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Comments ...

 +0  (nbme24#29)

Up to 80 percent of aortic aneurysms are caused by "hardening of the arteries" (atherosclerosis). Atherosclerosis can develop when cholesterol and fat build up inside the arteries. ... Elevated blood pressure through the aorta can then cause the aortic wall to expand and bulge.

https://www.uwhealth.org/heart-cardiovascular/aortic-aneurysm-causes-symptoms-and-concerns/10971

Also, FA 2019 pg300 says complications of atherosclerosis includes aneurysm

almondbreeze  I was dumb and went for marfan..

 +0  (nbme23#4)

FA2019 pg.479 + spina bifida occulta: failure of cudal neuropore to close, but no herniation + anencephaly: failure of rostral peuropore to close --> no forebrain, open calvarium


 +0  (nbme23#49)

Testosterone--> dihydrotestosterone (DHT)

DHT + early - differentiation of penis, scrotum, prostate + late - prostate growth balding, sebaceous gland activity


 +2  (nbme23#22)

other answer choices

black fly - onchocera volvulus (river blindness) tsetse fly - trypanosoma brucei (african sleepling sickness) deer fly - F. tularensis


 +0  (nbme22#20)

FA 2019 pg 455 on avascular necrosis of bone: Infarction of bone and marrow, usually very painful. Most common site is femoral head (watershed zone) (due to insufficiency of medial circumflex femoral artery). Causes include Corticosteroids, Alcoholism, Sickle cell disease, Trauma, SLE, "the Bends" (caisson/decompression disease), LEgg-Calve- Perthes disease (idiopathic), Gaucher disease, Slipped capital femoral epiphysis- CASTS Bend LEGS.


 +0  (nbme22#34)

uw: EBV commonly infects B cells, stimulating them to enter the cell cycle and proliferate continuously ("transformation or "immortalization"). this is accomplished when EBV-encoded activate proliferative and anti-apoptotic signaling pathways w/i the infected B cell. ... the immortalized B cells maintain the ability to secrete Ig and B-cell activation products (eg. CD23), with very few of them releasing virus particles at any one time.


 +1  (nbme22#28)

UW: the short gastric vv drain blood from the gastric funds into the splenic vein, pancreatic inflammation (e.g. pancreatitis, pancreatic ca.) can cause a blood clot w/i the splenic vein, which can increase pressure in the short gastric veins and lead to gastric varies only in the funds

almondbreeze  b/c pancreatic causes can form blood clot in splenic v, b/c splenic v runs behind pancreas


 +1  (nbme20#14)

'round, semitransparent nodules'

FA2019 p.473 says BCCs are waxy, pink, pearly nodules





Subcomments ...

submitted by karljeon(49),

A man with a Hx of EtOH dependence and chronic abd pain as well as X-ray findings of "calcifications in the mid-upper abdomen" is most likely referring to a chronic pancreatitis.

This leads to a lack of lipase secretion hence, pale, foul-smelling stools with oil droplets per pt Hx. This pt's pancreas also doesn't secrete other enzymes, such as amylases, proteases, nor trypsinogen (to activate other enzymes), so the answer is "generalized malabsorption".

karljeon  p. 367 (FA 2018) +1  
usmlecrasherss  pancreatic insufficiency FA 2019 p375 , +1  
almondbreeze  FA 2019 p391 on chronic pancreatitis +  
almondbreeze  UW: in chronic alcoholic pancreatitis, alcohol induced secretion of protein rich fluid precipitates in pancreatic duct--> forms ductal plugs that calcify +  


submitted by karljeon(49),

A man with a Hx of EtOH dependence and chronic abd pain as well as X-ray findings of "calcifications in the mid-upper abdomen" is most likely referring to a chronic pancreatitis.

This leads to a lack of lipase secretion hence, pale, foul-smelling stools with oil droplets per pt Hx. This pt's pancreas also doesn't secrete other enzymes, such as amylases, proteases, nor trypsinogen (to activate other enzymes), so the answer is "generalized malabsorption".

karljeon  p. 367 (FA 2018) +1  
usmlecrasherss  pancreatic insufficiency FA 2019 p375 , +1  
almondbreeze  FA 2019 p391 on chronic pancreatitis +  
almondbreeze  UW: in chronic alcoholic pancreatitis, alcohol induced secretion of protein rich fluid precipitates in pancreatic duct--> forms ductal plugs that calcify +  


submitted by mousie(126),

"dronates" are Bisphosphonates, commonly used to prevent/treat osteoporosis. Most common adverse effects are Esophagitis (patients should take with water and be upright for at least 30minutes), Osteonecrosis of the jaw, and atypical femoral stress fractures. -taken right from FA 2018 pg 471

almondbreeze  FA 2019 pg 248 pill-induced esophagitis : bisphosphonates, ferrous sulfate, NSAIDs, potassium chloroide, tetracyclines +  


submitted by neonem(366),

I think metastasis was the best option here because there are multiple malignant neoplasms... primary cancers tend to start as a single mass in the tissue of origin. In the lung, metastases are more common than primary neoplasms.

dbg  I seriously could not figure out whether those white opacities were actual lesions or reflections from the actual picture (flash light) ... mind went all the way maybe this is the shiny pleura so they're going after mesothelioma. smh +2  
dbg  shiny pleura with tiiiiny granulations if you look closely. but obviously was far off +  
et-tu-bromocriptine  "Multiple cannonball lesions" is indicative of a metastatic cancer. I think if they were leaning towards a mesothelioma, they'd show the border/edge of the lung ensheathed by a malignant neoplasm (see image): https://library.med.utah.edu/WebPath/jpeg1/LUNG081.jpg +1  
bullshitusmle  guys something I learned from NBMEs is that if there is a clinical vignette dont even look at the images they give you ,they are all useless and time-consuming +1  
goaiable  The way i narrowed it down was that the patient had signs of weight loss since three months whereas her cough developed recently (3 weeks). If the cancer arose in the lung then I think the cough or other pulmonary symptoms should emerge earlier. +  
almondbreeze  FA2019 pg 669 in the lung, metastasis (usually multiple lesions) are more common the primary neoplasms. most often from breast, colon, prostate, and bladder ca. +  


submitted by colonelred_(66),

Looked it up and found that because you’re in a supine position for a long time you’re going to have increased venous return which leads to increased CO. This negatively feedsback on RAAS, leading to decreased aldosterone. As a result, you’re going to have increased diuresis which leads to decreased blood and plasma volume.

medstruggle  Doesn’t supine position compress IVC leading to decreased venous return? (This is the pathophys of supine hypotension syndrome.) There was a UWorld questions about this ... +3  
tea-cats-biscuits  @medstruggle *Supine position* decreases blood pooling in the legs and decreases the effect of gravity. *Supine hypotension syndrome*, on the other hand, seems specific to a pregnant female, since the gravid uterus will compress the IVC; in an average pt, there wouldn’t be the same postural compression. +3  
welpdedelp  this was the exact same reasoning I used, but I thought the RAAS would inactivate which would lead to less aldosterone and less sodium retention +1  
yotsubato  You gotta be preggers to compress your IVC +2  
nwinkelmann  Could you also think of it in a purely "rest/digest" vs "fight/fright/flight" response, i.e. you're PNS is active, so your HR and subsequently your CO is less? But the explanation given above does make sense. Also because I think just saying someone is one bed rest leaves a lot up for interpretation, maybe not with this patient because his pelvis is broken, but lots of people on bed rest aren't lying flat.... ? +1  
urachus  wouldnt low aldosterone cause low plasma sodium? choice B +2  
kpjk  could it be that, while low aldosterone levels decrease plasma sodium levels- there is also decrease in blood volume(plasma),so there wont be a decrease in the "concentration" of sodium +  
almondbreeze  FA 2019 pg 306 on Lt heart failure induced orthopnea - Shortness of breath when supine: increased venous return from redistribution of blood +  
almondbreeze  if there was no HF, it would lead to increased CO --> decreased aldosterone +  


submitted by colonelred_(66),

Looked it up and found that because you’re in a supine position for a long time you’re going to have increased venous return which leads to increased CO. This negatively feedsback on RAAS, leading to decreased aldosterone. As a result, you’re going to have increased diuresis which leads to decreased blood and plasma volume.

