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 +6  (nbme24#38)

"Blood flow to various organs increases during pregnancy to meet the increased metabolic needs of tissues. Thus, venous return and cardiac output increases dramatically during pregnancy. Cardiac output gradually increases during the first 2 trimesters with the largest increase occurring by 16 weeks of gestation.3 The increase in cardiac output is well established by 5 weeks of gestation and increases to 50% above prepregnancy levels by 16 to 20 weeks of gestation. The rise in cardiac output typically plateaus after 20 weeks of gestation and remains elevated until term. The increases in cardiac output are associated with significant increases in stroke volume and heart rate (HR)"

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3802121/


 +0  (nbme24#46)

I have an issue with this question which also conflicts with UWorld. In order to be degraded by proteosomes the misfolded protein would need to be present in the cytosol for ubuination. It it accumulated in the RER then how does it get tagged? Honestly, so conflicted...

sajaqua1  So ordinarily a misfolded protein does undergo ubiquitination and proteolysis. It is noteable that CFTR misfolding doesn't even allow it escape the ER, so it accumulates in the ER

 +0  (nbme24#37)

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paanvaannd  lollll this doesn't exactly come through on desktop but it sure is funny on a mobile browser.

 +7  (nbme24#28)

A- primary motor cortex = wrong side of body (deficit of UMN on left side body)

B - Thalamus = sensory information conduit - motor deficits unlikely to originate from here

C - Pons - CNs 8,7,6,5, likely result in "locked in syndrome" or complete loss of motor function on right side + facial features.

D. Vermis - central body coordination. Damage results in ataxia

Not complete but maybe helpful..

yotsubato  C - Pons - CNs 8,7,6,5, likely result in "locked in syndrome" or complete loss of motor function on LEFT side + RIGHT sided facial features. Decussation occurs in medulla

 +1  (nbme24#25)

I thought this was a type 1 RTA but I was wrong. Any suggestions?

seagull  It looks like it was a type II RTA. The difference is incredibly subtle from the info given in this question.
gonyyong  He has Fanconi syndrome which is generalized reabsorption defect in PCT which leads to metabolic acidosis and hypophosphatemia → can lead to rickets Also, does lead to type II RTA
duat98  Also the proximal tubule is the place with the highest phosphate absorption rate. That's why PTH works here mostly and a little bit in the distal tubule.

 +3  (nbme24#35)

This infant has oxygen toxicity due to free radical generation. Free radicals damage the lung parenchyma leading to fibrosis and dysplasia (abnormal growth).

link981  Per American Lung Association: Bronchopulmonary dysplasia (BPD) is a form of chronic lung disease that affects newborns (mostly premature) and infants. It results from damage to the lungs caused by mechanical ventilation (respirator) and long-term use of oxygen. Most infants recover from BPD, but some may have long-term breathing difficulty. + Prematurely born infants have very few tiny air sacs (alveoli) at birth. The alveoli that are present tend to not be mature enough to function normal, and the infant requires respiratory support to breathe. Although life-saving, these treatments can also cause lung damage.

 +1  (nbme24#4)

https://en.wikipedia.org/wiki/Blastomycosis#/media/File:Blastomyces_dermatitidis_GMS.jpeg

I believe this is actually disseminated Blastomyces due to the "Broad Based Budding" as seen in the picture.

seagull  However, given the stain and some of the features I now see that this is most likely Crypto. THey like similar. my bad
mjmejora  oh what a catch! I also thought this was Blasto until you explained otherwise

 +9  (nbme24#11)

Another approach. Diabetes causes non-enzymatic glycosylation which may negatively impact the function of neurons mainly due to altered blood supply among other things. These glycosylate deposits typically occur peripherally at the legs. The only peripheral answer choice was a nociceptor in the legs. all the other answer choices are at least more centrally located with larger blood supplies.

Again, not perfect but a way to reason out this answer but it does work.

sam1  I believe this concept is referring to peripheral sensitization. Peripheral nerves that have sustained damage (such as through non-enzymatic glycosylation in DM) cause sensitization of their neighboring nerves, thus leading to lower thresholds for activation. This sensitization is thought to be accomplished through mediators such as PGE2.
sam1  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3701208/ ^ Section on peripheral sensitization

 +3  (nbme24#6)

This is a nice approach to identifying and treating factitious disorder.

https://www.google.com/search?q=backhand+slap+text&tbm=isch#imgrc=kvpORbo68F6X2M:

cinnapie  Not all heros wear capes
privwill  Mother of mine strongly believes in this method of treatment...


 +4  (nbme24#36)

This is either a hypertropic scar or keloid. Both arise due to over-expression of TGF-beta.

charcot_bouchard  i think its a foreign body granuloma

 +1  (nbme24#48)

The semantics of this question made me vomit blood.

At least one day a patient will look me in the eyes and ask " where are tripetides broken down at". I will smile at them and say "the intestinal mucosa and not the duodenum". They'll smile back and then i'll then i'll walk away and think of this moment as I jump from the window.


 +46  (nbme24#48)

The semantics of this question made me vomit blood.

One day a patient will look me in the eyes and ask, "Where are tripetides broken down?" I will smile at them and say, "the intestinal mucosa and not the duodenum." They'll smile back and I'll walk away and think of this moment as I jump from the window.

sympathetikey  Too real.
mcl  how do i upvote multiple times
trichotillomaniac  I made an account solely so I could upvote this.
dragon3  ty for the chuckle
cinnapie  @trichotillomaniac Same

 +11  (nbme24#49)

at BMI 15 not only has she never had a period but she never had a meal.

sympathetikey  You're on fire man lol

 +1  (nbme23#5)

The underlying mechanism is usually a problem with connective tissue due to a lack of type I collagen. This occurs in more than 90% of cases due to mutations in the COL1A1 or COL1A2 genes. These genetic problems are often inherited from a person's parents in an autosomal dominant manner or occur via a new mutation.

-Wiki

Basically, good f***ing luck!


 +3  (nbme23#2)

Another way to approach this is asking yourself which of these cell types are likely undergoing the most mitotic activity. The granulocyte precursors are likely dividing more than nerves or lymphocytes (in absence of infection). This was my approach.


 +2  (nbme23#28)

B12 deficiency leads to demylination of the DCML and ALS pathways (i.e. posterior cord syndrome).


 +3  (nbme23#49)

So, T1/2-T5/6 are the sympathetic level for the heart. The stellate ganglion are cervical sympathetic ganglion. This question seems more incorrect (or a huge leap) to me. But hey, I know people will disagree.

dentist  you're right! heart rate is the only option under sympathetic control.

 +1  (nbme23#19)

https://en.wikipedia.org/wiki/Proofreading_(biology)

Here is a little bit on proofreading.Hope it helps


 +2  (nbme23#34)

at the very least, there are multiple areas of cancer giving some indication that it maybe metastatic.


 +3  (nbme23#38)

Trauma lead to ARDS. ARDS developed exudate accumulation in lungs which brought on more inflammation.


