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 +0  (nbme23#2)

Why are "rotator cuff tear" and "rotator cuff tendnitis" wrong? is it bc both of these would show impingement sign? is there a way to DDx one from the other?


 +0  (nbme23#45)

why is plasma oncotic pressure wrong?


 +0  (nbme23#50)

which letter is CN IX in this diagram?

titanesxvi  A think is D, but it is not very clear

 +0  (nbme23#33)

can someone please explain this?

thomasburton  My reasoning was BC>AC so this must be a conductive problem (which to me means something middle ear or out) so usually I think something blocking air flow or impeding the ossicles. You can rule out all other answers as they are all causes of sensorineural (AC>BC).

 +0  (nbme23#7)

What's the echymoses supposed to be a clue about? Does this patient have DIC? Does DIC always cause hypovolemic shock?

drdoom  Disseminated intravascular coagulation (DIC) is a syndromic definition. (See tangent.) It does not “always” lead to shock but shock is definitely a possible sequela (since, by definition, DIC = “systemic thrombotic process”; anything systemic should get you a little worried), and so a patient with DIC should be monitored closely!

 +0  (nbme22#29)

Please help - how are you able to tell that the CT image is not at the level of duodenum?

I don't know what I'm looking for to compare and contrast a CT at the level of the duodenum vs the CT given in this Q.


 +0  (nbme22#1)

There has to be a better explanation for why ANP is wrong?


 +1  (nbme22#4)

Spironolactone and eplerenone are potassium-sparing diurectics that inhibit the Na/K ATPase. Na/K ATPase is on the basolateral membrane. None of the answer choices fit with this.

Amiloride and triamterene are also potassium-sparing diuretics. The mechanism is to block ENaC channels on the luminal membrane, this is choice "B."



 +0  (nbme22#41)

Patient has a hemithorax + CXR shows trachea deviates towards the hemithorax --> most likely diagnosis is spontaneous pneumothorax.

Epidemiologically, spontaneous pneumothorax is most associated with thin males

hello  Wait, maybe this is wrong logic? Please correct me regarding the exam findings if needed.
hello  Can confirm that this explanation is INCORRECT regarding trachea. Disregard this explanation.

 +0  (nbme22#48)

please help -- If catalase-positive bacteria neutralize their own superoxide, why isn't it the case for catalase-positive bacteria to infections in everyone?

I'm not understanding the connection to NADPH oxidase deficiency.

hello  to cause** infections in everyone

 +1  (nbme22#20)

Why isn't this a cohort study?

drdoom  This is a cohort study! (Since it involves splitting people into "groups"; group = cohort.) But the stem asks what "best describes" the design. So, yes, it's a cohort study but a more precise ("more specific") description is Open-label. In other words, "Open-label clinical trial" is a type of cohort study, and, in this case, "Open-label" is a more precise description of what is described in the stem.
drdoom  For a more technical explanation of "Cohort studies", see the definition from the National Library of Medicine: https://meshb.nlm.nih.gov/record/ui?ui=D015331
angelaq11  It is a cohort, just as @drdoom said, but it isn't an "Observational" one.

 +0  (nbme22#32)

For people asking why the data table was even included if it was not needed to answer this Q, here is a useful explanation:

The table was given because a 2x2 table is typically what you do see regarding data for case-control studies.

If the 2x2 table wasn't included, then literally everytone would pick Choice "E" as the correct answer b/c you can't calculate something without being provided numbers.

The difference in including the data-table is that:

  1. Again, you need to report a 2x2 table because that is typically what you will see regarding data for a case-control study

and

  1. by including the 2x2 table, it actually tests if the test-taker realized that the data in the 2x2 table does not help at all with calculating prevalence-- because case-control studies NEVER report on prevalence.
hello  I also want to add that the Q is asking about sinusitis in the GENERAL population, meanwhile the Q-stem discusses a case-control study that is studying the relationship of smoking (an exposure) to development of sinusitis. To then ask "what is the prevalence of sinusitis in the general population" totally disregards taking into account the exposure of smoking which was the entire reason for the study. In other words, asking prevalence would be very non-sensical.

 +1  (nbme22#9)

Patient has red lacy rash- this fits more with HHV-6 (Roseola virus), not Parvovirus.

HHV-6 causes deformation of erythoblasts, leading to anemia.

hyperfukus  Hey so i just looked in first aid and it says "diffuse Macular Rash for Roseola" and usually you have a super high fever and febrile seizures are almost always mentioned...I found in my notes from uworld that i mustve filled in a long time ago for Parvo: Infects Erythroid precursors + Replicates in BM Face/cheek rash followed by LACY Reticular rash on body...May get Rash from IC deposition...and then again i wrote replicates in erythrocyte progenitors causing reticulocytopenia which makes sense why dec Hb and dec Hct

 +0  (nbme22#43)

Patient cannnot extend wrist, which is innervated by radial nerve

Patient has been on crutches, which would affect axillary nerve --> this affects deltoid muscle, which does arm abduction 15-100º (so it can normally move arm above shoulder)

The only location in the given diagram to effect all of these nerves would be location "C"

Note: normally, arm movement above the horizontal is associated with serratus anterior muscle/long thoracic nerve. However, none of the diagram locations allow for inclusion of SALT. Since the patient has been on crutches for weeks, it suggests axillary nerve involvement --> deltoid is affected


 +0  (nbme22#14)

The patient is dehydrated. Need to give water to rehydrate.

Water follows solute. If sodium is added to the solution, water will follow the sodium. Now, enterocyte uptake of sodium is mediated by Sodium-Glucose transporter. Hence, the solution needs to contain sodium and glucose in order to have the enterocytes take up the sodium.


 +3  (nbme22#11)

The Q is describing the genitofemoral nerve, which runs on the external surface of the spermatic cord at the superficial inguinal ring

This Q is NOT referring to ilioinguinal nerve -- the ilioinguinal nerve exits THROUGH the superficial inguinal canal whereas this Q is asking about a nerve that is EXTERNAL to the superficial inguinal canal.

See http://www.groinpainclinic.co.uk/data/images/nervesaffected.jpg


 +0  (nbme22#34)

This the same as @keycompany's explanation with more explanation those that need it...

The patient is unaffected by the particular autosomal recessive disease and his brother has the autosomal recessive disease --> this means each of their parents carries the AR allele. Now, for the patient to be unaffected given that both his parents have the AR allele, it means that the patient has a 2/3 chance that he is simultaneously unaffected and a carrier.

The patient's partner is unaffected and normal Hardy-Weinberg genetics (as stated in the problem)..when this is specifically mentioned, you are to assume that the partner has a carrier frequency for the AR allele, which equal to 2pq.

The disease has a frequency in the population of 1/40000. This is q^2 --> q^2 = 1/40000. Solving for q, you get q = 1/200.

Carrier frequency is 2pq. However, for a rare disease, 2pq ≈ 2q. So, the carrier frequency for the partner = 2q = 2 * 1/200 = 1/100.

Now, the Q asks about an offspring of the patient and his partner being affected, so to have an affected child, there is a 1/4 chance of having an affected child (becasuse the patient and the partner both have a 1/2 chance of passing the allele --> you multiple these together 1/2 * 1/2).

So, multiply 2/3 * 1/100 * 1/4 = 1/600. This is P(patient being a carrier) * P(partner being a carrier) * P(having an affected offspring together).


 +0  (nbme22#35)

The grammar of the actual Q was confusing.

To make better sense, it should say "Which of the following is the most likely result on the transcription of genes that inhibit cell division and that contain the consensus sequeence TATA..."

So, the Q is asking about the tp53 gene and specifically about the tp53 gene promoter region.

Promoter regions have a TATA box (obviously, meaning rich in A-T base pairs). A-T base pairing has 2 hydrogen bonds, which makes them easier to cleave --> allows for DNA transcription to occur more easily. RNA Pol does transcription of DNA into RNA.

The entire Q-stem talks about how Li-Fraumeni is due to a mutation in tp53 gene, leading to a lack of tumor suppression activity.

So, if the promoter region TATA box of the tp53 gene is mutated, then the tp53 gene will not get transcribed --> this is why there will be decreased RNA Pol binding. RNA Pol will have a reduced ability to bind tp53 --> less tumor supressor gene transcription --> less tumor suppression.


 +0  (nbme21#29)

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.


 +0  (nbme21#29)

Please help

Why is valine incorrect?

An explanation below says that valine would be converted to glucose during regular metabolism?

Regular metabolism = fed state, so why would valine even be converted to glucose?


 +0  (nbme21#5)

This is the actual correct explanation:

PDA causes blood to flow from descending aorta to patent ductus arteriosus into pulmonary circulation ("right-to-left")

The "steal" from the aorta during diastole requires increased cardiac output to compensate to deliver adequate amount of blood to rest of body

Source: https://www.ncbi.nlm.nih.gov/books/NBK430758/


 +0  (nbme21#16)

Please help

Mid-systolic ejection click = pulmonic stenosis

How is pulmonic stenosis related to the patient's ASD -- does ASD cause pulmonic stenosis??

burak  ASD has typically 3 associated sounds according to UW, they are all about increased blood in RA. Increased blood in RA causes more blood do ejected from tricuspid (dşastolic rumble), and more blood to be ejected to pulmonary circulation which cause pulmonary flow murmur (midsystolic murmur in pulmonary region). It even can cause pulmonary regurgitaion like murmur, but most important murmur in ASD is typically midsystolic murmur. You can check it out on FA 2018 page 284
hello  Ok, what I learned: Extra blood in the right heart (due to ASD) doesn't lead to pulmonic stenosis? Instead, it's that pulmonic stenosis = most common comorbid heart association with ASD
burak  No it's not pulmonic stenosis, it doesn't lead. Murmur associated with ASD is pulmonic stenosis-like murmur, because it's caused by excess RA and RV volume ejecting to the pulmonary arteries. So it's same location with pulmonic stenosis, and it's systolic. You get it?
hello  @burak Yep!