medstruggle  Doesn’t supine position compress IVC leading to decreased venous return? (This is the pathophys of supine hypotension syndrome.) There was a UWorld questions about this ... +3  
tea-cats-biscuits  @medstruggle *Supine position* decreases blood pooling in the legs and decreases the effect of gravity. *Supine hypotension syndrome*, on the other hand, seems specific to a pregnant female, since the gravid uterus will compress the IVC; in an average pt, there wouldn’t be the same postural compression. +3  
welpdedelp  this was the exact same reasoning I used, but I thought the RAAS would inactivate which would lead to less aldosterone and less sodium retention +1  
yotsubato  You gotta be preggers to compress your IVC +2  
nwinkelmann  Could you also think of it in a purely "rest/digest" vs "fight/fright/flight" response, i.e. you're PNS is active, so your HR and subsequently your CO is less? But the explanation given above does make sense. Also because I think just saying someone is one bed rest leaves a lot up for interpretation, maybe not with this patient because his pelvis is broken, but lots of people on bed rest aren't lying flat.... ? +1  
urachus  wouldnt low aldosterone cause low plasma sodium? choice B +2  
kpjk  could it be that, while low aldosterone levels decrease plasma sodium levels- there is also decrease in blood volume(plasma),so there wont be a decrease in the "concentration" of sodium +  
almondbreeze  FA 2019 pg 306 on Lt heart failure induced orthopnea - Shortness of breath when supine: increased venous return from redistribution of blood +  
almondbreeze  if there was no HF, it would lead to increased CO --> decreased aldosterone +  


Fibronectin is an extracellular matrix glycoprotein, while lamin is an intermediate filament that specifically provides support to the cell nucleus. Don’t confuse lamin with laminin (science hates us clearly); laminin is like fibronectin, an ECM glycoprotein and a major component of the basal lamina of basement membranes.

masonkingcobra  Lamin looks like a "cross" and held up Jesus and the basal lamina is super important just like jesus (you bet there are people who believe this) https://answersingenesis.org/biology/microbiology/laminin-and-the-cross/ +7  
dr.xx  blasphemy @masonkingcobra +  
luciana  I clearly confused lamin with laminin, now I know +1  
almondbreeze  FA 2019 pg 48 lamin +  
almondbreeze  picked tubulin but i guess tubulin makes up microtubules and therefore is spherical +  


Fibronectin is an extracellular matrix glycoprotein, while lamin is an intermediate filament that specifically provides support to the cell nucleus. Don’t confuse lamin with laminin (science hates us clearly); laminin is like fibronectin, an ECM glycoprotein and a major component of the basal lamina of basement membranes.

masonkingcobra  Lamin looks like a "cross" and held up Jesus and the basal lamina is super important just like jesus (you bet there are people who believe this) https://answersingenesis.org/biology/microbiology/laminin-and-the-cross/ +7  
dr.xx  blasphemy @masonkingcobra +  
luciana  I clearly confused lamin with laminin, now I know +1  
almondbreeze  FA 2019 pg 48 lamin +  
almondbreeze  picked tubulin but i guess tubulin makes up microtubules and therefore is spherical +  


Up to 80 percent of aortic aneurysms are caused by "hardening of the arteries" (atherosclerosis). Atherosclerosis can develop when cholesterol and fat build up inside the arteries. ... Elevated blood pressure through the aorta can then cause the aortic wall to expand and bulge.

https://www.uwhealth.org/heart-cardiovascular/aortic-aneurysm-causes-symptoms-and-concerns/10971

Also, FA 2019 pg300 says complications of atherosclerosis includes aneurysm

almondbreeze  I was dumb and went for marfan.. +1  


submitted by famylife(49),

"Innervates the muscles of the medial compartment of the thigh (obturator externus, adductor longus, adductor brevis, adductor magnus and gracilis)."

https://teachmeanatomy.info/lower-limb/nerves/obturator-nerve/

famylife  Pics: https://www.google.com/search?rlz=1C1CHZL_enUS753US753&biw=1368&bih=809&tbm=isch&sa=1&ei=W6P6XJa3NMSQggfa35YY&q=obturator+nerve+adductors&oq=obturator+nerve+adductors&gs_l=img.3...9024.9024..9214...0.0..0.82.82.1......0....1..gws-wiz-img.rjc4GuKQAYo#imgrc=ZqWtUuDxpzeNMM: +  
almondbreeze  FA 2019 pg 444 +  


submitted by docred123(3),

Can anyone further explain this?! I could eliminate a few item choices and I guessed correctly, just need more information! Thanks

wired-in  Patient has 5 yr h/o hep C, so it is chronic. Chronic inflammation is characterized by presence of lymphocytes & plasma cells while neutrophils is more characteristic of acute inflammation (Pathoma Ch. 2). AFP is within reference range so probably not HCC. Choice D, palisading lymphocytes & giant cells suggests granuloma which isn't typical of hep C. +25  
almondbreeze  Fa2019 pg 215, 217 on acute/chronic inflammation +  


submitted by notadoctor(106),

According to Goljan, polycythemia vera is one of the most common causes of Budd-Chiari syndrome. According to FA, Budd-Chiari is associated more generally with hypercoagulable states, polycythemia vera, postpartum states, and HCC.

Hepatic cirrhosis can be ruled out based on the time course of the patient's presentation - he was fine 2 weeks ago and the abdominal pain started an hour ago.

krewfoo99  Also in cirrhosis, the liver wont be enlarged or tender on palpation +  
almondbreeze  @krewfoo99 Good job. accoring to FA2019 pg.368, congestive liver disease (hepatomegaly, ascites, varices, abdominal pain, liver failiure) seems to be the key in Budd-Chiari SD +  


submitted by sajaqua1(346),

Budd-Chiari syndrome occurs when there is occlusion of the hepatic vein or the hepatic vein fails to drain into the IVC. This can be caused by thrombosis of the hepatic vein, or by right sided heart failure (causing blood to 'back up' everywhere, but its manifestation through the hepatic vein are all the signs of Budd-Chiari syndrome). Anything that can increase the risk of thrombosis can then increase the risk of Budd-Chiari syndrome. This includes polycythemia vera, a hypercoagulable state. Our patient and PV but missed his appointment two weeks ago. He now presents with scleral icterus, an enlarged liver, and some signs of portal hypertension. Thrombosis of the only anatomical option presented that covers all of this is the hepatic vein ie our patient has Budd-Chiari. Remember that Budd-Chiari will have a "nutmeg liver" appearance on gross pathology.