 +0  (nbme23#25)

Did anyone think that influenza was right? I understand that Herpes-Z can cause pneumonia but why is this answer better over influenza?

jrod77  I believe it's the vesicular rash that gives it away. I thought it was influenza too, but i re-read the questions and I realized they included a rash which disqualifies influenza.
charcot_bouchard  Also h/o of immunsupression, disseminated VZV. Influenza itself doesnt cause severe disease. secondary PNA does. which u will see in elderly. usually

 +4  (nbme23#19)

This patient is tripping balls. Better do a drug screen which seems obvious.

sympathetikey  When the answer is so obvious that you pick a stupid answer instead of it. DOH
jooceman739  Funny thing I noticed is "he is alert and cooperative. He appears to be in pain" So he was so high that he was alert and cooperative during the basal ganglia hemorrhage
yotsubato  @sympathetikey That fucking guy who drinks 2 six packs a day with liver failure got me like that.
yogi  probably the "drug" have to be a stimulant or a hallucinogen which causes HTN & Tachycardia.
charcot_bouchard  Lol. I got the right answer but took long time
goodkarmaonly  The patient's B.P. and pulse are raised + Bilateral dilated pupils = Most likely use of a stimulant Thats how I reasoned it anyways

 +2  (nbme23#38)

Why is this not HUS? How did you guys approach the question?

joonam  I think if this was HUS (d/t a bacterial infection) the leukocyte count would be abnormal (11k<)
yotsubato  normochromic normocytic RBC thats why. You would see schistocytes

 +2  (nbme23#45)

This is a panic attack. Hyperventilation drops pCO2 leading to a respiratory alkalosis. po2 is relatively unaffected (don't ask me how?)

sympathetikey  Yeah haha I had the same conundrum.
sajaqua1  If she's breathing deep as she breathes fast, then oxygen is still reaching the alveoli , so arterial pO2 would not be effected.
imnotarobotbut  lmao i'm so freaking dumb i thought she was having alcohol withdrawals because it was relieved by alcohol
soph  Maybe Po2 is unaffected bc its perfusion (blood) limited not difusion limited (under normal circumstances).
charcot_bouchard  PErioral tingling- due to transient hypocalcemia induced by resp alkalosis.


 +4  (nbme23#49)

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


 +10  (nbme23#28)

This is a type II Renal Tubular Acidosis. My Medical School Never taught this to me. Did you also go to poverty med school? I'm surprised they even gave us toilet paper.

mousie  haha mine didn't either. But they usually leave out most high yield info so, to be expected I guess.
yotsubato  I didnt have physiology in my medical school. None, zip, zero, none. Nor did I have biochem. They said "you learned all this shit in undergrad, youll memorize it again for step 1 and forget it promptly" and then just moved on.

 +3  (nbme23#8)

Hardy-Weinberg equation = 1= P^2 + 2pq + q^2

P^2 = 1/10,000 = 1/100

Then remember P + q = 1 ------> 1/100 + q = 1 (q = 99/100)

Lastly plug back into Hardy-Weinberg Equation as:

2pq = Heterozygote carrier

(2 x 1/100 x 99/100 = 2/100 = 1/50)

link981  I think q should be 1/100. You got p and q mixed up.

 +4  (nbme23#48)

"why don't you stop what you're doing because it's ridiculous". --actual answer

sympathetikey  Mam--mam. Put down the egg, mam.
woodenspooninmymouth  I spent sometime in Guatemala last year, and someone told me that the egg thing is uncommon. What is common is giving their children a small gold bracelet. The bracelet is supposed to prevent the evil eye, dunno how.

 +2  (nbme23#39)

i'm still convinced this is irritable bowel syndrome. Change my mind.

mousie  haha I picked this too bc she's 44.... isn't celiac something that would present much younger?? but I don't think IBS would cause an iron deficiency anemia is the hint they were trying to give us.
sympathetikey  If it was IBS, they would have mentioned something about them having abdominal pain, different stool frequency, and then relief after defecation, me thinks.
aknemu  I was between celiac sprue and IBS but what pushed me towards celiac's was a few things: 1. The Iron deficency anemia (I think that would be unlikely in IBS) 2. Steatorrhea (which would also be unlikley in IBS) 3. Osteopenia- I was think vitamin D deficency 4. Lack of a psychiatric history
catch-22  IBS is a diagnosis of exclusion. If you haven't excluded Celiac (and this can't be excluded based on epidemiology alone), you can't diagnose IBS.

 +5  (nbme23#50)

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?
catch-22  You're looking at the ventral aspect of the brainstem.
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

 +0  (nbme22#15)

The mass is in the outer upper quadrant, this is why it want DCIS. Nice and simple

seagull  *wasn't

 +13  (nbme22#36)

Which of the following reasons is why this question is bull?

1) Using the word "cyclic" instead of tricyclic for clarity

2) Knowing all of epidemiology of all drugs

3) having to reason out that anticholinergic effects are probably the worst over alpha1 or H1 effects to no certainty.

4) The crippling depression of studying for days-to-weeks on end to probably do average on the test.

nlkrueger  yo, re-fucking-tweet
aesalmon  I agree, I picked H1 because such a common complaint for those on TCAs is Sedation, I figure it might be so commonly seen as to be the "most common" reason for noncompliance. I suppose the "hot as a hare...etc" effects would be more severe/annoying, but I didn't think they were more common.
fcambridge  I just like to pretend that there's a reason this question is now in an NBME and no longer being used for the test. Hopefully they realized the idiocy of this question like we all do
link981  Since it said cyclic, I thought of using, discontinuing, then using again. These people who write these questions need take some English writing courses so they can write with CLARITY. Cyclic is not the same as Tricyclic.

 +2  (nbme22#8)

So alpha was the answer so my fatigued mind put "A"...well done. You're going to be a doctor. lol

impostersyndromel1000  hope you dont have to write a prescription for me one day lol

 +13  (nbme22#35)

Did anyone need to read that last sentence like 50 times because the author refuses to use better grammar. Just frustrating.

link981  Author rationale: "What is grammar?"

 +4  (nbme22#30)

out of curiosity, how may people knew this? (dont be shy to say you did or didnt?)

My poverty education didn't ingrain this in me.

johnthurtjr  I did not
nlkrueger  i did not lol
ht3  you're definitely not alone lol
yotsubato  no idea
yotsubato  And its not in FA, so fuck it IMO
niboonsh  i didnt
epr94  did not
link981  I guessed it because the names sounded similar :D
d_holles  i did not
yb_26  I also guessed because both words start with "glu")))
impostersyndromel1000  same as person above me. also bc arginine carbamoyl phosphate and nag are all related through urea cycle.
jaxx  Not a clue. This was so random.
wolvarien  I did not
ls3076  no way
hyperfukus  no clue

 +3  (nbme22#43)

THis question is just critical thinking. The adrenals are bilaterally and symmetrically small. All other answer choices are not likely to be even bilaterally. Cancer won't equally spread in perfect symmetry nor infectious causes while maintaining the adrenal architecture.

slim23shady  Will TB be the answer if they'd mentioned the patient from developing world?

 +0  (nbme22#21)

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)!
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."

 +4  (nbme22#18)

The authors went out of their way to find thew worst photo of a granuloma they could. The threw on a stem that suggests that it would be granulation tisue. But little did we know...

amorah  I was between granulation tissue and granuloma. Then ruled out granulation tissue because this is a 10 week old wound. Assuming normal wound healing, granulation tissue would be replaced by type III collagen/resolution by 10 weeks.
sbryant6  Got this right because the exact same question is in Uworld.

 +1  (nbme22#24)

Im also convinced blocking IL-2 is also a treatment? WHy is TNF-alpha the better answer here?

amorah  FA P120-122. Immunosuppressants for RA are calcineurin inhibitor (cyclosporine and tacrolimus), 6MP, and TNFa inhibitors (adalimumab,infliximab, etanercept). It is important to distinguish that calcineurin inhibitors block t cell activation by preventing IL-2 transcription, not necessarily block IL-2 action. Sirolimus(rapamycin) blocks IL-2 action but it is used for kidney transplant rejection prophylaxis specifically.

 +0  (nbme22#15)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4989649/

According to this paper, Postpartum Thyroiditis presents with anti-TPO antibodies. The answer choice uses lymphocytes. So this is a transient Hashimotos Hyperthyroidism. Good Luck with that one!

seagull  EDIT: Lymphocytes are also present in this as well. My bad

 +1  (nbme22#41)

Couple ways to get the answer. 1. sensation of the anterior thigh and medial leg are by branches of the femoral nerve (L3, L4, L5). 2. Since the anterior thigh is affected the platellar reflex is likely affected which is a branch of L4.

medschul  Isn't the femoral nerve innervated by L2-4?

