duct* . pts bleed d/t *ectopic gastric mucosa* in the Meckel diverticulum --> secretes acid --> local ulceration & bleeding if it's painful and currant jelly stools --> intussusception.

Buzzword: Tc-pertechnetate used to make dx *recurrent*

Meckel diverticulum which is d/t persistent vitelline duct! Tc pertechnetate has high affinity for parietal cells of gastric mucosa & is used to dx Meckel which often has ectopic gastric mucosa (i.e. parietal cells)

What are the formulas for minute ventilation? alveolar ventilation? What about the physiologic dead space formula? *recurrent*

Minute ventilation: tidal volume * breaths/min Alveolar ventilation: (tidal volume -- dead space volume) * breaths/min if you see a diff b/w these 2 values it's d/t dead space!! :) this dead space is the anatomic dead space ~150 mL and any alveolar dead space (d/t well ventilated but poorly perfused alveoli i.e. perfectly good wasted alveoli) physiologic dead space: tidal volume * (PaCO2 - PECO2)/PaCO2 "paco peco over paco"

what are the nephritic (5) and nephrotic (6) syndromes? just names, we'll learn details as we go *recurrent*

Nephritic: 1. Post strep glomerulonephritis 2. Rapidly progressive (crescentic) glomerulonephritis 3. IgA nephropathy (Berger dz) 4. Alport syndrome (XL defect in type 4 collagen) 5. diffuse proliferative glomerulonephritis (lupus one) Nephrotic: 1. Minimal change dz 2. Focal segmental glomerulosclerosis (FSGS) 3. Membranous nephropathy 4. Diabetes mellitus glomerulonephropathy 5. Systemic amyloidosis (not technically but still) 6. Membranoproliferative glomerulonephritis (can be nephrotic or nephritic)

What is the differential for metastatic cancer that shows up in the bones? osteoblastic (3), mixed (2), osteolytic (5) how do you know if the lesions are osteoblastic or osteolytic? which is more aggressive?

Osteoblastic (*sclerotic*): 1. prostate cancer 2. small cell lung cancer 3. hodgkin lymphoma Mixed: 1. gastrointestinal 2. breast Osteolytic (*lucent*): 1. Multiple myeloma 2. Non small cell lung cancer 3. Non Hodgkin lymphoma 4. Renal cell carcinoma 5. Melanoma Osteolytic lesions indicate osteoclast stimulation and represent aggressive cancers

What is unique about P vivax and P ovale and what are they tx'ed w? *recurrent*

P vivax and P ovale are malaria bugs that *establish latent infxn* in liver in the form of *hypnozoites* and are thus responsible for *relapses* tx: primaquine is effective in eradicating hypnozoites from the system. the usual tx of chloroquine only removes malaria from the blood stream but not against latent hepatic infxns this is why we add primaquine you got confused w QUININE which can tx against chloroquine resistant strains.... the question gave that as one of the answer choices. it was like 'why do we add primaquine' and you said to tx chloroquine resistant strains but you should've said prevent dz relapse

What coronary artery is associated w rupture of posteromedial papillary muscle?! How long post MI is this usually seen? *recurrent*

POSTERIOR DESCENDING!!!! not left anterior descending (that one does anterolateral papillary muscle). Think: posterior papillary muscle & posterior descending! this is seen 3-5 days after MI. presents w *acute mitral regurg & pulm edema*

What is the PPV formula? how would we calculate it on a 2x2? what about NPV? action card: draw a 2x2 what question does it answer? *recurrent*

PPV: a/(a+b) Dz (outcome, etc) goes on the top Test result goes on the side NPV: d/(c+d) answers the question "given that pt has a _____ test result, what is the likelihood they actually have the dz?"

Buzzword: lamellar bone structure resembling a mosaic pattern Buzzword: osteoid matrix accumulation around trabeculae Buzzword: spongiosa filling medullary canals w no mature trabeculae Buzzword: trabecular thinning w fewer interconnections Buzzword: subperiosteal resorption w cortical thinning *recurrent*

Paget's dz of bone. the initial phase is d/t to *increased osteoclastic activity* not osteoblastic!! Vitamin D deficiency (osteomalacia) Osteopetrosis aka marble bone dz (persistent primary spongiosa w no mature trabeculae) Osteoporosis d/t estrogen decrease increased bone resorption d/t primary hyperparathyroidism

From what pathway/reaction does the majority of NADPH come from? what is NADPH used for? (3 things) *recurrent*

Pentose phosphate pathway (PPP) conversion of glucose 6 phosphate --> ribulose 5 phosphate releases 2 NADPH molecules USES: 1. cells that experience *high oxidative stress* i.e. RBCs! used to regenerate glutathione which is an antioxidant and thus helps maintain cell integrity 2. organs that are involved in *reductive biosynthesis* such as synthesis of FA (but not ketone production!), cholesterol, steroids. so organs like the liver & adrenal cortex. also needed for P450 in the liver bc P450 produces tons of free radicals. 3. phagocytic cells generating a respiratory burst via NADPH

On what end do you add the poly-A tail? What about the methylguanosine cap? *recurrent*

Poly A tail goes to the 3' end (this helps stabilize mRNA, not get degraded, and *helps it exit the nucleus*; added by polyadenylate polymerase) Methylguanosine triphosphate to the 5' end another post transcriptional modification is *removal of introns*

what are the 4 classes of antifungals? & their MOAs *recurrent*

Polyenes (amphotericin B and nystatin): bind to ergosterol molecules in fungal cell membranes --> create pores & cause cell lysis Azoles (-azole): inhibit *synthesis* of ergosterol Echinocandins (-fungin): inhibit the synthesis of *glucan* a component of the fungal cell wall Pyrimidines (flucytosine remember CUT the PY cytosine is pyrimidine): interferes w fungal RNA & protein synth

the 3rd (aka horizontal) portion of the duodenum is closely related to which artery? at what level does it course ? *recurrent*

SUPERIOR MESENTERIC ARTERY you got this wrong during HODI too lol now its time to learn it 3rd part is at L3 level 1st part is at L1; 2nd part is vertical and is L1-L3.

Aside from india ink and latex agglutination for the antibody, how can we confirm cryptococcus neoformans dx? *recurrent one*

Sabouraud agar (think Saumorai lol) sabouraud is also important for confirming coccidioides immitis

Why does TB lead to activation of MHC2 and not MHC1? *recurrent*

TB primarily replicates w/i phagosome (not cytosol) this means it will display on MHC 2 not MHC1 MHC1 is intracellular cytosolic viruses or some bacteria like listeria but mostly viruses this results in activation of CD4 and macrophages

What hormone do theca cells respond? what about granulosa cells? what do they each produce *recurring card*

Theca: LH. think of t*H*eca *interna* cells. theca create androstenedione in response to LH (theca externa just support follicle as CT. don't participate in steroid synth) Granulosa: FSH (think of granulosa as being the "grand" one that ppl always thing about. we always think about ovaries as doing everything for females. we also always think of FSH and not LH). granulosa creates *estrogen* in response to *FSH*

Buzzword: lots of colon polyps in a pt w hyperpigmented mouth, lips, hands, genitals *recurrent*

This is *AD Peutz Jeghers syndrome* which is excess hamartomas (polyps) thru out GI tract + hyperpigmentation. associated w higher risk of breast & GI cancers (colorectal, stomach, small bowel, pancreatic)

What drugs are commonly metabolized in CYP450 and thus prone to inducers or inhibitors? (4) *RECURRENT*

Warfarin Cyclosporine Tacrolimus Oral hypoglycemics

Buzzword: Atrophy of the mammillary bodies what are sx?

Werincke encephalopathy aka *thiamine* def (seen in chronic alcoholics!!) leads to classic triad of: ataxia, ophthalmoplegia (like horizontal nystagmus), confusion*

Hematuria + protenuria + urine RBC casts w hypercellular glomeruli on light microscopy. dx? what will you see in labs? LM? IF? EM? *recurrent*

You've had several questions on this ... take the time to learn it and make it as recurrent as need be. its okay if you don't get it all the first time around. youre only human Jen. PSGN anti-streptolysin O, anti DNase B, anti-cationic proteinase and *low C3 concentration* +/- cryoglobulins. C4 is usually normal LM: hypercellular glomeruli involving all lobules of glomeruli IF: "starry sky" appearance aka *granular deposits* of IgG and C3 (hence you have low C3 levels) EM: "humps" on the epithelial side of BM this is usually seen in kids :) remember this is a nephrotic syndrome.

What is the relative risk formula? *recurrent*

[a/(a+b)] / [c/(c+d)] but better than that is if you understand: RR = risk among the exposed (usually to a drug) / risk among the unexposed (i.e. go around living their life w/o tx) aka how many ppl took the drug and had an event OVER how many ppl did not take the drug and had an event. i.e. "how much better is it to take this drug than to not take it?" any effect?

Buzzword: ejection type systolic murmur *recurrent*

aortic stenosis!!

In what ligament is the uterine artery found? *recurrent*

cardinal ligament!!

What is the pathophys behind black pigment stone formation? *recurrent*

conditions that *increase* amount of unconj bilirubin in bile (commonly hemolysis! but also *ileal dz* where there is increased enterohepatic cycling of bilirubin) Unconjugated bilirubin --> promotes *calcium bilirubinate* precipitation

when might secondary lactose intolerance be seen?

d/t inflammation (celiac dz) or infxn (giardiasis)!! esp common after *giardial infxns* bc they damage intestinal lining --> damaged cells slough off --> replaced by immature cells w low lactase concentrations

are beta amyloid plaques in alzheimers intracellular or extracellular? *recurrent*

extracellular!!

Flattened diaphragm on xray means what? what would you see on PFTs? *recurrent*

hyperinflated lungs & flattened diaphragm is consistent w *chronic obstructive pulmonary dz* meaning you can't let all the air out. trapped inside. PFTs: "FRiCkin' RV needs some increased TLC, but it's hard w COPD!" elevated FRC, RV, and TLC d/t prematurely closing airway

Where does iron absorption occur and what procedure would cause poor iron abs? *recurrent*

majority of iron is abs in *duodenum & proximal jejunum* a *gastrojejunostomy* which is when you suture the stomach and distal jejunum together (i.e. cut out duodenum and proximal jejunum) would cause poor iron abs

What is painless obstructive jaundice and what should it ring a bell for? What is the most important risk factor associated w this dz? *recurrent*

obstructive jaundice is when you have *elevated bilirubin, dark urine, and pale stools* if this is accompanied by weight loss it should really put out a red flag for *pancreatic adenocarcinoma* *SMOKING* is the most important environmental risk factor!! it *doubles* the risk. other risk factors are age > 65, chronic pancreatitis, genetic predisposition like hereditary pancreatitis, peutz jeghers, MEN syndromes)

What cells does IL-2 activate? (4) *recurrent*

obviously T cells!! (bc hot T bone steak) but *also* NK cells, monocytes and B cells :o

painless midline mass close to the body of the hyoid bone *recurrent*

persistent thyroglossal duct cyst

What does "golden cytoplasmic granules that turn dark blue w prussian blue staining" on lung macrophages mean? *recurrent*

prussian blue stain detects intracellular iron. it's colorless but *turn blue-black* by iron. this means presence of *hemosiderin laden macrophages* aka siderophages this results from *chronic elevation of pulmonary capillary hydrostatic pressures* the high pressures in the alveolar blood vessels will leak out blood and cause macrophages to phagocytose the RBCs. macrophages then turn iron and hemoglobin to hemosiderin this is most commonly d/t high pulm pressure from left sided HF where the blood pushes back up to atria and back toward lungs

What are some examples of restrictive lungs dz? obstructive? *recurrent*

restrictive: can't get air in 1. pulmonary fibrosis (decreased compliance) 2. diffuse intra-alveolar hemorrhage--> alveolar atelectasis aka collapse 3. acute respiratory distress syndrome --> hyaline membranes --> reduce lung compliance 4. pneumothorax obstructive: 1. emphysema 2. asthma 3. chronic bronchitis

Buzzword: elevated IgA anti endomysial *recurrent*

screening for celiacs also anti tissue transglutaminase ab but i know this one

what are metalloproteinases? what is their fxn? what happens if they're too high?

substance secreted by lots of diff cells (fibroblasts, macrophages, neutrophils, synovial cells, some epithelial cells) Fxn: degradation of collagen & other proteins in ECM. it's important in *wound healing* bc it encourages scar tissue remodeling such as wound contraction if they're TOO high --> excessive wound contracture (when the scar rides up like Urbinelli always told them to rub it so it would heal better)

Buzzword: pt w lucid interval after getting hit on head what is it d/t?

this is *epidural* hematoma!! which means its above the dura mater and below the bone d/t rupture of *middle meningeal artery* seen after a *temporal bone* fracture

What type of drug is streptomycin? MOA? *recurrent*

this is an *aminoglycoside* NOT a macrolide. macrolides end in "thromycin" like arythromycin, clarithromycin, erythromycin and inhibit the 50S (buy AT 30, CCEL at 50; A in AT = aminoglycoside; E in CCEL = erythromycin) Aminoglycosides end in "mycin" or "micin" --> "Mean" (aMEANoglycoside) GNATS caNNOT kill anaerobes Gentamicin, Neomycin, Amikacin, Tobramycin, Streptomycin Aminoglycosides inhibit 30S

What are the DNA binding proteins? *recurrent*

this is another way of asking what proteins bind to intracellular receptors? aka which ones are the ROIDZZZ mnemonic from FA! "PET CAT on TV" Progesterone Estrogen Testosterone Cortisol Aldosterone T3/T4 Vitamin D

When do you see widened QRS complexes? *recurrent*

when there is a *bundle branch block* bundle branch conductivity determines duration of QRS complexes narrow QRS complexes mean the command is coming from the atria :)

What forms Guyon's canal?

where the ulnar nerve passes b/w pisiform and hamate

What are the 2 anti inflammatory cytokines? what is the fxn of TNF alpha or what does it cause?

2 anti inflammatory: IL-10 (inhibits TH1; i.e. comes from TH2) TGF-beta think: TGF*B* and IL*10* *b*oth at*ten*uate the immune response TNF alpha: causes *cachexia* in malignancy among other things. in fact sometimes its called 'cachectin'

This is kinda confusing but w God's help you're gonna learn it: what pathway does IGF-1 use to bind? What pathway leads to IGF-1 production? *recurrent*

According to FA, IGF-1 binds to receptor tyrosine kinase aka MAP kinase pathway UWorld said activation of JAK/STAT pathway leads to transcription factor activation and IGF-1 production... so i can only conclude that MAPK binds IGF-1 but JAK/STAT is what produces it....

What substances on amniotic fluid would you expect in a Down's pt? *recurrent*

low AFP normal AChE

Using combination oral contraceptive pills decreases risk for what type of cancer? Why is obesity a risk factor for endometrial hyperplasia? *recurrent*

ovarian cancer risk obesity is a risk factor bc it has aromatase which converts androgens to estrogen in adipose tissue. elevated estrogen w/o opposition by progesterone stimulates growth of the uterine lining

Mnemonic for live attenuated vaccines

"Attention! Please Vaccinate Small, Beautiful Young Infants w MMR Regularly" Adenovirus (military recruits) Polio (sabin) Varicella (chickenpox) Smallpox BCG Yellow fever Influenza (intranasal) MMR Rotavirus

what forms the wall of a cystic cavity months to years after a cerebral ischemic stroke?

*astrocyte* processes!! aka *glial scar* this wall forms bc it protects viable brain tissue from being damaged by the fibrotic inflammatory response that happens during healing!

What are the 5 2's for Meckels diverticulum?

1. 2% of population 2. 2 ft from ileocecal valve 3. 2 inches in length 4. 2% are symptomatic (rectal bleeding [d/t ectopic gastric tissue that can cause ulceration of adjacent mucosa --> melena or hematochezia] or intestinal obstrxn) 5. males are 2x more likely to be affected

what hormones can small cell carcinomas secrete? (3)

1. ACTH --> cushing 2. ADH --> SIADH 3. Ab against presynaptic calcium channels --> lambert eaton (muscle weakness that gets better w use)

"villi invading the myometrium on a hysterectomy specimen" "low B hCG level + normal fetal tissue and normal villi and trophoblastic tissue"

1. invasive mole!! 2. miscarriage :(

Ewing sarcoma usually affects children of what age? what part of the bone does it affect?

10-15 y/o so like allies age usually affects *diaphysis* of long bones most common *malignant* bone tumor in children after osteosarcoma!

hereditary hemochromatosis is most commonly what type of mutation in the HFE gene?

AR *MISSENSE mutation* in the HFE gene --> excessive intestinal iron abs

The left gonadal vein arises from the renal vein while the right gonadal vein arises from the IVC. what about the gonadal arteries?

BOTH of these come from aorta!

what ligand is needed for B cell isotype switching?

CD40 on activated B cells and CD40 Ligand on activated T cells. also modulated by cytokines from T cells :)

what comes out of the internal acoustic meatus?

Cn7 and 8

What immune cell is crohns related to ? UC?

Crohns --> Th1 --> non caseating granulomas UC --> Th2 --> IL5 and 13 --> inflammation & damage of intestinal mucosa

PT and PTT, which one is intrinsic and which is extrinsic?

PT = extrinsic (think about how warfarin inactivates factor 7 d/t vitamin K def) PTT = intrinsic

formular for renal plasma flow

RBF * (1 - hematocrit)

medullary thyroid cancer. what mutation?

RET activation (tumor promoter)

to calculate the standard deviation of a population, do you do SD divided by square root of n or just use SD?

SD/sqrt(n)!!

There are 2 types of T cells: Th1 and Th2 what roles do each play? *recurrent*

Th1: cell mediated immunity & type 4 hypersensitivity rxns Th2: allergin and type 1 hypersensitivity rxns

short stature, broad chest, amenorrhea

Turners (45, XO)

Macroorchidism, large jaw and ears

XL Fragile X

What is the cause of annular pancreas?

abn rotation (i.e. migration AND fusion) of the *DORSAL* bud (during 7th & 8th wk of fetal dev)

dacrocytes

aka target cells seen in primary myelofibrosis

Why do pts w SIADH have a clinically nl extracellular fluid volum e(i.e. euvolemic hyponatremia)

bc the excess fluid uptake leads to increased blood volume --> ANP activation --> natriuresis i.e. pee a lot but also pee the sodium so no edema

what is the pathophys behind alcohol induced hepatic steatosis?

decrease in free FA oxidation secondary to excess NADPH prodxn by the 2 major alcohol metabolism enzymes (alcohol DH and aldehyde DH)

pt w "blury vision, black spots, floaters, decreased periphearl vision"

diabetic retinopathy.

Buzzword: ovarian mass w fried egg cells

dysgerminoma. seen in adolescents. secretes beta hCG and LDH

Where is insulin-like growth factor 1 (IGF-1) released from? what triggers it?

from liver!! triggered by growth factor!!

What structures make up the basal ganglia? (3)

globus pallidus, caudate, putamen

what organs is at the level of the 12th rib?

kidney!! if 12th rib fracture --> kidney laceration spleen is at the 9-11th level of ribs

why is hep C so genetically unstable?

lacks proofreading 3' --> 5' exonuclease activity in its RNA polymerase so prone to frequent genetic mutation

Buzzword: numerous long, slender microvilli, and abundant tonofilaments from pleural biopsy

malignant mesothelioma

in a distribution that is not bell curved but rather positively skewed, what can we say about the mode, median, and mean? which one should we use?

mean is the most affected and shifted toward positive values. mode is affected the least. we should use median in these situations

what are the 2 drugs that tx gardnerella vaginalis?

metronidazole and CLINDAMYCIN!! (not in sketch :/ only metro in sketch but thats ok :) God has our back)

Acute extrapyramidal sx are d/t D2 block in what pathway?

nigrostriatal

is it common to see hepatocellular carcinoma?

no! more common to get malignant hepatic lesions to the liver from other places this is bc of its large size, dual blood supply, high perfusion rate, and filtration fxn of Kupffer cells

what are the drugs of choice for C diff tx?

oral Vancomycin: inhibits cell wall synth and is bacteriostatic fidaxomicin: macrocyclic abx that inhibits the *sigma subunit of RNA Polymerase* --> protein synthesis impairment cell death i.e. bactericidal!! (IV metronidazole can be used in pts w SEVERE C diff like megacolon, ileus, hypotension bc these pts often have delayed passage of oral abx)

what vessels are found in the infundibulopelvic ligament?

ovarian vessels!!

action card: draw the Gq, Gs, and Gi pathway

pg 234 FA

"segmental transmural inflammation w fibrinoid necrosis" in medium artery

polyarteritis nodosa

MHC 1 overexpression on sarcolemma w CD8+ lymphocyte infiltration in pt w symmetrical proximal weakness?

polymyositis you'll also always see *elevated muscle enzymes* like CK or aldolase

semen is composed of fluid from where?

primarily fluid secreted from *seminal vesicles and prostate* only 2-5% of fluid is semen. pts w vasectomies have normal volume of ejaculate

a penetrating injury to the second intercostal space at the left sternal border injures what?

pulmonary trunk

Buzzword: bug that is pyrrolidonyl arylamidase (PYR) positive

strep pyogenes! this has greatly replaced bacitracin!

large amplitude flinging movements affecting only proximal right arm. injury is where in brain?

subthalamic nucleus. this is hemiballismus sudden, wild flailing of *one* arm +/- ipsilateral leg "Half of body ballistic" commonly damaged d/t *lacunar stroke!!* [i.e. "long standing HTN" or "long standing HTN + DM"]

what does karyotype of CML show?

t(9;22) --> *short chr 22* & *long chr 9*

what virus is not enveloped and has a linear ssDNA

teacher/day care sketch. kid playing w david statue (naked/non enveloped) classroom has cool colors (DNA) single runway strip for parvo airplane (single stranded)

positive anti topoisomerase, anti RNA pol 3, anticentromere?

these are all highly specific for *systemic sclerosis*

what would be elevated in a pt that has schiller duval bodies on an ovarian biopsy?

this is endodermal sinu aka yolk sac tumor which is a germ cell tumor of the ovaries will see HIGH AFP levels not beta hCG. high beta hCG and LDH is seen in the other germ cell tumor aka the dysgerminoma

Buzzword: brain mass that's GFAP+ and has eosinophilic intracytoplasmic inclusions

this is pilocytic astrocytoma eosinophilic intracytoplasmic inclusions = rosenthal fibers

Where does negative selection for T cells happen?

thymic medulla

where is is the most oxygenated blood in fetal circulation? *recurrent*

umbilical vein! which drains into IVC via *ductus venosus*

what vessels are found in the cardinal ligament?

uterine vessels!!

What type of necrosis? "accumulation of fibrin like material in vessel walls" "deposition of fatty acid and calcium complexes" "formation of necrotic focus surrounded by epithelioid macrophages" "tissue necrosis w preservation of cellular architecture"

"accumulation of fibrin like material in vessel walls" --> fibrinoid necrosis. this is seen in vasculitis or HTN "deposition of fatty acid and calcium complexes" --> fat necrosis. this is seen in breakdown of adipose tissue d/t mechanical trauma or in acute pancreatitis d/t pancreatic enzyme release "formation of necrotic focus surrounded by epithelioid macrophages" --> granuloma!! seen in caseous necrosis. seen in mycopbacterial infxns or fungal infxns "tissue necrosis w preservation of cellular architecture" --> coagulative necrosis. d/t hypoxic cell death anywhere except CNS! d/t acute denaturation of structural and enzymatic cellular proteins. cells are anucleate w eosinophilic cytoplasm but preserve their structure. leukocytes eventually infiltrate and digest necrotic tissue

Buzzphrases: "autoimmune injury of the intrahepatic bile ducts" "decreased UDP glucuronosyltransferase activity" "defective Cl transport at epithelial surfaces" "defect transport and accumulation of Cu2+" "inherited def of a serine protease inhibitor" "unregulated GI iron abs"

"autoimmune injury of the intrahepatic bile ducts" --> primary biliary cholangitis. positive antimitochondrial antibodies!! "decreased UDP glucuronosyltransferase activity" --> mild would be Gilberts or severe would be Crigler Najjar syndrome type 1. it's when there's a def in the enzyme that converts uncoj bili to conj "defective Cl transport at epithelial surfaces" --> CF! "defect transport and accumulation of Cu2+" --> Wilson dz "inherited def of a serine protease inhibitor" --> alpha 1 antitrypsin def lung and liver probz "unregulated GI iron abs" --> hemochromatosis. heart commonly affected (cardiomyopathy) also pancreas ("bronze DM") and joints but not lungs

Buzzphrases: "bilobed nuclei and inclusion like nucleoli" "intercellular bridges and keratin pearls" "mucin secreting signet cells" "nests of epithelial cells w abundant clear cytoplasm" "sebaceous glands & keratinaceous debris"

"bilobed nuclei and inclusion like nucleoli" --> Hodgkin lymphoma bc those are reed sternberg aka owl eye cell description "intercellular bridges and keratin pearls" --> squamous cell cancer (skin, lung, esophagus) "mucin secreting signet cells" --> gastric cancer or krukenberg if found in ovary "nests of epithelial cells w abundant clear cytoplasm" --> renal cell carcinoma "sebaceous glands & keratinaceous debris" --> mature cystic teratoma w skin & hair follicles in this case

what dzs are associated w: "decreased choline acetyltransferase activity in the nucleus basalis" "decreased dopa decarboxylase activity in the substantia nigra" "decreased tryptophan hydroxylase activity in the raphe nuclei" "increased acetylcholinesterase activity in the caudate nucleus" "increased dopamine beta hydroxylase activity in the locus ceruleus"

"decreased choline acetyltransferase activity in the nucleus basalis" --> alzheimers!! "decreased dopa decarboxylase activity in the substantia nigra" --> parkinson dz and dementia w lewy bodies "decreased tryptophan hydroxylase activity in the raphe nuclei" --> this would be decreased serotonin which is involved in lots of stuff like depression, anorexia, sleep disorders "increased acetylcholinesterase activity in the caudate nucleus" --> huntingtons "increased dopamine beta hydroxylase activity in the locus ceruleus" --> normally makes NE [New Look] --> involved in panic attacks and panic disorder

what are the risk factors for gallstones? why esp in pregnancy?

"fat, fertile, female, forty" for pregnant women (or those on oral contraceptives), theres TONS of estrogen and progesterone which is a double whammy estrogen: increases cholesterol synth by *upregulating hepatic HMG-CoA reductase* progesterone: reduces bile acid secretion and slows gallbladder emptying

how do you describe cirrhosis on histo? what does it look like grossly?

"fibrosis and nodular parenchymal regeneration" grossly it looks like a bunch of blobs bc of the fibrous rings that have formed.

Pt w signet ring cells and hx of peptic ulcer dz. how would you describe their dz on histology?

"infiltrative growth w/i stomach wall" this is gastric adenocarcinoma. there are 2 types of gastric adenocarcinoma. 1. Intestinal type: look similar to colon cancers and show well formed glands that consist of columnar or cuboidal cells. 2. diffuse aka signet ring carcinoma type: they have signet ring cells and have "infiltrative growth w/i stomach wall". the diffuse involvement is d/t *E cadherin loss*

More buzzphrases :) "trophozoites containing RBCs" "dysplastic mucosal cells w variable degree of gland formation" "cytomegalic cels w inclusion bodies" "basophilic clusters seen on the surface of intestinal mucosal cells" "spindle shaped tumor cells w small vessel proliferation" "inflammatory infiltrate involving the mucosa & submucosa w crypt abscesses"

"trophozoites containing RBCs" --> entamoeba histolytica "dysplastic mucosal cells w variable degree of gland formation" --> adenocarcinoma "cytomegalic cels w inclusion bodies" --> cytomegalovirus "basophilic clusters seen on the surface of intestinal mucosal cells" --> cryptosporidium "spindle shaped tumor cells w small vessel proliferation" --> Kaposi's sarcoma... this would be d/t the HHV8 virus thing that causes vascular tumor. classically seen on skin but can also be seen in lungs or GI tract so on colonoscopy! "inflammatory infiltrate involving the mucosa & submucosa w crypt abscesses" --> UC!! :)

what is the #1 cause of death? #2? what 3 cancers are the MOST common (excluding skin) and which are the most common cause of death?

#1 cause of death is CVD #2 cause of death is cancer Most common cancers: 1. BREAST/prostate by farrrr 2. Lung 3. Colon Most common cause of death: 1. LUNG (bc no screening and doesn't present till late) 2. Breast/prostate 3. Still colon :) pathoma went over this and said it was important... AND THEN THERE WAS A UWORLD QUESTION!!

Essential fructosuria vs hereditary fructose intolerance which enzyme is missing in each? which one is worse? why?

*AR Essential fructosuria*: missing *fructokinase* this is a benign condition bc *hexokinase* is that cousin that picks up the slack. Fructokinase is missing but fructose can be metabolized thru hexokinase as fructose 6 phosphate (instead of fructose 1 phosphate) and go down the glycolysis, PPP, or glycogen synth pathway and be ok :) *Hereditary fructose intolerance*: missing *aldolase B* you'll see hypoglycemia & vomiting after fructose ingestion. Failure to thrive, liver & renal failure. once it goes past fructokinase and converts to fructose-1-phosphate, hexokinase can no longer rescue it and its only up to aldolase B to finish metabolism of fructose. so no aldolase B = no fructose metabolism at all and toxic build up of fructose 1 phosphate

This is gonna be a recurring card, but what is 1 important derivative from each of the following: Arginine (1) Arginine + aspartate (1) Glycine + succinyl CoA (1) Glycine + arginine + SAM (1) Glutamate (2) Glutamine + aspartate (1) Glutamine + aspartate + glycine (1) Histidine (1) Tyrosine (5) Tryptophan (3) Don't freak out. copy and paste this into tmrws flashcards and you'll practice it again. God loves you Jen. He won't let you down bc He chose this career for you. Take a deep breath

*Arginine*: nitric oxide *Arginine + aspartate*: urea *Glycine + succinyl CoA*: heme *Glycine + arginine + SAM*: creatinine *Glutamate*: GABA and glutathione *Glutamine + aspartate*: pyrimidines *Glutamine + aspartate + glycine*: purines *Histidine*: histamine *Tyrosine*: dopamine, epinephrine, NE, thyroxine, melanin *Tryptophan*: serotonin, melanin, niacin

Painless waxing and waning lymphadenopathy

*Follicular lymphoma*!! most common *indolent i.e. lazy/slow growing* non-hodgkin lymphoma in adults. B cell origin (duh bc follicles of lymph node lol) commonly see overexpression of bcl-2 oncogene d/t *14;18 translocation*

What is the reason of hypoketoic hypoglycemia? what is the most common cause?

*Reason*: defect in FA beta oxidation. our body should never get to a point where we have low sugar AND no ketones. unless super starved/death but our body will have low glucose and eventually make fatty acids in response if its been long enough (will try to use glycogen stores first etc) *Common cause*: medium chain *acyl-CoA DH def* which is an enzyme INSIDE the mitochondria involved in FA beta oxidation i.e. fatty acid breakdown to create ketone bodies which can be used to create glucose

Somatic sx disorder vs Malingering vs Factitious disorder vs conversion

*Somatic sx disorder*: excessive anxiety & preocupation *w* > 1 unexplained sx *Malingering*: falsification or exaggeration of sx to *obtain external reward* (like financial benefits, time off work) *factitious disorder*: intentional falsification of illness in the absence of *obvious* external reward. this is the typical nurse that likes to assume the sick role and will purposefully make herself sick. can include manipulating lab samples, ingesting a substance, altering med records, inducing illness. *Conversion*: *neuro* sx incompatible w a known dz

What are the 3 types of urinary incontinence and what is the problem in each?