 +0  (nbme21#17)

For anyone confused trying to follow @usmleuser007's comment

Slightly modified

Essential amino acids mnemonic "Ah, Three fans will try meth"the

Ah = arginine, histidine

Three = Threonine

Fans (phans)= Phenylalanine

Vill (will -- German accent pronouncing English word "will") = valine, isoleucine, leucine, lysine

Try = tryptophan

Meth = Methionine


 +0  (nbme21#36)

Multiple myeloma = neoplasm of plasma cells.

Plasma cells produce secretory Ab's (aka produce Ab's) -- plasma cells do not have membrane-bound Ig (aka do not have BCR').

To recap: membrane-bound Ig = BCR while secretory Ig = Ab.

Now, anti-idiotypic antibody = antibody against antibody.

Plasma cells do not contain surface Ig -- because plasma cells only be secrete Ab's.

Therefore, anti-idiotypic antibody would not work to target myeloma cells because myeloma cells = plasma cells aka plasma cells lack surface molecules that anti-idiotypic Ab's would need to bind to/target.

See diagram: https://qph.fs.quoracdn.net/main-qimg-ae42c5c9f839fc58a3ce10feaf14c02b


 +0  (nbme21#4)

The Q stem states FOXO is a transcription factor that responds to insulin signaling by altering the transcription of metabolic genes --> therefore, FOXO is a transcription factor involved in metabolism. This should make sense because insulin-receptor activation has a role in regulating metabolism.

This Q asks about reversible ways that insulin reguates FOXO transcrption factor activity.

Ubiquitin-mediated proteolysis is irreversible. Eliminate all choices except for B, D, and H.

Insulin-receptors function through PI3K signaling. PI3K signaling involves phosphorylation of serine --> serine phosphorylation is a reversible process. Eliminate H. FYI: protein/amino acid phosphorylation is always reversible.

You are left with choices B and D.

FOXO is a transcription factor --> transcription factors mediate gene activity by shuttling between the cytoplasm and nucleus. Regulating the location of FOXO transcription factor (i.e. cytoplasm vs. nucleus) will therefore reversibly modulate FOXO-mediated metabolic gene activity.

This leaves you with the correct answer: Choice B.


 +2  (nbme21#39)

q^2 = 1/900 --> q = 1/30

Carrier frequency per Hardy-Weinberg formula is 2pq.

Now, for rare autosomal recessive diseases the carrier frequency of 2pq ≈ 2q.

2q = 2(1/30) = 2/30 = 1/15

Answer = 1/15


 +0  (nbme21#10)

The patient has "cells arranged in infiltrating sheets" --> indicates malignant cancer cells.

The cells are neither glandular nor squamous --> the cancer is neither adenocarcinoma nor squamous cell lung cancer, respectively.

This leaves small oat cell lung cancer. SIADH is the most common paraneoplastic syndrome for small oat cell lung cancer --> leads to hyponatremia.


 +3  (nbme22#21)

Knowing the LR+ value = 10 does not help to solve this Q because estimating where "10" should fall on an axis is arbitrary. Also, the data points are coordinates -- they have an X-value and a Y-value (X, Y).

The way to approach this Q is to know that a high specificity means that a positive result is very, very likely to be a true positive.

Suppose that the specificity is 0.99 -- this is 99% specificity. Then, you look at the graph. The X-axis is "1-specificity." So, suppose the best test has a specificity of 99%. Then, calculate 1-specificity = 1 - 0.99 = 0.10. You would then chose the datapoint that corresponds to having an "X-value" that is closest to the origin. In this problem, it corresponds to data point "A."

You don't even need to know a specific specificity value to solve this problem. All you need to do is understand that if the specificity is extremely high, you will need to find a datapoint that is closest to the origin -- at least for the value in the X-axis in the coordinate of the data point -- because the X-axis corresponds to a calculation of "1-specificity".

link981  Excellent explanation but a minor typo. 1-0.99 = 0.01 not 0.10 :)

 +6  (nbme20#17)

Goljan had a lecture that mentioned that "If a patient has galactorrhea, review every drug they're taking since many drugs cause galactorrhea."

The only thing of possible relevance in this Q-stem is that she takes a medication, therefore the answer of "drug effect" is the most likely reason for her galactorrhea.


 +2  (nbme20#24)

Guyon Canal Syndrome is due to an Ulnar Nerve lesions and is associated with bicycle handlebar use.

Also FINGER abduction and adduction is mediated by ulnar nerve. The patient is having trouble with FINGER abduction and adduction.

The Froment sign is testing ADDUCTOR POLICIS ACTIVITY, which is mediated by the ULNAR NERVE activity. It is NOT testing thumb opposition, which would be mediated by the median nerve.

See Froment sign


 +1  (nbme20#50)

The reason "do not prescribe antibiotics until testing results are available" is incorrect is because we already have a gram stain that shows gram-negative diplococci in pairs. This is Neisseria gonorrhoeae. So, no need to wait for test results come back.

The Q-stem stating that "Testing for Neisseria and Chlamydia" is ordered" after already having done the Gram stain seems to be a distractor.


 +6  (nbme20#44)

Patient's symptoms began 30 min after mowing lawn (i.e. after doing physical activity). He has severe chest pain and is cool, clammy, diaphoretic. He has increased pulmonary artery pressure and increased left atrial pressure. Taken altogether, this is cardiogenic shock.

Cardiogenic shock is a heart pump problem -- the LV isn't working.

When the LV, isn't working, it causes a back up in the direction opposite to how blood normally flows. Therefore, blood will back up in the lungs.

This causes increased capillary hydrostatic pressure --> this drives more fluid into the interstitium --> this causes increased interstitial hydrostatic pressure --> there is now more fluid than normal in the interstitium --> this affects the protein ratio within the interstitum --> this causes decreased interstitial oncotic pressure.

targetusmle  awesomely explained :)

 +0  (nbme20#42)

Patient in hypovolemic shock - the clues are low BP and COOL skin. Hypovolemic shock is caused by fluid loss.

The patient has decreased preload b/c of fluid loss, i.e. there is decreased blood volume returning to heart --> thus decreased preload.

endochondral   why not dec SVR?
sup  @endochondral w/ hypovolemic shock you would see increased systemic arterial resistance as arteries will constrict to try and bring BP back up.
eacv  @endochondral dec SVR it typicaly of septic shock.

 +1  (nbme20#35)

Spleen is enlarged. Compare it to CT scan showing normal-sized spleen:

http://www.startradiology.com/uploads/scroll/18/14hiu6b3qot5.jpg





Subcomments ...

submitted by nwinkelmann(94),

Murmurs and maneuvers: 1st thought = how does it change with preload. All murmurs except HOCM, MVP, and atrial myxoma severity is directly proportional to change in preload (i.e. increased preload=worse murmur, etc.). Because of this, DDx can be narrowed down to HOCM, MVP, and atrial myxoma right away because the murmur worsened with decreased preload (i.e. standing up) when all but exceptions with improve.

Atrial myxoma = MCC primary cardiac tumor due to proliferation of connective tissue mesenchyme; a pedunculated mass connected via stalk to atrium septum that is suspended in the atrial blood volume and moves with the volume movement.

Presentation: triad of 1) mitral valve obstruction (i.e. malaise, symptoms of cardiac failure, syncope, etc.), 2) symptoms of embolism (i.e. facial and right arm hemiparesis in patient), and 3) constitutional symptoms (i.e. fever, weight loss, symptoms resembling connective tissue disease, because tumor releases IL-6). Others include neurologic symptoms, "pseudo-mitral valve disease" auscultatory findings (i.e. diastolic murmur), and atrial enlargement (which could compress underlying structures and cause symptoms also).

Not only does standing decrease preload, which means LA volume is lower so mass isn't as "suspended" but more mobile, standing also increases the downward gravitation force, which would contribute to the tumor moving towards the base of the atrial chamber, "plopping" on the mitral valve leaflets, and potentially extending through and causing a functional type of mitral stenosis (i.e. worsening diastolic murmur). This video explains it really well: https://www.youtube.com/watch?v=slIY64nViLg&t=161s

dentist  Sorry, you narrowed it down to HOCM, MVP, and LA myoxma, but I only see LA myxoma as an answer choice. Wouldn't you have been able to stop right there? +  
hello  @dentist, I appreciate this full answer b/c nwinkelmann is telling those of us that were wondering "how to ddx one from the other in case we need to"? +  
hello  @dentist btw, HOCM is an answer choice (RVOT is part of HOCM) +  


submitted by nwinkelmann(94),

Murmurs and maneuvers: 1st thought = how does it change with preload. All murmurs except HOCM, MVP, and atrial myxoma severity is directly proportional to change in preload (i.e. increased preload=worse murmur, etc.). Because of this, DDx can be narrowed down to HOCM, MVP, and atrial myxoma right away because the murmur worsened with decreased preload (i.e. standing up) when all but exceptions with improve.

Atrial myxoma = MCC primary cardiac tumor due to proliferation of connective tissue mesenchyme; a pedunculated mass connected via stalk to atrium septum that is suspended in the atrial blood volume and moves with the volume movement.

