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 +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.


 +0  (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 meningitis(201),

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 +  


submitted by gh889(41),

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(46),

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 +  


submitted by imgdoc(46),

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 +  


submitted by hayayah(508),

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 +  


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(103),

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?? +  


submitted by rogeliogs(2),

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(13),

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? +  
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. +3  
kernicterusthefrog  I had the same struggle and thought process. +  
eacv  There is a Uworld qx that explain this in detail> ID: 863 +1  
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. +  
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(13),

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? +  
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. +3  
kernicterusthefrog  I had the same struggle and thought process. +  
eacv  There is a Uworld qx that explain this in detail> ID: 863 +1  
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. +  
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(19),

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) +  


submitted by armymed88(19),

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) +  


submitted by calcium196(7),

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. +5  
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? +  
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(48),

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. +1  
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 +  
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? +  
almondbreeze  @ toxoplasmabartonella think you are right +  


submitted by hayayah(508),

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. +1  
almondbreeze  it's in FA2019 pg.110 +  
almondbreeze  but missing the full name for CCR5 +  


submitted by hayayah(508),

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. +1  
almondbreeze  it's in FA2019 pg.110 +  
almondbreeze  but missing the full name for CCR5 +  


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:( +  


submitted by mcl(276),

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? +6  
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. +  
almondbreeze  same. got it wrong bc the pt didn't have sx of hereditary angioedema - swollen lips and eyelids +  


submitted by readit(2),

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 +  


submitted by neonem(302),

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. +4  
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? +  


submitted by neonem(302),

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. +4  
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? +  


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. +6  
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/ +4  
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(2),

(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 +  


submitted by hayayah(508),

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 +1  
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. +1  


submitted by hayayah(508),

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 +1  
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. +1  


submitted by laminin(8),

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(508),

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(508),

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(75),

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 +1  


submitted by johnthurtjr(65),

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". +5  
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(440),

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 +  
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(440),

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 +  
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(78),

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(78),

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(123),

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 +  


submitted by xxabi(123),

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 +