 +4  (nbme22#44)

If you don't know what Dicumarol does like any normal human. The focus on what aspirin doesn't do, namely it's doesn't affect PT time and most pills don't increase clotting (especially with aspirin). This is how I logic to the right answer.

usmleuser007  If that's then thinking, then how would you differentiate between PT & PTT?
ls3076  Why isn't "Decreased platelet count" correct? Aspirin does not decrease the platelet count, only inactivates platelets.

 +2  (nbme22#50)

This is an incomplete hydatidiform mole. They contain incomplete fetal parts including stem cells which are trisomy and give rise to unstructured tissue.

kard  Can someone explain why the other choices are incorrect?, Thanks

 +1  (nbme22#33)

https://en.wikipedia.org/wiki/Reflex_syncope

Vasovagal Syncope. Much easier


 +2  (nbme22#41)

Why spontaneous? He's engaging in an active sport with an increased risk of Traumatic injury. So we really just assume hes not injured because the stem doesnt directly say he's injured? These questions lead to too many assumptions. (in my opinion)

nc1992  Spontaneous pneumothorax, as a condition, is significantly more likely than a traumatic pneumothorax from just about anything but a car crash (ok maybe if he was in a fight). The car crash or a stabbing is also more probable overall but there's no point in inferring something that isn't provided
nwinkelmann  I picked the traumatic injury also. After reading these comments I looked into it further. Traumatic pneumos occur because of blunt or penetrating chest trauma, and I found that the MCC form of blunt trauma (>70%) is motor vehicle acidents that cause significant trauma (i.e. rib fractures) or even blast trauma. Although it didn't say there were no chest wall fractures, at the same time it didn't indicate any rib fractures, which would be most like to cause the traumatic injury pneumo in the patient's case.
drdoom  The stem makes no mention of trauma.
hyperfukus  i guess the issue is that you have to assume what they mean by "strongest predisposing risk factor for this patient's condition" I think this is dumb bc the answer is completely different based on what you consider this patient's "CONDITION" to be? either way he has a pneumothorax so if you wan to know what caused that its prob him being active or bumping into someone but if you consider the etiology of the pneumothorax then its the bleb and that is from him being a skinny dude/smoker i went to this b/c he's also only 5/10 that's not tall in my head they could have been nicer and made him 6'1 at least...also i feel like i saw a lot of q's back in the day when i first learned this with a presentation of the person like tripping or something dumb but they already had the bleb and then got the pneumothorax

 +3  (nbme22#17)

https://singaporeosteopathy.com/2015/05/23/ankle-injuries-sprain-strains-and-fractures/

Figure 2. although figure 1 looks shockingly similar


 -2  (nbme22#20)

maybe someone can explain why this is avascular necrosis and not sepsis. It doesn't mention fever or absence of fever. The MRI has a small amount of hypodensity but to get avascular necrosis seems odd/

someduck3  Pg 455 of F.A. mentions that alcoholism can be a cause of avascular necrosis.
meningitis  I think the small dark area on the left head of femur and the darkened neck are the avascular sites. Neck: http://img.medscapestatic.com/pi/meds/ckb/15/19515tn.jpg Head: (obvious lesion on the RT femur, but similar discrete lesion on the left as seen on the practice NBME) http://radsource.us/wp-content/uploads/2005/11/1a.jpg
yotsubato  He wouldnt be playing golf if he had septic arthritis. Avascular necrosis is a more chronic condition that has a slow onset.

 +0  (nbme22#6)

True vocal cords are often damaged in singing or yelling. THis allows HPV to enter the underlying nucleated cells. HPV 16 and 18 are common subtypes that may cause SCC.

meningitis  Out of all of the virus', HPV has a predilection for stratified squamous epithelium and there is no indication of vesicles(HSV) or linear ulcers (CMV)in the question stem. But with HPV you usually get a big/small (depending on time) unilateral nodule. You are correct to say singing and yelling can cause nodules but these would be bilateral in the and would appear differently. So if a question stem could easily have included that as an option: maybe irritation or something like that.

 +0  (nbme22#10)

Splenectomy patients are vulnerable against encapsulated organisms. Which commonly include Strep Pneumo, Niesseria, H. Influenza.


 +7  (nbme21#2)

! I hate these with a burning F***ing passion. Thumbs up if you agree

mcl  Amen brother
praderwilli  Every morning: "I think i'll go over glycogen storage diseases, lysosomal storage diseases, and dyslipidemias after questions this afternoon." Every afternoon: Nah
mcl  oh my god are you me
praderwilli  I recently found a program called Pixorize. It's pretty much Sketchy for biochem. Wish I discovered it sooner cuz it has helped for a lot of the painful things like this!
tentorium  [special]
tentorium  [special]
tentorium  [special]
drhello  hello
burak  Cherry red spot basically means niemann-pick or tay sachs. Two differences between is: 1- No HSM in Tay Sachs, HSM in niemann-pick. 2- Both of them has muscle weakness but there is hyperreflexia in Tay Sachs, but areflexia in niemann pick disease. In stem cell HSM is not described and hyperreflexia noted.

 +2  (nbme21#36)

http://www.siumed.edu/~dking2/erg/GI178b.htm

Another histology slide with labels a few seconds ago

enbeemee  what are the other labeled structures? i can discern the parietal and chief cells, but not really the others...
hyperfukus  yea wth is A

 +0  (nbme21#14)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2270981/

This article fails to mention poor brain development in HYPERthyroidism. The author must have meant HYPOthyroidism.

This question upsets me to no end.

aesalmon  I agree, the article you linked states "signs of fetal hyperthyroidism such as tachycardia, intrauterine growth retardation, cardiac failure, and the development of fetal goitre" I chose answer E during the exam - "Thyroid gland enlargement" Still trying to understand how they linked cretinism to a case where the mother's hypothyroidism was well controlled, and then asked for the sequelae if her TSH increased. Maybe increased TSH is supposed to indicate worsening hypothyroid - low T3/T4 needing to be stimulated by TSH?

 +1  (nbme21#41)

Depression is very common in older populations, especially females. Common symptoms of depression include SIG E CAPS (including insomnia). THis question was very vague but depression was edged out because sleep apnea is more likely in overweight middle aged males.


 +1  (nbme21#36)

Idiotypic means --- antibody against antibody. B cells don't have surface antibodies but mere synthesize them.

hungrybox  This is wrong. PLASMA cells (mature B cells, the ones found in multiple myeloma) secrete antibodies, but IMMATURE B cells have antibodies that haven't switched classes yet (IgM and IgD).
hungrybox  To clarify - immature B cells have antibodies attached to their membrane.
seagull  I should have clarified that I was speaking about mature B cells. Thank You
sahusema  So because MM has mature B cells, exogenous antibodies can't attach to them. Am I getting that right?
cienfuegos  What is an Anti-Idiotypic Antibody? As shown in figure 1, an anti-idiotypic (Anti-ID) antibody binds to the idiotype of another antibody, usually an antibody drug. An idiotype can be defined as the specific combination of idiotopes present within an antibodies complement determining regions (CDRs). A single idiotope, is a specific region within an antibodies Fv region which binds to the paratope (antigenic epitope binding site) of a different antibody. Therefore, and idiotope can be considered almost synonymous with an antigenic determinant of an antibody. https://www.genscript.com/antibody-news/what-is-an-anti-Idiotypic-antibody.html
cienfuegos  @sahusema: almost exactly correct, but it's important to note they are talking about idiotypic antibodies specifically because by definition these bind the "idiotype" of another antibody (see definition above)

 +3  (nbme21#20)

The patient has a fever/infection. The picutre shows normal (1 immature) granulocytes (neutrophils). The immature might be part of the left-shift occuring in this patient. Therefore, this is simply a reactive immune process.


