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Contributor score: 26

Comments ...

 +2  (nbme22#6)

So do you ignore the distraction about his mother and consider which of the organisms can lead to nodule formation on the vocal cord?

neovanilla  yep _(ツ)_/¯

 +0  (nbme22#8)

Ataxia due to vitamin deficiency can only be caused by Thiamine or Vitamin E deficiency.

 +2  (nbme22#17)

Pott's Fracture: forced eversion of the foot➝ deltoid ligt avulses medial malleolus ➝ fibular fracture higher than tib fx

 +1  (nbme22#20)

the Fibularis Brevis is the only pure foot eversion muscle listed here. Everting his foot would exacerbate his injury and cause him more pain at the fracture

imo contraction of any of these muscles would be painful in this scenario

 +2  (nbme22#23)
  • enzyme deficiencys = AR

  • homozygous presence of CYP..."

QED: homozygous + AR = 25%

 +0  (nbme23#32)

I took the simplistic approach: I chose the opposite of whatever the kidney usually does and then lack of neg PTH feedback

 +1  (nbme23#22)

rheumatic hrt dz = mitral stenosis = pulmonary edema (bilateral crackles) = dyspnea

 +2  (nbme23#47)

found this super useful book on amazon about Budd-Chiari (check out the sick cover)

llamastep1  Thank you for that
focus  hahahahaha. DEAD.
anjum  I endorse clicking that link

drdoom  welcome, O great physician of the skull and oral cavity. we revere your intricate understandings of the face, jaw, maxilla and all their tiny and hidden foramina. teach us your ways.

 +0  (nbme24#16)

Follow the Calcium and work backwards. ↓Ca means ↓ Phosphate resorption in the PCT (which pulls Ca with it)

25-hydrovitD normal b/c its unrelated to PTH.

 +1  (nbme24#23)

duct through the bucc. (you can feel it with your tongue)

 +0  (nbme24#44)

To me: this seemed more straightforward. You'd want to follow up and check Gastrin levels on a patient who previously had 4x normal.

thotcandy  He could have 4x the normal because of current PPI use. the point was that you'd get him off, wait for it to normalize, then check again to see if it's due to neoplasm or PPIs

Subcomments ...

DKA is a state of decreased insulin; since we know that insulin causes a shift of K+ into the cells low levels of insulin will prevent this and result in hyperkalemia. In addition, due to hyperglycemia and high ECF osmolality water will shift out of the cells into the ECF and K+ shifts out with the water which will futher increase the hyperkalemia

dentist  I know Insulin cause shift K+ into cells due to closing of ATP-sensitive K channels (blocking K from leaving)? Does it increase K in the cells by another mechanism? +  
makinallkindzofgainz  @dentist - Insulin stimulates the Na+-K+-ATPase pump, this drives K+ into the cell (Source: Amboss) +  
castlblack  Another mechansim = acidosis causes hyperkalemia due to H+/K+ antiporters. H+ is high in blood so shifts into cells via this antiporter, which shifts K+ out. --potassium section of acid/base chapter in Costanzo physiology +  

submitted by mattnatomy(34),

Severe hypertension often leads to hyperplastic arteriolosclerosis (onion-skin appearance). Also see proliferation of smooth muscle cells.

meningitis  and explains the flame hemorrhages (Goljan) caused by malignant HTN +4  
taediggity  FA 2020 pg. 537 +  
dentist  FA 2020 pg 301* +  
ally123  The flame hemmorhages are also a good buzz word for recognizing he has hypertensive retinopathy 2e chronic, uncontrolled HTN. Pt's with hypertensive retinopathy can also present with "cotton wool spots" and "macular star". Pics on FA 2019, p. 299 +  

would anyone be able to clarify what the others would be? A) Allergen mediated vasoconstriction, leading to ischemic tissue injury: Type I B) Binding of antigen to IgE on the surface of mast cells leading to mast cell degranulation: Type I C) deposition of antigen-antibody complexes within postcapillary venules, leading to activation of complement: Not sure D) Phagocytosis of antigen by neutrophils, leading to oxidant mediated tissue damage: Type III?

sunny  i think C is type III +1  
sunny  i think C is type III +  
dentist  In Type III HS, First C happens then then D happens +  

submitted by bobson150(5),

Is the grey supposed to be a suture? If not why would this not be wound healing therefore granulation tissue?

asapdoc  If you look at the picture you can see the epithelioid and giant cells. I only picked granuloma because I remember seeing a similar picture in Uworld. +5  
dentist  granulation tissue is a part of the normal wound healing process, and happens within the first week. +  
castlblack  I agree I looked at that grey blob and thought foreign body --> granuloma +  

submitted by usmlehulk(3),

can someone please explain this question. i thought the patient is actually having cleft lip and palate, but why is the correct answer addressing only the cleft lip.

dentist  The question asks "the most likely cause of the facial finding involving the lip in this patient..." +4  
snripper  lmao. gottem +  
ace9yak  cleft lip = 'processes' clef palate = 'shelves' +  

submitted by welpdedelp(154),

It was scabies, which is transmitted person-operon.

welpdedelp  **person-person lol +4  
suckitnbme  NBME loves their scabies +6  
dentist  did you get scabies from "burrows" and "night itching" +  
pg32  My question is where do you get scabies originally? I knew it was transmitted person-to-person, but thought it has to originate somewhere (a pet possibly?) so I went with pets. The internet only seems to say that you get scabies from another person with scabies, so the question remains: where do people contract scabies from? +  

submitted by alexb(38),

Is the part with "constant studying" just supposed to support that she has a psych disorder related to perfectionism, which is why she's going to extremes to control her weight?

rrasha2  No, the constant studying is to trick you into thinking shes abusing amphetamines.Amphetamines decrease appetite so a lot of people abuse them for weight loss. That combined with increased concentration to study all day errrday.. #onehellofadrug +  
rrasha2  forgot to mention, another side effect of amphetamines would be increased BP due to the increased catecholamines..don't forget to keep an eye out for that +1  
dentist  would amphetamines influence electrolytes at all? +  

Increased Levels of Myeloid cells ( Erythrocytosis, thrombocythemia, and granulocytosis) plus Dizziness and Headache increase the suspicion for Polycythemia vera.