*Stress*: leakage of urine while coughing, lifting, sneezing. Urethral hypermobility & low urethral sphincter tone commonly d/t pelvic floor laxity *Urge*: sudden overwhelming urge to urinate. Detrusor hyperactivity [i.e. uninhibited bladder contraction] *Overflow*: incomplete emptying & persistent *involuntary* dribbling. Impaired detrusor contractility or bladder outlet obstruction (like tumor obstructing urethra)

in terms of psych, what is transference? what is displacement? what is projection?

*Transference*: shifting of emotions or desires associated w a *person from the past* to another person in the present (i.e. pt saying ' i feel as tho u aren't interested in listening to me like i am not ur priority' when the psychiatrist cancelled the appt) *Displacement*: person expresses unacceptable feelings intended for one person to a more neutral person (i.e. if the pt didn't express his anger to his father and instead berated the psychiatrist. in the question stem it said the pt has talked to his dad the weak before and had disclosed his anger for his father to his father directly) *Projection*: misattributing ONE'S own unacceptable feelings to another person (i.e. if the pt were unable to acknowledge his disappointment toward his psychiatrist about canceling and instead perceived his psychiatrist as being upset w him)

disproportionate loss to f/u b/w exposed and unexposed groups in a study leads to what type of bias?

*attrition bias* which is a subset of *selection bias* important to note that these loses in subjects have to be of one group type in particular. if the losses happen randomly b/w exposed & unexposed that's just a smaller study population. not bias.

what is the main MOA behind DM1?

*cell mediated immunity* that leads to INFILTRATION of islet pancreatic beta cells by inflammatory cells called *insulitis* antibodies against islet antigens are present, but this is NOT the primary MOA!! DM1 happens in genetically susceptible pts, but is not genetic itself. it gets triggered by environmental events

What is the biochemical abn in alzheimers? where is the neurotransmitter made?

*decreased ACh level!!* d/t def of choline acetyltransferase Nucleus basalis of Meynert (*A Ch*oice *May not* *be sal*ient another structure commonly involved in alzheimers is the hippocampus (nl fxn is formation of new memories)

aside from HLA B27 positive, fusion of sacroiliac joints, stiffness that improves thru out day. what is helpful in monitor pts w ankylosing spondilitis?

*degree of chest expansion* !! pts w ankylosing will get limited chest expansion and spinal mobility as their dz progresses. pts can also present w *enthesitis* which is pain, tenderness, and swelling at sites of tendon insertion into bone like achilles tendon DOUBLE BONUS AKA COMPLICATIONS: -respiratory: thoracic spine can be involved --> limiting chest wall expansion and leading to hypoventilator. this is why ankylosing pts should be monitored regularly!! -cardio: most common cardio complication is *ASCENDING AORTITIS* --> dilation of aortic ring & aortic insufficiency!! -eye: anterior uveitis (unilateral pain, blurry vision, photophobia, and conjunctival erythema)

What bug has intrinsic resistance to 3rd generation cephalosporins (aka cefotaxime or ceftriaxone)

*listeria monocytogenes*! d/t presence of *penicillin binding proteins* that have a *low affinity* for this drug class. other cephalosporin resistant organisms are MRSA, enterococci, atypicals like mycoplasma or chlamydia bc no cell wall! thats why you gotta tx listeria meningitis in babies w *ampicillin* (sound amp in santa/xmas sketch) otherwise cefotaxime + vanco (empiric anti meningitis tx given to all babies w meningitis sx) would cover the most common culprits including strep pneumo, n meningitidis, h flu, group B strep, and e coli

pt was recently dx'ed w superficial thrombophlebitis on left lower and upper extremities. sx get better w NSAIDs few days later comes in w erythema and tenderness from right forearm to anterior the right antecubital fossa. dx? next step?

*migratory thrombophlebitis* he had them in his left arm and leg and now he has them in the right forearm. migratory thrombophlebitis should raise the *visceral cancer* flag in your head. esp pancreatic cancer!! (but also like colon or lung) hypercoagulability is a very common paraneoplastic syndrome! in adenocarcinomas its bc of thromboplastin like substance that gets produced by adenocarcinomas that can disseminate and cause chronic intravascular coagulation migratory superficial thrombophlebitis is called *trousseau syndrome* funny enough arman trousseau (the dude that discovered the associated w cancer) diagnosed his own visceral cancer when he developed the syndrome!!

cocaine use in pregnant women increases risk for?

*placental abruption* !! but also preeclampsia, spontaneous abortion, fetal demise :o

what hormone causes endometrial bleeding during regular periods? what process are these cells undergoing?

*removal* of progesterone i.e. sudden drop at the end of the cycle --> vasoconstriction of spiral arteries- the cells undergo *apoptosis* --> fxnalis layer sloughs off

failure of septation in the heart leads to what congenital defect?

*truncus arteriosus* where there is a single arterial trunk overriding a large VSD so blood that goes out will go thru aorta and pulm arteries

How does scurvy present? (3 classic sx)

-"swollen tender gums" -red spots on legs that look like dots --> perifollicular hemorrhages. that one classic picture you couldn't figure out lol -hematomas like subperiosteal hematoma -petechial hemorrhages so really bleeding all over the place. why? bc you need vit C to hydroxylation of proline and lysine in collagen synthesis. poor collagen = poor blood vessel walls --> widespread microvascular bleeding

This one might be painful, but you gotta know it. it will be recurrent and God will give you the memory jen <3 its okay. I can do all things thru Christ who strengthens me. What do you see on histology post MI: 1. 0-4 hrs 2. 4-12 hrs 3. 12-24 hrs 4. 1-3 days 5. 3-7 days 6. 7-10 days 7. 10-14 days 8. 2wks - 2 months

1. 0-4 hrs --> normal tissue 2. 4-12 hrs --> wavy fibers w narrow, elongated myocytes 3. 12-24 hrs --> myocyte hypereosinophilia w pyknotic (shrunken) nuclei 4. 1-3 days --> coag necrosis (i.e. loss of nuclei & striations) and *LOTS of neutrophils*!! 5. 3-7 days --> disintegration of dead neutrophils & myofibers d/t *macrophage infiltration* esp near borders 6. 7-10 days --> ROBUST phagocytosis of dead cells by macrophages which will look full of *degenerating myoglobin pigment & hemosiderin NOT foam cells which indicate lipid engulfment* --> *start* forming granulation tissue (pre scar) 7. 10-14 days --> *well developed* granulation tissue w *neovascularization* (well formed pre scar) 8. 2wks - 2 months --> progressive collagen deposition & *scar* formation

this is another long one, but itll be ok :) God will make a way: what happens in the brain after an ischemic stroke: 12-24 hrs 24-72 hrs 3-7 days 1-2 wks > 2wks

1. 12-24 hrs: red neurons!! (i.e. regular apoptosis --> eosinophilic cytoplasm, pyknotic nuclei, loss of Nissl substance [ER]) 2. 24-72 hrs: neutrophilic infiltration 3. 3-7 days: macrophage and microglia infiltration & phagocytosis 4. 1-2 wks: *reactive gliosis* & vascular proliferation around necrotic area. this is when we see lots of *astrocytes* which are like the moms of the CNS bc they do everything. they act like buffers, remove excess neurotrans, support, repair, etc --> liquefactive necrosis seen grossly!! 5. > 2 wks: glial scar formation --> *cystic area surrounded by dense glial cells* grossly

what are some things down syndrome pts are at increased risk for/complications (6)

1. ASD 2. duodenal atresia 3. imperorate anus 4. hirschsprung dz 5. tracheoesophageal fistula 6. celiac dz

What are the steps in PI3K/Akt/mTOR pathway? (6)

1. Binding of *growth factor* 2. autophosphorylation of tyrosine residues 3. activation of phosphoinositide 3 kinase (PI3K) 4. activation of protein kinase B (Akt) 5. activation of mTOR 6. gene changes: cell growth, proliferation, survival (aka anti apoptosis)

Buzzphrases: "Bronchial hyperractivity" "Interalveolar septa destruction" "interstitial infiltration" "intraalveolar substance accumulation" "Pulm congestion" "pulm vascular obstrxn"

1. Bronchial hyperactivity --> chronic asthma 2. Interalveolar septa destruction --> alpha 1 antitrypsin 3. Interstitial infiltration --> interstitial pneumonitis 4. intraalveolar substance accumulation --> alveolar proteinosis 5. pulm congestion --> CHF 6. pulm vascular obstrxn --> pulm embolism or vasculopathy

main role of: 1. C3a 2. C5a 3. C3b

1. C3a: anaphylatoxins --> trigger mast cell degranulation, results in histamine mediated vasodilation and increased vascular permeability 2. C5a: same as C3a PLUS chemotactic for neutrophils 3. C3b: opsonin for phagocytosis (IgG is also another important opsonin!). can also bind to C3b convertase to form C5 convertase and ultimately trigger the MAC attack!

rank the 5 major organs in order from MOST susceptible to infarction post occlusion of an artery to least susceptible

1. CNS (delicate little thing) 2. Myocardium (hearts are delicate :3) 3. Kidney 4. Spleen 5. Liver liver is the least susceptible d/t DUAL BLOOD SUPPLY. gets blood from portal vein AND from hepatic artery. so if artery is occluded still ok d/t vein! it also gets bonus collateral blood supply from stuff like inferior phrenic, adrenal, intercostal arteries etc this is NOT true in pts w transplanted livers bc the collateral blood supply is severed during transplantation :/

What 2 things increase secretion of pancreatic enzymes?

1. Cholecystokinin (CCK) 2. cholinergic stimulation

What protein is associated w each of the following: Gap jxn Tight jxn Adherens jxn Desmosomes Hemidesmosomes

1. Gap jxn: connexins 2. Tight jxn: claudins, occludin 3. Adherens jxn: cadherins 4. Desmosomes: cadherins (desmogleins, desmoplakin) 5. Hemidesmosomes: integrins

"myxomatous valve thickening and elastin fragmentation" "subendocardial granulomatous lesions w fibrinoid necrosis and subsequent fibrosis" "thrombus formation on inflammed valvular endothelium" "differentiation of valve fibroblasts into osteoblast like cells"

1. Mitral valve prolapse 2. Rheumatic heart dz 3. Non bacterial thrombotic endocarditis (also called marantic, verrucous, of libman sacks if on both sides of leaflet) 4. calcific aortic valve dz!! most common cause of AS in aging pts!!

What are the 4 mechanisms behind reperfusion injury?

1. Oxygen free radical generation by parenchymal cells, endothelial cells, leukocytes 2. severe irreversible mitochondrial damage classically described as "mitochondrial permeability transition" 3. Inflammation which attracts circulating neutrophils that cause additional injury 4. activation of the complement pathway --> more cell injury and further inflammation

What are these things? 1. "branching papillae w cells containing empty appearing nuclei" 2. "dense fibrous tissue extending beyond the thyroid capsule" 3. "follicular hyperplasia w tall cells projecting into the follicular lumen" 4. "intense lymphoplasmacytic infiltrate w active germinal centers" 5. "widespread inflammatory infiltrates, giant cells, and disrupted follicles"

1. Papillary thyroid cancer. usually seen as an enlarging nodules in a clinically *euthyroid* pt. the papillary structures also usually have concentric calcifications aka psamomma bodies. the ground glass or empty appearing nuclei are orphan annie eyes. 2. Riedel thyroiditis. usually a hard thyroid and fixed to surrounding structures. resembles malignancy. 3. Graves dz. this shows hyperthyroidism. 4. Hashimoto's. hypothyroidism. Sometimes seen in Hurthle cells which are follicular epithelial cells that have undergone metaplastic change in response to inflammation 5. Subacute granulomatous de Quervain thyroiditis. pts usually show after viral URI w fever & painful tender thyroid gland

"presystolic sound immediately preceding S1 sound" "postsystolic sound immediately after S2"

1. S4 heart sound! this is normal in healthy *older* adults and is d/t *forced* blood into stiff ventricle so you'd see increased stiffness of the left ventricular wall. this is heard immediately after *atrial contraction!!* not a ventricle thing! 2. S3 heart sound! this is d/t sudden cessation of filling as ventricle reaches its elastic limit. heard during rapid *passive FILLING of ventricles* not an atrial thing!

Important fungal buzzphrases: 1. "round or cigar shaped budding yeasts" 2. "thick walled spherules filled w endospores at 37" 3. "oval yeast cells w/i macrophages" 4. "large, round yeasts w doubly refractile wall and *single* broad based bud" 5. "cells covered in budding blastoconidia"

1. Sporothrix schenckii (the thorn one; garden lady smoking cigar 2. Coccidioides immitis (san juaquin sketch w bushes in sphere shapes w red dots inside them) 3. Histoplasma capsulatum (the bat and bird droppings one so like chicken coops, caves; sketch of explorer in cave w macrophage looking puddles w spots inside) 4. Blastomyces dermatidis (the 2 cannon balls close together in the war/statue sketch) 5. Paracoccidioides brasilensis (pirate of brazil sketch w a map of central and south america behind him)

Classic associations for: Sturge-Weber syndrome Von Hippel Lindau dz Tuberous sclerosis Osler Weber Rendu syndrome

1. Sturge Weber. also called encephalotrigeminal angiomatosis and that name is helpful. *cutaneous facial angiomas* aka port-wine stain of face in the CN5.1 or 5.2 distribution. leptomeningeal angiomas (brain abn) other not as defining ones: mental retardation, seizures, hemiplegia, skull radiographs w "tram track" calcifications. FROM FA: STURGE *S*poradic port win *S*tain *T*ram track calcifications *U*nilateral *R*etardation *G*laucoma *G*NAQ gene *E*pilepsy 2. Von Hippel Lindau dz. AD condition. -capillary hemangioblastomas in the retina or cerebellum (described as "angiomatous lesion involving the cerebellum) -congenital cysts or neoplasms in the *kidney, liver, pancreas* -renal cell carcinoma (bilateral) WE HAD THIS PT FOR CSA!! FROM FA: HARP *H*emangioblastomas in retina, brain stem, cerebellum, spine *A*ngiomatosis bilateral *R*enal cell carcinomas *P*heochromocytomas 3. Tuberous sclerosis from FA: HAMARTOMAS -*H*amartomas in CNS & skin (NOT angiomatous lesions like in von hippel lindau) -*A*ngiofibromas *M*itral regurg *A*sh leaf spots cardiac *R*habdomyoma *T*uberous sclerosis [name of dz] autosomal d*O*minant *M*ental retardation renal *a*ngiomyolipoma *S*eizures *S*hagreen patches 4. Osler Weber Rendu syndrome. also called hereditary hemorrhagic telangiectasia. remember pathoma showed pic of guy w telangiectasias on his lips. sx are ruptures of telangiectasias on skin, nose, or GI --> hematuria, etc. no cysts

what are normal changes in TLC and FVC and RV in normal aging pts?

1. TLC is *unchanged* (bc chest wall compliance decrease counterbalances increased lung compliance) 2. FVC is low (bc you can't breathe out as much even if you try hard to) 3. RV is high (d/t diminished elastic recoil of lung i.e. it's a little stiffer so don't collapse as much and thus has residual air even after youve finished breathing out)

what are the 4 important pharmacokinetic equations?

1. Vd = drug IV / plasma concentration of drug 2. Clearance = rate of elimination / plasma concentration AKA Cl = (0.7)x(Vd)/ t 1/2 3. Loading dose = Concentration of steady state (i.e. desired concentration) x Vd 4. Maintenance dose = Concentration of steady state (i.e. desired dose) * Cl

what are the basic elements of informed consent? (4)

1. accurate description of the intervention 2. alternative treatments 3. risks and benefits of said alternatives 4. assessment of pts understanding and preference

what are 4 drugs you can't use while being on benozodiazepines?

1. alcohol 2. barbiturates 3. neuroleptics 4. 1st gen antihistamines BONUS: diazepam is a *long acting* benzo and its used for the following 4 things 1. anxiolytic (GAD and panic attacks) 2. sedative hypnotic (short term tx of insomnia) 3. anticonvulsant (status epilepticus. seizures from alcohol withdrawal) 4. muscle relaxant (stop the spasticity caused by UMN disorders like MS, strokes, spinal cord trauma) and tetanus

repeat this one till you know it bc you struggle w lung stuff: what are the 5 major causes of hypoxemia i.e. low PaO2? which have normal A-a gradient?

1. alveolar hypoventilation 2. low partial pressure of inspired oxygen 3. ventilation perfusion mismatch 4. diffusion impairment 5. right to left shunting NORMAL A-a gradient is seen in *alveolar hypoventilation & low partial pressure of inspired oxygen!!* whenever the A-a is normal it's bc you're not getting enough air in so the diff in the alveoli and the blood is normal versus air being trapped in alveoli and not able to pass thru to blood

What sx/presentation would make you think of each as the cause for stroke? 1. arteriovenous malformation 2. cardiac embolism 3. carotid artery atherosclerosis 4. cerebral amyloid angiopathy 5. charcot bouchard aneurysm 6. hypertensive encephalopathy 7. hypoxic encephalopathy 8. saccular aneurysm

1. arteriovenous malformation. commonly seen in *kids* and it's a single lesion. not multiple and not in older pts. 2. cardiac embolism. usually see multiple *infarcts* (so ischemic stroke. no lighting up on CT) and spontaneous hemorrhagic transformation 3. carotid artery atherosclerosis. also ischemic stroke so nothing on CT but apprents w *sudden onset* neuro sx 4. Cerebral amyloid angiopathy. most common cause of *multiple spontaenous lobar hemorrhages* esp in elderly. usually have gradually worsening sx. *focal neuro deficits* reflecting which cortex went man down 5. Charcot bouchard. hemorrhagic. chornic HTN. deep brain structures so really small. (similar to lacunar stroke but this is not hemorrhagic) 6. Hypertensive encephalopathy. *progressive* hx and confusion. n/v 7. Hypoxic encephalopathy. global interruption of cerebral blood supply like during cardaic arrest. --> rapid coma and vegetative state. not focal neuro deficits 8. saccular aneurysm rupture. "worst HA of my life" subarachnoid hemorrhage.

what drugs are proven decrease in mortality in pts w CHF? (4)

1. beta blockers (sketch w the muted bugle symphony w the angle playing the harp) [altho beta blockers should NOT be introduced during decompensation attack bc further slow heart and drown it. they should be introduced slowly after the pt has been stabilized!!] 2. angiotensin 2 receptor blockers ('sorry it's taken' ACE casino sketch w angel officiating the casino wedding lol) 3. ACE inhibitors (again ACE casino sketch w angel officiating the casino wedding) 4. aldosterone antagonists (little girl dressed as an angel next to the angry apple teacher [eplerenone] and the spiral investigator [spironolactone])

In immuno comp pt, what are the following: 1. "patches of adherent, grey/white pseudomembranes on erythematous mucosa. microscope finds yeast cells & pseudohyphae invading mucosal cells" 2. "small vesicles in esophagus --> "punched out ulcers" w eosinophilic intranuclear inclusions in multinuclear squamous cells at ulcer margins" 3. "linear ulcerations of esophagus w intranuclear and cytoplasmic inclusions"

1. candida albicans 2. HSV1 (cowdry type A on microscopy) 3. CMV

if a pt comes in w cushing like sx, what is the algorithm you go thru to determine what the cause is?

1. check ACTH levels. (screen w *low dose dexamethasone* if it doesn't suppress it then go on in the algorithm.) 2a. Suppressed? -adrenal adenoma (i.e. making too much cortisol and feeds back to ACTH so ACTH will be low) -adrenal malignancy -exogenous glucocorticoid intake 2b. normal or elevated? give HIGH DOSE dexamethasone suppression test 3a. suppression of ACTH & cortisol levels --> pituitary adenoma (also called cushing DZ [vs syndrome]) 3b. ACTH & cortisol levels unchanged --> ectopic ACTH prodxn (like small cell lung cancer. aint no cancer listening to high dose glucocorticoid lol. won't suppress)

what are common complications of vericose veins (5)

1. chronic edema 2. stasis dermatitis 3. skin ulcerations!! 4. poor wound healing 5. infection **NOT** DVT or PE bc varicose veins are usually in the SUPERFICIAL venous system not deep!

How do you assess someone for decision making capacity to ignore/refuse tx? (4)

1. communicates a choice. pt is able to *clearly* indicate preferred tx option 2. Understands information provided. pt understand his/her conditions & tx options 3. Appreciates consequences. pt *acknowledges* having condition & likely consequences of tx options 4. Rationale given for decision. pt is able to weigh risk & benefits & offer reasons for decision *notice that a dx of mild cognitive impairment does NOT automatically indicate lack of decision making capacity!! if they aren't orientated to date and month that doesn't mean they can't make their own decisions* *however, intoxicated pts* like a severe alcoholic that says hes fine and he'll sue if you keep him against his will does NOT have decision making capacity & thus should NOT be allowed to leave ED

what would you see sx wise w damage to: 1. Base of pons 2. caudate nucleus 3. frontal cortex 4. posterior limb of internal capsule

1. contralateral weakness & ataxia d/t descending motor tracts (corticospinal, corticobulbar) and pontocerebellar fibers being there 2. behvarioral abn (agitation, psychosis), speech/language disturbances, movement dirsorders (choreoathetosis) like huntingtons 3. social disinhibition and deficits in attention and executive fxn (planning, organizing, decision making) 4. posterior 1/3 of posterior limb has the *sensory fibers* like thalamocortical tract. anterior 2/3 of posterior limb has the *motor fibers* like corticospinal tract most commonly posterior limb of internal capsule causes pure motor lesions. sometimes combined sensorimotor deficits

what are the 3 pathways/steps pyruvate can go thru in metabolisis?

1. down the TCA pathway if there's O2: -acetyl CoA w the help of pyruvate DH 2. down the lactate pathway if no O2: -lactic acid w the help of lactate dehydrogenase 3. down the gluconeogenesis pathway: -oxaloacetate w the help of pyruvate carboxylase

ToF is commonly associated w what 3 syndromes?

1. downs 2. alagille 3. digeorge

in what circumstances can the following be injured: 1. accessory nerve 2. ansa cervicalis 3. inferior thyroid arteries

1. during surgery involving the posterior triangle of the neck 2. penetrating trauma to the neck *above* cricoid cartilage 3. thyroid surgery

What are the diff subtypes of delusional disorder? (5)

1. erotomanic: believing someone is in love w you 2. grandiose. believing you have great talent, insights, achievements 3. jealous: believing your partner is unfaithful 4. persecutory: believing they are being cheated, spied on, poisoned, harassed (commonly confused for schizophrenia) 5. Somatic: believing bodily fxns and sensations are abn

association time! :) 1. yellow papules that abruptly appear 2. linear xanthoma lesions in skin folds 3. soft eyelid or periorbital plaques

1. eruptive xanthomas. appear when there's an increase in TG and lipids! 2. Plane xanthomas. *strongly associated w primary biliary cirrhosis*

Protein defect. elevated lipoprotein. and major sx of each: 1. Familial chylomicronemia syndrome (type 1) 2. Familial hypercholesterolemia (type 2a) 3. Familial dysbetalipoproteinemia (type 3) 4. Familial hypertriglyceridemia (type 4) *recurrent*

1. familial chylomicronemia: missing *LPL* aka *ApoC2* elevated: chylomicrons Sx: *acute pancreatitis* 2. Familial hypercholesterolemia: missing *LDL receptor* aka *ApoB100* can't bring LDLs into liver. elevated: LDL Sx: *premature coronary artery dz* 3. Familial dysbetalipoproteinemia: missing: ApoE elevated: chylomicrons and VLDL remnants Sx: premature coronary artery dz Familial hypertriglyceridemia: missing: ApoA-V elevated: VLDL sx: associated w obesity & insulin resistance. increased pancreatitis risk

What complications can you commonly see in a pt w AR Friedreich ataxia?

1. hypertrophic cardiomyopathy (complications from cardiomyopathy is *most common cause of death* 2. DM 3. Skeletal abn like pes cavus, kyphoscoliosis (hunch back and horizontal shift/squiggle)

what are clinical features of ARDS?

1. hypoxia 2. bilateral pulmonary infiltrates 3. *NORMAL* pulmonary capillary wedge pressure (i.e. left atrium pressure) bc this isn't a heart problem. it's that excessive cytokine release led to endothelial activation --> neutrophil recruitment & degranulation in lung increased capillary permeability & alveolar fluid accumulation --> formation of hyaline membrane you'll see: -decreased lung compliance d/t atelectasis (i.e. collapse of alveoli) -increased capillary permeability from all the damage -increased work of breathing since it's harder to open collapsed alveoli -ventilation/perfusion mismatch d/t fluid filled and collapse alveoli being unable to deliver O2 despite continuing to receive adequate blood flow

where is sorbitol conversion to fructose slow and thus prone to sorbitol accumulation? (4)

1. retina 2. lens 3. kidney 4. peripheral nerves this is why we see cataracts in DM pts (opacification of lens --> loss of red reflex) soribtol accumulatioin increases cellular osmotic and oxidative stress. pathogenesisi behind DM retinopathy, neuropathy, and nephropathy!

What are the 5 effects of insulin? (think of them in terms of organ systems) What happens when you don't have enough insulin?

1. increase glucose uptake. This happens at *skeletal muscle, adipose tissue, liver* 2. increase glycogen synthesis AND decrease glycogenolysis. this happens at *liver* bc this is where glycogen is stored i think 3. decreased glucagon secretion. This happens in *alpha cells* of pancreas 4. decreased lipolysis and ketogenesis aka stop making energy from fatty acids. this happens in *adipose tissue and liver* 5. increase protein synthesis. bc we have lots of sugar so lets use it to build stuff :) this obviously happens in *muscle* NOT ENOUGH INSULIN: -hyperglycemia (polyuria, polydipsia, lethargy, polyphagia, anorexia) -ketosis/ketoacidosis bc continued breakdown of fats -muscle wasting and weight loss bc not building muscle. breaking it down instead Bonus: remember insulin comes from beta cells. glucagon from alpha cells of pancreas. they oppose each other and should always be in harmony

what can you dx w: 1. hydrogen breath test 2. rectal suction biopsy 3. terminal ileum biopsy?

1. lactose intolerance. lactose fermented by bacteria --> extra H+ exhaled 2. Gold standard for dx Hirschspurng dz 3. Crohn dz (focal inflammation & ulceration)

be patient w yourself. learn this one over time. and even if you don't learn them all God still has your back jen. youre not in control. God is. He always has been. what deficiencies/dzs cause impairment of the following conversions: 1. leucine --> acetoacetate 2. phenylalanine --> tyrosine 3. Tyrosine --> fumarate

1. leucine --> acetoacetate. Maple syrup urine dz. Isoleucine and valine are also increased bc these are all branched AA. urine will smell sweet. think: i love lucy and val love sweet maple on her pancakes 2. phenylalanine --> tyrosine. PKU, significant intellectual disability 3. AR alkaptonuria. excess buildup of oxidizable homogentisate which causes build up of tyrosine bc homogentisate is an intermediate in the break down of tyrosine to fumarate

what are 1st line tx for bipolar?

1. lithium 2. valproate (yes anti seizure but also FIRST LINE for bipolar!) 3. quetiapine (2nd gen antipsych)

RNA pol 2 is responsible for synthesizing what? (2)

1. mRNA 2. snRNA --> becomes snRNPs

tell the story about how neutrophils get recruited :D (5 steps)

1. margination: once upon a time there was a microvasculature leak. this led to improved contact of neutrophils w *endothelial lining* from inside the vessel 2. rolling: the neutrophils were on their way to work. just another day. when all of a sudden they ran into two super attractive guys called *L selectin* and *E selectin/P selectin* on the endothelial cells bc they were able to peak in from the vasculature rupture. 3. activation. once inside the girls were activated and started snooping inside the dudes house. the slow rolling allows leukocytes to sample chemokines secreted by inflamed tissue --> activates *integrins* that allows in conformational change in integrins necessary for binding 4. tight adhesion and crawling. neutrophils become *firmly attached* to endothelium via *CD18 beta 2 integrins* (*Mac1 and LFA1*). they attach to the guys *ICAM-1* on the endothelial cells 5. transmigration: finally the party can start when the neutrophils eventually migrate out of the vasculature by squeezing in b/w cells and into the damaged tissue. they do this via attachment to platelet endothelial cell adhesion molecule 1 (*PECAM1*) BONUS: there are 3 disorders that disrupt this process. 1. LAD (leukocyte adhesion def) type 1. absence of CD18. missing Mac-1 and lFA1 --> affects tight adhesion, crawling, & transmigration. *skin infxns w/o pus formation & delayed detachment of umbilical cord* 2. LAD type 2. milder. no delay in separation of ubmilical cord 3. LAD type 3. similar to type 1 but d/t diff integrin

what are 4 features of MDD w atypical features?

1. mood reactivity (mood improves in response to positive events) 2. leaden paralysis (pt's arms and legs feel extremely heavy) 3. Rejection sensitivity (overly sensitive to slight criticism) 4. Increased sleep and appetite MAO inhibitors like phenelzine (funnel) or tranylcypromine (come try some wine!) are good for pts w depression w atypical features or tx resistant depression

anti mitochondrial antibodies antiphospholipid antibodies

1. primary biliary cholangitis aka primary biliary cirrhosis 2. SLE and antiphospholipid antibody syndrome. both cause a hypercoag state w paradoxical PTT prolongation (which means blood is thin)

what are 6 *absolute* contraindications to the use of OCPs?

1. prior hx of thromboembolic event or stroke!! 2. hx of estrogen dependent tumor 3. women over 35 y/o that smoke *heavily* (> 15 cigarettes/day) 4. hypertriglyceridemia (LDL levels too) 5. Decompensated or active liver dz (impairs steroid metabolism) 6. Pregnancy

What are the 3 effects of angiotensin 2?

1. promotes release of aldosterone (increases BP) 2. systemic vasoconstriction (increases BP) 3. *efferent* arteriolar vasoconstriction (maintains GFR)

"fluid in alveolar spaces" "pleural space dz" "pulmonary vascular dz"

1. pulmonary edema 2. pneumothorax (accumulation of air pushing on lung and pushes trachea *AWAY* from affected lung) 3. not code for pulm HTN!! code for pulm *embolism* (usually have nl CXR)

damage to the following causes what: 1. putamen 2. internal globus pallidus 3. external globus pallidus

1. putamen --> contralateral tremor, bradykinesia, rigidity 2. internal GP --> excessive motion/movement 3. External GP --> decreased motion/movement

What 4 rxns in the TCA cycle use NAD? what vitamin def would impair this?

1. pyruvate --> acetyl CoA (pyruvate DH) 2. Isocitrate --> alpha ketoglutarate (isocitrate DH) 3. alpha ketoglutarate --> succinyl CoA (alpha ketoglutarate DH) 4. Malate --> oxaloacetate (malate DH) in general NAD+ --> NADH is used in a lot of reductases and dehydrogenases. vitamin B3 as seen w pellagra aka dementia, diarrhia, dermatitis (malar distribution of face, neck, back of hands worse w exposure to light aka a photosensitive rash)

what renal cancer affects collecting ducts? what does the cancer affecting renal pelvis, ureters, or bladder look like on histo?