 +7  (nbme21#40)

Examining patient from a urologist implies Berkson Bias which would skew the population mean of serum urea nitrogen away from the true accurate mean. Then, realize precision is dependent on statistical "Power" which is increased based on the size of the population of the study. (increased precision = increased statistical power). Therefore, an increase in population of a biased group with lead to inaccuracy with high precision.

forerofore  to add up, the urologist himself doesn't add or remove accuracy (since this is a blood test), what decreases the accuracy is the fact that in order to be sent to a urologist you probably are sick in the first place (selection bias), so your urea nitrogen is likely to be altered.




Subcomments ...

submitted by medstudied(2),

Can someone explain why the correct answer for the question here is conjugation but can’t be transposition?

catacholamine16  Transposition is when a segment of DNA (in this case, coding for resistance) jumps onto a plasmid within the same bacterial cell. That plasmid might then transfer to another nearby bacterial cell via conjugation. Transposition is happening WITHIN the bacterium. Conjugation is how that resistance gene gets transferred. +1  
lsmarshall  Also, E. coli is the classic example of a bug tat uses conjugation. ^but explanation above is correct^ +1  
seagull  I think he might have did what I did. I got Transformation mixed up with transposition. FML +2  


submitted by seagull(349),

Idiotypic means --- antibody against antibody. B cells don't have surface antibodies but mere synthesize them.

hungrybox  This is wrong. PLASMA cells (mature B cells, the ones found in multiple myeloma) secrete antibodies, but IMMATURE B cells have antibodies that haven't switched classes yet (IgM and IgD). +2  
hungrybox  To clarify - immature B cells have antibodies attached to their membrane. +  
seagull  I should have clarified that I was speaking about mature B cells. Thank You +1  
sahusema  So because MM has mature B cells, exogenous antibodies can't attach to them. Am I getting that right? +  
cienfuegos  What is an Anti-Idiotypic Antibody? As shown in figure 1, an anti-idiotypic (Anti-ID) antibody binds to the idiotype of another antibody, usually an antibody drug. An idiotype can be defined as the specific combination of idiotopes present within an antibodies complement determining regions (CDRs). A single idiotope, is a specific region within an antibodies Fv region which binds to the paratope (antigenic epitope binding site) of a different antibody. Therefore, and idiotope can be considered almost synonymous with an antigenic determinant of an antibody. https://www.genscript.com/antibody-news/what-is-an-anti-Idiotypic-antibody.html +  
cienfuegos  @sahusema: almost exactly correct, but it's important to note they are talking about idiotypic antibodies specifically because by definition these bind the "idiotype" of another antibody (see definition above) +  


submitted by sattanki(27),

Apparently there is a completely separate spinal cord reflex where direct penile stimulation leads to an erection. This reflex only needs an intact arc in S2-S4, so as long as this region is not injured, an erection can still occur. However, with transection at C8, then the psychogenic erection reflex cannot occur, as this requires descending fibers from the cortex.

lsmarshall  Just saw a good summary of nerves/vessels involved saying, "pelvic parasympathetic fibers from S2-S4 can cause cavernous arteriole vasodilation via the cavernous nerve without of central stimulation." +3  
seagull  S2-3-4 keeps the penis off the floor +8  
drdoom  Modifying @seagull into iambic pentameter: “S2, S3, and Number 4 / keeps the big ole penis / off the floor” +  


submitted by lsmarshall(181),

Urea Cycle Disorders > Isolated severe hyperammonemia (> 1000; i.e., no other severe metabolic disturbances

Ornithine transcarbamylase deficiency > (most common urea cycle dis.) orotic acidemia/aciduria, hyperammonemia

Organic Acidemias > Hyperammonemia, anion-gap acidosis, ketosis (from hypoglycemia)

Medium-chain acyl-CoA dehydrogenase deficiency > Hyperammonemia, hypoketotic hypoglycemia (seen in β-oxidation disorders, EXCEPT adrenoleukodystrophy)

Liver dysfunction > Hyperammonemia, LFTs messed up, older pt.

lsmarshall  Summary of metabolic issues relating to hyperammonemia +3  
seagull  i'm leaning towards Ornithine transcarbamylase deficiency. +2  
notadoctor  Not sure why this isn't considered a mitochondrial disorder since the issue is Ornithine transcarbamylase deficiency in the mitochondria? +  
charcot_bouchard  if it was mitochondrial disorder no one would escape +  
wowo  figure in OTC deficiency, they might have to explicitly mention the orotic aciduria AND typically presents earlier, around 24-48hrs of life after they've fed (at least per BB) + also per BB, propionic acidemia and MM acidemia have an onset of weeks to months and lead to build up of organic acids --> acidemia in addition to hyperammonemia (not sure why, but several aa enter the TCA cycle via propionyl CoA --> methylmalonyl CoA --> succinyl CoA, but now this is defunct d/t enzyme deficiencies...?). Anywho, propionic acidemia described on FA2019 p85, but doesn't list hyperammonemia +1  
artist90  i think it cannot be Ornithine transcarbamylase deficiency bc it is XR disease. this pt has a healthy 2yr old brother which rules out X-linked recessive disease correct me if i m wrong +  
artist90  it is 100% Propionic acidemia Uworld Q-id: 1340. it is an exact copy question of uworld. i got it wrong bc i forgot these are organic acids. But i am still confused on 2 things 1-how does acidosis cause Hypoglycemia and Ketosis. 2-why is Ammonia elevated in these pts bc urea cycle will be fine? +  
yb_26  1) hyperammonemia is seen in all urea cycle disorders except arginase deficiency 2) organic acids directly inhibit urea cycle => hyperammonemia (from UWorld) +  


submitted by colonelred_(43),

The diagnosis is strawberry hemangioma, commonly happens in kids, often resolves on its own as they get older.

shaeking  A strawberry hemangioma is normally pink or red (which is why it is named strawberry). The description has a flat purplish lesion which makes me think of a port wine stain on the face. How do you know to think of strawberry hemangioma over port wine based on this question stem? +  
sheesher  This sounds more like a nevus simplex, which is very similar to a port wine stain, though it regresses over time. +2  
seagull  the age is key here. Newborns have strawberry hemangiomas typically on their face. Sturge-Weber could also be the case but none of the answer choices matched to that description. +1  
vshummy  I would agree with Sturg Webber nevus flammeus but I also noticed First Aid says it's a non-neoplastic birth mark so I should have known not to pick malignant degeneration or local invasion. Also because capillary hemangiomas don't have to be flat but the nevus flammeus is consistently flat. But I'm also reading on Wiki that the nevus flammeus doesn't regress so they must be trying to describe strawberry hemangioma even though I don't agree with their color choice... +  
nala_ula  Maybe (and I can only hope I'm right and the test makers are not -that much of- sadists) they would have made sure to write "in a cranial nerve 5 (either ophthalmic or maxillary) distribution" if it were Sturge-Weber. +1  


submitted by brethren_md(39),

Stupid question, honestly just take your best guess and move on lol.

seagull  ░░░░░░░░░░░█▀▀░░█░░░░░░ ░░░░░░▄▀▀▀▀░░░░░█▄▄░░░░ ░░░░░░█░█░░░░░░░░░░▐░░░ ░░░░░░▐▐░░░░░░░░░▄░▐░░░ ░░░░░░█░░░░░░░░▄▀▀░▐░░░ ░░░░▄▀░░░░░░░░▐░▄▄▀░░░░ ░░▄▀░░░▐░░░░░█▄▀░▐░░░░░ ░░█░░░▐░░░░░░░░▄░█░░░░░ ░░░█▄░░▀▄░░░░▄▀▐░█░░░░░ ░░░█▐▀▀▀░▀▀▀▀░░▐░█░░░░░ ░░▐█▐▄░░▀░░░░░░▐░█▄▄░░░ ░░░▀▀▄░░░░░░░░▄▐▄▄▄▀░░░ THis Question ░░░░░░░░░░░░░░░░░░░░░░░ +2  


submitted by brethren_md(39),

Requires knowing how to calculate an anion gap - look it up. In this case, it is a normal anion gap metabolic acidosis. Know the mneumonics MUDPILES and HARDASS. Renal Tubular acidosis is the only answer choice that is an example of a normal anion metabolic acidosis.