Presentation: triad of 1) mitral valve obstruction (i.e. malaise, symptoms of cardiac failure, syncope, etc.), 2) symptoms of embolism (i.e. facial and right arm hemiparesis in patient), and 3) constitutional symptoms (i.e. fever, weight loss, symptoms resembling connective tissue disease, because tumor releases IL-6). Others include neurologic symptoms, "pseudo-mitral valve disease" auscultatory findings (i.e. diastolic murmur), and atrial enlargement (which could compress underlying structures and cause symptoms also).

Not only does standing decrease preload, which means LA volume is lower so mass isn't as "suspended" but more mobile, standing also increases the downward gravitation force, which would contribute to the tumor moving towards the base of the atrial chamber, "plopping" on the mitral valve leaflets, and potentially extending through and causing a functional type of mitral stenosis (i.e. worsening diastolic murmur). This video explains it really well: https://www.youtube.com/watch?v=slIY64nViLg&t=161s

dentist  Sorry, you narrowed it down to HOCM, MVP, and LA myoxma, but I only see LA myxoma as an answer choice. Wouldn't you have been able to stop right there? +  
hello  @dentist, I appreciate this full answer b/c nwinkelmann is telling those of us that were wondering "how to ddx one from the other in case we need to"? +  
hello  @dentist btw, HOCM is an answer choice (RVOT is part of HOCM) +  


submitted by ferrero(16),

A very similar question I have seen in Qbanks will ask why a patient with right heart failure does not develop edema and the answer is increased lymphatic drainage. I got this question wrong originally because I answered along this line of reasoning but I think in this case it all has to do with WHERE the extra pressure is coming from. In this question the pt has diastolic hypertension so you can think about the pressure as coming "forward" so constricting precapillary sphincters can prevent an increase in pressure in the capillary bed. However for right heart failure this extra fluid is coming from the OPPOSITE direction (backwards from the right heart) and constricting precapillary sphincters can do nothing (on opposite side of capillary bed) - the only way to prevent edema is to increase lymphatic drainage.

seagull  The question clearly lead us to think about Osmotic pressure by talking about protein and urine. I wonder how many people used that line of reasoning (like myself)? +11  
mousie  Great explanation, I chose lymphatic drainage for the same reasoning (similar Q on different bank) +1  
sympathetikey  My reasoning was much more simplistic (maybe too simple) but in my mind, systolic BP is determined by Cardiac Output and diastolic BP is determined by arterioles. Therefore, what comes before the capillary and regulates resistance? Arterioles. That's why I said that pre-capillary resistance. +13  
cr  the main difference between the 2 cases is that in this case the patient has high BP +  
link981  So in kindergarten language the question is essentially asking how high pressure in the arterial system is NOT transmitted to the venous system (which is where EDEMA develops). But you know they have to add all this info to try confuse a basic principle and make you second guess yourself. (Got it wrong by the way) because of what @ferrero said of Qbank questions. +  
hello  @ferrero what are you talking about? lymphatic drainage is the wrong answer... +  
hello  ok never mind. i got it. hard to understand b/c it was a big block of text. +  


submitted by ferrero(16),

A very similar question I have seen in Qbanks will ask why a patient with right heart failure does not develop edema and the answer is increased lymphatic drainage. I got this question wrong originally because I answered along this line of reasoning but I think in this case it all has to do with WHERE the extra pressure is coming from. In this question the pt has diastolic hypertension so you can think about the pressure as coming "forward" so constricting precapillary sphincters can prevent an increase in pressure in the capillary bed. However for right heart failure this extra fluid is coming from the OPPOSITE direction (backwards from the right heart) and constricting precapillary sphincters can do nothing (on opposite side of capillary bed) - the only way to prevent edema is to increase lymphatic drainage.

seagull  The question clearly lead us to think about Osmotic pressure by talking about protein and urine. I wonder how many people used that line of reasoning (like myself)? +11  
mousie  Great explanation, I chose lymphatic drainage for the same reasoning (similar Q on different bank) +1  
sympathetikey  My reasoning was much more simplistic (maybe too simple) but in my mind, systolic BP is determined by Cardiac Output and diastolic BP is determined by arterioles. Therefore, what comes before the capillary and regulates resistance? Arterioles. That's why I said that pre-capillary resistance. +13  
cr  the main difference between the 2 cases is that in this case the patient has high BP +  
link981  So in kindergarten language the question is essentially asking how high pressure in the arterial system is NOT transmitted to the venous system (which is where EDEMA develops). But you know they have to add all this info to try confuse a basic principle and make you second guess yourself. (Got it wrong by the way) because of what @ferrero said of Qbank questions. +  
hello  @ferrero what are you talking about? lymphatic drainage is the wrong answer... +  
hello  ok never mind. i got it. hard to understand b/c it was a big block of text. +  


submitted by seagull(423),

What a terrible picture. They they covered up part of it with lines. WTF

sympathetikey  Agreed. +  
catch-22  Start at the pontomedullary junction and count from superior to inferiorly (or medially to laterally): VI, VII, VIII, IX. +  
yotsubato  I looked at the left side (cause the nerves arent frazzled up). Saw 7 and 8 come out together nicely. Then picked the right sided version of 8 +  
lolmedlol  why is it not H or I on the right side; the stem says he has hearing loss on the right side, so the lesion should be ipsilateral no? +1  
catch-22  You're looking at the ventral aspect of the brainstem. +2  
catch-22  ^Also, you know it's the ventral aspect because you can see the medullary pyramids. +  
amarousis  think of the belly of the pons as a pregnant lady. so you're looking at the front of her +1  
hello  which letter is CN IX in this diagram? +  


submitted by seagull(423),

Epinephrine is the only G coupled receptor activator the list. The rest are either inter-cellular or a tyrosine kinase (insulin).

hello  intracellular* correcting in case it trips someone up +  


submitted by zpatel(6),

all the others a noncompetitive since they have specificity(specific ligands), NMDA is the only nonselective(hence competitive receptor), has a ligand site and ca , na and mg...hence competitive

hello  the question says competitive interactions, i think this is different from competitive binding. +  


submitted by hello(64),

Please help

Mid-systolic ejection click = pulmonic stenosis

How is pulmonic stenosis related to the patient's ASD -- does ASD cause pulmonic stenosis??

burak  ASD has typically 3 associated sounds according to UW, they are all about increased blood in RA. Increased blood in RA causes more blood do ejected from tricuspid (dşastolic rumble), and more blood to be ejected to pulmonary circulation which cause pulmonary flow murmur (midsystolic murmur in pulmonary region). It even can cause pulmonary regurgitaion like murmur, but most important murmur in ASD is typically midsystolic murmur. You can check it out on FA 2018 page 284 +1  
hello  Ok, what I learned: Extra blood in the right heart (due to ASD) doesn't lead to pulmonic stenosis? Instead, it's that pulmonic stenosis = most common comorbid heart association with ASD +1  
burak  No it's not pulmonic stenosis, it doesn't lead. Murmur associated with ASD is pulmonic stenosis-like murmur, because it's caused by excess RA and RV volume ejecting to the pulmonary arteries. So it's same location with pulmonic stenosis, and it's systolic. You get it? +1  
hello  @burak Yep! +  


submitted by dr.xx(42),

The hallmark of ITP is isolated thrombocytopenia.

https://emedicine.medscape.com/article/202158-workup

jboud86  Refer to page 419 in FA2019. +1  
hello  @dr.xx Compared to what? +  


Dec. NaCl - general volume loss Dec. K+ - Diuretic (most diuretics, except K+ sparing ones, cause hypoK+) Inc. HCO3-& pH - Volume loss -> RAAS -> aldosterone causes K+ & H+ wasting -> metabolic alkalosis; She may be vomiting as well, which is another possible cause of met. alk. Inc PaCO2 - respiratory compensation for met. alk.

hello  Patient has normal Na. +  
hello  Lab data indicates serum bicab not ABG bicarb. +  
hello  oops! just realized bicarb is never given as an ABG haha +  


Dec. NaCl - general volume loss Dec. K+ - Diuretic (most diuretics, except K+ sparing ones, cause hypoK+) Inc. HCO3-& pH - Volume loss -> RAAS -> aldosterone causes K+ & H+ wasting -> metabolic alkalosis; She may be vomiting as well, which is another possible cause of met. alk. Inc PaCO2 - respiratory compensation for met. alk.

hello  Patient has normal Na. +  
hello  Lab data indicates serum bicab not ABG bicarb. +  
hello  oops! just realized bicarb is never given as an ABG haha +  


Dec. NaCl - general volume loss Dec. K+ - Diuretic (most diuretics, except K+ sparing ones, cause hypoK+) Inc. HCO3-& pH - Volume loss -> RAAS -> aldosterone causes K+ & H+ wasting -> metabolic alkalosis; She may be vomiting as well, which is another possible cause of met. alk. Inc PaCO2 - respiratory compensation for met. alk.

hello  Patient has normal Na. +  
hello  Lab data indicates serum bicab not ABG bicarb. +  
hello  oops! just realized bicarb is never given as an ABG haha +  


submitted by usmleuser007(115),

This more likely to be diuretics rather than laxatives b/c

the lab study shows a renal dysfunction (BUN & Creatinine are elevated)