1. renal oncocytomas. gross path will show homogenous *brown tumor w a central stellate scar* no areas of necrosis like in renal cell carcinoma 2. urothelial carcinoma is the one that affects renal pelvis, ureters, or bladder. it will show *papillary tumors* w the classic fibrovascular stalk core

what vitamin is necessary in: 1. rxns that require FMN and FAD? 2. dehydrogenase enzymes 3. rxns that require NAD+ & NADP+ 4. carboxylase enzymes

1. riboflavin vitamin B2. these rxns involve dehydrogenase enzymes, but FMN and FAD 2. thiamine vitamin B1. examples: transketolase, alpha ketoglutarate DH, pyruvate DH 3. niacin vitamin B3. dehydrogenase enzymes that use NAD+ or NADP+ 4. biotin vitamin B7. all 4 carboxylase enzymes: pyruvate carboxylase, acetyl CoA carboxylase, propionyl CoA carboxylase, 3 methylcrotonyl CoA carboxylase

What 3 things control urination reflex? which one does normal pressure hydrocephalus affect?

1. sacral micturition center. found in S2-S4 and responsible for bladder contraction. Parasympath fibers from S2-S4 ventral white matter w/i pelvic nerves and stimulate cholinergic R in bladder wall 2. pontine micturition center. found in pontine reticular formation. coordinates relaxation of external urethral sphincter w bladder contraction during voiding 3. cerebral cortex. inhibits sacral micturition center so you don't pee yourself every time you gotta go normal pressure hydrocephalus affects the *cerebral cortex* part bc normal pressure hydrocephalus is d/t excess ventricle fluid so you'll get ventricular enlargement which stretches the cortical efferent & afferent fibers . the efferent fibers transmit impulses from the cortex to sacral micturition center.

What are the ADR of these drugs in pregnant pts? Tetracyclines Chloramphenicol TMP/SMX Aminoglycosides

1. tetracyclines (doxycycline): teeth staining yellow, gray, or brown (sketchy little baby in the biCYCLe race chewing on grey quarter medal) 2. Chloramphenicol: "gray baby" syndrome 3. TMP/SMX: neural tube defects 4. Ototoxicity, vestibulotoxicity

what meds are 1st line for HTN in general population? what rx is 1st line for pts w BPH + HTN? what rx is 1st line for pts w CAD or CHF + HTN? what rx is 1st line for pts w DM + HTN

1. thiazides (hydrochlorothiazide) 2. cardioselective beta blockers 3. alpha 1 blockers like doxazosin, prazosin, terazosin 4. ACE inhibitors

what does ALT > AST mean? what about AST > ALT usually 2:1 ratio

1. usually acute VIRAL hepatitis will also see rises in bilirubin and alk phos 2. AST > ALT is usually alcoholic hepatitis (think: *S*omeone likes to drink)

What is the order of channels being used during cardiac muscle excitation? (muscle not nodal) (4 steps)

1. voltage dependent L type Ca2+ channels on T tubules open & let Ca2+ into cytoplasm 2. Ca2+ binds ryanodine receptors of the SR and triggers more Ca2+ release 3. Ca2+ diffuses thru myofilament network and binds troponin C. moves tropomyosin out of the way so actin & myosin can interact 4. any extra Ca2+ still in cytoplasm gets either 1. taken up by SERCA back into SR (reqs ATP) *or* out to the T tubule via 3Na+/1Ca2+ exchange pump (this is myocyte relaxation :])

what are the derivatives of the aortic arches?

1st part of maxillary artery (think: 1st arch is maximal!) 2nd hyoid artery & stapedial artery (think: *S*econd is *s*tapedial) 3rd is Common carotid artery & proximal internal Carotid artery (think: C is the 3rd letter of the alphabet) 4th is the aortic arch on left and prox part of right subclavian (think: 4th arch = 4 limbs = systemic circulation) 6th proximal pulm arteries. ductus arteriosus on left!! (i.e. PDA!!)

What comes from the 1st and 2nd pharyngeal arches? 3rd and 4th?

1st: all about Ts and Ms CARTILAGE: Meckel's Cartilage (mandible, mandibular ligament, malleus & incus) Maxillary process (maxilla andn zygoMatic bone) MUSCLES Muscles of Mastication (Masseter, Medial pterygoid, lateral pterygoid, Temporalis) Mylohyoid Tensor Tympani Tensor veli palatini ant 2/3 of Tongue muscles NERVE Mandibular and Maxillary branches of Trigeminal 2nd: all about the Ss CARTILAGE: Stapes Styloid Process Stylohyoid process leSSer horn of the hyoid MUSCLES: Muscles of facial expression (bc CN Seven) Stapedius Stylohyoid NERVE: CN Seven 3rd: pharyngeal CARTILAGE: none MUSCLES: stylopharyngeus NERVE: glossopharyngeal (CN9) 4th: cricothyroid & larynx CARTILAGE: cricoid cartilage Thyroid cartilage cartilage of larynx MUSCLE: cricothyroid muscles Pharyngeal muscles (swallowing; superior laryngeal nerve) Laryngeal muscles (speech; recurrent laryngeal) NERVES: Vagus (bc 4+6 = 10) -superior laryngeal (cricothyroid muscles & pharyngeal muscles aka swallowing) -recurrent laryngeal (laryngeal muscles aka speech)

what comes from 1st pouch? 2nd pouch? 3rd pouch? 4th? pharyngeal poucehs

1st: middle ear structures middle ear cavity eustachian tubes mastoid air cells 2nd pouch: epithelial lining of tonsils 3rd pouch: inferior parathyroids thymus 4th pouch: superior parathyroids THINK: "ear, tonsils, bottom to top" 1 ear 2 tonsils 3 bottom aka inferior parathyroids 3 thymus 4 top aka superior parathyroids

what antibodies activate the complement system? which is the most effective?

2 molecules of IgM or IgG (remember GM makes classic cars) bind the *C1 complement component* but of these IgM is the most efficient bc it circulates as a pentamer which allows for increased complement interaction

What does 2,3 BPG do in the hemoglobin cells?

2,3 BPG causes release of O2. remember CADET? D = di phosphoglycerate high levels of 2,3 BPG means you'll have LOW affinity for O2 and thus drop off. if you DO NOT have 2,3 BPG (pts that have familial erythrocytosis w mutation in beta subunit) you'll have increased affinity for O2. these pts will then have hemoglobin most similar to HEMOGLOBIN F bc fetal hemoglobin has reduced 2,3 BPG allowing them to have higher affinity for O2 and thus be selfish like that to keep the O2 to themselves.

what type of rx is olanzapine and what should be monitored regularly in pts taking this rx?

2nd generation anti psych olanzapine and clozapine have *huge metabolic syndrome risks* thus pts should get their fasting glucose and lipid profile checked regularly also BP, waist circum, BP, etc Clozapine is the only antipsych that reqs routine monitoring of absolute neutrophil count ie WBC d/t the 1% chance of a granulocytosis

fxn of 5' to 3' exonuclease activity vs 3' to 5' exonuclease activity?

3' to 5' is the regular schmegular exonucleas activity that has "proofreading" activity (DNA pol 1, 2, and 3 have this) 5' to 3' is the cool unique feature that *removes RNA primers* (only DNA pol 1 has this)

What is empiric tx for suspected gonorrhea infxn? *recurrent*

3rd generation cephalosporin (ceftriaxone) PLUS azithromycin (macrolide) or doxycyline (fluoroquinolone)

What is the rule for SD's in a normal bell distribution?

68/95/99 68% w/i 1 SD 95% w/i 2 SD 99.8% w/i 3 SD

What is "normal" for umbilical cord separation ? i.e. how long?

< 1 month. if its more than 1 month we say its delayed separation are suspicious about neutrophil migration

what is the most common outcome of hep B infxn? hep C?

> 95% of the time --> full resolution altho the 3 options are a thing: 1. acute hepatitis w full resolution 2. chronic hepatitis w or w/i cirrhosis but increased risk for hepatocellular carcinoma 3. fulminant (severe/sudden) hepatitis w massive liver necrosis

Why do pts w bilateral renal artery stenosis get increase in creatinine when given ace inhibitor?

ACE inhibitor will DILATE efferent bc it will block angiotensin 2 which is constricting efferent but it will ALSO actually act on efferent arteriole well pts that have bilateral artery stenosis are SUPER DEPENDENT on angiotensin 2 to constrict efferent and maintain GFR since they're getting minimal blood flow. if you dilate it, you'll cause a big decrease in GFR

What is the trinucleotide repeat in huntingtons? what about myotonic dystrophy? what about fragile X? what about friedreich ataxia? *recurrent*

AD Huntingtons: CAG (*C*audate has low *A*Ch and *G*ABA) AD myotonic dystrophy: CTG (*C*ataracts, *T*oupee [early balding in men], *G*onadal atrophy) XD fragile X syndrome: CGG (*C*hin protruding, *G*iant *G*onads AR friedreich ataxia: GAA (ataxic GAAit)

what proteins are defective in NF1 and NF2? what chromosome mutation?

AD NF1 defect in chr 17 --> decreased prodxn of *neurofibromin* AD NF2 defect in chr 22 --> decreased prodxn of *merlin*

Buzzword: pink spider like lesions on oral and nasal mucosa, face, and arms + recurrent severe nosebleeds

AD Osler Weber Rendu syndrome aka hereditary hemorrhagic telangiectasia basically can have telangiectasias anywhere: lips, oronasopharynx, resp tract, GI, urinary tract... these can then rupture & cause bleeding anywhere --> nose bleeds, Gi bleed, hematuria

acute tubular necrosis vs acute interstitial nephritis?

AIN is d/t the 5 P offenders: Pee (diuretics) Pain free (NSAIDs) Penicillins & cephalosporins PPIs rifamPin they classically cause *eosinophilia* in urine sediment. also fever, maculopapular rash, acute renal failure that usually happens 1-3 wks after starting rx. you'll see "leukocyte infiltration and edema of the renal interstitium" Acute tubular necrosis is damage to the tubular lumen of kidney

Auer rods are seen in what cancer and what can they be stained w?

AML!! specifically APL auer rods are stained w myeloperoxidase

APC, BRCA1, RB, TP53... are these tumor suppressors or proto oncogenes? what about KRAS?

APC, BRCA1 , RB, TP53 are tumor suppressors!! KRAS is a proto oncogene so activating mutation = cancer. other proto oncogenes are ABL, BRAF, HER1, HER2, MYC, TGFA, SIS

Buzzword: increased level of neutral amino acids in urine (neutral aminoaciduria)

AR Hartnup dz metabolic disorder that affects *neutral amino acid transporter* --> impaired transport of neutral AA like *tryptophan* in small intestine & PCT of kidney tryptophan is essential to make *niacin, serotonin, and melatonin* so these pts will present w pellagra like sx!! (red rash on sun exposure, diarrhea) but w the added *cerebellar ataxia* in early childhood

Classic findings in AR Krabbe dz? (3) what builds up? Classic findings in XLR Fabry dz? Classic findings in AR Tay Sachs?

AR Krabbe: Neurodegeneration + *peripheral neuropathy* + *optic atrophy* DEF: galactocerebrosidase --> build up of galactocerebroside) XLR Fabry dz: *angiokeratomas* [small red spots on skin] + *peripheral neuropathy* + hypohidrosis (little sweating). later on in adults: *glomerulopathy* usually in adults DEF: alpha galactosidase A. build up ceramide trihexoside AR Tay Sachs: progressive neurodegeneration + cherry-red macular spot W NORMAL abn exam!! DEF: hexosaminidase A --> build up GM2 ganglioside Pts w AR Niemann Pick have hepatosplenomegaly (build up sphingomyelin) *look up photo on your phone*

Buzzword: blue-black spots on sclerae (dz and def)

AR alkaptonuria d/t def of *homogentisic acid dioxygenase* (involved in tyrosine metabolism) accumulation = pigment deposits in CT thru out body. in adults commonly seen as *blue black deposits* in the sclerae and ear cartilage. can also build up in large joints and spine --> ankylosis, motion restriction, significant pain

Buzzword: urine that turns black when exposed to air

AR alkaptonuria d/t def of homogentisic acid dioxygenase turns black d/t oxidization of homogentisic acid

pt w urine that turned black overnight. nothing shows up on urinalysis.

AR alkaptonuria!!!! tyrosine --> fumarate deficiency this is d/t accumulation of homogentisatic acid which accumulates in body and is excreted in urine. it can get oxidized --> turns urine black if it sits lot enough BONUS: the retained homogentisic acid will bind to *collagen* in CT, tendons, cartilate --> "*ochronosis*" which is a blue black pigmentation most evident in ears, nose, cheeks, and *ochronotic arthropathy* seen in ADULT HOOD even tho u can see the urine thing during childhood

elevated orotic acid crystals in urine. what's wrong? what other findings are common?

AR disorder that leads to *excess orotic acid*. orotic acid is an intermediate in uridine (pyrimidine) synthesis. deficit in *uridine 5' monophosphate (UMP) synthase* causes build up of orotic acid OR it can be d/t ornithine transcarbamylase def in the urea synthesis pathway, but the diff is that they'll have excessive ammonia building up. this is a common cause of megaloblastic anemia. yes we usually think of folate and B12 def bc they're involved in DNA synth but so is orotic acid! i.e. makes uridine! Tx: give uridine so they don't have to make it and thus UMP synthase def doesn't cause build up

urine test that's positive for copper reduction test but pt is asx?

AR essential fructosuria where fructokinase is deficient copper reduction test just detects reducing sugars (non specific for glucose, galactose, fructose etc) but in a pt that has no sx it can clue you into AR essential fructosuria which is very mild and usually presents w no sx since fructose can also be metabolized by hexokinase and shunted to the glycolysis pathway not all will get shunted tho so pts will have elevated fructose levels as seen in the copper test showing fructose in urine

buzzword: defect in repair of DNA cross links

AR fanconi anemia d/t mutations in genes resp for repair of interstrand DNA cross links . most common cause of *inherited* aplastic anemia --> short stature, *absent thumbs*, increased malignancy risk

what substance is directly responsible for activating the k+ channels that allow insulin release?

ATP!!! yes, glucose comes in to the cell via GLUT2 and we say "high glucose causes release of insulin" but it's not like the glucose has a binding spot. it has to get broken down via glycolysis and TCA cycle to create ATP. this ATP closes K+ channel which causes depol (bc of decreased K+ outflow) & allows *Ca2+* into cell. from there the Ca2+ teams up w cAMP (which was allowed to come in via GLP-1 receptor) and TOGETHER they create and release insulin!

who is the pacemaker in a 3rd degree block?

AV node! HR 45-55 bpm whereas other lower areas like purkinje fibers and such can be as slow as 20 bpm

What 3 sx does acute vitamin A excess result in? (4) chronic? (3) this will be a recurring card b/c you need to learn vitamin excess/deficiencies. its ok jen. take a deep breath. God has your back.

Acute: n/v vertigo vomiting blurred vision Chronic: 1. intracranial HTN (sometimes described as "papilledema w/o intracranial mass" bc papilledema just means high pressure in brain and it could be d/t mass so they have to say it's not d/t a mass) 2. Skin changes like dry skin 3. heptosplenomegaly d/t hepatic toxicity

What are classic withdrawal sx for the following: Alcohol Benzos Heroin Stimulates (cocaine or amphetamines) Nicotine Cannabis

Alcohol: delirium (also tremors, agitation, anxiety, psychosis). *seizures* Benzos: tremors, anxiety, perceptual disturbances, psychosis, insomnia. *seizures* Heroin: n/v, diarrhea. *dilated pupils!!!* *yawning* *lacrimation* Stimulants: *intense psychomotor retardation, severe "crash" depression*, hypersomnia (excessive sleepy), hyperphagia, vivid dreams Nicotine: *increased appetite* Cannabis: anxiety, depressed mood, irritability, decreased appetite

what artery/nerve are in the anterior, deep posterior, and lateral compartment of the leg?

Anterior: deep peroneal nerve * anterior tibial artery/vein Lateral: superficial peroneal nerve Deep posterior compartment: peroneal artery & veins AND tibial nerve w posterior tibial artery & vein nearby anterior compartment syndrome is the most common!!

ApoE = ? ApoC2? *recurrent*

Apo E is the marker for VLDL mostly. defect in Apo E = high VLDLs Apo C2 is the ligand marker for LPL so low Apo C2 means high chylomicrons since can't bind chylomicrons to LPL

a pt that comes from a village where they cover umbilical stumps w soil puts her baby at increased risk for what? how do we prevent?

C tetani! prevent by vaccinating *pregnant* women w inactivated tetanus toxin. this will provide baby w IgG transplacentally and set them up for success in the future :) babies get the diphtheria-pertussis-tetanus first dose at ~2 months. no earlier than 4-6 wks if in an endemic tetanus area but def wouldn't give if new born bc immature immune system won't be able to mount a proper memory response

CD31 cell marker is associated w what cancer? esp if exposure to polyvinyl chloride or arsenic?

CD 31 is an endothelial cell marker. specifically PECAM1 (platelet endothelial adhesion molecule) these are expressed by *endothelial cells* and fxn in leukocyte migration thru endothelium the vinyl chloride is BUZZWORD for angiosarcoma of liver!! used to make pipes out of PVC!! this is pathognemonic for angiosarcoma of liver in STEP 1 tests lol the added CD31 cluing you into endothelial i.e. blood vessels was nice but not necessary to know liver angiosacroma was the answer

What cells are responsible for creating giant cells seen in TB?

CD4+ !!! remember anything TB related is d/t macrophages, but who activates/call macrophages? T helper cells (Th1 --> IFN gamma) but still T helper so CD4+ !! Note: those "giant cells" made in TB are called "multinucleated Langhans giant cells" which are just fused activated macrophages (however, they can also be seen in other chronic infectious/inflammatory conditions like sarcoidosis or Crohns dz)

role of carcinoembryonic antigen in pts w colon cancer?

CEA levels are used to *monitor for tumor recurrence*. not for grading or staging or determining type of chemo or anything. CEA is elevated in other malignancies and benign dzs so not used to dx but helpful for detecting residual dz post op or recurrence altho elevated initial CEA levels are associated w a worse prognosis and failure to normalize following surgery suggests residual dz

immunocompetent pt w a heterophile antibody negative mononucleosis like sx. dx?

CMV!! if mono spot is positive then EBV but if negative twice on 2 separate occasions then CMV bc sometimes the 1st mono test will be negative but the 2nd will be positive this would be EBV but 2 negatives --> CMV

what comes out of the jugular foramen?

CN 9, 10, 11, jugular vein

What nerve comes out of the cerebellopontine angle?

CN8! vommonly injured in vestibular schwannomas! --> tinnitus & sensorineural hearing loss

What CN is responsible for afferent limb of carotid sinus baroreceptors? exactly where is this sinus found? what about afferent limb of aortic arch baroreceptor? what about efferent limb?

CN9 --> carotid (think aortic is higher up/before aortic arch and 9 is before 10). carotid sinus is found *just above bifurcation of common carotid artery* CN10 --> aortic arch EFFERENT is of both sinuses is carried by CN 10

what is the *most common cause* of spontaneous lobar hemorrhage? esp in elderly?

Cerebral amyloid angiopathy the question stem literally said CT has many small lobar hemorrhages of varying ages.... 2 yrs ago he had sudden right arm weakness and imaging showed small left frontal lobe hemorrhage so basically they gave us a hx of lots of lobar hemorrhages. and we were supposed to know it was *cerebral amyloid angiopathy* amyloid build up in arteries results in vessel wall weakening --> predisposition to rupture (this dz is NOT associated w systemic amyloidoses tho!)

What is the effect of cholinergic agonists like pilocarpine on eye aqueous humor prodxn and how does it get used for glaucoma?

Cholinergic agonists cause *miosis* by promoting *CONTRACTION of sphincter of the iris* --> anterior chamber angle gets wider --> trabecular meshwork has more accessible outflow they also *promote ciliary MUSCLE contraction* --> lens becomes more convex and allows for even more outflow BONUS: -acetazolamide also decreases aqueous humor *prodxn* -prostaglandin F2 like latonoprost and travoprost (LA Tan kid and travel boots kid) increase *outflow* of aqueous humor

DOC to prevent risk of cardiovascular events in pts w stable angina is daily aspirin. what do you give pts that have aspirin allergy?

Clopidogrel (ADP receptor inhibitor) is the DOC in pts that are unable to tolerate aspirin!! this is bc clopidogrel is *as effective as aspirin* for prevention in cardiovascular events!! recall clopidogrel (grill) blocks the P2Y12 component of ADP receptors on the platelet surface and prevents platelet aggregation (the point behind giving aspirin to to prevent risk of occlusive thrombus formation & subsequent MI)

What are the Cluster A personality disorders? Cluster B? Cluster C? *recurrent*

Cluster A = "weird" --> Accusatory, Aloof, Awkward: *Paranoid*: pervasive distrust and suspiciousness of others. profoundly cynical view of the world *Schizoid*: voluntary social withdrawal. limited emotional expression but happy this way. prefers to be a loner. *schizotypal*: magical thinking, interpersonal awkwardness Cluster B = "Wild" --> Bad, Borderline, falmBoyant, must be the Best *Antisocial*: disregard for and violation of rights of others. lack of remorse, criminality, impulsivity must be > 18 y/o otherwise its called conduct disorders. (big clue is conduct problems prior to age 15 i.e. Juvy) *Borderline*: unstable mood and interpersonal relationships. impulsivity, self mutilation, suicidality, *Histrionic*: excessive emotionality and excitability. attention seeking, sexually provocative *Narcissistic*: gradiosity, sense of entitlement, lacks empathy. must get the "best" service and doesn't respond well to criticism Cluster C = "worried" --> Cowardly, obsessive-Compulsive, Clingy *Avoidant*: hypersensitive to rejection, socially inhibited, feelings of inadequacy *Obsessive-compulsive*: preoccupation w order, perfectionism, etc. but its *ego syntonic* i.e. behavior is consistent w one's own beliefs and attitudes vs OCD where its ego dystonic *Dependent*: excessive need for support, low self confidence, pts gets stuck in abusive relationships

what are some distinguishing characteristics of crohn's (7) vs UC (4)

Crohn's: -transmural inflammation -thickened muscularis mucosa -cobblestoning -creeping fat -fissures -skip lesions -commonly in *terminal ileum* complications of crohns: -strictures (d/t bowel wall edema, fibrosis, and thickening) -fistulas (d/t penetration of ulcers thru the intestinal wall) -abscesses UC: -ulcers -superficial inflammation (mucosa and submucosa) -pseudopolyps -continuous in the colon only

Buzzword: spiral shaped mucus plugs

Curschmann spirals. seen in asthma

"phenylalanine deletion"

Cystic fibrosis!! remember its a phe deletion at F508 --> Cl- channel abn

What polymerase is the only one to have 5' to 3' exonuclease activity?

DNA pol 1!! used to remove the RNA primers and replace w DNA! also has 3' to 5' exonuclease activity but so does DNA pol 3 so the 5' to 3' thing is unique to DNA pol 1

pt w no evidence of liver failure but persistently high direct bilirubin (> 50% of total bilirubin)

Dubin Johnson syndrome

this might be painful but God has your back. Don't worry: Enveloped dsDNA virus Enveloped ssRNA virus Naked dsDNA virus Naked ssRNA virus

Enveloped dsDNA virus: viruses in the herpesviridae family like HSV1, HSV2, CMV, etc Enveloped ssRNA virus: influenza naked dsDNA virus: adenovirus (a den of lions w naked david statue) naked ssRNA virus: rhinovirus (common cold; sunny petting zoo thing w rhino. sunny = RNA. statue of david too = naked)

Draw the mechanism of alcohol (ethanol) metabolism. what 2 drugs can inhibit the diff steps?

Ethanol ---> acetaldehyde --> acetate 1. alcohol DH 2. acetaladehyde DH 1. *Fomepizole* inhibits Alcohol DH 2. *Disulfiram* inhibits acetaldehyde DH causing build up of acetaldehyde THINK: FOMEpizole --> antidoe *F*or *O*verdoses of *M*ethanol or *E*thylene glycol *Dis*ulfram *dis*courages *d*rinking by causing hangover sx d/t build up of acetaldehyde

what endocrine hormones use cAMP? mnemonic + 4 more what endocrine hormones use cGMP? What endocrine hormones use IP3 pathway? What endocrine hormones use intracellular receptors? What endocrine hormones use receptor tyrosine kinase? What endocrine hormones use nonreceptor tyrosine kinase? ITS OK IF YOU DON'T KNOW EVERYTHING JEN. So far you've only practice cAMP and GMP

FA P 330 FLAT CHAMP FSH, LH, ACTH, TSH, CRH, hCG, ADH (V2), MSH, PTH calcitonin, GHRH, glucagon, histamine (H2 receptor) __________________________________ BAD GraMPa (think vasodilators) BNP, ANP, eDRF (NO) __________________________________ GOAT HAG GnRH, Oxytocin, ADH (V1), TRH, Histamine (H1), Angiotensin 2, Gastrin __________________________________ PET CAT on TV Progesterone, Estrogen, Testosterone, Cortisol, Aldosterone, T3/T4, Vitamin D _________________________________ Think: growth factors. Receptor tyrosine kinase all use MAPK pathway (MAP kinase) Insulin, IGF-1, FGF, PDGF, EGF ___________________________________ PIGGlET (Think: acidophils & cytokines). Non tyrosine kinase so use JAK/STAT pathway Prolactin, Immunomodulators (cytokines like IL2, IL6, IFN), GH, G-CSF, Erythropoietin, Thrombopoietin

What is the clearance formula for kidney stuff? What do we use as GFR substitute when tryna calculate FF? What about RBF? *recurrent*

FF can be calculated from GFR/RBF GFR and RBF can be calculated from *clearance* of certain substances (see below) C = (urine concentration of S x urine flow rate) / plasma concentration of S GFR: creatinine or inulin whichever they give you RBF: PAH :)

What does FSH and LH do in males? *recurrent*

FSH --> sertoli cells. supportive actions for spermatogenesis including testosterone binding protein LH --> leydig cells --> testosterone production

What nucleus receives info from face ? what about DCML/ALS from body?

Face: ventral posterior *medial* [make up goes on face] nucleus of thalamus (from trigeminal pathway) Body: ventral posterior *lateral* nucleus of thalamus (from spinothalamic and DCML) together they make ventral posterior thalamus!! don't get tricked :)

What is hageman factor?

Factor XII - Activated upon exposure to sub endothelial or tissue collagen - Activates 1. Coagulation and fibrinolytic systems can have AR def but doesn't usually cause significant bleeding (tho it does prolong PTT)

what is genetic reassortment? what is antigenic drift? what is phenotypic mixing? antigenic drift?

Genetic reassortment: something that happens in *segmented* genomes like orthomyxoviruses aka influenza virus. it is when 2 diff strains of the same virus are able to get repacked into a new virion if there is a co infxn. so if a pt gets infected w a human type virus and an animal type virus the animal type virus wouldn't cause sx, but if during replication the animal segment and the human segment get repackaged now there is a combo that CAN infect! this whole phenomenon is called antigenic *shift* bc there are new antigens and they have shifted to affect a new organism (i.e. humans) Antigenic drift: talks about *point mutations* in the HA and NA genes [i.e. surface proteins hemagglutinin and neuraminidase] that slightly alter the product proteins allowing them to evade immune recognition and possibly increase infectivity. however this is NOT species to species transmission bc this is a MAJOR modification. this "drifts" from the normal but isn't a total SHIFT

Buzzword: pseudopalisading. brain tumor. adults.

Glioblastoma multiforme

Action card: look at phone pic about developmental stages and learn a couple at a time

God has your back jen. never forget.

Action card: go to page 85 of FA and start learning the glycogen regulation by insulin pathway. just a little at a time *recurrent*

God is w you Jen. You are doing your best. He will handle it. Have faith and peace.

Turn to page 324 in FA. try to work on learning that pathway

God loves you Jen, keep peace <3

what serologic marker tells you someone has chronic hep B infxn?

HBsAg (Hep B surface antigen) LONGER THAN 6 MONTHS

What does DKA do to K+ levels? how does this affect tx

HIGH extracellularly i.e. in serum --> "DO LAbSS" ("A" = acidosis so like diabetic keto ACIDOSIS & S = high blood Sugar d/t insulin def) LOW intracellular stores since they all go out in regards to tx: -initial rxn is to give insulin, but this will cause all the K+ to hide inside cells bc that's what insulin does. insulin puts K+ back into cells -SEVERE hypo K+ if you give pts insulin right away --> heart arryhthmias -timely administration of K+ supplementation is ESSENTIAL in pts w DKA

what does HIV pol gene do?

HIV pol gene mutations are responsible for *acquired resistance* to reverse transcriptase inhibitors, protease inhibitors, integrase strand transfer inhibitors (i.e. our medications!) if a pt has new mutations to the pol egne it's d/t INCONSISTENT USE... we usually prescribe combination therapy for this exact reason so they should be covered if they follow their regimen

what is the #1 risk factor for aoritc dissection?

HTN!! (not smoking! smoking, DM, and high cholesterol increase risk for atherosclerosis which predisposes to aortic aneurysm formation more so than aortic dissection)

how can you calculate mutant allele frequency from dz prevalence. i.e. if there's a dz and you get a donor to give you sperm and we don't know his phenotype but we know that the prevalence of dz is 1/40,000 how do we solve it i.e. how do we know what the chance of him donating the allele is?? this is an AR dz. sperm donor doesnt have the dz nor does his family

Hardy Weinberg!! q + p = 1 1/40,000 = rr (i.e. AR) square root to get q = 1/200 we also know that q^2 + 2pq + p^2 = 1 and 2pq is the carrier type. the pt doesn't have it so we don't only care about 2pq specifically we care about 2q since q = bad copy of gene so we would do 2(1/200) = 2/200 = 1/100, this is the probability the donor is a CARRIER (if we were told the mom is a carrier then you to 0.5 [chance the mother gives it] * 1/100 [probability the donor is a carrier] * 0.5 [chance the sperm donor gives it])

what is the most common cause of hypothyroidism in the US and how does it present on histo?

Hashimoto's! auto immune. also called chronic lymphocytic thyroiditis presents as "intense lymphoplasmacytic infiltrate w active germinal centers"

what is the pathophys of hemoglobin S? why does it cause more problems than HBC?

HbS promotes *hydrophobic interaction among Hb molecules* --> HbS polymerization & erythrocyte sickling this is bc normally the globin chains in the hb tetramer are folded in such a way that the polar glutamate which normally helps bind stuff is replaced w valine which is neutral --> forms *hydrophobic pocket* on beta globin surface --> interacts w another complementary non polar residue on another hemoglobin --> polymerization & subsequent erythrocyte sickling.

when do you see Heinz bodies? Howell Jolly bodies? Ring sideroblasts? Schistocytes?