mousie  Anion Gap: Na - (Cl + HCO3) = normally around 10-12 +1  
seagull  good to know. I keep looking up the urine values but all it said was "varies", then I threw my computer and yelled "does that vary Mother F****ers. I do feel better now. +12  
_yeetmasterflex  glad I wasn't the only one who got very pissed off at the urine values +1  
fulminant_life  Usually the first thing I look at is whether or not the Cl- is high. Generally if the Cl- is high its going to be a normal gap +1  
henoch schonlein  i think they gave you the urine values bc you can calculate the URINE anion gap which is (Na + K - Cl). In this case the Urine Anion Gap is positive (5). Boards and Beyond mentions that a positive UAG is due to Renal Tubular Acidosis Type 1 (inability of alpha intercalated cells to secrete hydrogen ions). just another approach to answer this q +5  


submitted by drdoom(163),

After the cuff is tied, the cells and tissue distal to the cuff will continue consuming ATP (ATP->ADP), but no fresh blood will be delivered to “clear” what will be an accumulating amount of ADP and other metabolites. ADP (=Adenosine) is itself a proxy of consumption and drives vasodilation of arteries! (Evolution is smart!) Increasing ADP/Adenosine in a “local environment” is a signal to the body that a lot of consumption is occurring there; thus, arteries and arterioles naturally dilate to increase blood flow rates and “sweep away” metabolic byproducts.

lispectedwumbologist  You're a good man. Thank you. +  
drdoom  So glad it helped! +1  
seagull  very well put, thank you +1  


Can anybody explain this one? I put repeated tests because I assumed an 83-year-old woman is an unusual demographic for syphilis.

m-ice  83 might seem an uncommon age, but we don't know for sure her sexual history. She only recently (8 months ago) started showing some signs of mild cognitive impairment. She has all these results implying that she has syphilis, so the most likely answer is that she has syphilis, so we should speak to her privately about her sexual history. The tests don't necessarily means she got syphilis very recently, it's possible she's had syphilis for a while and never got treated. +2  
mousie  I understand that she could possibly have syphilis but I also put repeat tests because I know there are a few things that can cause false positive VRDLs but if she also has a + RPR does this make a FP less likely? And also if she has mild cognitive impairment you still discuss with her not her daughter correct ...? +2  
m-ice  This definitely could be a false positive, but before we want to consider it to be a false positive, we should talk to the patient about it privately. Assuming that it's a false positive before asking the patient about it could delay treatment of her syphilis. There's a chance she didn't want to disclose her sexual history in front of her daughter or maybe she was embarrassed or didn't think it was important to mention. And you're absolutely right, she only has mild cognitive impairment, so we most definitely should talk to the patient alone without her daughter first. +  
seagull  She has dementia. She doesn't have the capacity to determine her own care (23/20 MME). I feel the daughter should have the word on the care since Grandma likely doesn't have the capacity to understand her actions. +1  
sajaqua1  From what I remember, dementia is typically a combination of impaired memory *and* impaired thought processes. There is nothing to indicate that the patient has impaired thought processes, and the memory impairment is only mild. The patient can still reasonably said to be competent, and so her private information should be discussed with her alone. +4  
yotsubato  Elder care homes or elderly communities actually have a high rate of STDs. Turns out, when you put a bunch of divorced/widowed adults together in a community they have sex. +2  
yotsubato  Additionally, you should respect the privacy of a competent adult with "Mild memory" impairment. I know I could have mild memory impairment considering the crap I forget studying for step 1 +4  
drdoom  @seagull dementia ≠ absence of competence -- the two are separate concepts and have to be evaluated independently. see https://meshb.nlm.nih.gov/record/ui?ui=D003704 and https://meshb.nlm.nih.gov/record/ui?ui=D016743 +1  
wowo  also important to note, d) repeated tests is also incorrect as the microhemagglutination assay is a confirmatory treponemal test (along the same lines as FTA-ABS) https://www.uofmhealth.org/health-library/hw5839 +1  


submitted by seagull(349),

I thought this was a type 1 RTA but I was wrong. Any suggestions?

seagull  It looks like it was a type II RTA. The difference is incredibly subtle from the info given in this question. +1  
gonyyong  He has Fanconi syndrome which is generalized reabsorption defect in PCT which leads to metabolic acidosis and hypophosphatemia → can lead to rickets Also, does lead to type II RTA +4  
duat98  Also the proximal tubule is the place with the highest phosphate absorption rate. That's why PTH works here mostly and a little bit in the distal tubule. +1  


submitted by karljeon(19),

I don't know if there is an equation for this, but I basically pumped out every division across the table to get ~5% on average.

Here they are: 400 / 6,000 = 0.067 250 / 5,600 = 0.045 300 / 5,350 = 0.056 300 / 5,050 = 0.059 250 / 4,800 = 0.052

The average of these %s for all the years = 5.58%. So that's close enough to 5%.

seagull  good work. I found this question annoying and gave up doing those considering the amount of time we are given. +1  
vshummy  Well just don’t include the intake year... because that messed me up.. +4  
_yeetmasterflex  How would we have known not to include the intake year? From average **annual** incidence? +  
lamhtu  Do not include intake year because the question stem is asking average annual incidence. The 4000 positives at intake could have acquired HIV whenever, not just in the last year. +1  
neels11  literally didn't think there was an actual way to figure this out. but my thought process was: okay incidence means NEW cases. so the annual average at the end of 5 years would be: (# of NEW people that tested positive at the end of year 5) / (# of people at that were at risk at the beginning of year 5) <--- aka at the end of year 4 250/5050 = 4.95% also if you look at year 5: you'll see that the at risk population is 4800 when 300 new cases were found the year before. 5050 at the end of year 4 MINUS the 300 new cases at the end of year 4 should give you 4750 as the new population at risk. but notice that end of year 5 we have 4800. idk if that means 50 people were false positives before or 50 people were added but in incidence births/death/etc don't matter it's kind of like UWORLD ID 1270. assuming average annual incidence is the same as cumulative incidence this was just a bunch of word vomit. sorry if it was unbearable to follow +  


submitted by seagull(349),

https://en.wikipedia.org/wiki/Blastomycosis#/media/File:Blastomyces_dermatitidis_GMS.jpeg

I believe this is actually disseminated Blastomyces due to the "Broad Based Budding" as seen in the picture.

seagull  However, given the stain and some of the features I now see that this is most likely Crypto. THey like similar. my bad +5  
mjmejora  oh what a catch! I also thought this was Blasto until you explained otherwise +  


submitted by mousie(74),

Is 45 minutes too long to be anaphylactic and would the absence of rash (urticaria, pruritus) RO anaphylactic?

hayayah  Yes! Allergic/anaphylactic blood transfusion reaction is within minutes to 2-3 hours. (pg 114 of the 2019 FA has a list of them ordered by time) +3  
hayayah  (also allergy / anaphylactic presents with more skin findings (urticaria, pruritus) +1  
seagull  The time through me off too. I though ABO mismatch since it occured around an hour. I thought TRALI would take a little longer. +4  
charcot_bouchard  Guys anaphylactic reaction to whole blood doesnt occur much except for selective IgA defi. so look out for prev history of mucosal infection. And it can have all feature of type 1 HS inclding bronchospasm. +2  
soph  I saw hypotension and though anaphylaxis........ -.- +  


submitted by lsmarshall(181),

"Parasternal heave (lift) occurs during right ventricular hypertrophy (i.e. enlargement) or very rarely severe left atrial enlargement." RV hypertrophy can be seen so easily because the RV is at the anterior surface of the chest.