Most likely the patient abused loop diuretics; also knows to cause contraction alkaloids, along with renal problems such as interstitial nephritis

endochondral1  would laxatives also have the low potassium? +1  
link981  My question exactly. And what if they were taking Potassium sparing diuretics? Then laxatives would be more likely or am I mistaken? +  
link981  Also creatine is normal, it's at the higher limit of normal so we can't say there is renal dysfunction. The BUN is elevated because patient has metabolic alkalosis with respiratory acidosis. +  
sweetmed  very important to Remember this: Diarrhea causes metabolic acidosis[from bicarb loss in stool], vomiting & loop diuretics cause metabolic alkalosis. +1  
hello  @usmleuser007 not sure your approach is the best way to think about it. The serum Cr is at the upper limit of normal (1.2). And, even if you calculate the ratio of BUN/Cr, it's 21, which would be a PRE-renal issue. +  


submitted by just_1more(1),

I got that it needed to be a potassium sparing diuretic. Is there a reason it cannot be an aldosterone antagonist? I chose blocks basolateral K+ channels as these decrease the basolateral K+/Na+/ATPase because the wording of the correct answer did not make sense to me -- assuming they were going for an ENaC blocker (and that decreased luminal permeability indicates that Na+ would be remaining in the lumen, not remaining in the principal cell as I originally thought).

luckeroo  I think the reason it’s a potassium-sparing diuretic rather than an aldosterone antagonist has less to do with why the aldosterone antagonist cannot be used and more to do with the fact that a potassium-sparing diuretic would be more of a “first-line” adjunctive diuretic treatment. +1  
luckeroo  As for the answer choice, potassium sparing diuretics achieve their overall anti-aldosterone effect by competitively inhibiting aldosterone receptors on the interstitial side (decreasing the Na/K-ATPase effect of shunting Na into the blood), thereby decreasing the gradient for sodium to enter the cell from the luminal aspect, blocking ENaC. +1  
yotsubato  There is no such thing as "Basolateral K Channel" there is only basolateral Sodium Potassium Pumps which are controlled by aldosterone. FA pg 573 +5  
nwinkelmann  @yotsubato LOL.... why didn't I think of it that what?! (by the way, that LOL is for me). The only basolateral K channel is the nephron (based on the first aid picture) is in the thick ascending limb of the loop of henle. +  
hello  Spironolactone and eplerenone are potassium-sparing diurectics that inhibit the Na/K ATPase, so I'm not sure what @luckeroo is referring to. Spironolactone and aplerenone are both ALDO antagonists. Na/K ATPase is found on the basolateral membrane. None of the answer choices fit with this. Amiloride and triamterene are also potassium-sparing diuretics; their mechanism is to block ENaC channels on the luminal membrane, this is choice "B." +1  


hello  Oops meant https://imgur.com/pD4amBJ +  


submitted by drdoom(192),

Nice schematic of how horizontal gaze is coordinated through the abducens/MLF/oculomotor pathway:

https://n.neurology.org/content/neurology/70/17/e57/F1.large.jpg

In the diagram, the system is coordinating gaze toward pt’s left, which (conveniently) is the same as in the stem.

Source article: https://n.neurology.org/content/70/17/e57

hello  Oops meant https://imgur.com/pD4amBJ +  


submitted by drdoom(192),

Nice schematic of how horizontal gaze is coordinated through the abducens/MLF/oculomotor pathway:

https://n.neurology.org/content/neurology/70/17/e57/F1.large.jpg

In the diagram, the system is coordinating gaze toward pt’s left, which (conveniently) is the same as in the stem.

Source article: https://n.neurology.org/content/70/17/e57

hello  Oops meant https://imgur.com/pD4amBJ +  


submitted by hello(64),

Patient has a hemithorax + CXR shows trachea deviates towards the hemithorax --> most likely diagnosis is spontaneous pneumothorax.

Epidemiologically, spontaneous pneumothorax is most associated with thin males

hello  Wait, maybe this is wrong logic? Please correct me regarding the exam findings if needed. +  
hello  Can confirm that this explanation is INCORRECT regarding trachea. Disregard this explanation. +  


submitted by hello(64),

Patient has a hemithorax + CXR shows trachea deviates towards the hemithorax --> most likely diagnosis is spontaneous pneumothorax.

Epidemiologically, spontaneous pneumothorax is most associated with thin males

hello  Wait, maybe this is wrong logic? Please correct me regarding the exam findings if needed. +  
hello  Can confirm that this explanation is INCORRECT regarding trachea. Disregard this explanation. +  


submitted by hello(64),

please help -- If catalase-positive bacteria neutralize their own superoxide, why isn't it the case for catalase-positive bacteria to infections in everyone?

I'm not understanding the connection to NADPH oxidase deficiency.

hello  to cause** infections in everyone +  


submitted by meningitis(154),

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. +  


submitted by burak(7),

Isn't it dependent on the location? I answered it coronary sinus because av node is located in Koch triangle; which composed of CSinus, Tendon of Todaro, Tricuspid annulus?

hello  The correct answer was atrioventricular BUNDLE-- it's also known as the Bundle of His. AV Bundle ≠ AV Node. +1  
burak  Now it's more confusing to me:) because av bundle is more inferior to the av node. +  
hello  Patient has ASD --> need to repair interatrial septum. AV bundle aka bundle of His is located neart interatrial septum. Coronary sinus opens into atria but is not located near the interatrial septum +2  


submitted by keycompany(115),

Flow Rate = Velocity x Cross-Sectional Area

2 cm^2 x 20 cm/sec x 60 sec/min x 1 L/1,000 cm^3 = 2.4 L/min

1,000 cm^3 = 1 L

seagull  Well, I missed this one. I don't even feel bad. +7  
link981  @keycompany a small typo, 100 cm^3 = 1 L not 1000cm^3. 1000 mL^3= 1 L +  
hello  @keycompany how did you edit your original comment to fix your typo? +  


submitted by keycompany(115),

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5290806/

Osler Sign is a low-sensitivity, low-specficity finding of Mockenberg Arteriolosclerosis (MA) characterized by "a palpable although pulseless, radial artery while the BP cuff is inflated above systolic pressure".

It is possible that either: a) The low-specificity of this test means it is also applicable to atherosclerosis (not just MA) b) The NBME incorrectly implies that MA is interchangable with atherosclerosis.

bubbles  This was my reasoning, too. I thought this was Mockenberg for sure +  
hello  I don't think think it's a type. According to 2 other comments: "It's atherosclerosis because it said “radial artery is NON-pulsatile BUT REMAINS PALPABLE even as the cuff is inflated”--> normally, you can’t feel the artery when the cuff is overinflated b/c overindlation occludes blood flow and arteries are squishy (compliant); BUT if you had atherosclerosis, which is literally hardening, you would not be able to compress the artery, and neither would you expect the normal radial (outward) expansion of an artery during systole. (that is, the pulses!): "If if something were to not be palpable then it would have to collapse -- atheroclerosis prevents this vessel collapse." +  


submitted by hello(64),

For people asking why the data table was even included if it was not needed to answer this Q, here is a useful explanation:

The table was given because a 2x2 table is typically what you do see regarding data for case-control studies.

If the 2x2 table wasn't included, then literally everytone would pick Choice "E" as the correct answer b/c you can't calculate something without being provided numbers.

The difference in including the data-table is that:

  1. Again, you need to report a 2x2 table because that is typically what you will see regarding data for a case-control study

and

  1. by including the 2x2 table, it actually tests if the test-taker realized that the data in the 2x2 table does not help at all with calculating prevalence-- because case-control studies NEVER report on prevalence.
hello  I also want to add that the Q is asking about sinusitis in the GENERAL population, meanwhile the Q-stem discusses a case-control study that is studying the relationship of smoking (an exposure) to development of sinusitis. To then ask "what is the prevalence of sinusitis in the general population" totally disregards taking into account the exposure of smoking which was the entire reason for the study. In other words, asking prevalence would be very non-sensical. +  


Why wasn’t the table enough to determine prevalence in the general population?

sacredazn  For the case control question, it’s taking that principle that you can’t use case control studies to calculate relative risk and applying it to prevalence. Basically with case control studies we start by saying okay, I’m going to find 200 people with sinusitis and 400 without. Then, you go back and look at the number exposed/unexposed and calculate the odds ratio. So you can’t use case controls to calculate prevalence because it all depends on how many cases you picked in the first place. Might make more sense to think about it with a rare cancer like craniopharyngioma or something- let’s say you chose 10 cases and 10 controls and wanted to look at how many people smoked. It wouldn’t make sense to then say the prevalance of craniopharyngioma is 10/20 = 50%. +5  
dr_trazobone69  Thank you, that makes a lot of sense! So we can use relative risk (cohort studies) to calculate prevalence? +  
sacredazn  @trazobone Hmm I think the wording would be key, you could use a prospective cohort to calculate incidence, but you wouldn’t be able to find prevalence of the gen population unless you had more info. I think the concept is that really to calculate prevalence you need a proper ecologic study looking at population-level data. The way it was worded in the question was tricky though lol since when has “cannot be determined from the info given” ever been a right answer. +3  
nwinkelmann  @sacredazn thank you! this was the best explanation to use the rare disease comparison. Made everything make so much sense and hopefully I'll actually just remember it now, instead of learning the factoid and failing to recall it all the time. +1  
hyperfukus  i guess this makes sense but i don't understand why we are asked to calculate it from tables like this then? is there more info in those? +  
hello  @hyperfukus The table was given because that a 22 table is typically what you do see regarding data for case-control studies. If the 22 table wasn't include, then literally everytone would pick Choice "E" as the correct answer b/c you can't calculate something without being provided numbers. The difference in including the data-table is that 1. again, you need to report a 22 table because that is typically what you will see regarding data for a case-control study and 2. by including the 22 table, it actually tests if the test-taker realized that the data in the 2*2 table does not help at all with calculating prevalence-- because case-control studies NEVER report on prevalence. +  


This one was a little tricky. For this one the key is the low radioiodine uptake. This patient has high T4 and low TSH which makes sense in a hyperthyroid patient, perhaps your first thought is that this patient has Grave’s disease. However, in Grave’s your thyroid is being stimulated to make more thyroid hormone from scratch and as such would have an increased radioiodine uptake because the thyroid is bringing in the required (now radiolabeled) iodine. This is why it is not Graves (“release of thyroid hormone from a thyroid stimulated by antibodies”).