Heinz bodies: seen after oxidant stress in pts w glucose 6 phosphate DH def!! remember fava beans w Heinz ketchup ;). they're inclusions of denatured hemoglobin Howell-Jolly bodies: these are *nuclear DNA remnant inclusions* so they're seen when the spleen isn't doing its job (post splenectomy or sickle cell pts whom's spleen has stopped working) Ring sideroblasts: precipitation of iron granules in developing RBCs d/t defects in heme synthesis. this COULD be seen in lead poisoning but they're only seen in *bone marrow* NOT peripheral blood smear!! so watch out how they ask the question!! Schistocytes: fragmented parts of RBCs formed from mechanical hemolysis via sheer force of blood flow. HUS, TTP, DIC, sickle cell and many others!!

why can hep D only exist in the presence of hep B?

Hep B provides hepatitis D w surface antigen for its envelope. Hep D also doesn't have replicase or RNA polymerase so it relies on the host cell machinery entirely. which would be fine except its also *replication defective* such that it doesn't encode for viral envelope proteins which are necessary to generate viral progeny.

During fasting, what enzyme lets the mitochondria of the liver gain access to TGs in order to make ketone bodies? what activates this enzyme? what inhibits it? *recurrent*

Hormone sensitive lipase this enzyme is found in *adipose tissue* and can catalyze the mobilization of *stored TG* into *free fatty acids + glycerol* Activated: stress hormones that let your body know you're in starving mode like catecholamines, *glucagon* (encourages sugar production. when glucose is gone you secrete glucagon), ACTH Inhibited: w *release of insulin* the FFA are used to make ketone bodies & keep us going the glycerol is used as a carbon source for gluconeogenesis aka make glucose and keep reasonable glucose levels to bring it all back around, the free fatty acids join w CoA in the liver *outside the mitochondria* and REQUIRE CARNITINE shuttle to get into the mitochondrial matrix --> further fatty acid breakdown (beta oxidation) and thus production of ketone bodies w/o hormone sensitive lipase or w/o carnitine you can't successfully make ketone bodies Finally, mitochondrial HMG-CoA synthase plays a role in creating ketones, but *DOES NOT* maintain blood glucose levels. that maintenance is d/t hormone sensitive lipase allowing formation of free fatty acids AND glycerol. the glycerol can go thru gluconeogenesis

what cytokine causes T cells to become Th1 cells? Th2?

IL 12 causes naive T cell --> Th1 IL4 causes naive T cell --> Th2

What is the first interleukin produced by T cells after contact w antigen?

IL-2 ! mostly from Th1 cells (remember Th1 cells release INF gamma and IL2) it stimulates T cells (CD4+ and CD8 and even a little B cells :])

Under what artery does horseshoe kidney get trapped?

INFERIOR mesenteric artery. i thought it was superior but its not!! :) during fetal embryogenesis the kidneys are in the sacral region!! they ascend to their position d/t very fast *caudal* fetal growth. it gets trapped by IMA which limits its ascent if it's a horseshoe kidney!

What is the fxn of IgA on mucosal surfaces?

IgA on mucosa and in secretions acts to *bind and inhibit* the action of pili so pts infected w Neisseria, strep pneumo or H flu which *cleave* IgA w IgA protease facilitates mucosal adherence of bacteria

What is the pathophys behind RA?

IgM antibodies against *Fc portion of human IgG* RA is a failure of immune tolerance d/t autoreactive immune response against joint components. CD4+ T helper cells become activated against self antigens & release cytokinase promoting chronic inflammatory synovitis CD4+ also induce *B cells to synthesize RHEUMATIC FACTOR* and anti-citrullinated protein (ACPA) antibodies. RA is usually IgM and it's specific for the *Fc part of IgG* --> form immune complexes --> deposit on synovium and cartilage --> activate complement in those locations and cause *chronic inflammation w joint destruction*

Drug distribution is not uniform. a highly lipophilic drugs will go where first? why? where will they take a while to reach?

Lipophilic gets sent to tissues. They go to well vascularized peripheral compartments first. think of blood just rushing them there. these include places like brain, kidney, liver, lung, heart (vital organs if you will) Poorly vascularized peripheral tissues are skeletal muscle, bone, fat. the drug reaches here too but later

MOA of selegiline?

MAO type B inhibitor (guy using sledge hammer to kill (inhibit) the type B mouse) selegiline can be used to delay progression of parkinson dz. usually start w selegiline, anticholinergics, amantadine and then after they don't help sx start levodopa/carbidopa

if wernicke or broca's is d/t ischemia, what artery is affected?

MCA

Lupus manifestation mnemonc?

MD SOAP BRAINS *M*alar Rash *D*iscoid rash *S*erositis (pleuritis and pericarditis or other heart probs like LIBMAN SACKS which is thickened valve leaflets w vegetations on BOTH surfaces) *O*ral ulcers *A*therosclerosis/arthritis (> 2 joints) *P*hotosensitivity *B*lood didsorders (anemia, thrombocytopenia, leukopenia d/t type 2 Hypersensitivty i.e. antibody mediated) *R*enal involvement (most common cause of death! diffuse proliferative glomerulonephritis commonly see "wire looping" of capillaries on LM) *A*NA+ *I*mmunologic markers: anti ANA, anti dsDNA, anti SM antibodies *N*eruologic: seizures or psychosis most of the damage done by SLE is immune complex mediated (i.e. hypersensitivity type 3)

What tumors are found in MEN 1, 2a, and 2b

MEN 1: -pituitary -pancreas -parathyroids MEN2: -parathyroids -medullary carcinoma aka thyroid CA -pheochromocytoma MEN3: -medullary carcinoma aka thyroid CA -pheochromocytomas -mucosal neuromas

why does an ice pack on face help myasthenia gravis pts?

MG pts have destruction of nicotinic receptors at NMJ d/t IgG antibodies destroying them. furthermore acetylcholinesterases are chopping away at Ach so you have even less ACh. if you give edrophonium which block acetylcholinesterases you improve sx by increasing ACh ice/cold makes acetylcholinesterases lower their acivity so sometimes pts will find that an ice pack on their face helps their eye lids open easier

What is the MOA of amphotericin B and what is the most notorious ADR?

MOA: bind ergosterol & alters cell membrane permeability amphoterrible!! --> really bad *renal toxicity* 1. reduce GFR d/t vasoconstriction 2. direct toxicity to renal epithelial cells (ATN, RTA, electrolyte disturbances) 3. *SEVERE HYPO K+ & MG2+*

Hiccups after a motor vehicle accident.. why hiccups?

MVAs most commonly damage abdomen structures and the most commonly damaged ab structure is the *spleen* abdominal processes that can cause irritation (like ruptured spleen! but also peritonitis, hemoperitoneum) can *irritate the phrenic nerve* around the diaphragm --> hiccups d/t spasmodic diaphragmatic contraction pulling air against a closed larynx

What is hibernating myocardium?

Metabolic adaptations (usually LV systolic dysfxn) in persistently ischemic tissue that promotes myocyte survival by avoiding myocardial necrosis until blood flow is restored.

i npts w lactate DH deficiency, what is responsible for the inhibition of glycolysis in skeletal muscle during exercise?

NAD+ depletion when we exercise we go thru anaerobic metabolism aka we take pyruvate and turn it into lactate. when we convert into lactate we *regenerate NAD+* w/o lactate DH can't regenerate NAD+ which is required for glycolysis. so you get muscle breakdown, pain, fatigue, d/t insufficient amounts of energy being produced bc remember when you are anaerobic youre doing the cori cycle of: glucose in muscle --> pyruvate --> lactate --> lactate to liver --> pyruvate --> glucose --> back to glucose in muscle --> pyruvate etc etc but can't breakdown glucose to pyruvate if you can't regenerate NAD+

"Dihydrorhodamine flow cytometry revealing an absence of green fluorescence that is characteristic of normal neutrophils"

NADPH oxidase deficiency! NADPH oxidase is a membrane bound complex that catalyzes the reduction O2 to superoxide w/i phagolysosomes --> facilitates intracellular killing of organisms ingested by phagocytes it can be dx'ed two ways: 1. nitroblue tetrazolium (NBT) testing. properly fxning neutrophils will produce reactive O2 species that reduce the yellow NBT to *dark blue* formazan 2. Dihydrorhodamine (DHR) flow cytometry which assesses prodxn of superoxide radicals by measuring the conversion of DHR to rhodamine, a fluorescent green compound that can be detected by flow cytometry machines. if NADPH oxidase def --> decreased green fluorescence *myeloperoxidase* deficiency will NOT show up w these tests. MPO is also involved in killing bacteria by catalyzing the prodxn of bleach from H2O2 but is not dx'ed w these tests!

what is the formula for number needed to harm?

NNH = 1 / absolute risk increase 1. calculate adverse event rate (i.e. death) in experimental and control groups. AER experimental = bad event / total pts in the experimental group AER control group = bad event / total pts in control group 2. find the absolute risk increase by *subtracting* the AER from control minus tx 3. now you can do 1 / absolute risk increase this means 40 pts need to be tx'ed in order for 1 additional person to experience an adverse event

what is first line tx for acute gout?

NSAIDs!! glucocorticoids can be given, but these are systemic and have a lot of ADR so only given if pt has contraindications for NSAIDs and colchicine

what are the voltages for the following: Na+ K+ Cl- Ca2+

Na+ = +60 K+ = -90 Cl- = -75 Ca2+ = +125

What ions make up the pancreatic juice? (4)

Na+, K+ HCO3-, Cl- As HCO3- increases the concentration of Cl- decreases so after having a meal we would expect low levels of Cl-! This is bc Cl- and HCO3- are exchanged for one another at the apical surface of pancreatic ductal cells

another name for von recklinghausen's dz?

Neurofibromatosis type 1!!

what are the 2 MOST important mediators of *coronary* vascular dilation w/i "normal" BP range i.e. what is in charge of autoregulation in nl pts that are exercising?

Nitric oxide and adenosine!!! NO --> large arteries and pre arteriolar vessels Adenosine --> small coronary arterioles pts that are exercising will have CORONARY vessels all the way DILATED bc they're tryna increase O2. exercise causes us to use up more O2. blood vessels in their normal dilation are ALREADY extracting 70% of O2 (pretty much as much as they can extract) so they can't extract more, instead, need more O2 so they vasodilate to increase blood flow and thus O2 they can grab on to

what are all the genes and proteins involved in the entry of HIV into cells? relax. say it until you get it. God has your back Jen. think of it as a story

Once upon a time there were 3 genes, env, gag, and pol. but we're only focusing on viral entry today so we'll focus on *env* 1. env codes for polyprotein gp160 2. gp160 is no good and must go thru *glycosylation* in the ER and golgi body to become *gp120 and gp41* 3. gp120 and gp41 are the best of friends and remain bound (noncovalently but still bound) on the surface of the HIV cell. 4. gp120 is the receptor part. gp41 is the transmembrane part 5. gp120 binds to CD4+ T cells *and* chemokine co receptor on T cells like CXCR4 or macrophages like CCR5. for this reason we say gp120 is responsible for *attachment to host CD4+ T cell* 6. when gp120 binds, it causes a conformational change that allows the *transmembrane one* i.e. gp41 whom it was guarding and defending finally get exposed 7. when gp41 is exposed it will mediate *fusion* of viral cell membrane and *entry of viral core into host cytoplasm* and now the virus is in :o the end :)

What is the fxn of the posterior limb of the internal capsule? (4)

POSTERIOR it separates the globus pallidus and putamen from the thalamus and carries corticospinal motor and somatic sensory fibers as well as visual and auditory fibers so in summary: 1. separates globus pallidus & putamen from thalamus 2. carries corticospianl motor fibers 3. carries somatic sensory fibers 4. carries visual & auditory fibers UWorld literally said the fxn of this limb of the internal capsule was the most important to know

PP blues, PP depression, PP psychosis in terms of days?

PP blues < 14 days. usually w/i 2-3 days of giving birth. no tx. reassure and monitor PP depression w/i 4-6 wks can be up to 1 yr. give anti depressants and psychothearpy PP psychosis is variable. antipsychotics, anti depre, mood stabilizers, don't leave mom alone w infant (hospitalization)

what is primary spontaenous pneumothorax and what is a predisposing condition? commonly described as "tall thin 20 y/o male w smoking hx"

PSP is a nontraumatic injury in pts w/o pre-existing pulm dz that results in *collapse of lung* it's d/t large change in alveolar or intrapleural pressure --> *break in visceral pleura & subsequent trapping of air b/w parietal & visceral spaces* this commonly leads to formation of SUBPLEURAL PLEBS bc superficial alveoli in the apices experience greater pressure changes d/t the weight of lungs pulling down on the apical tissue. the blebs can then spontaneously rupture thru visceral pleura commonly while pts are *at rest* and then the air from the intrapleural space (i.e. b/w visceral and parietal pleura) can cause "extrinsic compression" tall thin males are at higher risk d/t more negative intrapleural pressure since taller lungs. altho smoking is the most important risk factor

what is the winter formula? what is it used for?

PaCO2 = (1.5 * HCO3-) + 8 +/- 2 this is used when pts have metabolic acidosis (like DKA for example). we use this to check if their CO2 respiratory compensation is appropriate

What's the formula for checking metabolic acidosis compensation by resp system?

PaCO2 should = 1.5 (serum HCO3) + 8 +/- 2

Buzzphrase: "flow cytometry shows absence of CD55 on surface of RBCs" what would you see in these pts cells?

Paroxysmal nocturnal hemoglobinuria!! DAF (decay accelerating factor) is the thing that is required to be on your RBCs for your complement to know they're RBCs and thus shouldn't get attacked. Blood cells like RBCs, WBCs, platelets live very close to complement so they must be able to protect themselves. how? w molcules like MIRL and DAF (membrane inhibitor of reactive lysis and decay accelerating factor) which deactivate complement if it comes near by! CD55 is the marker for *DAF* DAF and MIRL are held on to by GPI FINDINGS: -hemosiderosis which is just accumulation of hemosiderin which is an iron-storage complex. this is bc of so much hemolysis that Fe2+ just starts pilling up

OD of what drug will cause*violent* behavior? what receptor does it act on?

Phencyclidine (PCP) MOA: N methyl D aspartate (NMDA) glutamate receptor antagonist. sx are agitation, hallucination, and *violent behavior*, loss of coordination, vertical nystagmus, memory loss. but the big buzzword here is violent behavior

What results from acid alpha glucosidase def?

Pompe dz... key features are *cardiomegaly* + *severe hypotonia* + *macroglossia* and biopsy will show accumulation of *glycogen in lysosomes* !! this glycogen storage in lysosmes is specific for Pompe dz. they will say "muscle biopsy shows enlarged lysoosmes w PAS positive material"

short stature, hypotonia, obesity

Prader Willi syndrome d/t 15q11-13 microdeletion affecting fathers genes and moms were deleted so only dads show thru

RBCs have a specific ion that's usually elevated. why?

RBCs in venous blood have a "chloride shift" d/t bicarb always diffusing out of RBCs into plasma. Cl- comes to the rescue and diffuses in to take their place if question asks what is responsible for this we would say *carbonic anhydrase* bc that's the enzyme that creates HCO3- in the first place. this is particularly important bc RBCs carry CO2 from tissues remember? yeah they carry O2 but also CO2 and what do they do w all this CO2? use carbonic anhydrase and water to make HCO3-!

Mnemonic for killed or inactivated vaccines?

RIP Always Rabies Influenza (injection) Polio (salk; sal*K* = Killed) hep A

B1: thiamine. primary fxn & def B2: riboflavin. primary fxn & def B3: niacin. primary fxn & def B6: pyridoxin. primary fxn & def B9: folate, folic acid. primary fxn & def B12. cobalamin. primary fxn & def C. primary fxn & def *recurrent*

Relax jen. its okay. you gotta learn the vitamins. one at a time B1: decarboxylation of alpha keto acids (carbohydrate metabolism). DEF: Beriberi (peripheral neuropathy, HF) or Wernicke-korsakoff syndrome B2: mtiochondrial electron carrier (FMN, FAD so stuff like electron transport chain, esp complex 2 aka succinate dehydrogenase. succinate DH also converts succinate into fumarate in TCA cycle). DEF: angular cheilosis, stomatitis, glossitis. Or normocytic anemia B3: electron transfer rxns (NAD/NADP). DEF: Pellagra (dermatitis, dementia, diarrhea). Or peripheral neuropathy B6: transamination of AA (amino acid synth). DEF: cheilosis, stomatitis, glossitis B9: hydroxymethyl/formyl carrier (purine & THYMINE synthesis). DEF: megaloblastic anemia. neural tube defects B12: isomerase & methyltransferase cofactor (DNA & methionine synthesis). DEF: megaloblastic anemia. Neuro deficits C: hydroxylation of proline & lysine (collagen synth). DEF: scruvy (poor wound healing, scattered ecchymoses, periodontal dz, hyperkeratotic hairs)

fetus w significant resp distress d/t pleural effusions & ascities dies soon after birth. hemoglobin was 6 and had positive direct coombs test. dx?

Rh alloimmunization aka hemolytic dz of the newborn aka erythroblastosis fetalis aka erythrocyte opsonization by *maternal antibodies*

Buzzword: glomerular capillary BM thickened w wire loop changes

SLE!! think "wire lupus"

What is the mnemonic for delivering bad news? *recurrent*

SPIKES *Set the stage*: make sure its private, comfortable setting, introduce eybody, maintain eye contact and sit at the same level *Perception*: use open ended questions to assess the pt's/family's perception of the medical situation *Invitation*: ask how much they wanna know *Knowledge*: warn the pt bad news is coming, speak in simple terms, deliver the news, stop and check for understanding, remain cognizant of cultural or educational/religious issues *Empathy*: express understanding and give support when responding to emotions *Summary & strategy*: summarize and create follow thru plan like end of life discussions if need be

what is the tx for status epilepticus?

STATUS EPILEPTICUS = single seizure lasting > 5 mins or occurrence of multiple *discrete seizures* w incomplete recovery of *consciousness* b/w episodes 1. Benzodiazepines (long acting like lorazepam) 2. Phenytoin (long acting anticonvulsant that inhibits high frequency firing by reducing Na+ channel's ability to recover from inactivation) you give benzos and phenytoin concurrently

what dzs need to reported despite HIPAA?

STIs like HIV, chlamydia, TB but not HPV!! so if they have genital warts no need to report!

What are the diff types of anginas? (3) *recurrent*

Stable aka chronic angina: -poorly localized chest pain -associated w physical exertion or emotional stress -relieved w/i 5 mins w rest and/or sublingual nitroglycerin - >75% occlusion d/t atherosclerosis NO THROMBOSIS Vasospastic aka Prinzmetal aka variant angina -d/t coronary artery spasm -*smoking* not HTN or hypercholest -can occur at rest, w physical activity or not, independent of HR & BP just bad all around Unstable -d/t thrombosis -new onset angina -or existing angina w increased frequency, intensity, or duration -or angina at rest

what bacterial meningitis benefits from glucocorticoids? why? what is the effect of glucocorticoids

Strep pneumo triggers *significant* inflammatory cytokines (TNF alpha, IFN gamma, IL12) --> loss of tight jxns, BBB, vasogenic edema, high ICP, leukocyte invasion) d/t their *CELL WALL* i.e. teichoic acid and peptidoglycan pts that are given glucocorticoids before abx can benefit d/t *reduction of levels of inflammatory cytokines* other bugs that cause meningitis are gram negative (N meningitis or H flu) so their wall is minimal and thus don't result in as much cytokine release/inflammation

What is the fxn of each rotator cuff? & nerve say them out loud until you get it right :) they're easy, just gotta practice

Supraspinatus --> abduction (suprascapular nerve) Infraspinatus --> external rotation (suprascapular nerve) teres minor --> adduction AND external rotation (axillary nerve) Subscapularis --> adduction AND internal rotation (upper & lower subscapular nerves)

in regards to candida: When are neutrophils important for fighting infxn? what about T cells?

T cells are important for *prevention of SUPERFICIAL candida infxn* like oral/esophageal thrush, vulvovaginitis, cutaneous candidiasis. Neutrophils prevent *hemaatogenous* spread of candida. disseminated candidiasis like candidemia, endocarditis etc is more likely see in *neutropenic* pts than any other immunocompromised pts this is specially seen in HIV pts. HIV pts are T cell poor so they often get thrush and stuff but rarely disseminated candidiasis unless they also have neutropenia

what is the usual tx for post herpetic neuralgia?

TCA! (like amitriptyline) or anticonvulsants like gabapentin or pregabalin otherwise if you want a more natural approach --> topical capsaicin (loss of membrane potential in nociceptive fibers) or topical lidocaine (decrease depol of neurons in peripheral nerves d/t Na+ block)

pt w hx of recurrent renal stones and bitemporal visual field defects. what should you screen for?

THIS IS MEN 1!!! you knew this jen! you literally had a flashcard on it the same day right before getting asked. but you didn't know how to apply it. well you're gonna learn. MEN 1 is: -parathyroid -pituitary -pancreatic yeah but what does that look like? theyre not gonna say pt comes in a parathyroid and pituitary tumor for parathyroid they'll say: "recurrent renal stones" bc this indicates high levels of calcium which is what happens when someone has hyper PTH. *this is usually the initial manifestation*!! for pituitary they'll classically give a prolactinoma or a bitemporal visual field defect to clue you into pituitary mass effect. for pancreas they're the entero-pancreatic neuroendocrine tumors that are commonly: gastrinomas, insulinomas, or nonfxnal tumors. again they're not gonna say "pt has pancreatic cancer" they're gonna give you a pt w really low sugars over and over or really high stomach acid levels.

What do S japonicum and S mansoni affect? What about S haematobium? what cell in our body mediates the damage?

These are schistosomiasis. d/t *infxn from swimming in infected freshwater from freshwater snails* thus this isn't possible to get in the US bc we don't have the fresh water snails that incubate the infectious larvae S japonicum and mansoni affect the *intestine and liver* --> periportal "pipestem" fibrosis (this is pathognomonic for hepatic schistosomiasis!!! sketchy w coral fibrosed liver thing) S haemotobium affects the *bladder* leading to marked fibrosis and ulceration and scarring of the bowel or bladder/ureters. this is mediated by *Th2 granulomatous response directed against the eggs* and its this activation that leads to the fibrosis SNAILS are the source of infxn

DUMBBELLSS

These sx are d/t ACh excess!! i.e. organophosphate poisoning bc organophosphates inactivate acetylcholinesterases and thus no one is chomping the AChs and keeping them on check Diarrhea Urination Miosis Bronchospasms Bradycardia Excitation of skeletal muscle/CNS (bc ACh also works on SNS and NMJ) Lacrimation Salivation Sweating

What gets compressed in a subfalcine herniation?

cingulate gyrus herniates under falx cerebri --> *ACA*

this is a little bit of a longer one. its ok and its important so don't worry about the time <3 GOD HAS YOUR BACK what is the Train of Four stimulation and what will you see in non depol NMJ blockers vs depol blockers?

Train of four is used during anesthesia to assess degree of paralysis. it's when a *peripheral nerve is stimulated 4 times quickly* the muscular response is recorded (literally looks like 4 bars) and the height of each bar represent the strength of each twitch *HIGHER BARS* mean activation of INCREASING NUMBER of INDIVIDUAL muscle fibers (myocytes) Nondepol NMJ blockers (vecuronium) are *competitive inhibitors* of POST synaptic ACh and will result in a *fading* ToF bc of decreased stimulation of the post synaptic ACh receptors. lets say there are 100 receptors and the competitive inhibitors block 50. well the 1st time you release Ach w the 1st stimulation of ToF you'll release lets say 100 ACh molecules bc you have all your vesicle. that will attach 25 of the available ACh receptors quick succession doesn't let your body repackage ACh fast enough so the next time you can only release 70 ACh molecules so now youre only gonna be able to activate 18 of the available ACh receptors the next activation you only release 40 ACh and activate even less post synaptic ACh so you get a fading pattern DEPOL BLOCK: -i wasn't able to fully understand the mechanism... but there are 2 phases: -Phase 1 is constant but diminished compared to normal. all 4 bars are the same reduced size. -Phase 2 looks like the nondepol block and will be a fade pattern BOTTOM LINE: *Nondepol block* like vecuronium --> fade *Depol block* like succinylcholine --> Phase 1: constant diminished Phase 2 (about 30 mins later): fade

what's the diff b/w a type A and type B aortic dissection? where is the dissection in each?

Type A is any aortic dissection involving the ascending aorta Type B is any aortic dissection involving the descending aorta Type B aka descending dissections almost always originate close to the *left subclavian artery* type A aka ascending aorta dissections usually originate in the sinotubular jxn

what is the number one tube that can be injured during a hysterectomy?

URETER........ /.-

pts w benign prostatic hyperplasia are at increased risk for what?

UTIs!! also bladder hypertrophy, hydroureter, hydronephrosis, CKD d/t obstructive uropathy. but main one is *UTI* not bladder transitional cell carcinoma!! the main risk factors for BTC is smoking and occupational exposure to aromatic amine containing dyes! also no increased risk for prostatic adenocarcinoma either! don't get tricked!

what is D-xylose?

a monosaccharide that is absorbed directly into the intestine w/o the need for pancreatic enzymes it can be used to test for brush border absorptive fxn independent of pancreatic fxn

injury to ventromedial nucleus leads to what? injury to anterior nucleus leads to what? injury to lateral nucleus leads to what? what about supraoptic & paraventricular?

Ventro medial injury makes you *V*ery *M*assive Anterior nucleus = cool off (think A/C like anterior cooling) so injury would make you hot Lateral injury makes you *l*ean supraoptic & paraventricular connect to posterior pituitary & produce vasopressin aka ADH and oxytocin . injury here means no ADH or oxytocin

"diminished thymidine synthesis" "impaired globin chain synthesis" "impaired pyruvate decarboxylation" "low rate of intracellular transamination reactions" "reduced iron availability for hemoglobin synthesis"

Vitamin deficiencies: "diminished thymidine synthesis" --> folic acid def "impaired globin chain synthesis" --> thalassemias "impaired pyruvate decarboxylation" --> thiamine pyrophosphate def (derivative from B1 thiamine) "low rate of intracellular transamination reactions" --> B6 (pyridoxine) def "reduced iron availability for hemoglobin synthesis" --> iron def anemia

"recurrent heart palpitations that start and stop abruptly. abn conduction pathway in this pts heart that bypasses the AV node" what is dx?

Wolff-Parkinson-White (WPW) syndrome classically see: -repeated episode of palpitations (paroxysmal supraventricular tachycardia) -accessory condxn pathway. i.e. part of the activation will go down the side of the ventricle instead of all down the AV node --> early ventricular activation EKG findings that are diagnostic if all 3: *-EKG short PR interval bc increased ventricle activation faster since not slowing down thru AV node -delta wave (early upslope of QRS complex) -widened QRS complex*

What pts are classically at increased sick for giardia lamblia infxns? why?

XL agammaglobulineamia pts!!! bc the main mechanisms against Giardia involve *CD4+ T cells* AND *secretory IgA production!!* (prevent adhesion to upper small bowel mucosa) this would be a problem in the primary lymphoid follicles and germinal centers which is where B cells mature

what is the significance of zinc fingers and how could this come up on step?

Zinc fingers are the most commonly identified DNA binding domain. many *transcription factors* use zinc finger motifs. in terms of hormones, only *intracellular receptors* can act as *transcription factors* so the way the way they asked this was telling you there was a zinc finger and asking what hormone was most closely related well it would be any of the PET CAT on TV ones: -Progesterone -Estrogen -Testosterone -Cortisol -Aldosterone -T3/T4 (thyroid hormone) -Vitamin D

explain the pathophys behind a fib in someone w severe aortic stenosis and how it specifically leads to pulm edema and acute HF

a fib = atria stop working. in pts w severe aortic stenosis that means their left ventricle has to fight against high afterload pressure --> concentric hypertrophy --> less space for EDV the left ventricle becomes *dependent on atrial kick aka atrial contraction* to fill it up. in a fib you lose the atria so you'll get a *SUDDEN DECREASE IN LEFT VENTRICULAR PRELOAD* and this is why you're gonna see severe hypotension, pulmonary edema, and just acute HF all around

what arrythmia is triggered by rapid electrical impulses originating the pulmonary veins?

a fib!! weird i know :o

What HIV medication is contraindicated in pts w HLA-B*57:01 positive results? what hypersensitivity does it cause?

abacavir (think of a vaca w the #57:01 on it) which is a nucleoside reverse transcriptase inhibitor (NRTI) known as *abacavir hypersensitivity rxn* that develops in 2-8% of pts and is strongly associated w HLA-B*57:01. this is a *type 4 hypersensitivity* Bonus snack facts: -fever, malaise, GI sx, and delayed rash are classic sx of toxicity -discontinuation = rapid improvement -negative HLA-B*57:01 usually means 100% no way you'll have rxn -genetic testing usually done before giving med

Buzzword: 3 Hz spike wave pattern on electroencephalogram

absence seizures. can be part of juvenile absence epilepsy if present w *tonic clonic seizures* too which is tx'ed w valproate. not ethosuximide.

retinal hemorrhages in an infant baby should trigger suspicion for? when does rolling over usually happen?

abusive head trauma aka shaken baby syndrome!! this is d/t rupture of congested retinal veins. HIGHLY SUGGESTIVE OF AHT!! also *posterior rib fractures* is very alarming for trauma by the perpetrator's grasp on torso! rolling over is seen ~4 months NOT 1 month old!! BONUS: AHT from vigorous shaking will present w *subdural hemorrhage* d/t tearing of bridging veins from the shaking motion :/

activation of what cells causes psoriasis?

activation of T helper cells & proliferation of keratinocytes --> epidermal hyperplasia --> erythematous plaques & hyperkeratosis --> scaling

fever + tinnitus + tachypnea ... what possible drug OD? what findings would you see in the blood?

acute aspirin intoxication you would see anion gap metabolic acidosis bc aspirin is acidic but only after 12 hrs you would also see respiratory alkalosis FIRST bc salicylates directly stimulate the medullary respiratory center --> increased ventilation --> loss of CO2 so after 12 hrs you would see a pH thats slightly acidic but no < 7.35 bc it was basic at first and now its coming down if you were to do the formula to check for metabolic acidosis compensation it PaCO2 would be *lower than predicted* bc it had a primary respiratory alkalosis so it was wayy down

Buzzword: patchy, bilateral airspace opacification w blunting of costophrenic angles

acute decompensated heart failure CXR. it looks all white and filled in tbh

how does dengue fever present?

acute febrile illness w H/A, retro orbital pain, joint, and muscle pain and hx of going to torpical or subtropical regions like Brazil, Mexico, south east asia, Caribbean, americas)

Buzzword: liver bx w spotty hepatocyte necrosis plus recent travel to south america. dx? what sx would you expect?

acute hepatitis A infxn! hep A will present w "spotty necrosis" w ballooning degeneration (hepatocyte swelling w wispy/clear cytoplasm), councilman bodies (eosinophilic apoptotic hepatocytes), and mononuclear cell infiltrates (i.e. look like a ton of infiltrates) sx expected would be: fever, anorexia, dark colored urine (d/t increased conjugated bilirubin levels)

most common leukemia in children

acute lymphoblastic leukemia (ALL; think ALL children get ALL) Sx: lymphadenopathy + hepatosplenomegaly + bleeding + *bone pain*

What type of chest pain *decreases* when pts lean forward? what is this d/t?

acute pericarditis!! it decreases pressure on the parietal pericardium you'll commonly hear a *friction rub* in these pts as the most specific finding fibrinous peri carditis is d/t many things like MI, rheumatologic dz (like SLE), uremia, viral infxn

Buzzword: lung cancer most common in non smokers + peripheral lung involvement *recurrent*

adenocarcinoma. think: addy is a no smoker human :) Risk factors include gene mutations and smoking (altho remember this is still the most common cancer in non smokers) MARKER: MET, ALK, RET, KRAS, EGFR, ROS

pt w bluish pigmentation at gum tooth line and wrist drop or foot drop?

adult lead poisoning!

what are the limbs of the corneal response?

afferent is CN5.1 efferent is CN7!! (not 3!!) the corneal response is TEARING in response to touching eye. lacrimation is done by CN7!