In this patient blood from LA to LV decreases in saturation, so it is going somehwere. From the O2 sat. we can deduce there is probably a VSD (increased RV pressure would cause RVH and parasternal heave). Furthermor, the vignette is likely describing tetralogy of fallot (caused by anterosuperior displacement of the infundibular septum). In Tet spells, RV outflow is too obstructed and patient gets cyanosis and R>L shunting Squats increase SVR, decreasing R>L shunting, putting more blood through pulmonary circuit and relieving cyanosis.

seagull  i'm pretty sure your a prof and not a student. +3  
nor16  nevertheless, we are greatful for explanation! +  


submitted by mousie(74),

is this subacute endocarditis associated Membrano-proliferative GN?

jus2234  The question describes how he had a strep infection 15 days ago, and now this is poststreptococcal glomeruloneprhitis, which can also be described as proliferative glomerulonephritis +6  
seagull  The question would be too fair if it just said PSGN. Instead we need to smell our own farts first. +24  
yotsubato  And they used terminology NOT found in FA +4  
water  who said they were limited to FA? +  
nbmehelp  FA uses the common nomenclature and the fact most of our other resources use the same nomenclature for this, I think we can agree that is is the accepted terms. If they're gonna decide not to use the nomenclature that most medical students are taught then they should provide their own study materials at that point for us to use. The test shouldn't be this convoluted for no reason. +1  


Why would it not be anemia of chronic disease with decreased serum transferrin concentration?

lispectedwumbologist  Nevermind I'm stupid as fuck I see my mistake +  
drdoom  be kind to yourself, doc! (it's a long road we're on!) +7  
step1forthewin  Hi, can someone explain the blood smear? isn't it supposed to show hypersegmented neutrophils if it was B12 deficiency? +  
loftybirdman  I think the blood smear is showing a lone lymphocyte, which should be the same size as a normal RBC. You can see the RBCs in this smear are bigger than that ->macrocytic ->B12 deficiency +8  
seagull  maybe i'm new to the game. but isn't the answer folate deficiency and not B12? Also, i though it was anemia of chronic disease as well. +  
vshummy  Lispectedwumbologist, please explain your mistake? Lol because that seems like a respectible answer to me... +  
gonyyong  It's a B12 deficiency Ileum is where B12 is reabsorbed, folate is jejunum The blood smear is showing enlarged RBCs Methionine synthase does this conversion, using cofactor B12 +  
uslme123  Anemia of chronic disease is a microcytic anemia -- I believe this is why they put a lymphocyte on the side -- so we could see that it was a macrocytic anemia. +  
yotsubato  Thanks NBME, that really helped me.... +  
keshvi  the question was relatively easy, but the picture was so misguiding i felt! i thought it looked like microcytic RBCs. I guess the key is, that they clearly mentioned distal ileum. and that is THE site for B12 absorption. +2  
sahusema  I didn't even register that was a lymphocyte. I thought I was seeing target cells so I was confused AF +  


submitted by sattanki(27),

Does anyone have any idea on this question? Thought it was ALS.

ankistruggles  I thought it was ALS too (and I think it still could be?) but my thought process was that a lower motor neuron lesion would be the more specific answer. +  
sattanki  Yeah makes sense, just threw me off cause ALS is both lower and upper motor neuron problems. Corticospinal tract would have been a better answer if they described more upper motor neuron symptoms, but as you said, they only describe lower motor neuron symptoms. Thanks! +1  
mousie  Agree I thought ALS too but eliminated Peripheral nerves and LMN because I guess I thought they were the same thing ....??? Am I way off here or could someone maybe explain how they are different? Thanks! +  
baconpies  peripheral nerves would include motor & sensory, whereas LMN would be just motor +6  
seagull  Also, a LMN damage wouldn't include both hand and LE unless it was somehow diffuse as in Guil-barre syndrome. It would likely be specific to part of a body. right??? +  
charcot_bouchard  No. if it was a peri nerve it would be limited to a particular muscle or muscles. but since its lower motor neuron it is affecting more diffusely. Like u need to take down only few Lumbo sacral neuron to get lower extremity weakness. but if it was sciatic or CFN (peri nerve) it would be specific & symptom include Sensory. +  


submitted by beeip(56),

Inability to elevate the palate suggests damage of the vagus nerve.

F. (CN X)

atstillisafraud  I guess F is the vagus nerve. Thanks to NBME I am also training to become a mind reader. +5  
seagull  Thanks to the NBME I have crippling depression +12  
drdoom  bonus cadaver diagram via @mcl +2  


submitted by sympathetikey(252),

Mad at myself for changing my answer.

Faulty logic made me wonder if hitting your head would caused increased ICP so, like a cushing ulcer, you would get increased Vagus nerve activity and maybe bradycardia + hypotension. But I guess the RAAS system would have counteracted that and caused vasoconstriction over 24 hours, so Hypovolemic shock is definitely the best choice.

Always should go with the obvious answer :)

seagull  I had the idea that this was a neurogenic shock and increasing intracranial pressure could affect the vagus too. I think the question really wants us to go that direction. +1  
uslme123  The Cushing reflex leads to bradycardia! +  
purdude  Wait I'm confused. I thought hypovolemic shock leads to an increased SVR? +1  
littletreetrunk  apparently, there's a thing called sympathetic escape that can happen after a while (i.e. he's been out for 24 hours): Accumulation of tissue metabolic vasodilator substances impairs sympathetic-mediated vasoconstriction, which leads to loss of vascular tone, progressive hypotension and organ hypoperfusion. +  
littletreetrunk  also also if he hit his head he could have loss of sympathetic outflow from a hypoxic medulla which could lead to vasodilation, which further reduces arterial pressure, but this was a hard one for me lol. I also put increased ICP wah. +  
catch-22  Any lack of sympathetic outflow/increased vagal outflow should reduce HR, not increase it. Further, you would expect brainstem signs if there was hypoxia to the brainstem. For example, if you had damage to the solitary nucleus, you wouldn't be able to regulate your HR in response to reduced BP. Since this patient has reduced BP and increased HR, this indicates that the primary disturbance is likely the reduced BP. He's also been in a desert for 24+ hours so. +  
charcot_bouchard  In a patient who develops hypotension following high-energy trauma, neurogenic shock is a diagnosis of exclusion that is made after hypovolemic and obstructive cardiogenic shock have been ruled out! Plus Absent Bradycardia rules it out +  


submitted by wired-in(22),

Maintenance dose formula is (CssCltau)/F where Css is steady-state target plasma conc. of drug, Cl is clearance, tau is dosage interval & F is bioavailability.

Neither dosage interval nor bioavailability is given, so ignoring those & plugging in the numbers (careful to convert units to mg/kg/day): (12 ug/mL * 1 mg/1000 ug) * (0.09 L/hr/kg * 1000 mL/1 L * 24 hr/1 day) = 25.92 mg/kg/day

...which isn't any of the answer choices listed. They must have rounded 0.09 L/hr/kg to 0.1 L/hr/kg, and doing so gives exactly 28.8 mg/kg/day (choice C)

lispectedwumbologist  That's so infuriating I stared at this question for 20 minutes thinking I did something wrong +14  
hyoid  ^^^^^ +2  
seagull  lol..my math never worked either. I also just chose the closest number. also, screw this question author for doing that. +2  
praderwilli  Big mad +3  
ht3  this is why you never waste 7 minutes on a question.... because of shit like this +3  
yotsubato  Why the FUCK did they not just give us a clearance of 0.1 if they're going to fuckin round it anyways... +4  
bigjimbo  JOKES +  
cr  in ur maths, why did u put 24h/1day and not 1day/24h? if the given Cl was 0.09L/hr/kg. I know it just is a math question, but i´d appreciate if someone could explain it. +  
d_holles  LMAO games NBME plays +  
hyperfukus  magic math!!!!! how TF r we supposed to know when they round and when they don't like wtf im so pissed someone please tell me step isn't like this...with such precise decimal answers and a calculator fxn you would assume they wanted an actual answer! +  


submitted by mousie(74),

Can someone please explain this to me? I don't understand why starting the other drug would not count as exclusion criteria?