B) Hepatic cirrhosis- it's entirely possible our patient does have hepatic cirrhosis for unrelated reasons, however the acute onset makes this less likely. C) Pancreatic carcinoma- pancreatic carcinoma obstruction of the common bile duct could cause a 'back up' of bile, ultimately causing some liver damage and scleral icterus. However once again the timing makes this unlikely. D) Portal vein thrombosis- portal vein thrombosis could cause some splenic enlargement and portal hypertension. However, its obstruction would not cause a tender, enlarged liver because it is upstream. E) Primary hemochromatosis- due to a defect in hepcidin production, this iron overload presents with darkened skin, insulin disregulation, hepatic damage (with the potential for hepatocellular carcinoma) and heart disease (restrictive or dilated cardiomyopathy, depending on your source). The only one of these signs that our patient has is an enlarged liver.

almondbreeze  FA 2019 pg 386 +  


submitted by defalty98(3),

Why are we complicating things? Change in the bases will destroy the palindromic sequence required for any restriction endonuclease to work. Methylation is the only option that makes sense.

arcanumm  This makes sense have reading what your comment. I overlooked this and just assumed the GATC was a mutation that allowed the restriction enzyme to work on the mutant only. +1  
arcanumm  it makes even more sense when looking at "numerous small fragments." Methylation is truly the obvious answer here in retrospect. +1  
bgiri  DNAse can also cause a change in base by breaking down dna at the GATC sequence? +  
almondbreeze  @bgiri Had the same reasoning - according to wiki, DNase catalyzes the hydrolytic cleavage of phosphodiester linkages in the DNA backbone, thus degrading DNA. +  


Patient is current breast-fed, so we can eliminate fructose (fructose is found in honey and fruits and some formula, but not in breast milk). Patient has reducing substances but no glucose in the urine, so he must some non-glucose sugar. My differential for reducing non-glucose sugars in the urine is disorders fructose metabolism or galactose metabolism. We have eliminated fructose, so that leaves us with galactokinase deficiency or classic galactosemia.

sympathetikey  & Galactokinase deficiency would be much milder. +5  
smc213  Big was soybean formula not giving any issues. Soy-milk can be used as a substitute formula in patients with Classic Galactosemia since it contains sucrose (->fructose and glucose). +1  
oslerweberenu  Why can't this be glucose 6 phosphatase deficiency Confused me +  
almondbreeze  @oslerweberenu G6PD - increased RBC susceptibility to oxidant stress (eg, sulfa drugs, antimalarials, infections, fava beans) -> hemolysis; has nothing to do with presence of reducing sugar +  
makinallkindzofgainz  @almondbreeze; Glucose-6-phosphatase deficiency is Von Gierke disease, they are not referring to G6PD deficiency (an entirely seperate disease) +1  


submitted by lfsuarez(114),

This question asks about the mechanism of phototherapy as it relates to neonatal jaundice. With phototherapy, bilirubin is simply converted to water soluble isomers that are then able to be excreted by the kidney. This however does not conjugate the bilirubin.

almondbreeze  FA 2019 pg 387 +  
abhishek021196  Physiologic neonatal jaundice At birth, immature UDP-glucuronosyltransferase = unconjugated hyperbilirubinemia = jaundice/ kernicterus (deposition of unconjugated, lipid-soluble bilirubin in the brain, particularly basal ganglia). Occurs after first 24 hours of life and usually resolves without treatment in 1–2 weeks. Treatment: phototherapy (non-UV) isomerizes unconjugated bilirubin to water-soluble form. +  


submitted by nwinkelmann(185),

@gh889 "Because the obstruction is above the alveolar regions there is a decrease in air flow, not lung volumes, which would make this an obstructive pathology" is the most helpful explanation. If you know the most basic definition/pathophysiology of obstructive vs restrictive (which I do, just didn't in that most simplified way), then you can figure anything out. If something is impacting airway flow = obstructive, if something is impacting airway volume = restrictive. THANK YOU!

burningmoon  How about emphysema? airway volume changed but it's obstructive. +1  
almondbreeze  i think OP meant to say that something DECREASING airway volume = restrictive +1  


submitted by asapdoc(31),

Dr.Goljan explains it really well on the audio. I will just give the basic idea. All the hemoglobins have alpha in it therefore you cannot notice it on hemoglobin electrophoresis

someduck3  Just to add to this; a-thal is due to a deletion. While b-thal is due to a mutation. If they had a b-thal there would be target cells. a-thal just presents as microcytic & hypochromic. +3  
almondbreeze  looks like a-thal can have target cells too. Individuals with alpha thalassemia trait (-α/-α or --/αα) are asymptomatic, with a normal CBC. The peripheral blood smear typically shows hypochromia, microcytosis, and target cells. (emedicine.medscape.com › article › 955496-clinical) +  


submitted by krewfoo99(40),

So basically what this is saying that DNA will be transmitted to the progeny not RNA. So DNA will replicate in the G2 phase and transfer of DNA material to progeny will occur in the M phase. The RNA may be mutated and making defective products, but this will not transmit into the progeny, thus not affecting species survival based on RNA mutations.

bk2458  makes sense!! +  
almondbreeze  good work +  


submitted by keycompany(183),

This question is disguised. What they are really asking is "what is the sole determinant of species survival"? The only answer is the ability to procreate. Because DNA Polymerase has proof-reading activity, progeny will be unaffected by RNA Polymerases lack of proof-reading activity.

ls3076  the phrasing of this explanation doesnt make sense to me. +3  
ls3076  oh wait sorry i just read it again. So instead of proofreading how are errors handled with RNA? +  
thomasburton  Think the point is basically although errors with RNA polymerase make make the bacterium not very good at infecting or killing or whatever it does not affect replication as it is not used during replication! +4  
almondbreeze  common sense asked in a very very convoluted way.. +  


submitted by monkd(6),

Am I crazy or did Uworld not have a question that stated Statins are the most effective drug regardless of baseline lipids. This logic threw my off.

adisdiadochokinetic  You are not crazy. I got this question wrong for the same reason but here's why I think NBME was going with fibrates. You can use the Friedewald equation to calculate LDL cholesterol from the values they give. This equation is LDL= Total Cholesterol-HDL Cholesterol-(Triglycerides/5). The Triglycerides/5 term is an estimate for VLDL. If you calculate it in this case you get an LDL of 120 which is firmly normal and thus the patient would ostensibly not benefit from statin therapy. +8  
hello36654  omg when the hell am I going to remember this equation? Jesuusssssss, this kind of details makes me want to give up on STEP +2  
almondbreeze  Her goal LDL should still be <100, bc she has 3 CHD risk equivalents (https://www.aafp.org/afp/2002/0301/p871.html#afp20020301p871-t3) CHD risk equivalent=the major risk factors that modify LDL goals 1) age(M>45, F>55), 2) smoking status, 3) hypertension(>140/90), 4) ow HDL level (<40), and 5) family history. (https://www.aafp.org/afp/2002/0301/p871.html#sec-4) +  
almondbreeze  *low HDL level (refer to table 3 of the article) +  
makinallkindzofgainz  These guys are hitting up attending-level cardiovascular risk factor calculations, meanwhile I picked statins because I think I remember that they help the heart +4  


submitted by monkd(6),

Am I crazy or did Uworld not have a question that stated Statins are the most effective drug regardless of baseline lipids. This logic threw my off.

adisdiadochokinetic  You are not crazy. I got this question wrong for the same reason but here's why I think NBME was going with fibrates. You can use the Friedewald equation to calculate LDL cholesterol from the values they give. This equation is LDL= Total Cholesterol-HDL Cholesterol-(Triglycerides/5). The Triglycerides/5 term is an estimate for VLDL. If you calculate it in this case you get an LDL of 120 which is firmly normal and thus the patient would ostensibly not benefit from statin therapy. +8  
hello36654  omg when the hell am I going to remember this equation? Jesuusssssss, this kind of details makes me want to give up on STEP +2  
almondbreeze  Her goal LDL should still be <100, bc she has 3 CHD risk equivalents (https://www.aafp.org/afp/2002/0301/p871.html#afp20020301p871-t3) CHD risk equivalent=the major risk factors that modify LDL goals 1) age(M>45, F>55), 2) smoking status, 3) hypertension(>140/90), 4) ow HDL level (<40), and 5) family history. (https://www.aafp.org/afp/2002/0301/p871.html#sec-4) +  
almondbreeze  *low HDL level (refer to table 3 of the article) +  
makinallkindzofgainz  These guys are hitting up attending-level cardiovascular risk factor calculations, meanwhile I picked statins because I think I remember that they help the heart +4  


submitted by hipster_do(5),

I’m going to say it’s X linked agammaglobulinemia rather than SCID, but the difference between these two are tiny but this is why I think it’s the former:

  • Boy (increased risk but both BA and SCID are x linked)
  • Recurrent bacterial infections but don’t mention diarrhea or thrush which is in SCID
  • Timeline is after 6 months, so the mother’s antibodies wore off.