Why can we see oxalate kidney stones in crohns pts?

again crohns is involved in the terminal ileum most commonly which is where bile acids are reabs. bile acids help fat reabs. impaired fat reabs means calcium will form *soap complexes* w the excess fat instead of binding to dietary oxalate like it should this leaves oxalate free to get abs by the gut mucosa. it makes it to the urine and promotes *oxolate kidney stones* aka enteric oxaluria

what is tetrahydrobiopterin and what is it used for? synthesis of 3 things

aka BH4!! remember the thing you always draw in the tyrosine pathway!! synthesis of: -tyrosine -dopamine (and thus NE, Epi bc w/o dopamine can't get NE or Epi) -serotonin this can be seen in phenylketonuria. usually PKU is d/t def of phenylalanine hydroxylase, but sometimes can also be d/t BH4 which is needed to go from phenylalanine --> tyrosine so you get a build up of phenylalanine

what is the specific viral component that allows them to infect humans vs animals etc? (i.e. tissue tropism)

antigenic glycoprotein affect tissue tropism the most!! these are things like hemagglutinin etc. this is how viruses get into cells! depending on which antigenic glycoproteins they have, they can bind or not bind to certain receptors in the human influenza virus hemagglutinin binds sialic acid receptors on human resp epithelial cells (other influenzas like avian/swin influenza they also code for hemagglutinin but don't have the proper antigens to bind to human cells!)

where does H pylori preferentially colinize?

antrum of stomach if they colonize in the gastric antrum --> duodenal ulcers if they colonize the gastric corpus --> gastric ulcers

"severe chest pain radiating to the back"

aortic dissection. commonly see intimal tear and medial degeneration aka "elastic tissue fragmentation and separation of the elastic and fibromuscular components of the tunica media by small cleft-like spaces"

ankylosing spondylitis has an increased risk of what heart murmur?

aortic regurg

what is the diff b/w aplastic crisis and aplastic anemia?

aplastic crisis is when you can't make RBCs aplastic anemia is when you can't make any bone marrow cells at all so you get pancytopenia

how can you tell if angioedema is d/t ACE inhibitor or hereditary C1 esterase inhibitor def?

apparently by age... hereditary C1 esterase inhibitor will show up during childhood or early adolescence if pt has hx of starting new ACE inhibitor and a couple months later presents w angioedema its D/T EXCESS BRADYKININ BUILD UP not d/t underlying hereditary C1 esterase inhibitor

it a pt has elevated arginine levels what is the deficiency and what pathway is involved?

arginase def urea cycle bc urea cycle takes arginine --> ornithine and urea via arginase "Ordinarily, careless Crappers Are Also Frivolous About Urination" Ornithine --Carbamoyl phosphate + ornithine transcarbamylase --> citrulline --- aspartate w arginosuccinate synthetase --> argininosuccinate --- argininosuccinase --> fumarate & arginine ---arginase--> urea & ornithine see pg 82 in FA

Digital clubbing is associated w what? What are some examples we can see digital clubbing (3 categories; 4, 5, 3)

associated w prolonged hypoxia (altho can be primary i.e. idiopathic too) LUNG STUFF: 1. *large cell* lung cancer 2. TB 3. CF 4. Suppurative (i.e. pus) lung dz's like empyema, bronchiectasis [purulent sputum, recurrent infxns], chronic lung abscesses HEART STUFF: the 5 T's of right to left shunts aka the cyanotic heart dz's 1. Truncus arteriosus (1 vessel) 2. Transposition (2 switched vessels) 3. Tricuspid atresia (3 = Tri) 4. Tetralogy of Fallot (4 = tetra) 5. TAPVR (5 letters in the name; total anomalous pulmonary venous connection) OTHER: IBD, hyperthyroidism, malabsorption

wide fixed splitting of S2?

atrial septal defect!!

what is primary biliary cholangitis?

autoimmune dz that destroys *small bile ducts in liver* can present w fat soluble vitamin def and pruritis d/t bile acid accumulation in skin visible jaundice usually doesn't appear until later in dz course

What should come to mind in a pt that has lung sx (SOB, wheezing, poor air movement) and elevated LFTs w a positive periodic acid-Schiff staining slide? what will their lungs look like?

autosomal *codominant* Alpha 1 antitrypsin (ATT) deficiency!! low alpha 1 antitrypsin (ATT) = excessive elastase activity breaking down elastin damage to liver AND lung LUNGS: panacinar emphysema aka "interalveolar septa distruction" since septa have large amounts of elastic LIVER: liver is responsible for creating this ATT. so you'll see *intrahepatocyte accumulation* of polymerized ATT molecules that never got released stain will show *hepatocytes* w reddish pink *intracellular granules* when using *periodic acid Schiff stain*

BRCA 1/2 mutations lead to increased risk of what 2 cancers?

breast and ovarian (mostly breast but still)

Buzzword: gram positive rods that form colonies resembling a "Medusa head" what is the virulence factor?

bacillus anthracis!! (viking ship w medusa looking head of ship) another clue is if they say he or she works in a *mail room* bc anthracis can be used for terorrism antiphagocytic D glutamate capsule!! this is a polypeptide not polysaccharide capsule! (viking w D's on his armor capsule) another clue is "mediastinum widening"!! (widened mediastinum looking pole on the viking ships). this is d/t hemorrhagic mediastinitis (bleeding axe)

why are downs pts at increased risk of developing early onset alzheimers?

bc amyloid precursor protein is on chromosome 21 in downs --> 3 copies of chr 21

why does oral glucose cause a greater peak in serum insulin compared to IV glucose? what hormones act like this?

bc gut mucosa produce *incretins* that stimulate pancreatic insulin secretion in response to sugar containing MEALS (i.e. thru mouth) this is independent of blood glucose levels bc it's associated w a meal. 2 hormones have *incretin like effects*: 1. GLP-1 (glucagon like peptide 1) 2. gastric inhibitory peptide aka GIP

young pt (26 yo no medical hx) w chest pain, palpitations, SOB, and sweating that 'feels like they're going to die' what is the next best step? EKG is normal

benzodiazepine administration!! apparently this is "classic" panic disorder. chest pain, tachycardia, SOB, sweating, tremulousness in a young otherwise healthy pt w a normal EKG are consistent w panic disorder. benzos are the DOC for emergency *rapid relief* of sx SSRIs and SNRIs are DOC for long term tx but if they present to ER, give them benzos i confused it for pheo but according to explanation pheo has episodic headaches and a higher HTN (this pt has 140/90 which is high but not that high)

what drug is a short term anxiolytic + muscle relaxant + anticonvulsant?

benzos! i.e. increased frequency of chloride channel opening Benzos are short term usually when pts are gonna start CBT to get immediate relief but short term bc of dependence risk Benzos are usually prescribed for 2 things: 1. short term use in anxiety disorders 2. alcohol withdrawal syndrome

what enzyme causes formation of 2,3 BPG in erythrocytes

bisphosphoglycerate mutase steals one of the glycolysis intermediates as its about to create ATP and uses that enzyme to create 2,3 BPG instead. this is important to we can lower the O2 affinity of hemoglobin w/i RBCs so they can unload, but it causes no prodxn of ATP to happen since RBCs don't have mitochondria so can't make it via TCA or oxidative phosphorylation.

What to ACE Inhibitors do to the following levels: Renin AT1 AT2 Aldosterone Bradykinin

block AT2 prodxn lowers Aldost increases bradykinin (weather they have the cough or not!!) loss of AT2 causes problems in the feedback mechanisms s actually *raises renin & AT2*

why can we sometimes see parasthesias in pts that have lost lots of blood and thus have gotten lots of blood transfusion at once?

blood transfusions have citrate added to them. if pts receive more than 5-6 liters of whole blood transfusions or packed RBCs in < 24 hrs they can have high levels of plasma citrate (anticoagulant) --> citrate chelates Ca2+ & Mg2+ thus reducing those levels in blood result? *parasthesias* or tingling sensation in toes/fingers d/t hypocalcemia

Buzzword: small bluish lesion under the nail *recurrent*

bluish neoplasm underneath nail bed can be 1 of 2 things: 1. glomus tumor 2. subungual melanoma a glomus tumor is a tumor of modified SM cells called "glomus bodies" which are involved in *thermoregulatory fxns*. these are found in the dermis of nail bed, pads of fingers & toes, ears shunts blood away from the skin surface in cold temps in order to prevent heat loss and directs blood to the skin in hot environments to facilitate dissipation of heat

DiGeorge vs velocardiofacial syndrome?

both are microdeletions of chromosome 22q11.2 DiGeorge is thymus + cardiac + hypocalcemia) Velocardiofacial is facial abn + cardiac + cleft palate Facial abn can include: *orbital hypertelorism* (wide set eyes), short palpebral fissures (kinda like downs), short philtrum (kinda like alcohol syndrome no?), cleft palate, bifid uvula

what part of the kidney does ADH act on?

both medullary and cortical, but the medullary segment is of particular important to create the *maximally concentrated urine* bc this is the area w the highest osmolarity so if you increase H2O reabs here you have a really good strong gradient to pull out lots of H2O (its as concentrated as the loop of henle at the bottom!) the cortex on the otherhand is closer to 300 instead of 1200 osmolality so if you pull water there you don't have as good of a gradient

Buzzword: schiller duval bodies on ovarian tumor

endodermal sinus high AFP. aggressive

"late diastolic collapse of the right atrium" what is it and what is the classic triad. what is another classic finding seen w it? why does it happen?

cardiac tamponade. classic sx aka Beck triad: hypotension + elevated JVP + muffled heart sounds *pulsus paradoxus* and thus *narrowing of pulse pressure during inspiration* is an important physical finding. remember this is *exaggerated drop in SBP* during inspiration. > 10 mmHg. during inspiration you get more pre load into the right atrium and right ventricle. bc there is cardiac tamponade its restricting the ability of rt ventricle to expand --> has to accommodate the increased preload somehow so it pushes on septum toward left ventricle. left ventricle EDV and stroke volume decreases --> decreased systolic pulse pressure during inspiration

"saddle anesthesia"?

cauda equina syndrome!! emergency!!

what is the striatum?

caudate + putamen this has low metabolic activity on PET scans in pts w huntingtons bc of decreased ACh in caudate nucleus

what does a drop in PaCO2 do to our brain vessels?

causes vasoconstriction!! --> decreased ICP & cerebral blood volume high CO2 levels = vasodilation bc your body thinks we're in trouble and brain uses ~20% of ALL your body's oxygen --> high CO2 means low O2

how are celiacs and PTH related?

celiac dz pts have malabsorption fo dietary fats and fat soluble vitamins ADEK this results in *vitamin D deficiency* w/o vitamin D --> intestinal abs of calcium and phosphorus *decreases* which in turn STIMULATES PTH... vitamin D also directly inhibits PTH release so deficiency would cause a significant rise bc you stop the inhibition AND you activate release this would lead to *low serum Ca2+ low serum PO4- and high serum PTH*. apparently not high Ca2+ bc in pts w celiacs its a chronic thing so their PTH has been high for a while and this leads to depleted bone stores. esp if the pt is complaining of diffuse bone pain/generalized weakness. that's a clue you've probably depleted your bones

Buzzword: acute and painless monocular vision loss w a cherry red macula

central retinal artery occlusion!! vision loss includes the entire visual field and is often permanent :( central retinal artery comes from ophthalmic artery which comes from internal artery. athero and thromboembolism (in the setting of a fib for example) are common causes of central retinal artery occlusions

What is ataxia telangiectasia?

cerebellar ataxia + telangiectasias ("distended capillaries on sun exposed areas of the skin") + recurrent pulmonary infxns (d/t IgA def) this is AR d/t mutation in ATM gene (ataxia telangiectasia mutated) this gene is responsible for DNA break repair

what getes compressed in tonsillar herniation?

cerebellar tonsils displace thru foramen magnum & compress medulla --> breathing problems

Buzzword: pearly mass behind tympanic membrane. pt has conductive hearing loss. dx?

cholesteatoma aka squamous cell debris collection d/t overgrowth of desquamated keratin debris don't get confused by the name. it doesn't contain any cholesterol or lipid component

Yes, fibrates upregulate lipoprotein lipase (LPL) but they also inhibit what? what is the result?

cholesterol 7 alpha hydroxylase! which is the rate limiting step in the synthesis of bile acids --> leads to *gallstone formation* (pile of rocks where seagulls are sitting in gemfibrozil jelly fish sketch)

Buzzword: bluish black gelatinous material behind tympanic membrane?

cholesterol granulomas. these can form in the middle ear after hemorrhage

What is the most common eye manifestation of CMV in utero?

chorioretinitis! usually you associate this w toxo and there's no sketchy symbol for it but just something you gotta know :/ (sketchy's symbol is the pie w retinitis in AIDS pt w cane)

pt w lung transplant 8 months ago now presents w lowered FEV1 and normal forced vital capacity. she has non productive cough and worsening SOB w exertion. she hasn't missed any doses of her transplant rx. dx?

chronic transplant rejection!! this is by far the most common complication in pts w lung transplants ~5 yrs after transplant! you'll see drop in FEV1: FVC ratio d/t drop in FEV1 you'll also see *bronchiolitis obliterans* bc chronic rejection affects the small bronchioli BONUS: -on histo: lymphocytic inflammation --> fibrosis --> destruction of bronchioles -to be considered acute rejection its usually w/i 6 months (usually no sx & only seen on surveillance bx. will see perivascular & interstitial mononuclear cell infiltrates)

What is an imperforate hymen?

d/t incomplete degeneration of the central portion of the fibrous tissue band connecting the walls of the vagina. vaginal secretions stimulated by the mother's estrogen can cause accumulation of mucus in the vaginal canal (mucocolpos) which can manifest as a *bulging introitus* it's usually reabs and the child will be asx until menarch. classic sx: primary amenorrhea cyclic abdominal or pelvic pain d/t accumulation of menstrual blood in the vagina & uterus (hematocolpos) secondary sexual development is NORMAL might see a bulge coming out of the vagina commonly "palpated anterior to the rectum"

what is the MOA behind heparin induced thrombocytopenia (HIT)?

d/t to *antibodies* against heparin and platelet factor 4 --> *thrombosis rather than bleeding* (hunter shooting platelets & beaver making his fibrin clot dam around the broken plates)

what does a prolactinoma do to estrogen levels?

decreases them! thats why you see olig/amenorrhea you can also see the usual menopause sx like decreased bone density, vaginal atrophy etc this is bc excess prolactin suppresses GnRH secretion and thus leads to reduced LH and FSH

what is the problem in Chediak Higashi syndrome? defect in ________?

defect in *neutrophil phagosome lysosome fusion* neutrophils can absorb the bad guys, but can't make lysosome to kill it so neutrophils will have giant cytoplasmic granules. also triad of albinism + nystamus + recurrent skin & resp infxns

what is the foramen cecum?

depression on the tongue that represent the embryological remnant of the superior end of the obliterated thyroglossal duct

Buzzword: anti Jo 1

dermatomyosisits. auto immune dz characterized by inflammatory myopathy (proximal muscle weakness; trouble climbing stairs.. combing hair) and cutaneous manifestations like *heliotrope rash* rash around the eyes esp upper eyelids) and *gattron papules* (flat topped papules over joints and bony prominences in hands) BONUS: -commonly associated w adenocarcinoma and can be a clue of underlying occult malignancy esp if develop this after age 50

What is the "Ghon complex'?

describes the *2 initial sites* aka injuries caused by primary tb... lower lobe of lung usually + ipsilateral hilar lymph node when these sites become calcified and fibrosed they can be visualized on gross pathology & radiographic imaging as the *ranke complex*

what is the tx for a pt w von willebrand dz? why? what is the fxn of vWF or how does it enhance clotting? (2)

desmopressin!! it increases release of vWF from Weibel palade bodies of endothelial cells enhances bc: 1. augments platelet binding 2. augments stabilization of factor 8 which is used to activate factor 10 which is the main meat of the coag cascade

what causes aortic aneurysms in syphilis?

destruction of vasa vasorum by bacteria (sketch w aorta looking tree w destroyed roots representing the vasa vasorum) --> inflammation, ischemia, & weakening of adventitia --> vessel wall prone to aneurysm commonly see w mediastinal widening if it dilates the aortic valve ring leading to aortic regurg

What is an ANOVA aka analysis of variance test used for?

detect differences b/w the MEANS of 2 or more groups if its just two groups --> two sample t test. but if its more we have to do anova. if its *categorical* variables like yes or no. high or low then its a chi square test.

what is the MOA behind tetralogy of fallot?

deviation of the infundibular septum d/t abn NCC migration during embryo dev --> PROV Pulm infundibular stenosis Right ventricular hypertrophy --> boot camp heart on CXR Overriding aorta VSD tet spells are d/t the pulmonary stenosis (pulm infundibular stenosis) bc it will cause the VSD to switch from left to right --> right to left d/t increased pressure in RV. squatting increases SVR aka afterload to switches back to L to R shunt

What's one cause of hyperosmotic volume depletion? give other 2 causes

diabetes insipidus. this is when your body is throwing away all the *water* d/t vasopressin decrease. it's a water wasting situation where you lose water only. all your ions are still the same so you would have hyperosmolality, but low intracellular and extracellular fluid. other causes: -profuse sweating d/t hypotonic nature of sweat -decreased fluid intake i.e. dehydration

Phrenic nerve carries pain fibers from what areas in the lung?

diaphragmatic and mediastinal pleura (remember visceral pleura has no pain fibers) inspiration makes it worse

"pulse w 2 distinct peaks"

dicrotic pulse. one during systole the other during diastole. usually seen in pts w severe systolic dysfxn and high systemic arterial resistance

Guillain Barre is d/t cross reacting of AB (i.e. molecular mimicry) but where do these ABs attack? i.e. what's the pathology?

endoneurial inflammation --> segmental demyelination & axon damage

"glomerular capillary wall thickening w no increase in cellularity" in a pt that has nephrotic sx when stained w methenamine silver, "irregular spikes protruding from glomerular BM are seen"

diffuse thickening WITHOUT increased cellularity is also buzzword those irregular spikes are code for "spike and dome" appearance when stained w a silver stain which is a buzzword for *membranous nephropathy* this is d/t *immune complex deposition* in subepithelial portion of glomerular capillary wall this is the most common cause of nephrotic syndrome in adults. commonly d/t SLE (altho SLE also has a nephritis syndrome called diffuse proliferative glomerulonephritis and it's buzzword is "wire looping" of capillaries on LM think SLE wire lupus; causes proliferation of lymphocytes and endothelial cells w/i capillary loops so it DOES have cellularity) another one that has "diffuse thickening" and is nephrotic is membranoproliferative glomerulonephritis. but a good clue or how to tell them apart is that this one (like the name suggests) DOES have proliferation of cells. often associated w hep B or C

when do we see a large gradient b/w alveolar and capillary PO2?

diffusion limited dz's like emphysema or pulm fibrosis! "capillary PO2" is also called "pulmonary venous PO2"

AD mutation in TTN gene resulting in truncated titin is diagnostic of what?

dilated cardiomyopathy!! not hypertrophic cardiomyopathy!! AD HOCM commonly has mutations involving beta myosin heavy chain or myosin binding protein C

what causes the delayed onset of long acting insulins?

dimer and hexamer formation. these take time to dissociate after injection and thus have delayed abs

young female sexually active has joint pain. knee joint yield 20 mL of cloud fluid w a leukocyte count of neutrophils. likely pathogen?

disseminated N gonorrhoaea! this pt had no vaginal sx but had a "vesciopapular rash" that increases suspicion even tho staph aureus is the most common cause of septic arthritis, in YOUNG sexually active pts N gonorrhoae should be the one you choose

Yes you can get campy infxns from undercooked poultry, but what other unique contact can cause it?

domesticated animals like dogs!!! :o particularly puppies from kennels

kid w palpable purpura over his buttocks & thighs dx and pathophys?

dx is Henoch Scholein purpura aka IgA vasculitis pathophys: *deposition of IgA immune COMPLEXES* !! i.e. type 3 hypersensitivity

if researchers are tryna study multi country studies and are using data from 14 countries what type of study is this?

ecological study. automatically. bc ecological studies are studies of *populations* not individuals!!

pt w recent wrist drop w high eosinophil count. also hx of asthma. serum AB against neutrophil myeloperoxidase. dx?

eosinophilic granulomatosis w polyangiitis aka churg strauss. small to medium vessel vasculitis clues here are *late onset asthma* like if it was dx in college asymmetric neuropathy (wrist drop in this case but can also be foot drop; this is called mononeuritis multiplex) eosinophils and *neutrophil myeloperoxidase* aka pANCA

Buzzword: perivascular pseudorosettes. brain tumor in child.

ependymoma. very rare. lines ventricle and commonly occupies the 4th ventricle --> hydrocephalus obstructing flow of CSF

Calcineurin is responsible for what? what drugs can inhibit it?

essential protein that activates IL2 to activate T cells. immunosuppressants like cyclosporine and tacrolimus work by inhibiting calcineurin activation

Yes alpha agonists cause vasoconstriction leading to increased BP and reactive bradycardia but what does that do for conduction velocity of the heart?

examiners can say "decreased atrioventricular node conduction velocity"!!! bc the baroreceptors in the carotid sinus and aortic arches will cause a reflexive increase in vagal influence which will result in inhibition of pacemaker activity of the SA node!!

hemolytic anemia increases risk for what type of gallstones? why?

excessive hemolysis = excess unconjugated bilirubin increased risk of pigmented gallstones d/t increased calcium bilirubinate

What is the first step when a ligand binds to a Gq protein?

exchange of GDP for GTP on the alpha subunit this activated alpha subunit undergoes conformational change and exposes *phospholipase C* and you know the rest from there :) PLC will cause PIP2 --> DAG & IP3 DAG --> protein kinase C IP3 --> Ca2+ Ca2+ will activate protein kinase C the most even tho DAG directly activates it too, Ca2+ is the one for major effect activated protein kinase C will phosphorylate proteins and cause stuff to happen like *SM contraction*

what branch is particularly at risk during a thyroidectomy involving the superior pole? what muscle does it innervate?

external branch of superior laryngeal nerve bc it's very close to the *superior thyroid artery and vein* which need to be ligated during surgery when working on the superior pole of thyroid innervates *cricothyroid muscle* (internal branch of laryngeal does supraglottic sensation and is not commonly injured) the left recurrent laryngeal does all other muscles (posterior cricoarytenoid, lateral cricoarytenoid, oblique arytenoid, transverse arytenoid, thyroarytenoid). injured when working on removal of the *inferior pole of the thyroid*

pt w facial weakness/drop that spares the forehead muscles. what does that mean?

facial weakness is d/t CENTRAL lesion affecting UMN such as the corticobulbar tract... not direct damage of CN7

What is the deficiency in XLR hemophilia A?

factor 7 def!! will see normal bleeding time, normal PT, and prolonged PTT (bc factor 7 is extrinsic pathway!)

failure of vitamin K to fix prothrombin time indicates what?

factor 7 deficiency

what defect leads to bicornuate uterus?

failure of *lateral fusion* of the paramesonephric ducts

At what stages is oogenesis arrested?

from belly (primary oocytes completely developed by 5th month of gestation!) until before puberty @ prophase 1 from puberty until fertilization @ metaphase 2

in ppl that are well fed, what is inhibiting fatty acid synthesis?

fatty acid synthesis can't happen w/o the carnitine shuttle when we're in a well fed state there's no need to cause fatty acid breakdown. that would lead to ketones used for energy. so in a well fed state we have the *citrate shuttle* which makes fatty acids to store them. rate limiting step here is *acetyl CoA carboxylase* which converts acetyl CoA to malonyl CoA the end product is *malonyl CoA* and it's the excess malonyl CoA that will INHIBIT carnitine acyltransferase necessary to start the carnitine shuttle

what is the genetic problem in lynch syndrome?

faulty DNA mismatch repair genes --> nucleotide mismatches that escape repair

what is rifaximin?

fisherman removing fish. its a poorly abs abx that removes NH3 producing bacteria!! this was a question on Uworld and God was mighty and helped you answer correctly but you didnt recognize the drug at all... rifaximin is used in tx of hepatic encephalopathy bc it's a nonabsorbable antibiotic that alters GI flora to decrease intestinal prodxn and abs of ammonia. usually added to *lactulose* which is catabolized by intestinal bacterial flora to short chain fatty acids --> lowers colonic pH --> increases conversion of ammonia to ammonium which can be peed out Lactulose: increases conversion of ammonia to ammonium Rifaximin: decreases intraluminal ammonia prodxn

what is another name for transverse carpal ligament? what muscle tendons are found in the carpal tunnel?

flexor retinaculum! this is what gets cut to tx median nerve MUSCLES: 1. flexor digitorum profundus 2. flexor digitorum superficialis 3. flexor pollicis longus

where does the thyroid gland arise from embryologically?

floor of foregut!! it gives rise to thyroid diverticulum which migrates caudally to neck --> thyroid :)

what is the first line tx for bulimia nervosa?

fluoxetine (girl at the office throwing up)

What nerve is in charge of foot eversion? what about dorsiflexion? what if both are affected?

foot eversion is by superficial fibular (peroneal) dorsiflexion is by deep fibular if both are injured in a pt then the injury is of the *common peroneal*

Buzzword: auer rods

found in acute myeloid leukemias!! commonly described as "myeloid cells w azurophilic rodlike granules"

Falling on outstretched hand causes fracture of what and dislocation of what in the hands? how can you detect each on Xray?

fracture of scaphoid and dislocation of lunate bone XRAY: both touch the radius (the big based bone that touches the wrist) -scaphoid is the most lateral touching the big base bone i.e. radius) -lunate is the 2nd (most medial) bone touching the radius

what monosaccharide is metabolized the fastest by the liver?

fructose! bc it can get metabolized into fructose 1 phosphate --> glyceraldehyde --> glyceraldehyde 3 phosphate and continue glycolysis bypassing phosphofructokinase which is a rate limiting enzyme stuff like galactose gets modified to enter at the 2nd step of glycolysis (glucose 6 phosphate step) mannose getes modified to enter at the 3rd step of glycolysis (fructose 6 phosphate) these are UPSTREAM from the rate limiting step that involves PFK so they still have to go thru the RLS

What enzyme is absent in pts w classic galactosemia? How does it present and what do you avoid?

galactose 1 phopshate uridyltransferase. presents in *neonates* w jaundice, vomiting, poor feeding, lethargy, hypoglycemia, and *galactose 1 phosphate accumulation* avoid galactose and lactose

if a breastfed newborn or very young like 5 day old pt comes to your office d/t inability to feed and presents w jaundice, lethargy, sunken fontanelle, hepatomegaly, hx of negative rods in urine, what should you be thinking?

galactose problems. lactose in milk gets broken to galactose & glucose from there galactose needs to get processed and there are 2 main galactose metabolism problems: 1. *galactose 1 phosphate uridyl transferase* think: long name, long list of sx. this is the really bad one. this is the one w jaundice, vomiting, hepatomegaly, renal dysfxn (AA in urine, metabolic acidosis), E coli sepsis, cataracts, hemolytic anemia. the list goes on. this is the bad one. 2. galactokinase def. cataracts & rarely pseudotumor cerebri lets continue the story: once upon a time there was milk in the breast which is mostly made of *lactose* from there it says goodbye to its best friend and they break up. glucose goes away and *galactose* must continue on. galactose is faced w 2 options. it can turn into *galactitol* or it can push further and pursue phosphate school. it can add phosphate to itself by meeting w the all mighty *galactokinase [GALK]* and become *Galactose 1 phosphate*. galactose 1 P misses glucose tho and can't stop thinking about her so she becomes *glucose 1 phosphate* w the help of *galactose 1 phosphate uridyl transferase [GALT]* glucose 1 phosphate can finally become Glucose 6 phosphate after 5 long hard years of med school + a path year and is now ready to enter the glycolysis cycle

What is the pathophys behind gallbladder outflow obstrxn causing cholecystitis

gallstone obstructing the cystic duct leads to *hydrolysis* of luminal lecithins to lysolecithins which disrupt the mucosal layer. luminal epithelium gets exposed to detergent action of the bile salts --> irritation and prostaglandin release increasing distension and internal pressure w/i GB --> ischemia. bacteria (E coli, enterococcus, klebsiella, etc) --> invade the injured and necrotic gallbladder wall --> infxn also gallbladder hypomotility d/t inflammation of mucosa. but the first step is *gallstone obstruction of outflow*

what artery found on the posterior wall of the duodenal bulb?

gastroduodenal this is commonly ruptured/eroded by posterior duodenal ulcers --> severe upper GI hemorrhage (anterior duodenal ulcers are more likely to perforate but not associated w major blood vessel)

alpha fetoprotein can be used to track what tumor? what about hCG? what about CA 125? CA 19-9?

germ cell (duh) but also!! hepatocellular carcinoma!! :o this is normally elevated in pts w chornic viral dz but a dramatic elevation or sudden rise --> HCC ____________________________ hCG can monitor *choriocarcinoma* and *germ cell* _____________________________ CA 125 --> ovarian _____________________________ CA 19-9 --> pancreatic

how does the CNS respond to irreversible neuronal damage? basophilic nuclei show up, neurons shrink, and there's intensely eosinophilic cytoplasm but what else happens?

glial cell hyperplasia. this is called gliosis. *astrocytes* will proliferate at site of injury to restore tissue integrity (similar to how fibroblasts do that outside the CNS) they replace lost neurons and compensate for their volume overtime form a closely connected firm meshwork called a *gliotic scar*

what is the DOC for beta blocker OD?

glucagon!! this is bc glucagon acts via the cAMP pathway and increases cAMP in the cardiac myocytes. increase cAMP = increased Ca2+ = increased muscle contraction major ADR of beta block is the super depression in myocardial contractility, bradycardia, and varying degrees of AV block!!