seagull  This has to do with Intention-to-treat analysis. Essentially, when participants are non-adherent but the data shouldn't be lost. They just undergo another statistical model to account for their changes. Here is a nice video https://www.youtube.com/watch?v=Kps3VzbykFQ&t=7s +5  
dr.xx  Where does the question mention "intention-to-treat"? +  
notadoctor  They seem to be pretty obsessed with "intention-to-treat" it's been asked in one way or another in all the new NBMEs that I've done. (Haven't done 24 as yet) +2  
wutuwantbruv  They don't, intention-to-treat is just the best way to go about it @dr.xx +  
smc213  Great for ITT: https://www.youtube.com/watch?v=Kps3VzbykFQ +  
yex  I agree with @notadoctor !! +  


How is this the answer if there is no family history of recurrent fractures? I thought osteogenesis imperfecta was autosomal dominant?

seagull  Exactly!! it's an autosomal dominate disease! +  
emcee  Autosomal dominant diseases are variably expressive. Still, I think this was a badly written question (should have given us some family history). +  
wutuwantbruv  Also, FA says that fractures may occur during the birthing process, which is what I believe they were going for. I don't believe these findings would be seen at birth with any of the other choices. +  
d_holles  Yeah I thought I outsmarted NBME by selecting Rickets bc it said no family history ... guess I got played lol. +3  


submitted by nlkrueger(6),

.... would we really take the word of a friend who definitely can't be confirmed? I feel like this is misleading

lispectedwumbologist  All the other answer choices make you come across as an asshole. Easy way to ace ethics questions is to just not be an asshole +2  
seagull  I would be a bigger asshole when the family came I'n after I pulled the plug...opps...but the friend said +2  
dr.xx  The patient has no wife, children, or close relatives... +  
nwinkelmann  @lispectedwumbologist this is going to be my technique, because I've gotten a couple of these wrong, but I completely agree with everyone else's sentiments of suspicion of going off what a friend said without any confirmation about state of advance directives, etc. It's really dumb. +  


submitted by welpdedelp(63),

I chose this b/c its the most common pathogen for skin infections

seagull  same here +2  
sympathetikey  Some bowlsheet +2  


submitted by lfsuarez(63),

20 of the 100 men without prostate cancer have abnormal test results.

Specificity = FP/FP+TN = 20/100 = 0.8 = 80%

seagull  almost. 100/120 = 83% roughly 80% +  
amirmullick3  Not sure what lfsuarez and seagull above mean. Here is my explanation. Specificity = TN/(TN+FP). This test gave 20 false positives out of 100 people, and only 15 true negatives out of 50 men. Specificity also equals 1-FPrate, and here the FP rate seems 20% so 100%-20%=80%. +3  
yb_26  abnormal test result means pt has cancer => TP = 35, FN = 15 (50-35), FP=20, TN =80 (100-20) => specificity = TN/(TN+FP) = 80/100 = 0.8 (in % will be 80%) true negatives are 80 out of 100, not 15 out of 50 +2  
bulgaine  If you replace the values from the question in the table of page 257 of FA 2019, yb_26 explanation is correct. Abnormal test = patient has cancer = test + Question says 35/50 men with prostate cancer (so all 50 have cancer) only 35 have abnormal test results, meaning that TP=35 (disease + test +) and FN= 15 (disease + test - because they do have cancer but the test was not abnormal for them ). 20/100 men without prostate cancer have abnormal test results meaning all 100 DONT have cancer but 20 show that they have cancer when its not true so FP=20 (disease - test +) and TN =80 (disease - test -) +  


submitted by ferrero(15),

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)? +10  
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. +10  
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. +  


submitted by seagull(349),

The mass is in the outer upper quadrant, this is why it want DCIS. Nice and simple

seagull  *wasn't +  


submitted by haliburton(74),

FA 2017: H pylori is associated with gastric adenocarcinoma and MALT lymphoma

seagull  I might be mistaken but I also thought Epstein Bar Virus was also implicated in gastric lymphomas? +  


submitted by seagull(349),

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4989649/

According to this paper, Postpartum Thyroiditis presents with anti-TPO antibodies. The answer choice uses lymphocytes. So this is a transient Hashimotos Hyperthyroidism. Good Luck with that one!

seagull  EDIT: Lymphocytes are also present in this as well. My bad +1  


submitted by mattnatomy(20),

I thought initially we were dealing with post-partum psychosis, but on re-reading, this looks more like either Generalized Anxiety Disorder or OCD or both. Either way, treatment should be an SSRI (Sertraline).

seagull  OCD for sure +1  


submitted by oznefu(7),

I’m having trouble understanding why this is a better choice than Paget disease, especially with the increased ALP?

zelderonmorningstar  Paget’s would also show some sclerosis. +1  
seagull  ALK is increased in bone breakdown too. Prostate loves spreading to the lumbar Spine. It's like crack-cocaine for cancer. +1  
aesalmon  I think the "Worse at night" lends itself more towards mets, and the pt demographics lean towards prostate cancer, which loves to go to the lumbar spine via the Batson plexus. I picked Paget but i think they would have given something more telling if they wanted pagets, histology or another clue +  
fcambridge  @seagull and aesalmon, I think you're a bit off here. Prostate mets would be osteoblastic, not osteolytic as is described in the vignette. +5  
sup  Yeah I chose Paget's too bcz I figured if it wasn't prostate cancer (which as @fcambridge said would present w/ osteoblastic lesions) they would give us another presenting sx of the metastatic cancer (lung, renal, skin) that might point us in that direction. I got distracted by the increased ALP too and fell for Paget :( +  
kernicterusthefrog  @fcambridge, not exactly. Yes, prostate mets tends to be osteoblastic, but about 30% are found to be lytic, per this study: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2768452/ Additionally, the night bone pains point to mets, and Paget's is much more commonly found in the cranial bones and appendicular skeleton, than axial. This could also be RCC mets! +  
sweetmed  I mainly ruled out pagets because they said the physical examination was normal. He would def have other symptoms. +1  


submitted by moloko270(28),

https://www.ncbi.nlm.nih.gov/pubmed/7058822

"syndrome of "dilutional hypo-osmolality" in severe congestive heart failure may be caused by an inappropriately high ADH secretion in which the osmoreceptor system is dominated by nonosmolar stimuli"

hayayah  Apparently, in chronic CHF you see hyponatremia. Because CHF causes a decrease in cardiac output and circulating blood volume, which in turn triggers a compensatory response aimed at preserving blood pressure. This stimulates the body to retain both water and sodium. +2  
seagull  i agree with Hayayah... the RAAS system is activated due to poor perfusion to the kidney due to decomp heart failure. +3  


Alkylating agents (merchlorethamine) (the other drugs listed are microtubule inhibitors) increase the risk of AML.

keycompany  Additionally, AML is the only answer choice that has multiple blast forms (myeloblasts, promyelocytes, etc.). ALL is characterized by a single blast form (lymphoblasts). +6  
seagull  CML has blasts too but they tend to favor mature forms. +3  
kash1f  You see numerous blast forms == AML, which is characterized by >20% blasts +2  
keycompany  The answer choices are all of lymphoid origin except for AML and Hodgkin Disease. We know Hodgkin Disease is a lymphoma (not leukemia) and would present with lymphadenoapthy. So the answer must be AML #testtakingstrategies +6  
impostersyndromel1000  @atstillisafraud thanks for mentioning the merchlorethamine increasing risk for AML, i was trying to make a connection with the drugs but couldnt. Had to lean on the test taking skills just like key company +  
sweetmed  Procarbazine is alkylating as well. +  


submitted by keycompany(103),

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. +6  
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 neonem(227),

From centerwatch.com (never heard of it before but seems like a good explanation):