SCID should be immediately because they just don’t have the IL2 receptors. CVID shows up when they’re 20-40 years old. You get absent germinal centers in both. No mention of absent thymic shadow which is in SCID.

placebo079  “Uniformly” low is also a clue; in CVID they are not. +3  
tea-cats-biscuits  This makes sense, though what really threw me off was that in Classic Bruton’s Agammaglobulinemia there’s near-zero B counts though (or at least that’s what FA and UTD says, “Absent B cells in peripheral blood” FA 116, 2018). The Q says the leukocyte count was normal though. Wouldn’t the leukocyte count include lymphocytes in the differential? And wouldn’t lymphocytes be low due to the near complete lack of B cells in peripheral circulation if it was BA? +1  
partybrockk  @tea-cats-biscuits Bruton’s is a failure of B cells to /MATURE/. So you get normal lymphocyte counts, decreased levels of immunoglobulins, and absent germinal centers. +3  
tea-cats-biscuits  @partybrockk That makes sense to me, but I keep getting hung up on how that’s not what either FA or UTD says about the classic lab findings of XLA. UTD specifically says this: “Laboratory findings include hypogammaglobulinemia/agammaglobulinemia, deficient antibody responses to immunizations, and absent or markedly reduced B cells in the blood,” and I previously quoted FA. I suppose it doesn’t really matter, but it’s definitely a bit frustrating unless I’m missing something about how absent B cells in the blood wouldn’t correlate to a decreased lymphocyte count ... +2  
temmy  please correct me if i am wrong cos i might be but my logic was there is decreases immunoglobulin uniformly meaning the B cells are uniformly absent and since they develop in the germinal center, the germinal center will be absent. +1  
almondbreeze  Picked 'decreased # of CD4 lymphocytes'.. ->Both CD4 and CD8 T lymphocytes were affected; the decrease was most pronounced for naïve T cells. (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1809006/) +  


submitted by meningitis(267),

hydrocholorothiazide is DOC for Nephrogenic Diabetes insipidus because it paradoxically causes an increase in BP by increasing sodium absorption and thus water absorption, Pathoma explains this nicely.

Desmopressin is incorrect because upon fasting (fluid restriction) ADH is increased meaning ADH is being released Centrally but is not working in the kidneys at the V2 receptors of the epithelial renal cells at Collecting duct.

On that note, Amiloride is used for Lithium induced nephrogenic DI.

hello  Where in Pathoma? I couldn't find it. +1  
almondbreeze  also sketchy says that thiazide s decrease the amount of lithium cleared--> lithium toxicity +1  
paperbackwriter  Agh confused as well because FA2019 (pg 562) says that thiazides are implicated in lithium toxicity D: +  
paperbackwriter  OOPS, please ignore last comment. I just realized that this Q stem never mentioned lithium. And on top of that @meningitis mentioned that amiloride is used if lithium induced. Apologies. +  


submitted by gh889(55),

according to uptodate thiazides cause a mild hypovolemic state thus your PCT will see more Na and H2O --> by principle that the PCT always reabsorbs 60% of what it sees, it will reabsorb more water and Na.

almondbreeze  in sketchy as well +  


submitted by imgdoc(71),

I think alot of people might have over emphasized how important ANP and BNP really are, yes it is important to know these peptides get secreted by the atrial/ventricular myocardium during heart failure. However their overall effectiveness in treating heart failure is zilch, a preceptor told me that if ANP and BNP were so useful in natriuresis then why do we give diuretics? It's because RAAS overpowers this system hence causing negative effects and the endless loop of heart failure. AKA why we give ACE inhibitors.

Knowing that ANP gets neutralized by the RAAS system, we can shift our focus back to heart failure in this patient, where cardiac output is decreased, leading to ADH secretion and finally dilutional hyponatremia.

almondbreeze  a concept continuously emphasized by uw, but I get always wrong :'( +  
almondbreeze  good work done! +  
raffff  why does the body make anp at all since its so useless +2  
makinallkindzofgainz  @raffff - at least BNP gives us a good marker for heart failure exacerbations :) thanks body! +  
mdrahimi7  Also read my answer mdrahimi7. I think it seems logical... +  


submitted by imgdoc(71),

I think alot of people might have over emphasized how important ANP and BNP really are, yes it is important to know these peptides get secreted by the atrial/ventricular myocardium during heart failure. However their overall effectiveness in treating heart failure is zilch, a preceptor told me that if ANP and BNP were so useful in natriuresis then why do we give diuretics? It's because RAAS overpowers this system hence causing negative effects and the endless loop of heart failure. AKA why we give ACE inhibitors.

Knowing that ANP gets neutralized by the RAAS system, we can shift our focus back to heart failure in this patient, where cardiac output is decreased, leading to ADH secretion and finally dilutional hyponatremia.

almondbreeze  a concept continuously emphasized by uw, but I get always wrong :'( +  
almondbreeze  good work done! +  
raffff  why does the body make anp at all since its so useless +2  
makinallkindzofgainz  @raffff - at least BNP gives us a good marker for heart failure exacerbations :) thanks body! +  
mdrahimi7  Also read my answer mdrahimi7. I think it seems logical... +  


submitted by hayayah(599),

This is a patient case of postpartum thyroiditis. Can arise up to a year after delivery and has lymphocytic infiltrate.

almondbreeze  FA 2019 pg 338 +1  


UW: the short gastric vv drain blood from the gastric funds into the splenic vein, pancreatic inflammation (e.g. pancreatitis, pancreatic ca.) can cause a blood clot w/i the splenic vein, which can increase pressure in the short gastric veins and lead to gastric varies only in the funds

almondbreeze  b/c pancreatic causes can form blood clot in splenic v, b/c splenic v runs behind pancreas +  


submitted by welpdedelp(137),

It was a Ferruginous bodies--> asbestosis. Ferruginous bodies are believed to be formed by macrophages that have phagocytosed and attempted to digest the fibers.

almondbreeze  info about ferruginous bodies being mf can't be found on FA/UW :'( they just say it's 'material' +  
taediggity  FA 2020 677, FA 2019 659... mf?? mofos?? +  
69_nbme_420  Just to add: The question asks what cell type initiated the Fibrosis → Alveolar macrophages engulf the particles and induce fibrosis (same pathophys for all Pneumoconiosis). Pathoma 2019 Pg 92 +1  


submitted by rogeliogs(6),

My approach to this question was more just focusing in the info they are giving. None of the other option makes sense because there is not evidence to talk about them. I was very tempted to pick the "decrease leptin production" but I remembered Dr Goljan saying "Think simple, think cheap, they are not trying to trick you." So, chubby parents = chubby kids.

almondbreeze  thought his words on "think cheap" had to do with treatments - i.e. exercise +  


submitted by jooceman739(15),

Retinoblastoma:

The physician said the boy is unlikely to develop any other neoplasms, so he doesn't have the inherited Rb mutation.

In this case, he has the sporadic retinoblastoma. Sporadic retinoblastoma requires two somatic mutations of Rb in the same retinal cell.

Just as a side note: Inherited retinoblastomas tend to be bilateral. Sporadic are unilateral.

carls14  aren't retinal cells a type of somatic cell? Why not is the mutation not considered in the somatic cell of the child? +4  
omerta  Although this mutation would be considered somatic, I believe the question is just asking you to be specific as to which cells. If you answered "somatic cells of the child," that's quite broad and could apply to almost anything. +6  
kernicterusthefrog  I had the same struggle and thought process. +1  
eacv  There is a Uworld qx that explain this in detail> ID: 863 +2  
arcanumm  I read the answer options too fast so got this wrong. It is a somatic cell type, but somatic in general implies a higher risk for developing other cancers. The hint here is that the physician stated he is unlikely to develop any other neoplasms, so it is a specific double hit mutation in the retina. +2  
almondbreeze  wouldn't she have any possibility of developing osteosarcoma as well? :( +  
almondbreeze  did some reading and it seems like osteosarcoma only occurs in familial retinoblastoma with RB mutation +  


submitted by jooceman739(15),

Retinoblastoma:

The physician said the boy is unlikely to develop any other neoplasms, so he doesn't have the inherited Rb mutation.