What other deficiency presents similarly to G6PD deficiency w bite cells?

glutathione reductase deficiency. it will cause build up of oxidized glutathione which is damaging to RBCs bc RBCs are susceptible to oxidative damage

What is McArdle dz?

glycogen storage dz type 5. this is d/t def in *myophosphorylase* an isoenzyme of *glycogen phosphorylase* which breaks down glycogen during EXERCISE These pts will present w *exercise intolerance* plus muscle cramps and rhabdomyolysis THINK: M dz painful Muscle cramps Myoglobinuria (red urine) w strenuous exercise Myophosphorylase is missing McArdle = Muscle

Action card: draw the JVP wave and explain what the a wave, c wave, x descent, v wave, and y descent are

google or pg 282 in FA a wave: highest peak. *a*trial contraction. this is *missing in a fib* !! c wave: RV *c*ontraction (closed tricuspid valve bulging into atrium) x descent: downward displacement of closed tricuspid valve during rapid ventricular ejection phase. aka right atrial relaxation. reduced or absent in tricuspid regurg and right HF bc pressure gradients are reduced v wave: "*v*"illing of right atrium against closed tricuspid *v*alve you'll see an increase in right atrial pressure (i.e. line curves up) y descent: RA empt*y*ing into RV. prominent in constrictive pericarditis and absent in cardiac tamponade

Buzzword: phosphoribosyl pyrophosphate synthetase def

gout!! this is bc PRPP (which PRPP synthetase makes) is responsible for the purine salvage pathway preventing full breakdown of purines if you can't stop breakdown of purines you lose them as uric acid --> excess uric acid = gout

Buzzword: coffee bean nuclei or call exner bodies on ovarian mass histo

granulosa cell tumor. high inhibin

You'll learn more about these w pathoma hopefully but what cancer is related to a "dry tap"?

hairy cell leukemia. an indolent B cell neoplasm (usually in middle aged men) that infiltrates the bone marrow & reticuloendothelial system. dry tap is b/w it infiltrates the bone marrow --> fibrosis and bone marrow failure --> pancytopenia classically this leukemia is described as "lymphocytes w cytoplasmic projections" bc they legit look like hairy cells lol

what do cystine stones look like under the microscope?

haxagonal!! think: "*SIX*tine stones have SIX sides commonly seen in defects where there is loss of cystine reabs fxn @ PCT that defect also results in poor reabs of COLA: *C*ystine *O*rnithine *L*ysine *A*rginine aka the *dibasic* amino acids thus you would see AMINOACIDURIA in these pts. sneaky way to ask it.

How are the 5 hepatitis viruses transmitted?

hep a: fecal oral (shellfish, travelers, day care) hep B (blood, baby making i.e. sexual contact, and birthing i.e. mom to child) hep C: blood like blood transfusion or IV drug use hep D: parenteral, sexual, perinatal Hep E: fecal oral, esp waterborne water sanitation would thus be helpful for reducing incidence of hep A or Hep B but not Hep B, C, or D. also remember you can't have hep D w/o B so if we can vaccinate against B and C we would be good :)

Buzzword: developed aversion to smoking

hepatitis A infxn!!

Buzzword: fever + fatigue + joint pain + urticarial skin rash w elevated liver enzymes

hepatitis B this is the CLASSIC triad!! called *serum sickness-like syndrome* esp increased suspicion if hx of multiple sex partners! compare that to hep C which is usually *asymptomatic* altho has the most risk of turning into chronic hepatitis! also this one is *almost exclusively* d/t IV drug use not much sexual transmission

moldy grains that cause mutations in gene p53 increase risk for what cancer?

hepatocellular carcinoma!! "moldy grains" = aspergillus flavur and aspergillus parasiticus producing *aflatoxins* which are STRONGLY associated hepatocellular carcinoma (crab [cancer] shaped spot on van next to cow w liver stain) esp in areas w/i asia and africa where aflatoxin B1 exposure is high

hepatocyte apoptosis vs necrosis on histology?

hepatocyte apoptosis --> cellular shrinkage and eosinophilia Hepatocyte necrosis --> cellular swelling and cytoplasmic emptying (ballooning degeneration) acute viral Hepatitis (low grade fever, nausea, dark colored urine, RUQ ab tenderness) causes hepatocyte necrosis AND apoptosis w mononuclear infiltration

mutations in MLH1 and MLH2 cause what?

hereditary non polyposis colorectal cancer aka Lynch syndrome... this is the *microsatellite instability* pathway... not the usual AK-53 pathway

BMPR2 mutation

hereditary primary pulmonary HTN (commonly affects 20-40 y/o females) no left heart failure or hypertrophy present

what RBC disorder requires splenectomy as the tx?

hereditary spherocytosis bc the RBCs work fine, they're just shaped funny so the spleen continues to knock them out when it shouldn't if you remove spleen they'll be just fine (just have howell jolly bodies i.e. fragments of nuclear material) since no spleen to remove the nucleus anymore

buzzword: defect in spectrin or ankyrin

hereditary spherocytosis! this is a hemolytic anemia d/t scaffolding protein defect which leads to cells not being "right" so the spleen doesn't recognize them and kills them. not autoimmune or anything. increased risk of pigmented gallstones d/t excess bilirubin from so much heme breakdown precipitating w calcium --> calcium bilirubinate BONUS: will see *increased mean corpuscular hemoglobin concentration* bc the spleen keeps removing some of the membrane to try and edit the defective RBC so the hemoglobin becomes more and more concentrated w/i the RBC

what virus has an envelope and is ds linear DNA? (3)

hermes on the road w 2 yellow straight lines (ds linear) and outside w the blue cool sky (DNA). he has a white robe on (envelope) herpesviridae family so like HSV1 and 2, epstein barr virus, cytomegalovirus and others but know those for now

what happens to pH, H+ secretion, and HCO3- at high altitudes over days?

high altitude = no oxygen so hyperventilation --> *respiratory alkalosis* meaning *high pH* kidneys overtime compensate so *lower HCO3- reabs* to try and create more acidic environment what you didn't know is that H+ *secretion* decreases. This makes sense since the goal is to create acidic environment but you just didn't directly know that :) if it's been several *weeks* the kidneys will also respond by increased EPO which increases RBCs to help abs more oxygen also if its been weeks --> *increased 2,3 BPG prodxn* which will make RBCs more willing to release O2 to tissues we can give carbonic anhydrase inhibitors to speed up the decrease in HCO3- reabs by kidneys and help sx (H/A, fatigue, lightheadedness)

What should "high pitched bowel sounds" make you think of? what about if they told you they also removed a cholesterol mass that was obstructing the ileocecal valve? what classic finding would you see on xray?

high pitched bowel sounds = small bowel obstruction this pt would be suffering from *gallstone ileus* which is d/t huge gallstones eroding the gallbladder wall and lodging into the ileocecal valve. you would see air in the biliary tree bc of retrograde passage of intestinal gas thru the fistula that was made

Buzzword: mutation in BMPR2

inactivating mutation commonly seen in pts w *primary pulmonary HTN* classic pt is young adult female leads to *proliferation of SM* think: BMPR2 --> Big smooth Muscle PRoliferation 2

What virus is enveloped and has partially double stranded circular DNA w an RNA-dependent DNA polymerase?

hippie sketch. hippie wearing white robe (enveloped), in a partial double stranded circle of hippies (double stranded circular DNA), w blue/green cool colors (DNA). another hippie w "reverso transcripto" book bc this virus has RNA dep DNA polymerase which can make DNA from RNA. hepatitis B the partial dsDNA comes into nucleus, gets fully finished as complete dsDNA. this can then serve as template to create viral mRNAs one of the mRNAs along w the reverse transcriptase gets encapsulated and can then re-make partial dsDNA to infect more cells. the "mature" capsids will have the partial circular dsDNA + reverse transcriptase. we can thus say *replication* happens w/i newly synthesized capsids w the help of reverse transcriptase

what is a consequence of having high homocysteine levels?

homocysteine is PRO THROMBOTIC (literally saw that in like 3 questions today so just know it!) if you have vit 12 or folate def or vit 6 def (bc need B6 to convert into cystathione to convert into cysteine) you'll have build up of homocysteine predisposing to thromboemoblic events

what hormone is responsible for insulin resistance in pregnancy 2nd and 3rd trimesters? what else does this hormone do? (3 things total)

human placental lactogen (hPL). comes from *syncytiotorphoblast* this is necessary to: 1. increase glucose levels in maternal circulation so fetus can get enough energy 2. hPL also increases lipolysis which results in free FA and ketons which provide energy for the MOTHER leaving the glucose and AA from protein breakdown to baby 3. increases insulin prodxn from beta cells in pancreas. this is why normally mothers DON'T get gestational DM. gestational DM happens when pancreatic fxn is NOT sufficient to overcome pregnancy related increase in insulin resistance

what is the most important host factor in preventing influenza infxn in pts that are mostly uninfected (i.e. 70% of pts are uninfected)?

humoral response antibodies against *hemagglutinin* bc this is what allows for viral entry into our bodies we wouldn't choose against neuraminidase bc antibodies against that would *prevent exit* of virus but if majority of pts don't even have the virus that would offer as much immunity

Strongest risk factor for completed suicide in psych pts?

hx of suicide attempt!! (not access to firearms)

What is the pathophys behind lung rejection in hyperacute, acute, and chronic settings?

hyperacute: preformed host antibodies to donor ABO or HLA --> "white graft" reaction d/t fibrinoid necrosis w hemorrhage & ischemia acute: cell mediated response to mismatched donor HLA --> small lung vessel & submucosal infiltrates in alveolar walls chronic: chronic, low-grade, cell mediated response to HLA *antigens* --> *bronchiolitis obliterans* aka small airway inflammation

what labs might be elevated in a pt w renal cell carcinoma?

hypercalcemia and erythrocytosis d/t paraneoplastic syndromes which are common in RCC. secretion of Parathyroid hormone related peptide --> hyper Ca2+ excessive erythropoietin prodxn --> erythrocytosis classic sx are hematuria (painless), ab mass, flank pain if late, weight loss

what is the genetic cause behind fragile x syndrome? yes its trinucleotide repeats but what happens genetically

hypermethylation bc of so many repeats your body tries to shut it up so it hypermethylates it and *inactivates* FMR1 preventing transcription & prodxn of fragile X mental retardation protein (FMR1 gene) --> impaired neural development

Ehlers danlos is d/t defect in what? sx?

hypermobile joints, overelastic skin d/t to COLLAGEN SYNTHESIS defect!! not elastin defect!! if elastin were defective you wouldn't be able to stretch skin jen lol

non fusion of urethral folds in boys leads to?

hypospadias!! this is an abn opening of the urethra in the inferior (ventral) part of the penis proximal to the distal tip of glans penis

Can you have von willibrand dz if the platelets are low?

i mean technically yes, but if platelet count is low it's likely not von willibrand dz bc von willibrand doesn't affect platelet number, you have normal platelets just can't bind them to cause platelet aggregation also PTT will be increased since vWF stabilizes factor 8 (part of intrinsic pathway)

What causes K+ to shift out of the cell?

i.e. what causes hyperkalemia? "Hyperkalemia? DO LAbSS" Digitalis (blocks Na/K) leading to lots of K+ outside cells hyperOsmolarity Lysis of cells Acidosis (like DKA!!) beta blockers high blood Sugar (insulin def) Succinylcholine (increase risk in burns/muscle trauma)

bug that is able to "produce insoluble extracellular polysaccharides"

idk if there are others but an example would be *dextrans* production which is by *viridans strep species* like strep mutans or strep sanguinis they use sucrose as substrate

superinfxn vs coinfxn w Hep D and B?

if Hep B and D at the same time --> coinfxn if pt was chronic Hep B pt and now gets hep D --> superinfxn superinfxn is worse and increases risk of cirrhosis and hepatocellular carcinoma more than purely hep B virus

Weber test is when you vibrate the thing on forehead to test hearing. what do the results mean?

if sensorineural --> lateralizes to unaffected ear if conductive --> lateralized to affected ear (this is bc the conduction deficit *masks the ambient noise in the room* and allows the vibration to be heard better/longer you start w rinne test (bone conduction) to determine sensorineural vs conductive. if normal air conduction > bone --> sensorineural or normal. if weber lateralizes --> sensorineural bc weber should never lateralize

Prevalence is affected by what 2 things?

incidence (new cases) and duration of dz (prevalence = incidence * duration of dz) think about the drops and sink full of water and drain analogy. drops is the incidence (i.e. new cases). sink full of water is new cases. drain is how many deaths. if incidence is staying the same, that means the only thing affected the level of the water is the drainage. i.e. how fast are ppl dying from this dz. this in turn is affected by quality of care. if prevalence is increasing that means less ppl are dying --> improved quality of care. increased accuracy of diagnostic testing affects prevalence AND incidence bc it changes rate at which new cases are added

What type of infarct affects the internal capsule? what is the main cause of this type of infarct?

if the question stem says the internal capsule was affected you wanna think LACUNAR INFARCT. esp if they're < 15 mm (question stem said 9mm) lacunar infarcts are most closely related to *HTN* so in these pts you would see *hypertensive arteriolar sclerosis* which is a consequence of LONG STANDING HTN. this is bc lacunar infarcts affect the *small penetrating arterioles* which like the name says are tiny. if something is thickening/hardening the vessel wall --> super easy to occlude vessel other ways they could ask this is by putting: lipohyalinosis or microatheroma formation bc these are also consequences of long standing HTN. so again. lacunar infarct --> HTN probs lacunar infarct is a *ischemic stroke* i.e. no blood on CT bc its just the vessel getting occluded

claudication of aortoiliac branches (i.e. branches that affect leg but more proximal) are commonly associated w what sx?

impotence or gluteal claudication! this is called Leriche syndrome this is bc the aortoiliac is the area right as soon as the artery branches off the aorta kinda like common iliac but right at aorta... thus affects external iliac and all it's branches plus internal iliac and all its branches (superior gluteal & internal pudendal commonly)

how does lead toxicity present, what does it inhibit, and who is at risk?

in children commonly see *language regression + anemia* inhibits aminolevulinic acid (ALA) dehydratase aka ALAD which is 2nd step in making protoporphyrin. w/o it --> anemia and ALA accumulation. also inhibits ferrochelatase which is the last step in making heme --> can't incoroporate iron into protoporphyrin so incorporates zinc instead --> *elevated zinc protoporphyrin levels* young kids that live in home built *before 1978* are at increased risk!! esp if live in poverty

what arteries are most susceptible to atherosclerosis?

in order: CAPI Coronary arteries Abdominal aorta (lower ab aorta) Popliteal arteries Internal carotid arteries the coronary arteries and abdominal aorta will develop atherosclerosis early in life even in the 20s! factors that encourage atherosclerosis: areas w bends and branch points that encourage turbulent blood flow bc it will disrupt vascular wall integrity. and turbulent flow will also prolong endothelial contact w cholesterol particles

solve the TPR for 4 vessels that are in parallel where each resistance = 2

in parallel its: 1/TPR = 1/R + 1/R + 1/R + 1/R 1/TPR = 1/2 + 1/2 + 1/2 + 1/2 1/TPR = 4/2 1/TPR = 2 TPR = 1/2 the key and what you always mess is up is that it's not TPR = asdlfkajs;dlf it's 1 OVER TPR = as;klfjasd

What is the fxn of Cl- channels in the respiratory & intestinal epithelium? How does this affect nasal transepithelial diagnostic tests? *recurrent*

in the respiratory epithelium, CFTR Cl- channels *secrete* Cl- this secretion of Cl- *downregulates* ENaC Na+ channels. if CFTR mutation (i.e. CF) you'll have *decreased Cl-* secretion which lets the ENaC reign free. This means increased Na+ reabsorption and thus H2O reabs into epithelial cells. this leads to dehydrated mucous in nasal transepithelial tests they put saline (i.e. Na+ and Cl- rich solution) on the nasal epithelium. this excess Na+ is like xmas for ENaCs so they suck it all right in and only leave the Cl- behind (since Cl- channels aren't working). when the probe measure the potential, it'll be *more negative* since it's only measuring all the negative Cl- outside compared to all the positive Na+ inside. this can be diagnostic in mild CF pts where sweat test is negative

what findings are suggestive of septic shock and what interleukins would be elevated?

in the setting of infxn especially: 1. hypotension 2. tachycardia 3. tachypnea 4. super high or super low body temp one of the most important mediators of sepsis is *TNF alpha* which is from activated macrophages. this one then activates other cytokines will also see high IL1 and IL6 bc they too induce systemic inflammatory response think: all the fever mediators!

How are Cl channels diff in the sweat ducts vs respiratory/intestinal epithelium? What do CFTR mutations do to electrolytes in pancreatic ducts? *recurrent*

in the sweat ducts Cl- channels work *along w* ENaCs and both *reabsorb* their respective ion (as opposed to resp epithelium where Cl- secreted limited ENaC abs) this is why pts have positive Cl- sweat tests. they can't reabs Cl- and this limits Na+ reabs too --> salty sweat. ultimately this results in *hyponatremia* and you'll see dry mucous membranes as well as sunken fontanelle and lethargy/vomiting in a 1 month old or young baby bc hypovolemic Pancreatic ducts: *lower rate of bicarb* secretion --> mucin precipitation --> intraductal concentrations

DNA methylation is responsible for what genetic phenomenon?

inactivating gene transcription, commonly seen in *genomic imprinting* (other things too but this could be an example they give) the methylation occurs by DNA methyltransferase often the addition of methyl groups happens to adenine and cytosine nucleotide residues Genomic imprinting is just the phenomenon in which offspring's genes are expressed in a *parent specific* manner. i.e. an allele from the father might be inactivated or "imprinted" by methylation so that only the allele from the mom is expressed (prader willi, angelman, etc)

Yes, we have "water under the bridge" meaning the ureter is under the uterine artery, but take it a step further. whats directly *posterior* to the ureter? *recurrent*

internal iliac artery!! this is in the *true pelvis* look up pic of need be if the question asked at the level *midway from the kidney* the vessels anterior to the ureter would be the *gonadal vessels* if in the true pelvis the vessels anterior to the ureter it would be uterine artery

cavernous hemangioma pts are at greatest risk for developing what complication?

intracerebral hemorrhage! cavernous hemangiomas are just malformations of vessels that occur w/i the brain parenchyma thus can rupture --> intracerebral hemorrhage

premature baby w weak high pitched crying, prominent scalp veins, and tense fontanels

intraventricular hemorrhage damaging the germinal matrix bc this part of brain has thin walled vessels lacking glial fibers that normally support blood vessels so they're extra weak this germinal matrix is less prominent around 24-32 wks so preemies are high risk bc theyre young

What is a frequent complication of a premature baby weighing < 1500 g?

intraventricular hemorrhage which affects the fragile "germinal matrix" it can cause long term neurodev

spliceosomes remove introns containing introns. how do they know where to cut?

introns containing *GU at the 5' site* or *AG at the 3' site* will get cut"

what is the most common ligament involved in an inversion of foot sprain?

inversion sprain results in *lateral* ankle damage most commonly injured is the *anterior talofibular ligament* name says it all. fibula is the lateral leg bone and talo bc ankle

what is a common ADR of isoniazid and how can it be prevented?

isoniazid is chemically similar to pyridoxin i.e. vit B6. this can result in increased urinary excretion of pyridoxine and a frank deficiency of this vitamin can eventually develop --> peripheral neuropathy. prevent by giving vit B6 in conjxn w isoniazid BONUS: vit B6 is involved in synthesis of tones of stuff like serotonin, epi, NE, dopamine, GABA

decreased activity of intracellular catalase peroxidase would lead to resistance in what drug?

isoniazid! some TB trains have decreased myocabacterial catalase peroxidase --> resistance to isoniazid

How does adenosine affect the heart? what other substance works similarly?

it doesn't allow Ca2+ in (required to create action potential) and keeps K+ around (longer repol/resting). i.e this affects *phase 4* of cardiomyocytes! this results in *slowing of sinus rate* and increase the AV conduction time! Acetylcholine works similarly by increasing outward K+ conductance while decreasing inward Ca2+ & Na+

What is the MOA of tetanus toxin? i.e. how does it prevent infxn?

it is an inactivated tetanus toxoid vaccine --> stimulates *HUMORAL ANTIBODY* response "circulating antibodies that neutralize bacterial products"

What does "very large arteriovenous concentration gradient" mean in terms of anesthetics? what would that do for onset of action?

it means it has high TISSUE solubility so the tissues keep it. large arteriovenous gradient means arteries have more of the product than veins. why? bc arteries will be taking it to tissues and instead of getting it back in the veins the tissues steal it. this means it would delay onset of action bc takes more to saturate tissues in order to have excess in blood which will finally allow for blood to saturate enough to make it to make it to brain and anesthetics start to work when they get to the brain

what does high lipophilicity mean for anesthetics?

it means it will have a rapid set of onset bc this rides on the blood flow distribution don't confuse this for solubility. apparently solubility =/= lipophilicity if it's lipophilic it will be rapidly cleared from plasma into organs receiving the high blood flow i.e. the brain so the onset would be very fast but then it gets redistributed to rgans receiving less blood flow so the half life is pretty short too an example of this is propofol

what does M protein do for group A strep?

it's a major virulence factor that *prevents phagocytosis, inhibits complement binding, and mediates bacterial adherence* it's also similar to mammalian tropomyosin and myosin. this is what can lead to rheumatic carditis

what is thet MOA of minimal change dz?

it's d/t to systemic T cell dysfxn that leads to excess *glomerular permeability factor* that causes podocyte foot process fusion/effacement it is NOT antibody mediated or antibody complex mediated or any sort of attack on your membrane.. its the glomerular permeability factor that causes the podocyte effacement and thus loss of anion charge --> albumin can filter thru bc its small enough (usually the negative charge keeps it from filtering tho)

what is the fxn of beta glucuronidase?

it's released by *damaged hepatocytes and bacteria* in infected bile it deconjugates bilirubin and the free bilirubin precipitates w Ca2+ in bile to form *pigmented gallstones*

How do hormone contraceptives work to prevent pregnancy? what contraceptives are combined contraceptives?

it's the *progestin* (aka synthetic progesterone) that prevents pregnancies. estrogen is often thrown in there to improve bleeding profile regardless, they *suppress GnRH in the hypothalamus* --> decreases synthesis of LH and FSH. remember we NEED the LH spike to stimulate ovulation!! --> ovulation is thus inhibited w/o the LH spike --> no ovulation = no baby COMBINED: pill, transdermal patch, vaginal ring

thru what foramen does CN9 exit? what are its fxns (4)

jugular foramen 1. stylopharyngeus muscle (elevates larynx during swallowing) 2. inferior salivatory nucleus --> CN 9 --> otic ganglion --> travels along auriculotemporal nerve (CN5) --> *parotid gland secretion* 3. general sensory for: tympanic membrane, eustachian tube, posterior third of tongue, tonsillar region, upper pharynx (including afferent part of gag reflex), carotid body, carotid sinus 4. posterior third tongue taste

what is the most common jxn in the circle of willis for saccular aneurysms?

jxn of anterior communicating artery & anterior cerebral artery. will result in bitemporal hemianopia if pt presents w CN3 sx it would be the posterior communicating artery

lung mass that is anaplastic and undifferentiated. giant cells w various pleomorphisms

large cell carcinoma. risk factor is also smoking. it's ini peripheral lung and has very poor prognosis

pt w hx of new construction job, constipation, decreased concentration, microcytic anemia. dx? what do you see on histo? moa?

lead poisoning!! microcytic anemia + constipation + mental status changes esp in the setting of construction work screams *lead poisoning* from metals commonly used in manufacturing (construction, mining, smelting, chemical processing, recycling, spray painting, radiator repair, etc) HISTO: basophilic stippling!! (but this is also seen in thalassemias and myelodysplastic syndrome) MOA: lead *inhibits heme synthesis pathway* specifically the aminolevulinate DEHYDRATASE (not the rate limiting step aka ALAS) and ferrochelatase --> inhibits protoporphyrin formation i.e. *microcytic, hypochromic anemia*

What murmur *radiates to left axilla*? what murmur *radiates to carotid*? what is the most common cause of this murmur? *recurrent!! very HY*

left axilla: mitral regurg and tricuspid regurg carotid/neck: aortic stenosis!! most common cause is *calcific degeneration* esp of biscupid valves (which aorta should be tricuspid)

why is pressure in the left renal vein usually higher than in the right renal vein? what is a complication of this in males?

left renal vein runs b/w the SMA and the aorta! left gonadal vein plugs into left renal vein and can lead to varicocele if the pressure of the SMA is too much squishing the left renal vein and thus causing back up of flow of the left spermatic vein ("nutcracker effect")

Buzzword: brown pigment w hemosiderin on lung histo

left sided HF --> pulmonary edema and extravasation of RBCs into alveolar parenchyma "heart failure cells" from pathoma!!!

Pneumonia w diarrhea should make you think of ..? common lab finding seen?

legionella pneumophilia!! (legionare tryna propose but pooping his pants and coughing) seen w hyponatremia (legionares throwing salt overboard) seen in pts w exposure to *contaminated water* (legionares are at sea in a docking thing) so like cruise ship hx, spas, hospitals, air conditioned hotels!!

what is the best indicator of mitral stenosis severity?

length of time b/w S2 (specifically *A2* component which represents aortic valve closure) and the opening snap (OS) short A2-OS interval indicates more severe stenosis . OS is d/t abrupt tensing of the valve leaflets. as MS worses, left atrial pressures increase d/t impaired movement of blood into left ventricle. A2-OS interval becomes shorter as left atrial pressure increases from a more intense stenosis causing the forceful opening remember S1 = closure of mitral and tricuspid (happens at same time) S2 = closure of aortic first then pulmonary (bc of the inspiration thing causing pulm to delay a little bit)

"nonblanchable lesions over bilateral lower extremities. hx of penicillin use d/t sore throat"

leukocytoclastic vasculitis... also called cutaneous small cell vasculitis. classically involves the *lower extremities* usually seen d/t drug or pathogen exposure (penicillins, cephalosporins, sulfonamides, phenytoin, allopurinol)

MOA of: -leuprolide -ketoconazole -finasteride -flutamide, cyproterone

leuprolide: GnRH agonist. inhibits LH release Ketoconazole: inhibits testosterone synth at leydig cells Finasteride: 5 alpha reductase inhibitor at peripheral tissues so prevents conversion of testosterone to DHT. used for benign prostatic hyperplasia and male pattern baldness Flutamide, cyproterone, spironolactone: androgen receptor binding (doesn't inhibit testosterone prodxn just a classic competitive testosterone receptor inhibitor)

what muscle and nerve is responsible for keeping your eyelid from drooping?

levator palpebrae innervated by CN3

pt that had severe sepsis now has right upper quadrant ab pain, nausea, recurrent fever. what's going on ?

likely acalculous cholecystitis aka inflamed and enlarged gallbladder W NO GALLSTONES this is classically seen in *critically ill pts* like those w sepsis, severe burns, trauma, immunosuppression associated w high mortality! thought to arise d/t gallbladder stasis and ischemia --> inflammation of and injury to the gallbladder wall

clef palate results from what? clef lip results from what?

lip: maxillary prominences fails to fuse w intermaxillary segment palate: palatine shelves fail to fuse w one another or w the primary palate

what type of necrosis would you see in a pt that had an ischemic stroke? what is characteristic of it?

liquefactive necrosis this is the classic necrosis seen in the CNS ~1 week after injury characterized by immune cell migration & *hydrolytic enzyme release*

What organ is the MOST important for cholesterol level homeostasis?

liver!! tons of other cells (SM, adrenocortical cells, fibroblasts, lymphocytes, etc) have high affinity LDL receptors, but hte LIVER handles ~70% of the plasma LDL this is impaired in *AD Familial hypercholesterolemia*

Action card: you might not like this, but itll be worth it. Go thru the TCA cycle and write it out at least once (will repeat this card a lot; don't star)

look at pic on your phone. uworld is good bc it has all the intermediates created and such

What are the lung findings regarding BREATH SOUNDS (normal, increased, absent, decreased), TACTILE FREMITUS (normal, increased, decreased) and PERCUSSION (resonance, dullness, hyperresonance) in the following: 1. normal lung 2. consolidation 3. pleural effusion 4. pneumothorax 5. atelectasis

look at uworld image on your phone

Draw what the globus pallidus and putamen look like on a CORONAL cross section of the brain

look up a google pic if need be (kenhub is really good) but from the outside in it goes: putamen --> globus pallidus external segment --> globus pallidus internal segment INTERNAL CAPSULE --> thalamus right under the ventricle space

what is erythema multiforme most commonly associated w?

looks like target lesions! associated w *herpes simplex virus* (hermes the deliver guy w target stamps on his arm). CD8+ mediated (duh bc HSV is virus) don't confuse w chronicum erythema migrans!! that's lymes!! "bulls eye"

how do you tx congenital adrenal hyperplasias?

low doses of exogenous corticosteroids to suppressive excess ACTH secretion in pts w 21 hydroxylase def (most common CAH) there is an inability to produce cortisol and aldosterone. aldosterone can be produced elsewhere so its not a big deal i think. however, cortisol can only be produced here so if we have LOW cortisol prodxn, the hypothalamus goes crazy and causes increased prodxn in ACTH by the anterior pituitary. this results in adrenal cortex and androgen over prodxn if you give a little (physiologic doses) of corticosteroids (i.e. glucocorticoids + mineralocorticoid) you can turn down the ACTH and thus reduce stimulation of adrenal cortex! :)

what are the pH, HCO3-, and H2PO4- levels like in a pt w DKA in their URINE after 2 days?

low pH bc DKA is acidic crisis and you're peeing out ketones low HCO3- bc tryna compensate by ABSORBING as much HCO3- as you can so not peeing any out HIGH H2PO4- bc when you reabs more HCO3- you have to throw away an H+ ... where does this H+ go ? binds to HPO4 that gets filtered at glomerulus combines to form H2PO4- that gets excreted in urine BONUS: -they didn't ask in this question, but NH4+ would also be increased in urine bc that's another urine buffer (like H2PO4-) that helps in acid excretion -also free H+ increases in urine but that changes the pH very fast and limits more H+ to come out so thats why our body uses buffers like NH4+ and H2PO4- to be able to pull out more acid

do uric acid crystals precipitate at high or low pH? what part of the kidney

low pH. they come out in acidic urine. this is why in the carbonic anhydrase sketchy you see calcium phosphate stone formation d/t high pH from bicarb... but they said high bicarb can solubize uric acid and cystine stones (no symbol) :/ stones form at *DCT and collecting ducts* bc these are the most acidic places in nephron d/t alpha intercalated cells

what causes the precipitation of calcium oxolate kidney stones?

low urinary citrate!! nothing to do w pH :) also hypercalciuria (like in hyper PTH), hyperoxaluria (d/t malabs like crohns or low calcium diet bc you need calcium to bind and trap oxalate in gut and not let it get reabs) MOA of urinary citrate: prevents stone formation bc citrate will bind to free calcium! thus preventing its precipitation and facilitates its excretion! :) common to see hypocitraturia in the setting of *chronic metabolic acidosis* bc of enhanced renal citrate reabs BONUS: -ingestion of calcium IS NOT a risk factor for renal stone formation bc dietary calcium is ingested w oxalate in food and forms insoluble calcium oxalate salts! this results in decreased gut abs and thus reduced renal excretion of oxalate

What is a "low Vd" and what does that mean in terms of drug characteristics (4)

low volume of distribution is around 3-5 L these drugs have: 1. high molecular weight 2. high plasma protein binding 3. high charge 4. hydrophilicity they tend to trap the drug in the plasma and thus don't distribute as much

"air fluid level" on lung xray is code for what what cells play a role in this ? how/moa? ADR? *recurrent*

lung abscess formation other clues to watch out for are *several days of fever* and a productive *copious foul smelling sputum* cough common cause is aspiration pneumonia (i.e. aspiration of anaerobic bacteria from oropharynx) *neutrophils* play a role in formation of lung abscess! activated neutrophils *release cytotoxic granules* like lysosomes containing myeloperoxidase and other digestive enzymes to destroy extracellular bacteria & recruit additional immune components to the area potentially bad side effect is that it can cause *liquefying necrosis* (pg 5 of pathoma if you need a refresher) but liquefactive necrosis is just necrotic tissue that becomes liquefied d/t enzymatic lysis of cells. this is most characteristic of the brain (proteolytic enzymes from microglial cells liquefy the brain) but can also be seen in *abscess* formation d/t proteolytic enzymes *from neutrophils* liquefying tissue. or *pancreatitis* proteolytic enzymes from pancreas liquefy parenchyma

MOA behind toxic shock syndrome is mediated by what 2 cells?

macrophages and T lymphocytes massive release of cytokines (IL2 from T cells and IL1 and TNF alpha from macrophages)

what is the main fxn of alanine?

major AA responsible for transferring *nitrogen* to the liver for disposal. amino groups (w nitrogen) almost always get transaminated i.e. transfered to alpha ketoglutarate which then forms glutamate. glutamate is processed in liver to form urea which is the primary disposal form of nitrogen in humans.