"Phase IV studies, often called Post Marketing Surveillance Trials, are conducted after a drug or device has been approved for consumer sale. Pharmaceutical companies have several objectives at this stage: (1) to compare a drug with other drugs already in the market; (2) to monitor a drug's long-term effectiveness and impact on a patient's quality of life; and (3) to determine the cost-effectiveness of a drug therapy relative to other traditional and new therapies. Phase IV studies can result in a drug or device being taken off the market or restrictions of use could be placed on the product depending on the findings in the study."

seagull  Well, I was not smart and put phase 1 since it was talking alot about adverse effects and withdrawl from the patients. But now I see I have 2 extra chromosomes...my bad. +  
link981  Phase 1- Determine if drug is SAFE Phase 4- Continous surveillance of a drug that is already on the market. The vignette clearly states the drug is marketed. That means it passed the clinical trials. Marketed drugs have passed Phase 3 +  


submitted by mcl(167),

This image is very helpful.

seagull  http://www.siumed.edu/~dking2/erg/GI178b.htm Another histology slide with labels +  
masonkingcobra  I like to think that the parietal cells look like "fried eggs" classically +  


It’s acute alcohol consumption so fatty change more likely. Cellular swelling indicates alcoholic hepatitis which requires chronic alcohol consumption (See FA 2019 pg 385). At least that’s the logic I used to pick fatty change.

seagull  Seems like fatty change would require more than 1 weekend. I choose swelling since it's reversible and seems like something with a quick onset. +7  
nc1992  I think it's just a bad question. It should be "on weekends" +4  
uslme123  https://webpath.med.utah.edu/LIVEHTML/LIVER145.html +1  
uslme123  So his hepatocytes aren't dying ( ballon degeneration ) vs just damaged/increased FA synthesis due to increased NADH/citrate +  
sympathetikey  @seagull I agree! +  
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. +  


"Upon application of pressure to the internal end of the cervix, oxytocin is released (therefore increase in contractile proteins), which stimulates uterine contractions, which in turn increases pressure on the cervix (thereby increasing oxytocin release, etc.), until the baby is delivered.

Sensory information regarding mechanical stretch of the cervix is carried in a sensory neuron, which synapses in the dorsal horn before ascending to the brain in the anterolateral columns (ipsilateral and contralateral routes). Via the median forebrain bundle, the efferent reaches the PVN and SON of the hypothalamus. The posterior pituitary releases oxytocin due to increased firing in the hypothalamo-hypophyseal tract. Oxytocin acts on the myometrium, on receptors which have been upregulated by a functional increase of the estrogen-progesterone ratio. This functional ratio change is mediated by a decrease in myometrial sensitivity to progesterone, due to an increase in progesterone receptor A, and a concurrent increase in myometrial sensitivity to estrogen, due to an increase in estrogen receptor α. This causes myometrial contraction and further positive feedback on the reflex.[1]"

https://en.wikipedia.org/wiki/Ferguson_reflex

seagull  https://www.ncbi.nlm.nih.gov/pubmed/8665768 a counter argument for PGE if you chose that answer. However, the author believes oxytocin is superior. +  
usmleuser007  1) PGE rises initially that causes the uterine contractions= this would be equivalent to when someone say #of contractions per time period. 2) Oxytocin is increased when the cervix is manipulated (ie. the birth canal reflex). +2  


submitted by jotajota94(10),

PDA flows from aorta to pulmonary artery decreasing afterload. Therefore cardiac output increases

seagull  doesnt pre-load also decrease which would drop the C.O.? +  
hungrybox  @seagull I think it would increase preload b/c more blood is going into the pulmonary arteries -> lungs -> pulmonary veins -> eventually more blood in left atrium/ventricle -> inc preload +3  


submitted by mcl(167),

Deltoid is innervated by axillary nerve, which comes from roots C5/C6. Actions of the deltoid include abduction of the upper extremity.

seagull  I hope everyone memorized every single part of the brachial plexus and all the roots of each, No detail let untouched!!! +3  
mcl  In case anyone else has purged the whole brachial plexus from your memory (like me), this is a great resource linked by another user. https://geekymedics.com/nerve-supply-to-the-upper-limb/ +  


Multiple myeloma is an neoplastic proliferation of plasma cells, and since plasma cells don’t have surface Ig bound innately, that was the only “true” option.

seagull  Idiotypic means --- antibody against antibody. B cells don't have surface antibodies but mere synthesize them. +1  


submitted by haliburton(74),

Bullous pemphigoid antigen must be hemidesmosome. FA: bulla are "bullow" the dermis (subepidermal blister). BP also yield "tense" bulla.

seagull  I love how this cant be straight forward. All the other proteins are either subunits of desmosomes or cytoskeletal components. Because I know molecular biology that well on top of the majority of medicine....FML +1  
cienfuegos  @seagull: excellent comment, literally loling right now +  
cienfuegos  or sobbing and threatening to hold my breath if they don't make it stop +  


submitted by beeip(56),

I might be the only person on earth who got this one wrong, but regardless:

"ITT analysis includes every subject who is randomized according to randomized treatment assignment. It ignores noncompliance, protocol deviations, withdrawal, and anything that happens after randomization."[1]

yo  You're not. I also goofed. +1  
seagull  https://www.youtube.com/watch?v=Kps3VzbykFQ This video is a pretty decent explination worth your time on the subject. +1  
hungrybox  I got it right but I was only like 50% sure. So I appreciate it. +  


submitted by rocmed(-3),

Can't renal cell carcinoma cause invasion of the renal artery, obstructing blood flow (resulting in a bruit), thereby upregulating RAAS and increasing blood pressure?

rocmed  And isn't smoking also a risk factor for RCC? +  
lispectedwumbologist  It is but RCC tends to present later in life (6th or 7th decade). In a 55 year old smoker, atherosclerosis of the renal artery is am much more common cause of bruits +  
seagull  Hypertension is also a risk factor of an atherosclerosis leading to more inflammation. Eventually dilation (aneurysm) might occur... if im wrong then ignore this +  
seagull  Hypertension is also a risk factor of an atherosclerosis leading to more inflammation. Eventually dilation (aneurysm) might occur... if im wrong then ignore this +  
illogical  Renal Cell Carcinoma has a tendency to invade the Left Renal **Vein** (Pg 134, Pathoma 2018). Thus it has an association w/ obstructed drainage of the Left Spermatic Vein leading to a varicocele. Renal artery stenosis is more commonly due to atherosclerosis (almost 85-90%) or fibromuscular dysplasia. +6  
ratadecalle  With RCC and renal vein invasion you would see B/L lower edema and venous collaterals in the abd wall (Uworld). Also he has a severe headache and confusion which are signs of a hypertensive emergency. +  


submitted by rocmed(-3),

Can't renal cell carcinoma cause invasion of the renal artery, obstructing blood flow (resulting in a bruit), thereby upregulating RAAS and increasing blood pressure?

rocmed  And isn't smoking also a risk factor for RCC? +  
lispectedwumbologist  It is but RCC tends to present later in life (6th or 7th decade). In a 55 year old smoker, atherosclerosis of the renal artery is am much more common cause of bruits +  
seagull  Hypertension is also a risk factor of an atherosclerosis leading to more inflammation. Eventually dilation (aneurysm) might occur... if im wrong then ignore this +  
seagull  Hypertension is also a risk factor of an atherosclerosis leading to more inflammation. Eventually dilation (aneurysm) might occur... if im wrong then ignore this +  
illogical  Renal Cell Carcinoma has a tendency to invade the Left Renal **Vein** (Pg 134, Pathoma 2018). Thus it has an association w/ obstructed drainage of the Left Spermatic Vein leading to a varicocele. Renal artery stenosis is more commonly due to atherosclerosis (almost 85-90%) or fibromuscular dysplasia. +6  
ratadecalle  With RCC and renal vein invasion you would see B/L lower edema and venous collaterals in the abd wall (Uworld). Also he has a severe headache and confusion which are signs of a hypertensive emergency. +