So if its not Grave’s what could it be? For this you’d have to know that Hashimoto’s Thyroiditis (also known as Chronic Lymphocytic Thyroiditis and is often referred to as such on board exams to throw you off) has three phases - first they are hyperthyroid, then euthyroid, then the classic hypothyroid that you would expect with low T4 and high TSH. This was the key to this question. The reason for this is that antithyroid peroxidase antibodies in Hashimoto’s cause the thyroid to release all of its stored thyroid hormone making the patient hyperthyroid for a short period of time. After this massive release of thyroid hormone, the antibodies make them unable to make new TH and therefore they become euthyroid for a short period and then hypothyroid which you would expect! Since they can’t make new TH, the thyroid will not take up the radioiodine and therefore there will be low radioiodine uptake. Hence, “release of stored thyroid hormone from a thyroid gland infiltrated by lymphocytes.” aka “Lymphocytic (hashimotos) thyroiditis”.

I think “release of thyroid hormone from a lymphomatous thyroid gland” is referring to some kind of thyroid cancer in which case you would expect them to be describing a nodule on radioiodine uptake.

​Summary video here and also a great site in general: https://onlinemeded.org/spa/endocrine/thyroid/acquire

aesalmon  pg 338 of FA lists it under hypothyroidism but it does present as transient hyperthyroidism first +3  
hyperfukus  yep that was the key! Goiter is "HOT" but the remaining answer choices were still kind of bleh D was distracting the hell out of me i spent so long to convince myself to pick C and move on +1  
hello  Pasting nwinkelmann's comment as an addition: Choice "D" is wrong b/c "lymphomatous thyroid gland" = primary thyroid lymphoma (typically NHL, which is very rare) or Hashimoto's thyroid progression. Hashimoto's thyroiditis = lymphocytic infiltrate with germinal B cells and Hurthle cells, which upon continued stimulation, can lead to mutation/malignant transformation to B cell lymphoma. Both of these present with hypothyroidism with low T4 and high TSH (opposite of this patient). +  


submitted by nwinkelmann(94),

Can someone explain how to rule out the other answer choicers?

warbyparker1  you can r/o SMA because as kidneys ascend they get stuck low in the INFERIOR MA (L3 level). So I guess there should be no problem w SMA +  
hello  I think friability of vascular tissue would indicate in inflammatory process (the one I can think of is strawberry cervix) -- so i think that's why you can rule out choice C. +  


submitted by pparalpha(18),

Can someone please explain why it would not be glycogen depletion? I thought the question was talking about the Warburg phenomenon... so why not breakdown of glycogen to glucose?

I guess it would not explain the edema?

hello  Glygocen stores are depleted within 24h. This person has signs and symptoms of longterm nutritional deficiences. +1  


hello  Adding to this... The Q is describing the GENIOFEMORAL nerve, which runs EXTERNAL TO of spermatic cord at the superficial inguinal ring This Q is NOT referring to ilioinguinal nerve, which exits THROUGH the superficial inguinal canal +  


submitted by keycompany(115),

Mandelian Genetics:

Man has 2/3 chance of being a carrier. (He does not have the disease). Woman carrier risk must be calculated with p^2 + 2pq + q^2. q^2 = 1/40,000 q = 1/200, p is roughly = 1 2pq = 1/100 = Carrier frequency .

Risk of having a child thus equals 2/3 x 1/100 x 1/4 = 1/600 Because: 2/3 = Man Carrier risk 1/100 = Female Carrier Risk 1/4 = Chance they each pass on the recessive gene to their offspring.

hello  See my explanation if you need more words to explain this explanation +  


submitted by burak(7),

Isn't it dependent on the location? I answered it coronary sinus because av node is located in Koch triangle; which composed of CSinus, Tendon of Todaro, Tricuspid annulus?

hello  The correct answer was atrioventricular BUNDLE-- it's also known as the Bundle of His. AV Bundle ≠ AV Node. +1  
burak  Now it's more confusing to me:) because av bundle is more inferior to the av node. +  
hello  Patient has ASD --> need to repair interatrial septum. AV bundle aka bundle of His is located neart interatrial septum. Coronary sinus opens into atria but is not located near the interatrial septum +2  


submitted by hello(64),

Please help

Mid-systolic ejection click = pulmonic stenosis

How is pulmonic stenosis related to the patient's ASD -- does ASD cause pulmonic stenosis??

burak  ASD has typically 3 associated sounds according to UW, they are all about increased blood in RA. Increased blood in RA causes more blood do ejected from tricuspid (dşastolic rumble), and more blood to be ejected to pulmonary circulation which cause pulmonary flow murmur (midsystolic murmur in pulmonary region). It even can cause pulmonary regurgitaion like murmur, but most important murmur in ASD is typically midsystolic murmur. You can check it out on FA 2018 page 284 +1  
hello  Ok, what I learned: Extra blood in the right heart (due to ASD) doesn't lead to pulmonic stenosis? Instead, it's that pulmonic stenosis = most common comorbid heart association with ASD +1  
burak  No it's not pulmonic stenosis, it doesn't lead. Murmur associated with ASD is pulmonic stenosis-like murmur, because it's caused by excess RA and RV volume ejecting to the pulmonary arteries. So it's same location with pulmonic stenosis, and it's systolic. You get it? +1  
hello  @burak Yep! +  


submitted by assoplasty(39),

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. +  


submitted by didelphus(19),

Any idea why hyperchloremia isn't an answer? The diarrhea would cause an normal anion gap (hyperchloremic) metabolic acidosis.

charcot_bouchard  this is the problem bet uw and nbme. in uw it would be for sure a gotcha ques. but in nbme they are usually looking for most obvious. also look what they are asking "most likely". baby would dev low Na before acidosis. Thats my 2 cents +2  
temmy  hyperchloremia will not account for the seizure that brought the patient to the hospital. seizures according to first aid is caused by hypocalcemia and hyponatremia +  
cry2mucheveryday  Children with diarrhoea who drink large amounts of water or other hypotonic fluids containing very low concentrations of salt and other solutes, or who receive intravenous infusions of 50% glucose in water, may develop hyponatraemia. This occurs because water is absorbed from the gut while the loss of salt (NaCl) continues, causing net losses of sodium in excess of water. The principal features of hyponatraemic dehydration are: there is a deficit of water and sodium, but the deficit of sodium is greater; serum sodium concentration is low (<130 mmol/l); serum osmolality is low (<275 mOsmol/l); the child is lethargic; infrequently, there are seizures. https://rehydrate.org/diarrhoea/tmsdd/2med.htm#CONSEQUENCES%20OF%20WATERY%20DIARRHOEA +  
cry2mucheveryday  Also, why is this being given formula...? May be lactase deficiency...which leads to osmotic diarrhea...leads to hyponatremia(goljan) Aren't newborns supposed to be kept on exclusive breast milk till 6 months?? +  
hello  @cry2mucheveryday Don't read too much into it. The fact that the baby is receiving formula isn't relevant to answering the Q. Btw, not everyone breast feeds. Additionally, the Q wouldn't make much sense if it said "they ran out of breastmilk"... +  
hello  @cry2mucheveryday Being on formula then the parents running out of formula is more of a clue for water intoxication. This is typically the scenario that water intoxication presents. However, I suppose if for some reason the baby was being breastfed and the parents switched to exclusively waterfeeding (and no other foods), then water intoxication would also result. +  


submitted by didelphus(19),

Any idea why hyperchloremia isn't an answer? The diarrhea would cause an normal anion gap (hyperchloremic) metabolic acidosis.

charcot_bouchard  this is the problem bet uw and nbme. in uw it would be for sure a gotcha ques. but in nbme they are usually looking for most obvious. also look what they are asking "most likely". baby would dev low Na before acidosis. Thats my 2 cents +2  
temmy  hyperchloremia will not account for the seizure that brought the patient to the hospital. seizures according to first aid is caused by hypocalcemia and hyponatremia +  
cry2mucheveryday  Children with diarrhoea who drink large amounts of water or other hypotonic fluids containing very low concentrations of salt and other solutes, or who receive intravenous infusions of 50% glucose in water, may develop hyponatraemia. This occurs because water is absorbed from the gut while the loss of salt (NaCl) continues, causing net losses of sodium in excess of water. The principal features of hyponatraemic dehydration are: there is a deficit of water and sodium, but the deficit of sodium is greater; serum sodium concentration is low (<130 mmol/l); serum osmolality is low (<275 mOsmol/l); the child is lethargic; infrequently, there are seizures. https://rehydrate.org/diarrhoea/tmsdd/2med.htm#CONSEQUENCES%20OF%20WATERY%20DIARRHOEA +  
cry2mucheveryday  Also, why is this being given formula...? May be lactase deficiency...which leads to osmotic diarrhea...leads to hyponatremia(goljan) Aren't newborns supposed to be kept on exclusive breast milk till 6 months?? +  
hello  @cry2mucheveryday Don't read too much into it. The fact that the baby is receiving formula isn't relevant to answering the Q. Btw, not everyone breast feeds. Additionally, the Q wouldn't make much sense if it said "they ran out of breastmilk"... +  
hello  @cry2mucheveryday Being on formula then the parents running out of formula is more of a clue for water intoxication. This is typically the scenario that water intoxication presents. However, I suppose if for some reason the baby was being breastfed and the parents switched to exclusively waterfeeding (and no other foods), then water intoxication would also result. +  


submitted by jjubilee(0),

Per google symptoms of hypochloremia and hyponatremia are very similar; however, hyponatremia includes seizures and spasms. But per my quick google search hypochloremia does not. Hypochloremia also can present with respiratory difficulties, but I didn't see that with hyponatremia.