In this case, he has the sporadic retinoblastoma. Sporadic retinoblastoma requires two somatic mutations of Rb in the same retinal cell.

Just as a side note: Inherited retinoblastomas tend to be bilateral. Sporadic are unilateral.

carls14  aren't retinal cells a type of somatic cell? Why not is the mutation not considered in the somatic cell of the child? +4  
omerta  Although this mutation would be considered somatic, I believe the question is just asking you to be specific as to which cells. If you answered "somatic cells of the child," that's quite broad and could apply to almost anything. +6  
kernicterusthefrog  I had the same struggle and thought process. +1  
eacv  There is a Uworld qx that explain this in detail> ID: 863 +2  
arcanumm  I read the answer options too fast so got this wrong. It is a somatic cell type, but somatic in general implies a higher risk for developing other cancers. The hint here is that the physician stated he is unlikely to develop any other neoplasms, so it is a specific double hit mutation in the retina. +2  
almondbreeze  wouldn't she have any possibility of developing osteosarcoma as well? :( +  
almondbreeze  did some reading and it seems like osteosarcoma only occurs in familial retinoblastoma with RB mutation +  


submitted by armymed88(29),

Wound healing inflammatory for up til 3 days (clots, PMNs, macros) Proliferative 3days til weeks- granulation tissue, new vessels, new epithelium, contraction (repair and regeneration) Remodel 1wk til 6m- replace collagen III with I, increase strength (up to 60-70% original strength possible)

john055  it looks like the patient has new onset erythema which points to infection and I think neutrophils make sense. I myself have marked angiogenesis but I did it offline. Is angiogenesis the right answer ? +  
almondbreeze  yup +  
almondbreeze  according to FA 2019 pg217, neutrophil is present during inflammatory phase- i.e. only up to 3d after the wound. After that we have the proliferative phase with granulation tiss. and angiogenesis, epithelial cell proliferation, dissolution of clot, and wound contraction (involved cells: fibroblasts, myofibroblasts, endothelial cells, keratinocytes, mf) +  
mitchell_to_lakers  why not fibrosis? +  


submitted by armymed88(29),

Wound healing inflammatory for up til 3 days (clots, PMNs, macros) Proliferative 3days til weeks- granulation tissue, new vessels, new epithelium, contraction (repair and regeneration) Remodel 1wk til 6m- replace collagen III with I, increase strength (up to 60-70% original strength possible)

john055  it looks like the patient has new onset erythema which points to infection and I think neutrophils make sense. I myself have marked angiogenesis but I did it offline. Is angiogenesis the right answer ? +  
almondbreeze  yup +  
almondbreeze  according to FA 2019 pg217, neutrophil is present during inflammatory phase- i.e. only up to 3d after the wound. After that we have the proliferative phase with granulation tiss. and angiogenesis, epithelial cell proliferation, dissolution of clot, and wound contraction (involved cells: fibroblasts, myofibroblasts, endothelial cells, keratinocytes, mf) +  
mitchell_to_lakers  why not fibrosis? +  


submitted by calcium196(10),

Ubiquitin-mediated proteolysis is not reversibly affected by insulin. The question asks for reversible ways that insulin affects it, and ubiquitination would lead to degradation via proteases, which is not reversible. Nuclear/cytoplasmic shunting makes sense because FOXO is a transcription factor, so it can’t do its job if it is in the cytoplasm!

meningitis  Thank you for your explanation! One question: How about the serine phosphorylation? Is it answered by pure memorization that the FOXO TF is serine phosphorylated, or is it a general fact that all TF's are serine-threonine phosphorylated? +  
tsl19  I'm not sure, but it may be as simple as this: ubiquitin-mediated proteolysis is irreversible, but both N/C shuttling and phosphorylation are generally reversible processes. +  
didelphus  I also guessed that FOXO must be a part of the PI3K pathway, since insulin regulates metabolism through PI3K and the question stem specifically mentions that. Phosphorylation is a major part of that pathway, so even indirectly phosphorylation would regulate FOXO. Frustrating question. +6  
niboonsh  yes, FOXO is affected downstream of the activation of PI3K. This is a really good video that explains the whole cascade https://www.youtube.com/watch?v=ewgLd9N3s-4 +  
alexb  According to wikipedia (https://en.wikipedia.org/wiki/FOXO1) phosphorylation of FOXO1 is irreversible. This is referring to phosphorylation of serine residues on FOXO by Akt, which occurs in response to insulin. But the NBME answer suggests it's reversible. What's up? +1  
almondbreeze  could wiki be wrong on phosphorylation being irreversible? according to this article, it is a reversible process: regulation of FoxO transcription factors by reversible phosphorylation and acetylation (https://www.sciencedirect.com/science/article/pii/S0167488911000735#s0010) some wiki info, however, is helpful : In its un-phosphorylated state, FOXO1 is localized to the nucleus, where it binds to the insulin response sequence located in the promoter for glucose 6-phosphatase and increases its rate of transcription. FOXO1, through increasing transcription of glucose-6-phosphatase, indirectly increases the rate of hepatic glucose production.[19] However, when FOXO1 is phosphorylated by Akt on Thr-24, Ser-256, and Ser-319, it is excluded from the nucleus, where it is then ubiquitinated and degraded. The phosphorylation of FOXO1 by Akt subsequently decreases the hepatic glucose production through a decrease in transcription of glucose 6-phosphatase. +  


submitted by assoplasty(64),

Fats are ketogenic (except odd chain FA), so they produce ketones for energy production (Acetyl-CoA) rather than glucose. If the question asked what the primary source of energy production was, it would still be glycogen (and not ketones), because this is within 24 hours. However after 24 hours the answer could be ketone bodies. Regardless, the question specifically said the pt had a serum glucose of 100, indicating that we are looking for something that provides a substrate for gluconeogenesis.

During periods of starvation, substrates for gluconeogenesis come from two sources: (1) breakdown of existing muscle, or (2) via odd-chain FA through propionyl-CoA. (*Valine also feeds into propionyl CoA, but is not involved during starvation --> see below)

(1) The alanine-pyruvate cycle provides this (glutamine in muscle + pyruvate --> alanine --> goes to liver --> transamination to alpha-ketoglutorate --> pyruvate is separated from glutamine --> glutamine goes to urea cycle, pyruvate goes on to gluconeogenesis). Lactate can also be used (this could have been a right answer if it were listed).

(2) Odd chain FAs are also glucogenic, but stearic acid (provided in the answer choice) isn’t odd chain, so it is only ketogenic and can be ruled out.