What is the urea cycle i.e. what does it get rid of? what do you need to avoid if impaired?

major disposal of nitrogen waste aka ammonia which is produced by *catabolism of amino acids* defects usually cause neuro sx (lethargy, vomiting, seizures) d/t accumulation of ammonia. if defect in urea cycle (like if defective ornithine transport) pts should *avoid protein excess* bc that will reduce the amount of AA turn over :) still need to eat the essential amino acids and stuff but not in excess and must be very well regulated

what's another word for "serum paraproteins"?

monoclonal immunoglobulins!!! just love to trick you :) :) :) :) technically it's immunoglobulins or chain fragments. that's why they use that general broad term word. this is seen in multiple myeloma! which is excessive Ig*G* not IgM!! sometimes its IgA IMPORTANT:!! even tho youre making excess IgG, in the *urine* you would see excess LAMBDA LIGHT CHAINS [or kappa] bc the kidney (myeloma kidney) getes damaged D/T THE LIGHT CHAINS since immunoglobulins are *too large* to pass thru glomerulus!!!! not IgA, IgM, IgG or heavy chains!

how does CMV present in immunocompetent pts?

mononucleosis like illness (mom at the CMV mega-lo prices pulling on the back of son's shirt making his throat hurt; monospot test helps rule out mono. monospot is also called heterophile antibody) in immunocomp pts CMV sx: -esophageal ulcers -retinitis -hepatitis & hepatosplenomegaly -viral pneumonia (esp after transplants)

What are sx of Henoch-Schonlein purpura (HSP)? *recurrent*

most common vasculitis in children!! d/t IgA immune complex deposition w/i small blood vessels of *skin, kidneys (hematuria), intestines, and joints* but the big buzzword is "palpable purpura" in kids on butt & legs!! bc it's IgA deposition commonly see *after an upper respiratory infxn bc IgA fights against & protect mucosal lining

what is a charcot bouchard aneurysm?

most commonly caused by *chronic HTN* so easily confused by lacunar stroke bc they're also < 1 mm however, they cause *intraparenchymal hemorrhage* which DOES show up on CT (lacunar strokes don't) it affects the deep brain structures so like basal ganglia, cerebellar nuclei, thalamus, and pons. don't confuse for berry aneurysms or subarachnoid hemorrhage which can look similar but will have "Worst H/A of my life" charcot bouchard is a *hemorrhagic stroke*

Buzzword: pseudomyxoma peritonei on ovarian mass

mucinous cystadenocarcinoma (epithelial ovarian neoplasm)

whats a good clue that makes you lean toward SCID vs other immunodef?

mucocutaneous candidiasis. oral thrush is d/t T cell def. other common immunodeficiencies are diff bc: Chediak hagashi: albinism. Wiskott: T and B cell missing but will have eczema X linked agammaglobulinema: normal T cells but absent B cells

What is hemoglobin C?

mutation in the Beta globin chain that causes the NORMAL negatively charged glutamate w *lysine* (remember in sickle cell Hemoglobin S replaces glutamate w *valine*)

what mutation can human tumor cells induce that make that make them resistant against chemo?

mutation in the human multidrug resistance gene (MDR1) codes for P glycoprotein which is an ATP dependent efflux pump protein that can reduce the *influx of drugs* into cytosol and increase *efflux from the cytosol* . esp removes hydrophobic agents like anthracyclines this P glycoprotein is nl'ly in intestinal and renal tubular epithelial and capillary endothelium of BBB cells and fxns to eliminate foreign compounds from the body

G:C --> T:A transversion mutation in gene p53 on codon 249

mutation that greatly increases risk of developign hepatocellular carcinoma d/t *dietary aflatoxin exposure*

What does attachment of ATP specifically cause in the skeletal muscle?

myosin head *detachment* from the actin filament w/o this ATP the muscle will be fixed in a *contracted state* & cross bridge will occur b/w myosin & actin --> which we can see in rigor mortis :o why dead ppl are rigid

Bean shaped diplococci is code for? gram negative rod causing meningitis?

n meningitidis! second most common cause of meningitis in adults (strep pneumo #1!!) gram neg rod causing meningitis would be e coli

what is the first line pharm tx for moderate to severe alcohol use disorder? MOA?

naltrexone! which is mu-opioid receptor blocker works by *blocking the rewarding and reinforcing* effects of alcohol --> reduces craving for it Disulfram is an acetal aldehyde DH inhibitor that *dis*courages drinking, but does so in an aversive way... causes acetaladehyde accumulation --> n/v, flushing, sweating, H/A, dyspnea, low BP, palpitations. also doesn't tx craving.

is gout negative or positive birefringent?

negative!! needle shaped crystals. yellow when parallel. these are also called monosodium urate crystals

What cells are increased in COPD?

neutrophils, macrophages, and CD8+ lymphocytes. These cells release enzymes & proteases like elastase --> impair fxn of protease inhibitors like alpha 1 antitrypsin --> alveolar damage --> reduced ciliary motion --> increased mucus secretion by goblet cells. another way to say this is *protease-antiprotease imbalance* even tho asthma is an obstructive lung dz it is NOT COPD!! COPD = chronic bronchitis and emphysema

what type of granulomas do we see in crohns?

non caseating :) remember caseating is only seen in TB and fungal infxns! so if ever in doubt go w non caseating lol

Crohn dz on histology?

noncaseating granulomas!! remember these are Th1 mediated bc Th1 = IFN gamma = macrophages and macrophages do granulomas

what is the most common cause of viral gastroenteritis in pts that are fully vaccinated?

norovirus!! it'll present w diarrhea thats water and w/o blood or mucus. also fever. norovirus presents very similarly but is in pts that are not vaccinated as new vaccinations have greatly decreased the number of ppl infected

talk about the histone organization of DNA. which one is outside the core?

nucleosomes are structural subunits w/i nucleus of eukaryotic cells. they help warp DNA around core histone proteins and make it compact. 5 major histones: H1 H2A H2B H3 H4 they're all positively charged and thus attract negatively charged DNA *the only one that lies outside* the histone core is *H1*!! we call this the linker segmenet and it helps in *packaging* of nucleosomes into even more compact structures

complete collapse of a lung usually happens as a result of ...?

obstruction of a *mainstem* bronchus (central lung tumors in chronic smokers) bc it'll prevent ventilation

what is the MOA behind obstructive sleep apnea causing pulmonary HTN?

obstructive sleep apnea is seen in obese pts. when they sleep their airway will collapse and this leads to constant transient hypercapnia and hypoxemia at night. this leads to *vasoconstriction* of pulmonary capillaries --> pulm HTN and eventually right heart failure additionally, this hypoxic state stimulates *sympathetic cardiac stimulation* which leads to systemic HTN d/t sympathetic constantly being on

omphalocele is associated w what trisomies? what about myelomeningocele? what about duodenal atresia? holoprosencephaly?

omphalocele --> trisomy 13 and 18 myelomeningocele --> 18 duodenal atresia --> trisomy 21 holoprosencephaly --> trisomy 13

what is hepcidin? talk thru the iron abs story :)

once upon a time there was a receptor called *DMT1* on the surface of ENTEROCYTES near the lumen where food is. this receptors job is to let iron into the cell and hand if off to the back door guard *ferroportin* which has favor w the hepatocytes Ferroportin lets iron in to the hepatocyte side and from there it hands the job to the *transferrin receptor* which is modulated by the *HFE* gene. once transferrin has let in enough iron, the hepatocyte will sense that and let out *hepcidin* to say STOP! ENOUGH IRON! the hepcidin goes over transferrin and it yells directly at *ferroportin* in the enterocyte to shut it up and not let it transfer anymore iron to hepatocytes in hemochromatosis, HFE is defective ruining some *transferrin* receptors. this means hepatocytes think we have *low* iron so it'll *decrease* hepcidin release bc remember we said hepcidin was the tattle tale saying STOP! WE HAVE ENOUGH! (note transferrin is full/saturated bc it's binding the iron, it just can't bring it in so hepatocytes think we're low on iron) that means ferroportin wont get the memo that it's absorbing too much so it'll keep absorbing and keep absorbing from the intestine so the pathophys of hemochromatosis is double whammie: 1. increased intestinal iron abs via DMT1 (since ferroportin isn't inhibited and it gets its stuff from the sourcer aka DMT1) 2. decreased hepcidin which again isn't telling ferroportin to stop

gradual loss of peripheral vision

open angle glaucoma will see increased intraocular pressure commonly d/t increased secretion or decreased outflow of aqueous humor. will see *pale optic disc* d/t loss of ganglion cell axons

"protruding tongue, excessive skin at the nape of the neck, upslanting palpebral fissures" "low set ears, webbed neck, wide spaced nipples" "micrognathia, low set ears, clenched hands w overlapping fingers"

pay attention to this bc you got it wrong in uworld... this is classic description of downs!! think about excessive skin at nape of neck (don't confuse for turners where they have a mass at nape of neck) ________________________ this is turners! ________________________ this is Edwards aka trisomy 18

permissiveness vs synergistic effect vs additive effect in terms of pharmacodynamics?

permissiveness: the second drug given DOES NOT have a direct effect but allows another to exert its maximal effect. synergistic effect: drug A + B have a bigger result than the theoretical addition of the two alone [i.e. if drug A increases glucose by 20 and drug B by 30 alone, you would expect increase of 50 when combined, but if they increase by 80 then its synergistic additive: when two drugs are like the sum of their individual effects. see synergistic explanation

Action card: draw the lung volumes and capacities *recurrent*

pg 646 FA

Action card: draw on the board what an obstructive vs restrictive loop curve looks like *recurrent*

pg 656 FA

What ratio do we use to measure lung maturity?

phosphatidylcholine TO sphingomyelin aka lecithin TO sphingomyelin ratio aka L/S i got the question wrong bc i put sphingomyelin to phosphatidylglycerol ....... mature surfactant is 2x phosphatidylcholine to sphingomyelin

pt has a lesion in temporal lobe. what does the result in terms of visual changes?

pie in the sky!!! upper quadrantanopia. this is also called injury to meyers loop in the temporal lobe *PARIETAL lobe lesion* = lower quadrantanopia aka pie on the floor lol

Buzzword: cerebellar mass in a kid that is cystic and solid

pilocytic astrocytoma

What is the most common brain tumor in children? what part of the brain is most commonly affected?

pilocytic astrocytoma. well circumscribed *cerebellar* mass remember "Prepubescent Minds Eaten w Cancer" Pilocytic astrocytoma Medulloblastoma Ependymoma Craniopharyngyoma

What eye findings can you see in opioid OD? How do we tx opioid OD and what receptors does it bind to? *recurrent*

pin point !! tx w *naloxone* which antagonizes all opioid receptors but *especially* mu receptors which are involved in respiratory and cardiac depression. and reduced GI motility so blocking them brings pts back to life w/i minutes

what is the tx of pituitary apoplexy?

pituitary apoplexy = pituitary hemorhage this happens in pts w preexisting pituitary adenoma tx is obvi surgery but also *urgen tx w glucocorticoids* to prevent adrenal crisis bc you'll have severe ACTH deficiency and thus adrenocortical insufficiency so supplement w glucocorticoids

removal of placenta "in pieces" suggests what? what is a potential risk factor?

placenta accreta!! pts w scar tissue from prior surgery like C section can result in malformed or *absent decidual layer* allowing for *direct myometrial attachment* by the villous tissue and prevents normal placental separation after fetal delivery

bugs that produce extended spectrum beta lactamases do so by what MOA?

plasmids w drug resistance gene thus they can be transmitted b/w organisms thru plasmid conjugation

pleiotropy vs mosaicism

pleiotropy is when 1 gene mutation leads to lots of seemingly unrelated phenotypic abn. mosaicism is when there is the presence of 2 populations of cells w diff genotypes in one pt (like in that weird Downs phenomenon where some cells has nl ch21 and other have 3 ch21 cells)

how can you tell if aspiration pneumonia is d/t true pneumonia or pneumonitis?

pneumonia is d/t aspiration of oral microbes like anaerobes commonly. seen w lung parenchyma INFXN. presents days after aspiration event. fever and smelly sputum. causes abscess. usually seen in *right lower lobe of lung* bc the right bronchus is less angled pneumonitis is d/t aspiration of gastric acid which causes direct tissue injury and so youll see inflammation. usually in one of both lower lobes. resolves w/o abx. presents *hours* after aspiration event

"transmural inflammation of arterial wall w fibrinoid necrosis?"

polyarteritis nodosa other sx: -intermittent ab pain -periph neuropathy -renal insuff -*severe* HTN

pt w sx all over the place like fever, weight loss, muscle pains, asthma, high TGs, but has "ab discomfort and black stools" and GI endoscopy doesn't find any abnormalities dx? what is the classic association?

polyarteritis nodosa!! this is a medium vessel vasculitis that affects multiple organs but lungs are classically spared! classically associated w *serum HBsAg* so it's the most likely predisposing factor to this condition!!

what's a good clue into ARDS? (acute resp distress syndrome) what is the pathophys on histo?

pt w sepsis that suddenly becomes hypoxic very quickly and requires mechanical ventilation w/i hours this rapid onset resp failure suggests ARDS. there are lots of causes for ARDS tho. can be d/t direct pulm trauma like inhaled irritants or indirect like sepsis, burns, pancreatitis. result is pulm epithelial or endothelial damage. basically any time there is a lot of cytokine release they can get to your lungs and cause damage. in sepsis there is a HUGE release of cytokines and some make it to lungs and cause damage! ARDS MOA is "leakage of protein rich fluid that leads to edema" so you'll see fluid accumulation in the alveolar spaces. there are 3 phases of ARDS tho: 1. Exudative phase: inflammatory cytokines (IL-1, IL-6, TNF alpha) activate pulm endothelium and recruit neutrophils to lung tissue --> endothelial damage leading to increased capillary permeability and *leakage of protein rich fluid into alveolar space* --> formation of hyaline membranes!! 2. Proliferative phase: 1-2 wks later endothelial cells, pneumocytes, fibroblasts proliferate to try and repair damaged lung. collagen is deposited and scarring can happen. edema is reabs 3. fibrotic phase: sometimes excess collagen deposition can happen --> irreversible pulm fibrosis

if you see hypertrophic right ventricle on biopsy what should be your gut association?

pulmonary arterial HTN for the RIGHT ventricle to get hypertrophied is super rare and it means there's some serious pushing its been having to do right ventricle feeds into lungs so it must mean there's some pulmonary arterial HTN going on if its of primary cause i.e. no other medical problems like left heart failure or chronic lung dz we call it *pulmonary arterial HTN (PAN)* vs just pulmonary HTN PAN is classically seen in young women 20-40 y/o question stem girl was 32!

"slow rising low amplitude pulse"

pulsus parvus et tardus. commonly d/t aortic stenosis

allopurinol inhibits breakdown of what type of drugs?

purine drugs! (pure nun w pure as gold necklace rosemary thing around her neck) purine drugs are like *azathioprine* and *6MP* this is bc xanthine oxidase metabolizes it so if you give allopurinol you'll cause them to build up in toxic levels azathioprine and 6MP (azathioprine becomes 6MP) are used for immunosuppression (sometimes even for UC) this can also be good bc it means if you give a pt a lower dose of azathioprine but combine w allopurinol you can increase the effects of azathioprine by increasing the build up since you've inhibited the breakdown of it. lower dose = lower ADR. but if you don't know pt is on allopurinol you can increase deaths and opportunistic infxns d/t lowered immune system

WBC casts on urine sediment are pathognomonic for what?

pyelonephritis!! esp in the setting of UTI like urinary frequency and urgency otherwise might be acute interstitial nephritis but this doesn't have any urinary sx or transplant rejection

what cells of the brain are most vulnerable to ischemic injury and affected first?

pyramidal cells of hippocampus and Purkinje cells of cerebellum but tbh 5-10 mins of interrupted blood supply leads to syncope and permanent damage to brain tissue happens in 4-5 mins so

What is the first step in pyruvate going back up to become glucose? i.e. gluconeogenesis?

pyruvate has to become *oxaloacetate* does this w the help of *pyruvate carboxylase* and CO2 w Acetyl CoA and biotin once its become oxaloacetate it needs to become malate. go thru malate shuttle out the mitochondria and outside the mitochondria into cytosol it turns back into oxaloacetate and then it becomes phosphoenolpyruvate (PEP) to go back up to glucose *Acetyl CoA is very important* acetyl coa is what determines whether the cell is gonna go gluconeogenesis or TCA to make ATP. when there is a lot of fatty acid oxidation that leads to high levels of Acetyl CoA. this tells the body we are in starving mode and pyruvate carboxylase becomes activated to enter gluconeogenesis. we need to make sugar! when *acetyl CoA* is low that means we aren't doing beta oxidation so we must have glucose and thus should make ATP i.e. go down the TCA cycle. decreases activation of pyruvate carboxylase

Buzzword: sodium cyanide nitroprusside test

qualitive screening test taht detects presence of urinary cystine. helpful in dx of cystinuria where you see hexagonal flat yellow stones d/t excess cystine in urine this test will be postiive if *red purple discoloration*

Buzzword: pts goes on a field trip to study bats. later develops spasms, progressive paralysis, coma, dies. bug?

rabies!!! bats makes you think of caves and histoplasma fungi but NOT ALWAYS. bats (most commonly actually!!), raccoons, skunks, foxes are rabies reservoirs! in the developing world dogs, but thats very rare here in US

What is ramelteon what what is it used for?

ramelteon is lame-el-ton it's a melatonin agonist that's used in *elderly pts for insomnia* usually insomnia can be tx'ed w benzos, antihistamines (1st gen), or sedating antidepressants like amytryptalins but these are contraindicated in elderly d/t their ADR

what is the physiology behind pure red cell aplasia? what's the buzzword association? (3)

rare form of bone marrow failure where there are *IgG autoantibodies or cytotoxic T lymphocytes* that cause inhibition of erythropoietic precursors this will cause only RBCs to be low. so low hemoglobin, low reticulocyte, low RBC count but normal WBCs and platelets etc ASSOCIATIONS -*thymomas* (sometimes the thymomas can be the cause and thus everyone should get CT to see if this is the cause and get it removed for full recovery of sx!!) -*lymphocytic leukemias -*parvovirus B19 infxns*

when do you use relative risk and when do you use odds ratio?

relative risk is when you're doing cohort studies or other "incidence measure" studies. when you pick the ppl and then follow them to see if they got the dz you do odds ratio for case-control studies which is where you identify people that already have the dz and compare to those that don't have the dz. (i.e. cases of women that just delivered babies w neural tube defects and compare those to controls of women who delivered normal babies. then you ask about how much ibuprofen they used during the 1st 3 mo of pregnancy) if that were a cohort study you would have gotten women that took ibuprofen early in pregnancy and then followed them to see who delivered healthy babies and who had defects. slight difference but case control = odds ratio

if a pt has hx of MI and needed stents and has high blood pressure and kidneys are small.... what is the likely dx?

renal artery stenosis that's actually how they asked the question. they gave pt w hx of 2 stents in LAD (read: atherosclerosis hx) that was on all sorts of anti HTN rx (thiazide, amlodipine, lisinopril) and BP still 180/110. renal US showed kidney at 7cm and other at 11cm (normal is ~11cm) and asked why the kidneys were like that... in majority of pts renal artery stenosis is d/t atherosclerosis (> 90% of cases). only in younger women is it d/t fibromuscular dysplasia ("string of pearls")

Many cancers metastasize to lung, but which cancer appears like clear cells w a prominent nucleus on bx and looks like "cannonball metastases" on CXR? and has high hematocrit?

renal cell carcinoma!! renal cell carcinoma has REALLY non specific sx like fever and weight loss and commonly get detected accidentally they very frequently metastasize to lung. grossly they look yellow bc of high glycogen & lipid content. on histo kinda look like fried eggs but the technical description is "polygonal clear cells filled w abundant clear cytoplasm" another clue is increased hematocrit (i.e. polycythemia d/t EPO excess)

sudden onset hematuria in an otherwise young healthy pt w family hx of sickle cell dz?

renal papillary necrosis!! the pt is likely a carrier and some of the sickle cells must have obstructed the small kidney vessels --> ischemia can also see in NSAID rx pts bc it decreases renal blood flow --> ischemia, can also be seen in DM pts d/t renal vasculopathy from excessive nonenzymatic glycosylation. or also pyelonephritis and UTI obstrxn but would see fever or costovertebral angle tenderness (i.e. back tenderness where the ribs meet the vertebra at the level of the kidney)

basic pathophys of tetani toxin?

retrograde axonal transport to CNS --> *blocks inhibitory interneurons* @ anterior horn cells --> spams esp lockjaw

what artery causes inferior surface of heart infarction?

right coronary artery!! altho more specifically its the *posterior descending artery* which in 90% of ppl comes from the right coronary artery (i.e. right dominant circulation) this is also bc the inferior surface of the heart is majority left ventricle and the PDA supplies the left ventricle :)

Blockage of right brachiocephalic vein would look like what?

right face and arm swellin and engorgement of subQ veins. this is bc the jugular and axillary/subclavian all drain into brachiocephalic. if you block brachiocephalic blood can't go back in if you blocked SVC it would look the same except bilaterally. also note the right brachiocephalic vein drains right lymphatic duct. which drains right upper extremity, right face and neck, right hemithorax, right upper quadrant of abdomen

a penetrating injury at the left sternal border in the fourth intercostal space injures what?

right ventricle

Buzzword: ring enhancing lesions in parietal or frontal lobes vs Buzzword: hemorrhagic necrosis of the inferior and medial temporal lobes

ring enhancing = toxoplasma gondii hemorrhagic necrosis of inferior and medial TEMPORAL lobes = HSV1 encephalitis! it results from *primary oropharyngeal infxn* or *reactivation of latent virus* --> goes olfactory tract --> olfactory cortex in the temporal lobe and causes mayhem classic sx w HSV-1 encephalitis is the usual h/a, fever, AMS, seizure but also *aphasia and personality changes* since its affecting temporal lobe

what is the antibody drug for CD20 cells?

rituximab! this is the tx for follicular non hodgkin's lymphoma!!

what ligament maintains the anteflexion of the uterus?

round ligament

hCG has similar structure to what other hormones?

same alpha subunit as FSH, LH, and TSH it has very very similar beta subunit w TSH! pts w testicular germ cell tumors can develop high hCG and can stimulate TSH receptors --> paraneoplastic hyperthyroidism!

What is statistical power? (formula and what it means or when we would want it to be high) what is beta? what is a type 2 error? type 1?

statistical power is 1 - beta it represents a study's ability to *detect a difference when one exists* typically set to 80% so there will be an 80% chance of rejecting the null when it's actually truly false another way they could say that is "rejecting the null hypothesis when it is truly false" i.e. the probability of finding a true relationship beta is the probability of committing a type 2 error. remember type 2 error is when you *fail to reject* the null when it's actually false (so you say nope there is no difference when there truly is. or you say no giving drug A isn't better than the gold standard when it actually is) Type 1 error: when you reject the null hypothesis but it was actually true. you say there IS a difference when there wasn't (false positive). oh yeah giving tx A is so much better than the gold standard! when its not

what causes production of prolactin? what inhibits it?

stimulation by thyrotropin releasing hormone (TRH) so pts w hypothyroidism might start lactating!! inhibition by progesterone

HOCM is genetic... AD... what does the mutation affect specifically?

structural proteins (i.e. beta myosin heavy chain, myosin binding protein C, etc, etc) of the *cardiac sarcomere* on histology you can see cardiomyocyte hypertrophy w *haphazard cellular arrangement* & interstitial fibrosis

What foramen does the CN7 exit thru?

stylomastoid foramen and courses w/i substance of the parotid gland --> branches into 5 (temporal, zygomatic, buccal, mandibular, cervical)

Capsaicin causes decrease in activity of what neurotransmitter? how does it decrease pain (2 moa's)

substance P! which is a neurotransmitter involved in transmission of pain signals! this can be used to tx postherpetic neuralgia by reducing pain over time (at first it'll cause burning, stinging, erythema) but persistent exposure --> pain reduction over time capsaicin also causes *defunctionalization* which is excessive activation of channel that causes *buildup of intracellular Ca2+* --> long lasting dysfxn of nociceptive nerve fibers

high frequency deep brain stimulation of what area can lead to suppression of neuronal activity and thus tx Parkinsons pts?

subthalamic nucleus!! or globus pallidus INTERNUS suppressing either of these removes the inhibition from the thalamus and thus allows movement again :)

What does sucrose, lactose, and maltose break down to?

sucrose = fructose + glucose lactose = galactose + glucose (gla + glu = la) Maltose = glucose + glucose (aka G^2)

What amino acid does keratin contain?

sulfur containing CYSTEINE forms disulfide bonds b/w cysteine residues --> additional rigidity & toughness (hair, nails)

Superficial peroneal nerve is found where and provides sensation for what part of the lower extremity? what about the deep fibular?

superficial fibular aka peroneal is in the lateral compartment of the leg. responsible for eversion. *sensory for DORSUM OF FOOT [not sole of foot]* deep fibular aka peroneal is in the anterior compartment of the leg. responsible for dorsiflexion. *sensory for region b/w 1st & 2nd digit of foot!!*

What forms the femoral triangle?

superiorly: inguinal ligament medially: adductor longus muscle sartorius muscle: laterally

what is the most specific non-cardiac finding that would indicate a pt has left sided heart failure

supine dyspnea that is relieved by sitting up aka *orthopnea* (i was confused bc i thought that was a right HF sx but its NOT!! God just reminded me it's a PULM HTN sx!! and whats the most common cause of PULM HTN?! LEFT HF!!!)

how does estrogen in oral contraceptives prevent pregnancy? what about progesterone?

suppress the midcycle gonadotropin surge --> inhibit ovulation progesterone is mostly added to counteract the increase risk of endometrial cancer associated w unopposed estrogen (altho it also thickens mucous and can be used as contraceptive alone bc there are some progestin only contraceptives so!)

if pt has severe PP hemorrhage that isn't responding to rx like uterine massage or uterotonic meds, what is the next step?

surgery!! ligate the *internal iliac arteries* this would preserve fertility bc it would prevent you from having to do a hysterectomy! it would stop uterine flow and thus hemorrhage, but the uterus has collateral blood flow from ovarian arteries and thus will be able to maintain uterine fxn after the ligation

what is the most common cause of kidney infarction?

systemic thromboembolism of the left atrium or ventricle commonly d/t *a fib* !! BONUS: -brain and kidneys are more likely than other organs to suffer embolic infarctions d/t perfusion rate being higher

Thyroglossal duct cyst vs branchial cleft cyst

thyroglossal duct is *midline* and moves w swallowing branchial cleft cyst is in lateral neck near SCM and doesn't move w swallowing

What are the following: t(15;17) t(8;14) t(9;22) t(14;18) inv(16) t(12;21) t(11; 14)

t(15;17) --> Acute promyelocytic leukemia (APL) which is a subset of Acute myeloid leukemia (AML) t(8;14) --> Burkitt lymphoma! myc from chromosome 8 to immunoglobulin promoter site on chr 14 t(9;22) --> chronic myelogenous leukemia (CML) there is a BCR-ABL fusion protein that results. BUT ALSO in a small subset of B-ALL pts!! t(14;18) --> non-Hodgkin follicular small cleaved cell lymphoma. takes BCL2 from cr 18 and puts it near the immunoglobulin heavy chain promoter region on chr 14 inv(16) --> eosinophilic subtype of AML (ME4o) t(12;21) --> B cell acute lymphoblastic leukemia (B-ALL) t(11;14) --> mantle cell lymphoma which is a type of non hodkins. driven by *cyclin D1* activaiton

What is used as the surgical landmark when operating a pt w appendicitis?

teniae coli!! not haustra bc they don't span the entire colonic circumferences. teniae coli are 3 separate SM ribbons that travel longitudinally on the outside of the colon and converge t the root of the vermiform appendix so perfect landmark that is very specific to appendix. where the teniae coli end that's the appendix

Target cells on smear?

thalassemias

"bilateral wedge shaped strips of necrosis over the cerebral convexity parallel to and a few cm lateral to longitudinal cerebral fissure" what is this code for? what is the result ?

that's code for watershed zone and if its a wedge shape strip that means ischemia of the watershed zone this would result in **hypoxic ischemic encephalopathy* which is global cerebral ischemia d/t profound cerebral hypoperfusion

what vitamin is deficient in pts that have: peripheral neuropathy + heart failure?

that's wet beri beri and it's d/t B1 thiamine def dry beri beri is peripheral neuropathy but no cardiac problems

what is the MOA of benzodiazepins?

the bind to the benzodiazepine binding site on GABA receptors which *allosterically* increases the *frequency of Cl- channels opening* (which is what GABA channels are. GABA channels are Cl- channels that bind GABA to open) its the influx of Cl- not GABA that causes the inhibitory effects seen w GABA. influx of Cl- ions --> neural hyperpolarization & inhibition of the action potential

What is the airway pressure at the center of the airway pressure-volume curve? what is the intrapleural pressure?

the center of pressure-volume curve is the fxnal residual capacity of the lungs. it's 0 airway pressure it's -5 cm H2O intrapleural pressure bc lung pleura is always in a negative state holding our lungs and stuff. if you injure the intrapleural space like in a pneumothorax the lung will collapse bc it has equilibrated w the atmosphere

are conjugated vaccines strong or weak? why?

they are STRONGLY immunogenic esp in kids < 2 y/o!! d/t B and T cell recruitment they provide higher longer lasting antibody titers relative to only polysaccharide vaccines (esp in infants bc they have immature humoral antibody response) so we can give adults the regular polysaccharide one since they already have a mature humoral immune system. this one mainly produces IgM (Adults in *M*essanine) and we give kids < 2 y/o that have an immature humorsal system the conjugated one to help them produce T cell immunity and IgG (*G*round level for Kids)

what would proteasome inhibitors lead to in cells?

they called this "drugs that have a high affinity for proteasome catalytic site" so watch out cuz that's code for proteasome inhibitors. normally proteasomes degrade old proteins that are damaged, cytotoxic, misfolded etc if you inhibit proteasomes you would cause build up of toxic stuff w/i cells and that would lead to *apoptosis* of cells!!