hello  That answer choice is hypERchrloremia, not hypochloremia. +  


submitted by hayayah(400),

Catheter placement:

https://aneskey.com/wp-content/uploads/2016/08/image00804.jpeg

Recall that the lung apex extends above the first rib.

hungrybox  His expression is so blissful. U can tell they're shootin up some full u-opioid agonist codeine type of shit and not some shitty partial u-opioid agonist buprenorphine type of shit or some shit like loperamide that doesn't even act on the CNS +6  
rerdwins  even better, if you recall that the esophagus is RETROperitoneal ( its in like half the answer choices). hence, to get to it you have to go WAAYYYYY deep ( like rick and morty smuggling shit). after that, the lung option makes the most sense. +4  
hello  Also, pulmonary artery is way too far away to be damaged by internal jugular vein catherization. +  


submitted by nosancuck(37),

Yo dawg we all about PVT TIM HaLL

Phenylalanine, Valine, TryptoDANK, Threonine, Isoleucine, Methionine, Histidine, Leucine Lysine

meningitis  I don't understand what the question is asking... can someone please explain it to me? Patient doesnt eat protein, shes chubby. What does methionine have to do with this? +2  
charcot_bouchard  Just basically asking which is essential amino acids. +1  
usmleuser007  Essential amino acids (something i came up with) 1. "Three HAL fans will try meth" a. Threonine = Three b. Histidine; Arginine; Lysine = HAL c. Phenylalanine = fans d. Valine; Isoleucine; Leucine = will e. Tryptophan = try f. Methionine = meth +1  
nala_ula  They're saying there is a lack of good quality protein -> slight nutritional deficiency. She may have acquired weight but it's not because of protein. So they're specifically asking what amino acid she might be missing due to her subpar diet. Since essential amino acids are those that the body cannot make itself, out off those listed, methionine is the essential amino acid. It's on page 81 of FA 2019. +6  
nala_ula  correct me if I'm wrong please :) +  
hello  For anyone confused trying to follow @usmleuser007's comment -- slightly modified Essential amino acids mnemonic "Ah, Three fans will try meth" Ah = arginine, histidine Three = Threonine Fans (phans)= Phenylalanine Vil (Will -- German accent pronouncing English word 'will') = valine, isoleucine, leucine, lysine Try = tryptophan Meth = Methionine +  


submitted by youssefa(17),

Wouldn't acute alcohol consumption even in moderate amount cause reversible hepatic cellular injury characterized by cellular ballooning? It should be the right answer unless the question stem means "Weekends"

hello  No. The order of liver damage due to alcohol is: fatty changes --> cellular swelling (cellular balooning) --> necrosis. This Q stem states to the patient consumed large amount of alcohol on a weekend -- he has acutely drank a large amount of alcohol on one weekend --> this corresponds with fatty changes +  
et-tu-bromocriptine  It's not in pathoma, but I have it written in (so he or Dr. Ryan may have mentioned it) - Alcoholic hepatitis is generally seen in binge drinkers WITH A LONG HISTORY OF CONSUMPTION. +  
krisgsxr600  Its kind of in pathoma Chapter 1, "free radical Injury", Section 2 "examples of free radical injury" goes over how free radicals (caused by drinking) lead to fat accumulation +  


submitted by temmy(26),

please help according to winters equation the patient has a normal anion gap

ergogenic22  winter's formula is to look at the compensation to see if it is appropriate. PCO2 = 1.5[HCO3-] + 8 +/- 2 In this case, 1.5* 10 (Pt's bicarb) +8 +/-2 = 21 to 25 Pt's PO2 is 23, so compensation is appropriate. If PCO2 was below 21, it would be concomitant respiratory alkalosis +1  
ergogenic22  in other words, winter's formula is not necessary for this question +1  
the_sacramento_kings  lol unless you want to make sure its not A. +1  
hello  @ergogenic22 Someone might use Winter's formula to rule out choice A. +  
maxillarythirdmolar  respiratory depression of alcohol should rule out "A" +  


submitted by cantaloupe5(35),

Histology showed coagulative necrosis (preserved architecture of myocardial fibers) with neutrophil infiltration which hinted that the MI was within 24 hours. Most likely cause of death within first 24 hours of MI is arrhythmia. Myocardial rupture would also be visible on gross appearance of the heart, which they described in the stem.

bighead478  in FA it shows softening of the myocardium to happen at 3-14 days. Do you think this was overly misleading people (like me) into choosing myocardial rupture? I understand the histo features are consistent with < 24 hours, but the stem should also match this in every detail +3  
sbryant6  Myocardial rupture would not happen until 3-14 days. Since this shows signs of <24 hrs, the answer is arrythmia. +1  
hello  @bighead478 You have to look at the whole picture. Histo shows preserved architecture, which indicates coagulative necrosis -- coagulative necrosis is a histo finding only in the first 24h. The most common causes of MI-related sudden death are: arrythmia > cardiogenic shock (heart pump problem) > rupture. +  


submitted by dragon3(4),

What's the difference between reactive granulocytosis vs lymphocytosis?

whossayin  Yes I’m at a loss for this one too. Still can’t figure out how we’re expected to differentiate those based on this slide shown. The only logical explanation that I can think of is that reactive lymphocytes may be seen in LYMPHOMAS as opposed to granulocytes which are seen in LEUKEMIAS Such a shitty way to trick us, hah! +  
henoch280  reactive lymphocytes are seen in EBV infection. you would see lymphocytes in the slide not neutrophils FA2018 pg 165 +3  
whossayin  That makes sense.. but was the question talking about EBV infections or hematological malignancies? Just a vague question I wasn’t really sure what exactly was it trying to teach us, I guess the reactive lymphocytosis just threw me off! Anyways, thanks for the clarification buddy! +  
ratadecalle  They way I thought about it was: Granulocytes: multi lobed nucleus Lymphocytes: single lobe +2  
hello  @whossayin - it's not reactive lymphocytosis because there are no buzzword type symtoms of EBV in the Q stem. Also, reactive lymphocytes look way different. +  


submitted by hungrybox(235),

some wrong answers:

*makes sense b/c myeloblasts are precursors to granulocytes, which use MPO to fight off infections

temmy  Hungrybox aka life saver +  
hello  Thank you!!! +  


submitted by dr.xx(42),

In sarcoidosis, hypercalcemia normally suppresses the release of PTH and therefore the production of calcitriol (1,25-dihydroxycholecalciferol), but in sarcoidosis and other granulomatous diseases, activated mononuclear cells (particularly macrophages) in the lung and lymph nodes produce calcitriol (1,25-dihydroxycholecalciferol) from calcidiol (25-hydroxycholecalciferol) independent of PTH.

https://www.uptodate.com/contents/hypercalcemia-in-granulomatous-diseases

dr.xx  ~~In sarcoidosis,~~ +  
hello  Probably a typo in the first 2 words of the explanation -- not sure what they meant to say instead +  
drdoom  I believe @dr.xx meant to strikeout "In sarcoidosis" from his comment; double-tilde is the markdown plaintext that usually accomplishes that. +  


submitted by cantaloupe5(35),

Hypo/hyperthyroidism is diagnosed with TSH w/ reflex to T4 (this just tells the lab if TSH is normal don’t check T4 but if TSH is abnormal, check T4 too). TSH wasn’t an option so T4 is the best answer.

hello  I don't get why this was downvoted... +  
maxillarythirdmolar  To take it a step further, Goljan mentions that there are a myriad of things circulating in the body, often in a 1:2 ratio of free:bound, so in states like this you could acutally see disruption of this ratio as the body maintains its level of free hormone but further increases its level of bound hormone. Goljan also mentions that you'd see the opposite effect in the presence of steroids and nephrotic syndromes. So you could see decreased total T4 but normal free T4 because the bound amounts go down. +  


submitted by chillqd(7),

The Stem is describing hemochromatosis, characterized by abnormal iron sensing and increased intestinal absorption. This increases Iron, increasing ferritin. In response, TIBC is decreased, which increases transferrin saturation as there is less circulating carrier molecules.