Although valine (and other branched a.a.) feed into Propionyl-CoA, they are not used in starvation because starvation strictly relies on hepatic gluconeogenesis. These a.a. are not metabolized in the liver because the liver lacks branched-chain a.a. transferase enzyme. In First Aid, Biochem section, under Fasting/Starvation, in both the “fasting state” (which is within the time frame of this question), or the “starvation state,” both utilize hepatic gluconeogenesis. My assumption is that valine is used during regular metabolism, and not during periods of starvation.

hello  I want to re-emphasize something that @assoplasty has already stated :). The Q-stem states serum glucose = 100, and the Q asks why the patient is able to maintain normoglycemia. Therefore, you can immediately eliminate choices A and C because acetoacetate and beta-hydroxybutyrate are sources of energy during ketogenesis -- ketogenesis does not provide glucose energy sources. +2  
chandlerbas  ^ this checks out: valine and isoleucine are broken down in the muscle into branched chain 2 oxo acid via branched chain aminotransferase (reversible) then the valine and isoleucine leave the muscle and swims to the liver to be acted on by branched chain 2 oxo acid DH (irreversible). So bascially the process from taking BCAA valine and isoleucine requires 2 enzymes. the first enzyme is in the muscle, and the second enzyme is in the liver (for simplification purposes --> both organs contain both enzymes but dont have the same affinity for their substrate). source: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1147506/?page=4 so you're right to say that the liver +2  
toxoplasmabartonella  Thank you for such a great explanation. Isn't it glutamate instead of glutamine that combines with pyruvate in muscle to yield alanine for Cahill cycle? +1  
almondbreeze  @ toxoplasmabartonella think you are right +  


submitted by hayayah(599),

Cysteine-cysteine chemokine receptor 5 (CCR5) is a protein found on the surface of CD4 cells.

yotsubato  Note, this is NOT in FA +  
sbryant6  It is in UWorld. +2  
almondbreeze  it's in FA2019 pg.110 +1  
almondbreeze  but missing the full name for CCR5 +1  


submitted by hayayah(599),

Cysteine-cysteine chemokine receptor 5 (CCR5) is a protein found on the surface of CD4 cells.

yotsubato  Note, this is NOT in FA +  
sbryant6  It is in UWorld. +2  
almondbreeze  it's in FA2019 pg.110 +1  
almondbreeze  but missing the full name for CCR5 +1  


Question asked for gram positive cocci in CHAINS. S. aureus forms clusters, eliminating it. This leaves Enterococcus faecalis and Group A strep. E. faecalis is associated with UTIs.

almondbreeze  get the clinicals but got thrown off by 'chain'. FA2019 pg.137 also says coccus = berry, strepto =twisted (chain), differentiating the two:( +1  


submitted by mcl(375),

Patient may have hereditary angioedema, which is associated with "recurrent attacks of intense, massive, localized subcutaneous edema involving the extremities, genitalia, face, or trunk, or submucosal edema of upper airway or bowels". The article goes on to say "C1-esterase inhibitor works directly on the complement and contact plasma cascades to reduce bradykinin release" which is also probably good to know.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3666183/

notadoctor  Thought this was a trick question as C1 esterase deficiency also results in a decrease in C4. However, the second answer choice was not referring to C4 but to C4 binding protein, which I now know is different. I also didn't realize C1 esterase was technically a complement protein. +4  
youssefa  Based on many sources hereditary angioedema does NOT cause a rash (urticaria) which is a main differentiating point between angioedema and allergy. This mislead me in this question. Any clarification? +10  
ergogenic22  +1 on the above because uptodate states that c1 esterase inhibitor deficiency, both acquired and nonhereditary, are both non-urticarial, non-pruritic, and that is confirmed by the above linked article +1  
sahusema  Question writer probably didn't know the difference between cutaneous urticaria and subcutaneous edema. +3  
almondbreeze  same. got it wrong bc the pt didn't have sx of hereditary angioedema - swollen lips and eyelids +1  


submitted by readit(8),

Why is is not pseudo aneurysm?

"Aortic pseudoaneurysms typically occur as a result of trauma +/- intervention, a considered subset of traumatic aortic injury in the majority of cases. They can be acute or chronic."

https://radiopaedia.org/articles/aortic-pseudoaneurysm?lang=us

readit  *same goes for saccular aneurysm, which also is usually 2/2 trauma +  
samsam3711  In the question stem there is no indication of trauma so it would be hard to just assume that +  
almondbreeze  see my comment above for marfan syndrome. might help +  
drzed  This is because a pseudoaneurysm is between the media and adventitia, and is incited by trauma; a dissection is between the intima and the media and is a result of hypertension causing an intimal tear. The history points toward cocaine -> hypertension rather than penetrating trauma. +  


submitted by neonem(366),

Major risk factor for aortic dissection is hypertension, and in this case might be due to cocaine use, which causes marked hypertension. Dissections cause a tear in the tunica intima -- blood can flow backwards into the pericardium and cause tamponade. This manifests as crackles in the lung due to poor left ventricular function (filling/diastolic problem due to compression).

forerofore  there is another clue, the man has diminished pulses in just one arm, which means that the left subclavian artery must be involved somehow, and an aortic dissection would be the best answer explaining this. +5  
temmy  please why is there where a diastolic mumur? +1  
whoissaad  @temmy Aortic dissection especially near the root of aorta can lead to dilatation of the aortic valves, which can lead to Aortic regurgitation (diastoic murmur at left sternal border) +6  
garibay92  Does anyone know why is this patient's tepmerature elevated? +1  
ratadecalle  @garibay92, not important for this question I think but cocaine can cause malignant hyperthermia +1  
almondbreeze  judging by his heart murmur, he probably has marfan syndrome. that's the only place where FA talks about dissecting aneurysm +  
almondbreeze  he's only 28 - another clue for marfan? +  
turtlepenlight  did anyone else think it was weird his only sx was SOB? I always think of radiating pain as being a good clue for dissection +1  
cmun777  @almondbreeze his heart murmur is at the LSB (aortic regurg) and not consistent with MVP plus no other sx/indication of Marfan. I think the only association of RF you should think about in this question is the cocaine use and consequent HTN. +1  
ibestalkinyo  @turtlepenlight I agree. I chose another answer because I was like, there's no way this guy doesn't hurt if he's got a dissection. +  


submitted by neonem(366),

Major risk factor for aortic dissection is hypertension, and in this case might be due to cocaine use, which causes marked hypertension. Dissections cause a tear in the tunica intima -- blood can flow backwards into the pericardium and cause tamponade. This manifests as crackles in the lung due to poor left ventricular function (filling/diastolic problem due to compression).

forerofore  there is another clue, the man has diminished pulses in just one arm, which means that the left subclavian artery must be involved somehow, and an aortic dissection would be the best answer explaining this. +5  
temmy  please why is there where a diastolic mumur? +1  
whoissaad  @temmy Aortic dissection especially near the root of aorta can lead to dilatation of the aortic valves, which can lead to Aortic regurgitation (diastoic murmur at left sternal border) +6  
garibay92  Does anyone know why is this patient's tepmerature elevated? +1  
ratadecalle  @garibay92, not important for this question I think but cocaine can cause malignant hyperthermia +1  
almondbreeze  judging by his heart murmur, he probably has marfan syndrome. that's the only place where FA talks about dissecting aneurysm +  
almondbreeze  he's only 28 - another clue for marfan? +  
turtlepenlight  did anyone else think it was weird his only sx was SOB? I always think of radiating pain as being a good clue for dissection +1  
cmun777  @almondbreeze his heart murmur is at the LSB (aortic regurg) and not consistent with MVP plus no other sx/indication of Marfan. I think the only association of RF you should think about in this question is the cocaine use and consequent HTN. +1  
ibestalkinyo  @turtlepenlight I agree. I chose another answer because I was like, there's no way this guy doesn't hurt if he's got a dissection. +  


Arthropod for sure, but for the record I'm pretty sure this was Chikungunya Virus. Only got this from a UWorld question as I hadn't seen it until then, but apparently the arthralgia is really bad, which is what drew me to the answer.