How does strep pyogenes adhere to oral cavity/teeth?

they can produce dextrans (deck of cards) which binds to fibrin-platelet aggregates (holding a plate in his hand) that can bind to tooth enamel esp after dental procedures (donkey w big teeth) or previously damaged heart valves (green dude wearing Mitral hat)

ultimate MOA of opioids?

they close presynaptic Ca2+ channels --> reduced calcium influx which leads to reduced neurotransmitter release opioids also open postsynpatic k+ channels --> increased K+ efflux out of cells --> *membrane hyperpolarization* d/t K+ efflux they don't affect Na+ or Na+/Ca2+ exchange mechanisms from there theres full agonist, partial agonist, mixed agonist, antagonist etc

pt w hx of DVT... go get it tx... and then an MCA stroke 3 days later. whats going on? what would they have?

they have an ASD!! --> "wide splitting of S2 that does not change w respiration" aka "wide fixed S2 split" you would expect a DVT or any fragments seen after tx to go to lungs and cause a PE... if it goes anywhere else that's called "parodoxical embolism" and it's d/t ASD of some sort like patent foramen ovale or atrial septal defect or even VSD but most commonly associated w ASD

Where does the quadricep muscles insert?

they insert into the patella which inserts into the tibial tubercle by the patellar ligament so if you get injury of the quadriceps you would say the damage is in the tibial tuberosity this is commonly seen in adolescent athletes after a growth spurt and repetitive jumping motion. it's called osgood schlatter dz and it's d/t an overuse injury of the *secondary ossification center* of the tibial tubercle

How do thiazolidinediones (aka pioglitazone) work?

they're modulate transcription. bind PPAR gamma --> induce conformational change in PPAR gamma (fat kid in 2nd grade classroom cutting a circular "paper" PPAR gamma to give to his date.) PPAR gamma is an intracellular receptor taht regulates gene transcription

what is the CAAT sequence? what about TATA?

theyre BOTH promoters!! found upstream of the transcription site they're responsible for promoting the initiation of *transcription* and serve as a binding site for transcription factors and RNA pol 2

"TTAGGG" repeats represent what?

theyre the DNA repeats that are added by telomerase!! prevent loss of genetic material w every duplication

what things get reabsorbed at the PCT? what things do NOT get reabsorbed? this is basically asking that one line graph about kidneys and tubular fluid/plasma ultrafiltrate that gabby said she memorized

things that increase in concentration as the go thru the PCT (i.e. they DO NOT get rescued or they even get secreted) in order from most secreted: 1. PAH 2. Creatinine 3. Inulin (not secreted, just not reabs at all) 4. Urea 5. Cl- 6. K- 7. Na+ things that actively get saved at PCT in order from least rescued to most rescued: 1. HCO3- 2. Amino acids 3. Glucose (this is the furthest down in the curve!!) "Please Can I Unlearn Chronic Kidney Nonsense? Hi Appreciate Glucose

pt w contralateral motor weakness involving both arm and leg on passive extension there's initial resistance followed by a sudden release of tension. where is the lesion in the brain?

this is "clasp knife" spasticity seen w UMN lesions. these can be anywhere in the pyramidal system --> corticospinal tracts, internal capsule, primary motor cortex (aka precentral gyrus), medulla, pons, midbrain HOWEVER, the pt also has motor weakness which makes you think of corticospinal tract injury since this caries the corticospinal tract

a pt w hx of sickle cell dz comes in after a fever and has super low hematocrit (like 16% when normal is 36%). her reticulocyte count is 0.1% when normal is 0.5%. leukocytes and platelets are normal. what is going on and what is it d/t

this is *aplastic crisis* commonly seen in sickle cell pts. it's when pts get severe anemia following a minor febrile illness. it's most commonly d/t *parvovirus 19* in sickle cells pts which is a naked single stranded DNA virus. infxn of erythroid precursor cells in the bone marrow (plastic bone next to plane w sickle shape on it)

"erythematous, papulovesicular, weeping lesions" what is this and what is the classic histology finding?

this is *eczematous dermatitis* aka eczema but when it presents w rupturing blisters and stuff its called *acute allergic contact dermatitis* either way its a contact dermatitis so its a *type 4 hypersensitivity* acute eczematous dermatitis is classically seen w *spongiosis* which is accumulation of edema fluid in the *intercellular spaces* of the epidermis

pt w breast cancer given tx and now presents w blood in urine + anemia. what was given and how could it have been prevented

this is *hemorrhagic cystitis* they gave a *mustard based chemotherapy agent* like cyclophosphamide or ifosfamide. this gets metabolized into *acrolein* which is a toxic metabolite to kidneys --> hemorrhagic cystitis this is prevented w *aggressive hydration, bladder irrigation, and administration of MESNA* which binds to acrolein in urine

sharp chest pain made worse by swallowing or coughing

this is *pleuritic pain* commonly see in pericarditis commonly seen 2-4 days post MI (pathoma says 1-3) pleuritic pain can be made better when sitting up if made worse w swallowing --> clue that posterior pericardium is involved. if made worse w coughing and raidiates to neck --> inferior pericardium is involved bc thats adjacent to phrenic nerve which supplies the diaphragm and thats C3,4,5 neck area

young pt w NO HX of trauma has severe HA and vomiting. slips into coma and dies. autopsy shows ruptured cerebral aneurysm. what is a likely cause related to congenital cardiac anomalies?

this is *spontaenous intracranial hemorrhage* most common cause in young adults is arteriovenous malformations, rupture cerebral aneurysms (we were told this pt had this), or abuse of sympathomimetic drugs like cocaine berry aneurysms most commonly happen at *circle of willis* an association w ruptured cerebral aneurysm + congenital cardiac defect can be *coarctation of aorta* bc of the HTN in branches of aortic arch proximal to coarct (i.e. going up to brain)

autopsy finding of "masses composed of platelet rich thrombi but no organisms are present attached to the edges of the mitral valve leaflets" what is this a red flag for?

this is *sterile platelet rich thrombi* associated w *nonbacterial thrombotic endocarditis* NBTE is most commonly associated w *advanced malignancy* esp mucinous adenocarcinoma. also associated w SLE this is bc the pathophys of NBTE is d/t valvular endothelial injury caused by inflammatory cytokines which triggers platelet deposition in the presence of an underlying *hypercoag state* (and i think i remember ppl saying cancer usually leads to hypercoag state or something like that) systemic embolization can occur and is the most common *presentation* of NBTE so pt might come in w a large infarction or something

"acute hemorrhage in left temporal lobe --> compression of anterior medial temporal lobe against the free margin of tentorium cerebelli" what is this and what nerve is commonly affected?

this is *transtentorial aka uncal herniation* commonly compresses *CN3 aka oculomotor* bc it's right near the circle of willis and remember willis the spider has CN3 running near it BONUS: -CN3 compression --> down & out eye. also fixed & dilated. ipsilateral eye -can also compress PCA --> *contralateral* homonymous hemianopsia w macular sparing

"suprabasilar cells w perinuclear vacuolization only" seen on cervix

this is HPV infxn causing perinuclear vacuolization aka koilocytic change d/t viral proteins this doesn't reflect any malignant or pre malignant conditions just HPV infxn

HIV pt that is an IV drug user and now comes in w a blue-violet or brownish skin plaque. what virus is related?

this is Kaposi sarcoma. usually presents as blue violet or brownish skin plaque on the extremities and mucous membranes of HIV positive pts . highly associated w *human herpes virus type 8*

pt w oliguria and high serum creatinine level. hx of intranasal ulcer that has failed to heal. what antibodies would be present?

this is WEGENERS aka granulomatosis w polyangitis remember "C" --> nasopharynx, lungs, kidneys. the intranasal ulcer was our clue for nasopharynx (other clues could be sinusitis. if lungs then hemoptysis) recent renal failure is clue for kidney involvement recall wegners is *cANCA* positive which is cytoplasmic staining *antineutrophil* cytoplasmic antibodies so the antibodies would be against neutrophils!

what is the rate liming step of acyclovir? what does that mean practically?

this is a *guanosine analog* that has *phosphorylation* as the rate limiting step when it enters infected cells it has to be phosphorylated by a *virally encoded* thymidine kinase.. that's the rate limiting step. w/o this it's not effective this means it's effective against viruses that code for this thymidine kinase. namely: 1. HSV1 and 2 2. VZV *not* EBV or CMV

Buzzword: posterior neck mass composed of cystic space separated by CT

this is a cystic hygroma which is just a clogging of lymph or something. anyway characteristic of *turners*!!

buzzword: pts neutorphils fail to turn blue following exposure to nitroblue tetrazolium

this is a nitroblue tetrazolium test used to measure *neutrophil superoxide prodxn* it is deficient in G6PD pts --> prone to catalase+ organisms!

What is clostridium septicum toxicity MOA and risk factor?

this is a normal bug in the GI tract. usually non pathogenic but *breakdowns in the GI mucosa* can lead to invasion --> hematogenous dissemination --> *spontaneous gas gangrene* that's NOT d/t trauma (this is opposite of C perfrigens which is d/t trauma). will still present the same as like gangrene on the skin but there will be no hx of trauma! RISK factor: colonic malignancy like IBD or immunosuppression --> creates portal of entry for bacteria

What is bronchopulmonary shunting?

this is a normal pulmonary principle where there's a small drop in PO2 and small increase in PCO2 in the pulmonary veins d/t receiving deoxy blood from the bronchial circulation (dual circulation. only accounts for about a 4mmHg drop in PO2

"patchy epithelial necrosis of tubules, tubulorrhexis, and intratubular casts"

this is acute tubular necrosis which can be seen in the setting of ischemia like hemorrhage (GI bleed!), acute MI, sepsis, shock or d/t toxins like radiologic contrast agents, aminoglycosides, myoglobin regardless there will be 2 classic stages after the inciting event: 1. oliguric renal failure (~24-36 hrs after event): GFR goes down, urine output goes down, fluid overload 2. recovery phase (~1- 3 wks after event): gradual increase in urine output leading to high volume diuresis... but the kidney tubules are still impaired so you'll get *electrolyte wasting* all around --> low *K+*, Mg2+, Phos, Ca2+

if you see a granuloma w/i myocardial tissue what should you jump to?

this is an Aschoff body. granulomas inside myocardium are aschoff bodies they're pathognomonic for acute rheumatic fever if hx also says "new holosystolic murmur" then youre golden. (its probably acute mitral valve regurg) this is diff than VIRAL infxns which show tons of lymphocytic interstitial infiltrate in the myocardium. aschoff (granulomas) aren't seen. viral infxn is the most common cause of myocarditis in the general population

smoker w nagging right shoulder pain that's ipsilateral and weakness in same arm. comes in w right ptosis and asymmetric pupils in dim light but reactive to light. more symmetric in bright light. lesions involves what?

this is apparently horners. even tho we classically see ptosis, anhidrosis, and miosis (constricted pupil) only seeing 2 of the 3 is enough. in a pt that's a smoker classically will be d/t *pancoast lung tumor* that is near superior sulcus --> supressing cervical sympathetic ganglia (i.e. "autonomic ganglia"). pt w shoulder pain is another clue that its compressing the brachial plexus i.e. a structure near the sulcus of lung.

review the rules of 4 for brain strokes... :)

this is at home so wait till you get home or look at pics on your phone

how does CCl4 affect cells?

this is carbon tetrachloride poisoning!! i.e. not something that our body is equipt to deal w CCl4 causes free radical injury. it gets oxidized by CYP450 in liver like normal, but it creates free radical CCl3. this can then react w structural lipids of cell membranes. this results in lipid degradation and hydrogen peroxide formation aka *lipid peroxidation* --> peroxides then make more new free radicals and the vicious cycle is started -->-->--> hepatocyte necrosis

Pt is triggered by *gliadin* where should you biopsy?

this is celiac dz. gluten gets broken down into gliadin. gliadin triggers an inflammatory reaction *duodenum and jejunum* are the most exposed to highest concentrations of gliadin --> next step would be to BIOPSY duodenum or jejunum! --> villus flattening and intraepithelial lymphocyte infiltration technically next best step is to check to *tissue transglutaminase IgA* antibodies before you biopsy.

2-10 y/o boy w palpable skin lesions on butt + abdominal pain + hematuria couple days after colicky ab pain... what else would you see and what is this?

this is classic Henoch Schonlein purpura aka IgA vasculitis you would see joint pain as well this is classically seen after strep or viral URI infxn HSP affects GI, kidneys, skin, joint so: GI: severe ab pain w upper or lower GI bleeding so hematemesis or bloody diarrhea Kidneys: mesangial prolif and crescent formation (can be confused w IgA nephropathy) Skin: "palpable purpura" on butt and lower extremities Joints: migratory arthralgias or arthritis

pt w SOB and histo shows "giant cell foreign body response in the lower lobe of the lung"

this is classic description of aspiration pneumonia

pt w asymmetric weakness, fever, h/a, myalgias. coarse hand tremo. flaccid paralysis of left lower extremity but sensation is ok PCR shows viral RNA. what is dx and how is it transmitted?

this is classic for West Nile virus that's neuroinvasive west nile is transmitted by *mosquitos* so insect bite is right answer commonly seen in warm climate like southern US (texas ;]), latin america, africa A good clue to make this dx is if there is *acute onset of asymmetric flaccid paralysis* + concurrent *parkinsonian features* (rigidity, bradykinesia, tremor, postural instability)

AIDS pt w "latex agglutination test positive for soluble polysaccharide antigen" bug and finding on light microscopy?

this is cryptococcus neoformans but the finding would be round or oval budding yeast the key in this question was that this was the only 'yeast' answer.. all the other options (including "germ tubes" which is candida albicans at 37 degrees and remember this one is yeast in the cold and mold in the heat)

falling d/t "knee buckling"

this is d/t femoral nerve injury patellar reflex is diminished, sensory over anterior and medial thigh and leg is lost as well

pathophys behind "leather bottle stomach"?

this is diffuse gastric adenocarcinoma!! loss of *E cadherin* --> large areas of infiltrate in stomach wall. also called linitis plastica

72 y/o lady comes w h/a, fatigue, diffuse muscular pain. prednisone leads to *marked and rapid* improvement of sx. dx? what do you see on histo?

this is giant cell arteritis. usually presents w jaw caludication but the big clue here is old lady and that glucocorticoids were given and there was a BIG & RAPID improvement in her sx. also polymyalgia rheumatica histo: granulomatous inflammation of the media

"diffuse medium sized lymphocytes and a high proliferation index represented by a high Ki67 approaching 100%" or "bx of mass reveals uniform, round, medium sized tumor cells w basophilic cytoplasm and proliferation fraction (Ki67) of > 99%"

this is just code for BURKITT LYMPHOMA t(11;14) you either know it or you dont, but you will :) associated w EBV infxn remember :) also described as "starry sky"

Low FVC and TLC but high FEV1/FVC ratio

this is key for RESTRICTIVE LUNG DZs tons of them poor breathing mechanics (poor muscular effort like polio, MG, guillane barre. or poor structural apparatus like scoliosis, morbid obesity) interstitial lung dzs like silicosis, asbestosis, sarcoidosis, 'honeycomb' lung and digital clubbing, drug tox, etc, etc regardless, end result is usually always pulmonary fibrosis

Buzzword: pt seeing double when walking down stairs *recurrent*

this is key for vertical diplopia. this is seen most when the eye is down & toward nose. examples are in walking down stairs (no trouble walking UP stairs), up close reading this is injury of the *CN4* --> superior oblique muscle

pt w poor dentition. 3 wks low grade fever, weight loss, productive cough. foul smelling sputum. what would be dx?

this is likely aspiration pneumonia. tx is *clindamycin* bc this covers oral anaerobes and aerobic gram positives like strep pneumo

Buzzword: yellow-brown in tissue of an old pt. what is it and pathophys? *recurrent*

this is lipofuscin!! this is normal "wear and tear" pigment. associated w *normal aging* but esp in malnutrition & cachexia formed by lipid peroxidation aka oxidation & polymerization of autophagocytosed organellar membranes

Buzzword: solid lesion in cerebellum. i.e. not cystic + solid

this is medulloblastoma. most common MALIGNANT childhood brain cancer. exclusively in the cerebellum and will compress 4th ventricle --> hydrocephalus. usually see homer wright rosettes. not cystic like pilocytic astrocytoma

pt w spinning sensation + ringing in ear + difficulty hearing in affected ear feels fine b/w episodes dx and pathophys?

this is meniere's dz!! which is recurrent vertigo + ear fullness/pain and tinnitus + unilateral sensorineural hearing loss the key is that these episodes are EPISODIC... and it'sd/t *increased pressure and volume of endolymph in the inner ear* BPPV is d/t otoliths in semicircular canals but is characterized by episodes brought on by head movement and no auditory sx.

How does TNF alpha (a pro inflammatory cytokine) induce insulin resistance? what other substances act by this mechanism?

thru serine kinases. these *phosphorylate serine residues* on the beta (intracellular tyrosine kinase domains) of the insulin receptor NORMAL: insulin --> insulin receptor --> receptor autophosphorylation --> tyrosine phosphorylation of IRS --> PI3K pathway & RAS/MAPK pathway --> GLUT 4 out on membranes to bring sugar in this inhibits tyrosine phosphorylation of IRS-1 by IR and thus hinders downstream signaling --> resistance to normal actions of insulin other substances that act similarly are: -phosphorylation of threonine residues -catecholamines -glucocorticoids -glucagon

pt w hx of diastolic murmur has a stroke in MCA and dies. autopsy shows diffuse fibrous thickening and distortion of the mitral valve leaflets, commissural fusion at the leaflet edges and narrowing of the mitral valve orifice. dx?

this is mitral stenosis d/t RHEUMATIC FEVER!! (apparently rheumatic fever accounts for 99% of MS cases in the developing world. but in "YOUNGER" pts.. calcification is the most common cause of AS in pts > 70 y/o) the autopsy didn't find any sort of calcification... rheumatic fever is a big cause of mitral stenosis in pts that have had it for a long time remember it goes mitral > atrial > pulmonary and regurg ---> stenosis but those findings of commissural fusion are that fish mouth thing you saw in that one path lecture pt likely had a fib bc MS can cause atrial enlargement which can lead to a fib --> dislodged to brain :/ fibrosis is what clues us in to RF bc "friable vegetations on the valve cusps" would have us think about infective endocarditis

What type of crystals would you see in a pt that has a swollen right knee that's red and painful w passive ROM? *recurrent*

this is pseudogout. you would see *rhomboid shaped calcium pyrophosphate crystals* they're blue when aligned parallel and yellow when perpendicular to the ray of the compensator (opposite of that in gout) Think: "the blue P's" --> blue when Parallel, Positive birefringent, calcium Pyrophosphate, Pseudogout the key here is that knee is involved (in gout its usually needle shaped and negatively birefringent and also big toe) & WBC is high but mostly *neutrophils*

pt w hx of smoking and working in industrial chemical manufactoring facility. US reveals mass of kidney. it looks yellow on gross image. what type of cancer and where did it originate?

this is renal clear cell carcinoma. most common type of renal CA (85%) it originates from *epithelium of proximal renal tubules* gross path will show *sphere like golden yellow tissue* d/t high lipid content. also areas of necrosis and focal hemorrhage BONUS: presents w paraneoplastic sx like *polycythemia* d/t EPO which makes sense. but also hyper Ca2+!

Buzzword: pt has extra rib and presents w decreased sensation of intrinsic hand muscles like medial fingers and hypothenar (pinky).

this is thoracic outlet syndrome!! Thoracic outlet is the space above the 1st rib and behind the clavicle. compression of the lower trunk of brachial plexus --> upper extremity numbness, tingling, weakness. we didn't see it in this pt but you can also see compression of *subclavian vein* --> upper extremity swelling. can also cause *subclavian artery* --> exertional arm pain. TOS most commonly happens w/i *scalene triangle* which is formed by ant and middle scalene muscles & 1st rib. you'll see the same sx in klumpke palsy. that's bc both of these are d/t compression of the lower trunk of the brachial plexus. but Klumpke is classically adult falling while tryna grab a tree branch and infant pulled upward forcefully during delivery

pt w recent travel to southeast asia, continuous fever for several days of like 104, slow HR, loose stools the last few days. faint erythematous skin rash over trunk & abdomen. peripheral blood smear is normal. dx?

this is typhoid fever from salmonella typhi. the buzzwords that should stand out is that: 1. high fever but LOW HR. usually you would expect high fever and high HR 2. faint or salmon colored erythematous rash is the "rose spots" (remember sketch!) 3. progressive high fever that has been going on for a few days 4. can present as constipation or diarrhea this is transmitted fecal orally from contaminated food or water. usually from 3rd world countries d/t poor sanitation

pt injures himself operating a motorized watercraft on the ocean near Floriday 2 days ago. physical exam shows small laceration on the dorsum of foot w surrounding edema, erythema, and hemorrhagic bullae. cultures show curved gram negative rods. greatest risk factor?

this is vibrio vulnificus which is a curved gram neg free living bacterium that is found in *marine* envinronments. increased risk of infxn in pts that have *liver dz or iron overload* to progress to necrotizing fasciitis. otherwise this infxn is mild cellulitis :)

What readings might we see on respiratory gas analysis that would make us think of physiologic intrapulmonary shunting?

this is what happens when an alveoli is plugged. you would see an alveolar PO2 of 40 (instead of the NORMAL 104 [remember 150 is in the upper airways]) you never see 0 bc our normal deoxy venous blood has 40 so it will at least equilibrate.

buzzword: dihydrorhodamine negative

this measures neutrophil superoxide prodxn if negative --> neutrophils aren't making superoxide --> prone to catalase+ bacteria

in a pt w noncaeating granulomas. what is the reason behind elevated calcium levels?

this question was in the context of a pt w sarcoidosis, but that was irrelevant bc they said the pt had 'noncaseating granulomas' noncaseating granulomas = macrophages. also from pathoma, non caseating granulomas are defined by the presence of *epitheliod histiocytes* which are ACTIVATED MACROPHAGES well these cells have 1 alpha hydroxylase which turns vitamin D into active form and *increases Ca2+* so in pts w sarcoidosis (or TB) or any other cause for increased non caseating granulomas you can see *hypercalcemia*!!

pt has noticed he has "difficulty releasing the doorknob lately" he also has cataracts, frontal baldness, and gonadal atrophy

this question was packed w buzzwords!! this is *Myotonic dystrophy* which is a CTG repeat (Cataracts, Toupee, Gonadal atrophy) on the myotonia protein kinase gene. Myotonia means sustained muscle contraction it's AD :) its abnly slow relaxation of muscles called myotonia has *anticipation* bc of increased # of repeats in subsequent generations!!

What is a potential deadly complication an RNA virus containing hemagluttinin cultured from a brain sample

this would be measles and the complication (i.e. if its made it to the brain) is subacute sclerosing panencephalitis (SSPE) which presents as various neuro deficits & dementia. weasle w white turban on his head watching the 'tails of SSPEnse' play

"white yellow plaques on colonic mucosa" in pt w ab pain and diarrhea

those are code of pseudomembranes!! aka these are seen in C diff!! pseudomembranes are made up of fibrin & inflammatory cells

where can we see cavernous hemangiomas?

typically in the liver, but also the brain!! Gross exam wil show "mulberry like" appearance bc they look purple since they're little vascular clusters. they're abnormally dilated capillaries separated by thin CT septa. they're just a bunch of dilated blood vessels. commonly cause recurrent hemorrhages d/t reduced structural support --> present as refractory seizures that don't get better w diff txs

t(14;21)

unbalanced robertsonian translocation for downs will result in 46, XX, t(14;21)

what does the ventral pancreatic bud give rise to? (2)

uncinate process portion of the *head* (little mitten of pancreas i.e. the small portion of head) & *main pancreatic duct*

What does struvite aka magnesium phosphate crystals look like in urine under the microscope but also grossly?

under the microscope: "coffin lid" they look rectangular w the top like a coffin grossly: brown dark looking w nephron that has yellow tissue d/t damage (xanthomatous changes)

pt has been dx'ed w S bovis endocarditis. whats the next step?

undergo colonscopic evaluation to exclude neoplasia!! greatly associated w colon cancer!!

sudden appearance of acanthosis nigricans in middle age/elderly pts is suggestive of what?

underlying malignancy most commonly *gastric adenocarcinoma* !! or other GI or genitourinary malignancies this is nl benign in younger pts or in DM pts bc its d/t insulin resistance (which increases FA build up; can also be d/t obesity, acromegaly)

vasopressin and desmopressin act on V2 to activate water reabs, but what else?

urea reabs!!! at the inner medullary collecting duct if a pt w central DI is given desmopressin/vasopresin you'll see increase in urea reabs! this is bc urea enhances the medullary osmotic gradient and allows for prodxn of maximally concentrated urine so your body allows it

what is the most common cause of unilateral fetal hydronephrosis d/t *obstruction*?

ureteropelvic jxn narrowing or kinking (i.e. at proximal ureter where the ureter inserts into pelvis of kidney) don't confuse this is vesicoureteral reflux which would also cause fetal hydronephrosis but would be *nonobstructive* bc basically it's just a regurg of urine from the bladder up the ureters as it contracts when we pee

buzzword: nitroblue tetrazolium test... what dz

used to dx chronic granulomatous dz

loss of support from what ligament leads to uterine prolapse into vagina?

uterosacral ligament

What is temporal (giant cell) arteritis and what is a feared complication? *recurrent*

vasculitis of the *large vessels* specifically the aorta but even more specifically the *carotid artery* it's the most common vasculitis in older adults and esp affects females. will present w H/A (i.e. temporal artery involvement), visual problems, *jaw claudication* feared complication is blindness (ischemic optic neuropathy d/t ophthalmic artery involvement) w/o tx!! tx is glucocorticoid therapy that SHOULD BE STARTED regardless of whether the biopsy results are back or not!

small intestinal bacterial overgrowth is characterized by overprodxn of ?

vitamin K and folate!! question stem literally said pt had small intestinal bacterial overgrowth so it was one of those you either know it or you don't kind of things... this is esp common in the setting of a gastric bypass bc they're commonly "roux-en-Y" where you cuz majority of stomach, seal top, and reattach to distal jejunum. you connect a tiny bit of the top stomach/esophagus to top part of small intestine (proximal jejunum usually)

What 2 vitamins are NOT present in breast milk? what's another unique mineral we should supplement w in breastfed babies? at what age? *recurrent*

vitamins D & K! vitamin K is usually supplemented by IM injection at delivery to prevent hemorrhagic dz in the newborn vitamin D should be supplemented in all infants breasfeeding to prevent rickets [inadequate bone & cartilage mineralization] (altho sunlight can provide sufficient vitamin D, babies are usually shielded to prevent sunburn!) *IRON* should be supplemented in babies breast fed > 4 months bc iron concentration in breast milk decreases over time. we can stop iron supplements when they begin solid food intake :)

in a pt w build up of methylmalonic acid, what would you expect to see in: -Urine propionic acid -serum glucose -urine ketones -serum ammonia?

we think of methylmalonic acid as a B12 def thing, and it is, but it can also be d/t *methylmalonyl CoA mutase def* Branched FAs like isoleucine, valine, threonine, methoinine, and odd chain fatty acids normally leads to formation of *propionyl CoA* which gets converted to methylmalonyl CoA and this methylmalonyl CoA will become succinyl CoA and enter TCA like we said if we can't make succinyl CoA this way we'll get build up of *propionic acid --> metabolic acidosis* Propionyl CoA is an organic acid that causes: -high urine propionic acid -low serum glucose d/t organic acids inhibiting gluconeogenesis -high ketones (bc of hypoglycemia body tryna compensate) -high serum ammonia d/t organic acids inhibiting the urea cycle

what is the weakest point of the urethra in men? what parts make up the posterior urethra? anterior?

weakest point: membranous segment posterior: membranous segment and prostatic segment. associated w pelvic factures anterior urethra: bulbous and penile segments. associated w straddle injuries trauma of the pelvis usually causes disruption of the membranous segment right at the bulbomembranous jxn

ataxia + nystagmus + opthalmoplegia + anterograde amnesia

wernicke encephalopathy!! commonly seen in pts w low thiamine levels like CHRONIC ALCOHOLICS giving these pts dextrose w/o prior thiamine supplementation = wernicke encephalopathy this affects the *mammary body* which is above the bump of the pons kinda

Uniparental disomy

when both chromosomes in a given pair come from ONE parent. pts will have full complement of chromosomes on karyotyping

why should beta blockers be used w caution in pts w DM?

when our body is low on sugar it lets us know in 2 ways: 1. neurogenic sx mediated by excess sympathetic release of NE and epi and ACh. NE and epi sx include tremulousness, palpitations, anxiety. ACh include sweating, hunger, paresthesias 2. neuroglycopenic sx (i.e. when its so bad our brain is low on sugar too): behavioral changes, confusion, visual disturbances, seizures beta blockers block sympathetics and thus block pt awareness of hypoglycemia (i.e. only present w Ach sx of like sweating and hungry). AND they make the it worse bc B2 normally increases gluconeogenesis so blocking B2 means blocking gluconeo! for this reason its better to give DM pts a *selective* B1 blocker

What is crigler najjar syndrome? recurrent

when pts don't have UDP-glucuronosyltransferase and thus lack the enzyme needed to catalyze bilirubin glucuronidation build up of unconjugated bilirubin --> deposition in brain --> symptomatic... die w/i a few years it's cousin Gilbert syndrome is a mild decrease in UDP glucuronosyltransferase. it's asx relatively common & benign

What is Kussmaul sign?

when we breathe in it decreases chest pressure so it allows more blood to go into right heart... this decreases JVP normally Kussmaul's sign is when JVP increases on inspiration. this is d/t *impaired right sided diastolic filling* d/t *constrictive pericarditis* or restrictive cardiomyopathy or tricuspid stenosis

what is the most common virus responsible for viral meningitis?

when we think of meningitis we usually think bacteria, strep pneumo, H flu, N meningitidis etc but if lymphocytes > neutrophils and protein is normal (not low) --> VIRUS most common is ENTEROVIRUSES!! (coxsackie, echovirus, poliovirus).... enteroviruses are resp for > 90% of aseptic meningitis cases!!

What artery runs w the radial nerve? what artery runs w the axillary nerve? what type of fracture might injure the brachial artery? *recurrent*

you keep getting this wrong, but you won't anymore :) deep brachial artery aka profunda brachii (branch of the brachial artery) runs w the radial nerve at the midshaft of the humerus w the axillary nerve runs the *posterior circumflex* near the surgical neck (also anterior circumflex but posterior is associated axillary nerve) brachial artery is injured in *supracondylar fractures of the humerus* i.e. funny bone area

in pts that have a contraindication to anticoagulation therapy but have had DVTs, what do you do for them to prevent embolization?

you place a IVC filter. IVC filters are designed to prevent embolization of DVT from legs to the lung vasculature and are used in pts who have contraindications to anti coagulation (like if pt has hx of GI hemorrhages that req extensive transfusions/hospitalizations)

what would you expect to see in plasma renin activity levels in a pt that was previously HTN and had normal plasma renin activity after you gave them ARBs and thaizide diuretic x3 wks?

you would expect an INCREASE in renin activity but a decrease in BP this is bc vasartan (or any ARB) would inhibit feedbackAG2 which normally feedbacks to lower renin. w/o AG2 your renin will increase thiazides also lower volume which makes JGA freak out which makes macula densa stimulate renin release the decrease in AG2 would cause vasodilation tho so BP would go down, despite plasma renin up if this doesn't happen its d/t *pt non compliance* w meds. effects should be seen @ 3 wks low sodium diet would also cause increase in serum renin and aldosterone levels