With excess iron in the blood, it will accumulate in tissues including the liver, skin, pancreas. Sequelae include dilated cardiomyopathy, hypogonadism, diabetes, arthropathy 2/2 calcium pyrophosphate deposition, nd Hepatocellular Carcinoma

hello  I think you made one slight mistake. TIBC = total iron binding capacity. It is synonymous with "transferrin saturation". This patient has increased transferrin saturation aka increased TIBC. The transferrin molecules are saturated -- it is incorrect to say "as transferrin saturation increases, there is less circulating carrier molecules." It is more correct to say that the amount of free (unbound) transferrin is decreased. +1  
hpsbwz  @hello Transferrin saturation and TIBC are not synonymous. Transferrin is calculated using total body iron / TIBC. While the serum iron level continues to increase, the transferrin level decreases. Thus, the amount of transferrin available to bind iron (TIBC) decreases and the amount of transferrin saturated with iron (i.e., percent transferrin saturation) increases. +  


submitted by ergogenic22(42),

why is hyperlipidemia secondary to cushing syndrome not a possibility?

hello  SIADH = MC paraneoplastic syndrome of small oat cell lung cancer. Also, Cushing syndrome would cause would weight gain, skin hyperpigmentation, and hypokalemia. Not, lyperlipidemia. +  
charmrooftops  You do get hyperlipidemia in cushing though? https://www.amboss.com/us/knowledge/Cushing_syndrome So still unsure why this is not a possibility. Is it just a "more common" thing for SIADH? +  


submitted by sympathetikey(303),

As stated below, the Left crus cerebri was damaged (see what it should normally look like below). This contains the corticospinal tract. Since the corticospinal tract decusates at the medulla, below the midbrain section we're looking at, you would see Contralateral (Right) Spastic Hemiparesis

sympathetikey  http://what-when-how.com/wp-content/uploads/2012/04/tmp15F11_thumb.jpg +4  
hello  What identifies that a cross-section is medulla vs midbrain vs pons? +1  
kernicterusthefrog  @hello I like to pay attention to the Cerebral Aqueduct (diamond/spade shape seen mostly in Midbrain, and transitioning to 4th ventricle in rostral Pons), and then the shape and size of the 4th ventricle as you move down Pons to rostral&middle Medulla, and eventual closing and absence of fluid space at caudal Medulla. +4  
hello  @kernicterusthefrog Thank you. +  


submitted by armymed88(15),

A little math here.. pH is low --> acidosis pCO2 is high --> respiratory Normal compensation should be roughly a 1 (acute) to 4(chronic) increase in bicarb per every 10 increase in pCO2.. Its lower here, so clearly not compensated and indicated additional drop in bicard --> add on metab acidosis

hello  Hm, what do you mean by "normal compensation?" Are you talking about the bicarb should be increased? Are you saying that a normal compensation would be metabolic alkalosis? Would metabolic alkalosis be an increase in bicarb? +1  
kateinwonderland  How do you know which one has bigger contribution in this situation where there's increased CO2 and decreased HCO-, both indicating acidosis?? +  
yb_26  normal kidney compensation would be an increase in bicarb reabsorption => increased serum bicarb. This pt has low serum bicarb => concurrent metabolic acidosis +  


submitted by seagull(423),

This is a likelihood ratio. LR+= Sens/1-Specif

Any value greater than 10 (per first aid) indicated "usefulness of diagnostic test" which is comparable to PPV (ruling in a dz). Point "A" is the closest mark to where 10 should be on the Y axis.

brise  The question is asking what point would be the most likely to rule in cancer, and high specificity when positive rules in cancer. The highest specificity value is A, bc the the X axis shows (1-specificity)! +4  
hello  brise is correct. Knowing the LR+ value = 10 does not help in this situation because estimating where "10" should fall on an axis is arbitrary. The way to approach this Q is to know that a high specificity is will mean that a positive result is very very likely to be a true positive. In theory, suppose that the specificity was 0.99. This is 99% specificity. Then, you look at the graph. The X-axis is "1-specificity." So, suppose the best test has a specificity of 99%. Then, calculating 1-specificity = 1 - 0.99 = 0.1. You would then chose the datapoint that corresponds to having an "X-value" that is closest to the origin. In this problem, it corresponds to data point "A." +2  


submitted by bobson150(3),

Is this saying there is vesicoureteral reflux? I could have sworm this same image was on form 20 or 21 and the answer was Wilms tumor

hello  Yes, it was. I think in both vignettes, the picture was basically irrelevant. Or another possible clue -- but definitely not needed to answer the Q. +1  
presidentdrmonstermd  My school uses old "retired" NBME questions for exams and I've also seen this exact same picture multiple times...w/ different scenarios I think. I tried remembering what the questions were but I guess it's mostly irrelevant. +1  
hyperfukus  SAME +  
hyperfukus  I also put wilm's tumor bc it felt really familiar wtf +  


The description of bilateral lower limb loss of vibration implies DCML damage, and the absent DTRs + Romberg seem to me to be implying that he possibly has tabes dorsalis from syphilis (or something very similar in presentation).

As for the other answers, A is wrong because his motor function is intact, B is wrong because pain and temperature deficits are not mentioned, C is wrong because it implies a specific nerve is entrapped, but he has lost bilateral sensation in his entire lower extremities

D is the trickiest, and I’m not 100% sure, but I would think radiculopathy of the anterior (ventral) roots would cause motor deficits since they carry motor efferents. You might also expect that motor dysfunction to be unilateral, since it would be unlikely to have a problem with the nerve roots on both sides. also the DCML is not located near the anterior roots of the spinal cord, so if the anterior roots were affected you really wouldn’t expect to see vibratory loss.

So basically process of elimination, I do feel like sensory neuropathy is an extremely vague answer though and I wasn’t a fan of the question.

keycompany  This is a great rationale. I would like to add on that D is wrong because Radicular Neuropathy of the anterior lumbar roots would (1) be painful [radicular neuropathy is characterized by radiating pain (hence the word “Radicular”); this patient has numbness and tingling, not pain] and (2) because the anterior lumbar roots are the motor roots and do not carry sensory innervation. This patient is having a problem with his dorsal spinal cord (not anterior/ventral). +4  
hello  Want to clarify that "radiculopathy" is not synonymous with pain. Radiculopathy can cause pain, weakness, or numbness. I think the only reason Choice D. was incorrect because it discussed the "anterior lumbar roots", which would affect motor function. +3  
niboonsh  Radiculopathy is damage to the actual nerve itself, wouldnt that make it a LMN lesion and babinski would be negative? +1  
link981  Great explanation guys +  


submitted by hayayah(400),

Neoplasia is new tissue growth that is unregulated, irreversible, and monoclonal.

Clonality can be determined by glucose-6-phosphate dehydrogenase (G6PD) enzyme isoforms. G6PD is X-linked.

*For more information check out Ch. 3 Neoplasia in Pathoma

hello  This is great, thank you. +4  
breis  Pathoma ch. 3 pg 23 "Basic Principles" +2  
charcot_bouchard  Shoutout to Imam Satter! Without him this question wasnt possible for me to answer in 10 sec. +3  


submitted by hayayah(400),

This patient has small cell carcinoma. This type of cancer is associated with paraneoplastic syndromes such as: Cushing Syndrome, SIADH, or antibodies against Ca2+ channels (Lambert-Eaton) or neurons. Amplification of myc oncogenes is also common.

SIADH (Syndrome of inappropriate antidiuretic hormone secretion) is characterized by:

  • Excessive free water retention
  • Euvolemic hyponatremia with continued urinary Na+ excretion
  • Urine osmolality > serum osmolality

Body responds to water retention with aldosterone and ANP and BNP. That is what causes the increased urinary Na+ secretion Žwhich leads to normalization of extracellular fluid volume Žand the euvolemic hyponatremia.

hello  Why would body respond to water retention with ALDO? ALDO would increase water retention... +2  
nala_ula  @hello, the body's response is to decrease Aldosterone since there is increased volume retention and subsequently increased blood pressure. This concept confused me a lot, but I ended up just viewing it as separate responses. First, the increased volume retention leads to increase ANP and BNP secretion that lead to decreased Na+ reabsorption in the tubules (page 294 in FA 2019) and second, this increased volume basically leads to increased pressure so lets also decrease aldosterone so there is no Na+ retention (since water comes with it)... I thought it was counterintuitive to secrete so much Na+ since you're already having decreased serum osmolality (decreased Na+ concentration) because of the water retention, but I'm guessing that this is just another way our body's well intentions end up making us worse XD +5  
compasses  see page 344 FA2019 for SIADH. +  
dickass  author pasted text straight from FA but the arrows didn't copy over, inverting the original meaning +  
medninja  The idea of increasing urine Na is getting rid of water, thats why this mechanism end increasing urine Na secretion even when there are very low serum Na levels. +  


submitted by hayayah(400),

Case of arteriolosclerosis.