https://www.cdc.gov/chikungunya/index.html

meningitis  More like Zika Virus (Same a. aegypti vector) since it says she has rash associated to her bone and muscle pain. I had Zika one time (i live in Puerto Rico). Remember also dengue and Zika are Flavivirus. Dengue can cause hemolysis (hemorrhagic), and Zika is associated with Guillen Barre and fetal abnormalities. +7  
nala_ula  I'm shocked that I found a fellow puerto rican on this site! Good luck on your test! +  
namira  dont be shocked! me too! exito! +1  
niboonsh  Dengue is also known as "bone break fever" which makes me think its more likely to be dengue due to the "excruciating pains in joints and muscles". https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4242787/ +8  
dr_jan_itor  I was thinking that its Murine typhus transmitted by fleas +  
monique  I would say this is more likely scenario of either Dengue or Chikungunya, not Zika virus. Excruciating pain is common in those, not in Zika. Zika has milder symptoms of those three infection. +1  
jakeperalta  Can confirm that Chikungunya's arthralgia is pretty horrible, from personal experience. +  
almondbreeze  UW: co-infection with chikungunya virus with dengue virus can occure bc Aedes mosquito is a vector of both Chiungunya, dengue, and zika +  


submitted by fatboyslim(5),

(From UW 11852) Some medications including opioids, radiocontrast dyes, and some antibiotics (e.g. vancomycin) can induce and IgE-INDEPENDENT mast cell degranulation by activation of protein kinase A and PI3 kinase, which results in release of histamine, bradykinin, and other chemotactic factors -> diffuse itching, pain, bronchospasm, and localized swee=lling (urticaria).

almondbreeze  just to add : more agents causing such reaction - beta-lactams, sulfonamide, aminoglycoside +  
drzed  Are those IgE dependent, or just allergic reactions (asking because the sketchy for beta-lactam penicillins mention acute interstitial nephritis as an allergic reaction)? +  


submitted by hayayah(599),

Sensitivity tests are used for screening. Specificity tests are used for confirmation after positive screenings.

Sensitivity tests are used for seeing how many people truly have the disease. Specificity tests are for those who do not have the disease.

A highly sensitive test, when negative, rules OUT disease. A highly specific test, when positive, rules IN disease. So, a test with with low sensitivity cannot rule out a disease. A test with low specificity can't rule in disease.

The doctor and patient want to screen for colon cancer and rule it out. The doctor would want a test with high sensitivity to be able to do that. He knows that testing her stool for blood will not rule out the possibility of colon CA.

sympathetikey  SeN Out (Snout) --> sensitive test; - test rules out SPec In (Specin) --> specific test; + test rules in +2  
usmlecrasher  can anyone pls explain why it is not << potential false- positive results >> ??? +  
almondbreeze  correct me if I'm wrong, but 'high FP (choice C)=low specificity (choice B)'. Whereas high specificity is required to rule in dz +1  
almondbreeze  picked positive predictive value myself. can anyone explain why not PPV? +  
williamfreakingosler  The principle @hayayah is talking about (a negative test being relied upon to reliably rule out) is negative predictive value ("NPV"). I don't see why "uncertain NPV" isn't the correct answer, particularly because NPV is predicated on the disease having the same base rate in the person(s) being tested as in the population that was characterized for the test statistic. Given that the patient has a strong family history of colon cancer, the NPV of FOBT is uncertain. Said another way, the sensitivity of a test does not change with the population, but the NPV does. The whole reason the doctor is denying FOBT is because of bayesian thinking (a priori information related to family history), and from my point of view bayesian logic is more relevant to PPV/NPV than to sensitivity, hence my confusion over why NPV isn't the right answer. +2  
ibestalkinyo  I thought negative predictive value for the same reasoning +  
raga7  AFTER THE RESULT OF TEST WE CAN USED PPV OR PPN, BUT FOR TEH FIRST TIME LOOKING ANY DESEASE USE SENSITIVITY OR SPECIFICITY. +  


submitted by hayayah(599),

Sensitivity tests are used for screening. Specificity tests are used for confirmation after positive screenings.

Sensitivity tests are used for seeing how many people truly have the disease. Specificity tests are for those who do not have the disease.

A highly sensitive test, when negative, rules OUT disease. A highly specific test, when positive, rules IN disease. So, a test with with low sensitivity cannot rule out a disease. A test with low specificity can't rule in disease.

The doctor and patient want to screen for colon cancer and rule it out. The doctor would want a test with high sensitivity to be able to do that. He knows that testing her stool for blood will not rule out the possibility of colon CA.

sympathetikey  SeN Out (Snout) --> sensitive test; - test rules out SPec In (Specin) --> specific test; + test rules in +2  
usmlecrasher  can anyone pls explain why it is not << potential false- positive results >> ??? +  
almondbreeze  correct me if I'm wrong, but 'high FP (choice C)=low specificity (choice B)'. Whereas high specificity is required to rule in dz +1  
almondbreeze  picked positive predictive value myself. can anyone explain why not PPV? +  
williamfreakingosler  The principle @hayayah is talking about (a negative test being relied upon to reliably rule out) is negative predictive value ("NPV"). I don't see why "uncertain NPV" isn't the correct answer, particularly because NPV is predicated on the disease having the same base rate in the person(s) being tested as in the population that was characterized for the test statistic. Given that the patient has a strong family history of colon cancer, the NPV of FOBT is uncertain. Said another way, the sensitivity of a test does not change with the population, but the NPV does. The whole reason the doctor is denying FOBT is because of bayesian thinking (a priori information related to family history), and from my point of view bayesian logic is more relevant to PPV/NPV than to sensitivity, hence my confusion over why NPV isn't the right answer. +2  
ibestalkinyo  I thought negative predictive value for the same reasoning +  
raga7  AFTER THE RESULT OF TEST WE CAN USED PPV OR PPN, BUT FOR TEH FIRST TIME LOOKING ANY DESEASE USE SENSITIVITY OR SPECIFICITY. +  


submitted by laminin(9),

Tetracyclines have a high affinity to form chelates with polyvalent metallic cations such as Fe+++, Fe++, Al+++, Mg++ and Ca++. Many of these tetracycline-metal complexes are either insoluble or otherwise poorly absorbable from the gastro-intestinal tract. Milk and other dairy products, antacids containing polyvalent cations, as well as various iron salts ingested simultaneously with tetracycline derivatives, might interfere with their absorption by 50 to 90% or even more. source: https://www.ncbi.nlm.nih.gov/pubmed/946598

almondbreeze  FA 2019 pg. 192: Do not take tetracyclines with milk (Ca2+), antacids (eg. Ca2+ or Mg2+), or iron-containing preparations b/c divalent cations inhibit drugs' absorption in the gut +  


submitted by hayayah(599),

Administration of Penicillin for Syphilis may lead to the Jarisch-Herxheimer reaction hours after treatment. Occurs due to lysis of spirochetes (so it can occur with Borrelia and Leptospirosis as well). The reaction is characterized by fever and chills.

The classical explanation of the Herxheimer reaction is that treatment results in the sudden death and destruction of large numbers of treponemes, with the liberation of protein products and toxins.

almondbreeze  FA pg.148 +  


submitted by hayayah(599),

Capitate and lunate are in the center of the palm. Capitate is not an option, so lunate is the answer.

Dislocation of lunate may cause acute carpal tunnel syndrome.

yotsubato  Lunate is the only carpal bone that is frequently dislocated. Scaphoid is frequently fractured. Hook of hamate is also frequently fractured. +3  
redvelvet  and also point tenderness in the anatomical snuffbox may indicate a scaphoid fracture. +1  
chandlerbas  yes lunate is the most common dislunated carpal bone ;) +2  
almondbreeze  FA 2019 pg. 439 : dislocation of lunate may cause acute carpal tunnel syndrome +  


submitted by monoloco(84),

This is the only choice that comes close to nicking the thoracic duct, specifically at its inlet, the left subclavian.

kpjk  why not midsternal thoracotomy? +  
wuagbe  because the thoracic duct ascends the thorax posteriorly, and enters venous circulation from behind. link to image: https://www.sciencedirect.com/topics/agricultural-and-biological-sciences/thoracic-duct +3  


submitted by johnthurtjr(79),

While I can get on board with Adjustment Disorder, I don't see how this answer is any better than Somatic Symptom Disorder. From FA:

Variety of bodily complaints lasting months to years associated with excessive, persistent thoughts and anxiety about symptoms. May co-appear with illness.

SSD belongs in a group of disorders characterized by physical symptoms causing significant distress and impairment.

savdaddy  I think part of it stems from the fact that this patients symptoms are occurring within the time-frame for adjustment disorder while SSD seems to have a longer timeline. Aside from that I find it difficult to see why SSD wasn't a possible answer. +1  
chillqd  To add to that, I inferred that the obsession with checking temp and with the tingling sensation were signs provided to him by the physicians of recurrence. He is anxious over his cancer recurring, and they are more specific than a variety of body complaints +  
hello  In somatic symptom disorder, the motivation is unconscious. I think for the patient in this Q-stem, his motivation is conscious -- he wants to make sure that recurrence of cancer is not going "undetected". +6  
cienfuegos  I also had issues differentiating these two and ultimately went with SSD, but upon further review it seems that a key differentiating feature was the timeline. His somatic symptoms would have had to have been present for at least 6 months per the DSM criteria https://www.ncbi.nlm.nih.gov/books/NBK519704/table/ch3.t31/ +  
almondbreeze  @chillqd Same! Why not OCD? He's fearful that something bad might happen (=cancer relapse; obsession) and calling his doc (=compulsion) +  


submitted by sympathetikey(606),

Choice A. would have been correct if this patient was immunocompromised. Per First Aid, "If CD4 <100, Bartonella...Findings: Neutrophilic Inflammation.

However, as this patient has a competent immune system, buzz words are stellate necrotizing granulomas.

yotsubato  Everyones choice A is different. +  
sugaplum  they mean- Diffuse neutrophil infiltration +1  
macrohphage95  what does stellate necrotizng granuloma means ? +  
krisgsxr600  always with the details! losing dumb points :( +1  
futuredoc12345  @sympathetikey Doesn't the biopsy finding vary with the biopsy location: Lymph nodes have stellate granulomas and Bacillary Angiomatosis (skin lesion) has neutrophilic inflammation. What do you think? +  
chextra  @sympathetikey Pathoma chapter 2 says cat scratch disease forms non-caseating granulomas +  
almondbreeze  @ chextra Same with FA 2019 pg. 218 +  
almondbreeze  Sketchy micro: Immunocompetent: regional LN in axilla in one arm (like our pt here) Immunocompromised: bacillary angiomatsis is transmitted by cat scratches +  


submitted by sympathetikey(606),

Choice A. would have been correct if this patient was immunocompromised. Per First Aid, "If CD4 <100, Bartonella...Findings: Neutrophilic Inflammation.

However, as this patient has a competent immune system, buzz words are stellate necrotizing granulomas.

yotsubato  Everyones choice A is different. +  
sugaplum  they mean- Diffuse neutrophil infiltration +1  
macrohphage95  what does stellate necrotizng granuloma means ? +  
krisgsxr600  always with the details! losing dumb points :( +1  
futuredoc12345  @sympathetikey Doesn't the biopsy finding vary with the biopsy location: Lymph nodes have stellate granulomas and Bacillary Angiomatosis (skin lesion) has neutrophilic inflammation. What do you think? +  
chextra  @sympathetikey Pathoma chapter 2 says cat scratch disease forms non-caseating granulomas +  
almondbreeze  @ chextra Same with FA 2019 pg. 218 +  
almondbreeze  Sketchy micro: Immunocompetent: regional LN in axilla in one arm (like our pt here) Immunocompromised: bacillary angiomatsis is transmitted by cat scratches +  


submitted by sugaplum(122),

B Hensele- Cat Scratch in immuno-compotent - http://www.pathologyoutlines.com/topic/lymphnodescatscratch.html Bartonella henselae in Immuno-compromised- Baciliary angiomatotsis Looks like kaposi sarcoma "Diffuse neutrophilic infiltrate" FA 2019 177

almondbreeze  FA 177 says Kaposi has lymphocytic inflammation whereas Bartonella spp has neutrophilic inflammation. I guess this does not apply when immunocompromised? But doesn't Bartonella usually affect the immunocompromised ppl? +  
almondbreeze  Got it after seeing that she's immunocompetent +  


submitted by sugaplum(122),

B Hensele- Cat Scratch in immuno-compotent - http://www.pathologyoutlines.com/topic/lymphnodescatscratch.html Bartonella henselae in Immuno-compromised- Baciliary angiomatotsis Looks like kaposi sarcoma "Diffuse neutrophilic infiltrate" FA 2019 177

almondbreeze  FA 177 says Kaposi has lymphocytic inflammation whereas Bartonella spp has neutrophilic inflammation. I guess this does not apply when immunocompromised? But doesn't Bartonella usually affect the immunocompromised ppl? +  
almondbreeze  Got it after seeing that she's immunocompetent +  


submitted by xxabi(142),

Broca’s aphasia: expressive (motor aphasia) with agrammatism (pts aware that they don’t make sense) - area A Wernicke’s aphasia: receptive (sensory) aphasia with impaired comprehension (pts lack insight)

breis  Why would B be incorrect? I realize Broca is "technically lower" but A seems too low to be causing weakness of the lower 2/3 of the face? Am I missing something? +  
shaeking  @breis B is incorrect because of the lower 2/3 of the face weakness. B isn't located on the motor cortex but in the premotor cortex, plus it isn't low enough for the lower two thirds of the face. https://thebrain.mcgill.ca/flash/a/a_06/a_06_cr/a_06_cr_mou/a_06_cr_mou.html https://www.sciencenews.org/blog/science-ticker/homunculus-reimagined +1  
cienfuegos  @breis, per UW: "a/w r. hemiparesis (face & UE) bc close to primary motor cortex" +  
almondbreeze  B is close to premotor cortex which is involved in learned or patterned skills & in planning movements. (i.e. two-hand coordination) slide 25/37 :https://www.slideserve.com/hal/the-motor-system-and-its-disorders +  
almondbreeze  B is also close to frontal eye field; eyes look toward the lesion FA pg. 499 +  
frijoles  I incorrectly picked C. When answering this, Broca's "broken speech" was my first thought, but I figured a lesion causing a facial droop would have to involve the motor strip so I prioritized that and chalked up the speech issue to dysarthria (I understand this is more of a "slurred speech" than broken, abrupt speech, but again, I simply misprioritized concepts.). So for the record, Broca area is part of the motor cortex? +  


submitted by xxabi(142),

Broca’s aphasia: expressive (motor aphasia) with agrammatism (pts aware that they don’t make sense) - area A Wernicke’s aphasia: receptive (sensory) aphasia with impaired comprehension (pts lack insight)

breis  Why would B be incorrect? I realize Broca is "technically lower" but A seems too low to be causing weakness of the lower 2/3 of the face? Am I missing something? +  
shaeking  @breis B is incorrect because of the lower 2/3 of the face weakness. B isn't located on the motor cortex but in the premotor cortex, plus it isn't low enough for the lower two thirds of the face. https://thebrain.mcgill.ca/flash/a/a_06/a_06_cr/a_06_cr_mou/a_06_cr_mou.html https://www.sciencenews.org/blog/science-ticker/homunculus-reimagined +1  
cienfuegos  @breis, per UW: "a/w r. hemiparesis (face & UE) bc close to primary motor cortex" +  
almondbreeze  B is close to premotor cortex which is involved in learned or patterned skills & in planning movements. (i.e. two-hand coordination) slide 25/37 :https://www.slideserve.com/hal/the-motor-system-and-its-disorders +  
almondbreeze  B is also close to frontal eye field; eyes look toward the lesion FA pg. 499 +  
frijoles  I incorrectly picked C. When answering this, Broca's "broken speech" was my first thought, but I figured a lesion causing a facial droop would have to involve the motor strip so I prioritized that and chalked up the speech issue to dysarthria (I understand this is more of a "slurred speech" than broken, abrupt speech, but again, I simply misprioritized concepts.). So for the record, Broca area is part of the motor cortex? +