Hyperplastic arteriolosclerosis involves thickening of vessel wall by hyperplasia of smooth muscle ('onion-skin appearance')

  • Consequence of malignant hypertension (>180/120 w/ acute end-organ damage)
  • Results in reduced vessel caliber with end-organ ischemia
  • May lead to fibrinoid necrosis of the vessel wall with hemorrhage; classically causes acute renal failure (ARF) with a characteristic 'flea-bitten' appearance
masonkingcobra  From Robbin's: Fibromuscular dysplasia is a focal irregular thickening of the walls of medium-sized and large muscular arteries due to a combination of medial and intimal hyperplasia and fibrosis. It can manifest at any age but occurs most frequently in young women. The focal wall thickening results in luminal stenosis or can be associated with abnormal vessel spasm that reduces vascular flow; in the renal arteries, it can lead to renovascular hypertension. Between the focal segments of thickened wall, the artery often also exhibits medial attenuation; vascular outpouchings can develop in these portions of the vessel and sometimes rupture. +  
asapdoc  I thought this was a weirdly worded answer. I immediately ( stupidly) crossed of fibromuscular dysplasia since it wasnt a younger women =/ +5  
uslme123  I was thinking malignant nephrosclerosis ... but I guess you'd get hyperplastic arteries first -_- +  
hello  The answer choice is fibromuscular HYPERplasia - I think this is different from fibromuscular DYSplasia (seen in young women); +7  
yotsubato  hello is right. Fibromuscular hyperplasia is thickening of the muscular layer of the arteriole in response to chronic hypertension (as the question stem implies) +2  
smc213  Fibromuscular Hyperplasia vs Dysplasia...... are supposedly the SAME thing with multiple names. Fibromuscular dysplasia, also known as fibromuscular hyperplasia, medial hyperplasia, or arterial dysplasia, is a relatively uncommon multifocal arterial disease of unknown cause, characterized by nonatherosclerotic abnormalities involving the smooth muscle, fibrous and elastic tissue, of small- to medium-sized arterial walls. http://www.medlink.com/article/fibromuscular_dysplasia +1  
smc213  *sorry I had to post this because it was confusing!!!*Fibromuscular dysplasia is most common in women between the ages of 40 of and 60, but the condition can also occur in children and the elderly. The majority (more than 90%) of patients with FMD are women. However, men can also have FMD, and those who do have a higher risk of complications such as aneurysms (bulging) or dissections (tears) in the arteries. https://my.clevelandclinic.org/health/diseases/17001-fibromuscular-dysplasia-fmd +1  
momina_amjad  These questions are driving me crazy- fibromuscular dysplasia/hyperplasia is the same thing, and it is NOT this presentation and it doesn't refer to arteriolosclerosis seen in malignant HTN! Is the HTN a cause, or a consequence? I read it as being the cause (uncontrolled HTN for many years) If it was the consequence, the presentation is still not classical! -_- +1  
charcot_bouchard  Poor controlled HTN is the cause here +  
charcot_bouchard  Also guys if u take it as Fibromuscular dysplasia resulting in RAS none of the answer choice matches +  


submitted by sympathetikey(303),

As stated below, the Left crus cerebri was damaged (see what it should normally look like below). This contains the corticospinal tract. Since the corticospinal tract decusates at the medulla, below the midbrain section we're looking at, you would see Contralateral (Right) Spastic Hemiparesis

sympathetikey  http://what-when-how.com/wp-content/uploads/2012/04/tmp15F11_thumb.jpg +4  
hello  What identifies that a cross-section is medulla vs midbrain vs pons? +1  
kernicterusthefrog  @hello I like to pay attention to the Cerebral Aqueduct (diamond/spade shape seen mostly in Midbrain, and transitioning to 4th ventricle in rostral Pons), and then the shape and size of the 4th ventricle as you move down Pons to rostral&middle Medulla, and eventual closing and absence of fluid space at caudal Medulla. +4  
hello  @kernicterusthefrog Thank you. +  


submitted by hayayah(400),

Renovascular disease is the most common cause of 2° HTN in adults. Can be d/t ischemia from renal stenosis or microvascular disease. Can hear renal bruits lateral to umbilicus.

Main causes of renal artery stenosis:

  • Atherosclerotic plaques—proximal 1/3rd of renal artery, usually in older males, smokers.

  • Fibromuscular dysplasia—distal 2/3rd of renal artery or segmental branches, usually young or middle-aged females.

Lab values based off:

  1. Stenosis decreases blood flow to glomerulus.
  2. Juxtaglomerular apparatus (JGA) responds by secreting renin, which converts angiotensinogen to angiotensin I.
  3. Angiotensin I is converted to angiotensin II (ATII) by angiotensin converting enzyme (ACE --in lungs)
  4. ATII raises blood pressure by (1) contracting arteriolar smooth muscle, increasing total peripheral resistance and (2) promoting adrenal release of aldosterone, which increases reabsorption of sodium (where Na+ goes H2O will follow) in the distal convoluted tubule (expanding plasma volume). Can lead to hypokalemia (seen in the labs for this question)
  5. Leads to HTN with increased plasma renin and unilateral atrophy (due to low blood flow) of the affected kidney; neither feature is seen in primary hypertension
uslme123  So both causes would result in increased aldo and MR is the only way to differentiate the two? +1  
hello  @USMLE123 I think both are causes of renal artery stenosis and that could be seen via MR angiography. It is asking what could help DIAGNOSE this patient -- and her most likely cause of the findings is fibromuscular dysplasia. So, yes, MR angiography would look different for the 2 different etiologies and thus could can be used to differentiate the two from one another. However, epidemiologically, we are looking to diagnose her with the suspected most probable cause. +1  
yotsubato  @USLME123 I think measuring Aldosterone is an incorrect answer because you already know its increased due to low K. Knowing she has high Aldosterone wouldnt provide you evidence for a final diagnosis. +2  


submitted by johnthurtjr(49),

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. +  
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". +3  
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/ +  


submitted by hayayah(400),

Definition of adjustment disorder:

Emotional symptoms (eg, anxiety, depression) that occur within 3 months of an identifiable psychosocial stressor (eg, divorce, illness) lasting < 6 months once the stressor has ended.

If symptoms persist > 6 months after stressor ends, it is GAD.

hello  Yep, and I think what we are supposed to take from this Q is: The only info. we have for this patient is that he ended chemo 2 months ago and has been calling the doctor a lot -- this is supposed to mean he has been calling a lot since ending chemo 2 months ago. His frequent calls starting after ending chemo and within 3 months of the stressor fits with the above-stated definition of "adjustment disorder" with anxiety. I stressor in this case could possibly be either the actual illness or the ending of chemo/treatment. It probably does not matter much in this case. +  
charcot_bouchard  I think doing uw done me wrong here. Adjustment disorder isnt diagnosed when symptom match another disorder --- it was like never a right answer. But ofc its right answer in nbme +1  
maxillarythirdmolar  Just to add to that, the tingling in his fingers may seem like a distraction/it probably is. Likely has some relation to his Chemo. +1  


submitted by hayayah(400),

Zollinger-Ellison syndrome: Gastrin-secreting tumor (gastrinoma) of pancreas or duodenum.

hello  Can you please explain how gastrin relates to the physical exam findings in the patient? +  
amorah  I believe the logic behind it is patient has pain and black stool, suggesting peptic ulcer with bleeding. Since pain is not relieved by antiacid and H2 blockers, it suggests ectopic source to stimulate the excessive acid. Among all, gastrin by ZE syndrome fits the most. +3  


submitted by beeip(63),

Thought this would be something regarding "bariatric surgery," but nope, just "no starchy foods, because you're pre-diabetic."

hello  Yep, seems that because the patient has prediabetes, he should avoid eating excessive starchy foods. +  
yotsubato  such a BS question IMO +3  
yotsubato  such a BS question IMO +  
breis  I put nuts thinking of "fats" and that with a bariatric surgery they may have problems with absorption.. +2  
teetime  This isn't right because the bariatric surgery will cure the prediabetes. It's dumping. +  
dr_jan_itor  Why should he avoid eating excessive starchy foods? To avoid gaining weight? It doesn't matter what macronutrients he eats if they are calorie controlled. +  


submitted by kentuckyfan(18),

Urea cycle: Decreased citrulline and hyperammonemia can differentiate it from orotic aciduria.

hello  As the poster indicates, the described patient has a defect in the urea cycle, specifically an ornithine transcarbamylase deficiency. Added for clarity to future readers. +  


submitted by drdoom(192),

The more general principle: endothelia vasodilate in the presence of high CO2; you gotta get rid of that acid somehow! Can’t let it accumulate, as lower pH within a “micro-environment” affects structure/efficiency of enzymes, proteins, etc. The more acidic a local environment, the more you expect nearby vasculature to dilate (as a means of increasing flow rate, thereby ferrying off accumulate acid).

The anesthesiologist can exploit this mechanism. By hyperventilating (blowing off CO2), the brain vasculature senses a low CO2 / “hunky-dory state,” which requires no vasodilation. In other words, the vasculature does not need to continue the ATP-consuming practice of synthesizing Nitric Oxide (NO).

hello  But, the Q-stem states the anesthesiologist is HYPOventilating the patient. +2  
drdoom  decreasing respiratory rate = retention of CO2 = vasodilation of brain arteries = more filling of tubes = greater intra-cranial pressure +1  
drdoom  @hello shoot, you're right! i ended my explanation with the example of HYPERventilation when i should have done the opposite! (sorry!) ... edit: "By HYPOventilating (retaining CO2), the brain vasculature senses a high CO2 environment and vasodilates = increases intra-cranial filling and pressure!" +  


submitted by loopers(2),

Vomiting blood and cool skin indicates this is a type of hypovolemic shock. To understand shock, remember that 1) BP = TPR x CO 2) CO = SV x HR 3) SV = EDV - ESV In hypovolemic shock, you are losing fluid, so stroke volume is decreased and end diastolic volume is decreased. Decreased EDV means that the "filling volume" is decreased, which also means the preload will be decreased (https://www.cvphysiology.com/Cardiac%20Function/CF007). Also, skin is cool because you're decreasing SV --> decreased CO --> Ang II/ADH/etc is released to vasoconstrict increaseing resistance. Since there is increased resistance, there is less blood flow causing skin to be cold/clammy.

hello  Patient in hypovolemic shock - the clues are low BP and COOL skin. Hypovolemic shock is caused by fluid loss. The patient has decreased preload b/c of fluid loss, i.e. there is decreased blood volume returning to heart --> thus decreased preload. +3