Low EPO in PV due to Negative feedback on EPO release by kidney.

dentist  This is where the timing of everything in the question trips me up. FA say PV mechanism is increase EPO (2019, p299) +  
paulkarr  Different types of Polycythemia have different effects on EPO levels. "Appropriate Absolute" and "Inappropriate Absolute" will both increase EPO levels (Inappropriate is caused by this EPO increase). Where as Polycythemia Vera has decreased EPO levels due to the negative feedback loop. FA2019 pg 425 hooks it up nicely. +1  

submitted by nwinkelmann(218),

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? +1  
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"? +2  
hello  @dentist btw, HOCM is an answer choice (RVOT is part of HOCM) +2  
thotcandy  @hello but since that's pseudo-aortic stenosis, it would present with a systolic murmur, correct? +  

submitted by mousie(135),

help with this one please.... is this because he has hyperTG AND Cholesterol AND chylomicrons.. only LL deficiency would explain all of these findings? I chose LDL R deficiency because I guess I though it would cause all of them to increase but is this type of deficiency only associated with high LDL?

sympathetikey  First off, do yourself a favor and check this out - https://www.youtube.com/watch?v=NJYNf-Jcclo The LDL receptor is found on peripheral tissues. It recognizes B100 on LDL, IDL, and VLDL (secreted from the liver). Therefore, an issue with that would cause an increase in those, but mainly LDL. Since in this question we see that Triglycerides and Chylomicrons are elevated, that points towards a different problem. That problem is in the Lipoprotein Lipase receptor. This is the receptor that allows tissues to degrade TGs in Chylomicrons. So, if it's not working, you get increased TGs and Chylomicrons. Additionally, you get eruptive xanthomas, which are the yellow white papules the question refers to. +7  
davidw  There is much easier way go to page 94 in first aid. This kid has Type 1 Hyper-Chylomicronemia which is I) Increased Chylomicrons, Increase TG and Increased Cholesterol. It can be either Lipoprotein Lipase or Apolipoprotein CII Deficiency +10  
bulgaine  The video sympathetikey referred to only mentions pancreatitis in type IV but according to page 94 of FA 2019 it is also present in type I Hyper-chylomicronemia which is what the question stem is referring to with the abdominal pain, vomiting and increased amylase activity +  
dentist  thats not the only difference in that video.... +  
paulkarr  Pixorize has a set of videos on all the lipid disorders that made it a breeze to answer. Pixorize is basically sketchy but for biochem and other basic science subjects. +  

submitted by seagull(838),

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. +  
drzed  The cervical ganglion is a fusion of the last few cervical levels and the first thoracic level, so it is plausible. +  

submitted by hopsalong(20),

I get this is a fluffy question and acknowledging the patient's reasons for missing insulin injections is the cuddliest, but I feel like this answer tows the line a bit. You don't want to say that missing doses is ok, but you also don't want to be mean to patient either. I thought this answer (A) was condoning her missing the injections, so I picked (C). In retrospect, I guess acknowledge means talk about/focus the conversation around.

dentist  I would say: "I understand why you are missing injections, but you're going to have a BAD TIME IF YOU KEEP MISSING INJECTIONS" +2  
alexxxx30  @dentist, I was searching for that answer as well, but it wasn't there so I picked C ahahaha +  

submitted by mousie(135),

Cholera = Fecal oral /Legionnaires = Legonalla pneumo = NO person to person only by inhalation of bacteria contaminated water /Lyme = tick bite /Meningiococcal = sharing respiratory and throat secretions (saliva or spit). Generally, it takes close (for example, coughing or kissing) or lengthy contact to spread these bacteria (CDC) /RMSF = tick bite

smc213  Also, when Meningococcal meningitis is treated ... close contacts are also treated prophylactically whereas the others typically are not. There's also a subunit vaccine for n. meningitis due to high infectivity rate especially in crowded establishments. +5  
dentist  So, Cholera is also p2p but Mening is more likely? +1  
usmlecharserssss  in cholera people to water => water to people +  
qball  Remember the fire sprinklers from Sketchy for M. Meningitis. as respiratory droplets are the easiest to transmit from person to person. +  
drschmoctor  but the poop water comes from people so.... +1  
llamastep1  Respiratory dropplets is easier than fecal-oral tho +  
lowyield  Can also reason that n. meningitidis is common in college students because they live in close quarters which suggests high rate of transmission even amongst immunocompetent individuals +  

submitted by mousie(135),

My understanding if BC>AC this is abnormal = conductive hearing loss = otosclerosis VS Sensoryneural hearing loss will have normal AC>BC = loss of hair cells

dentist  VS: progressive unilateral hearing loss, doesn't affect Rinne Test, associated with NF2 and actor Mark Ruffalo Otoslcerosis is (usually....) progressive bilateral hearing loss, BC > AC. source +  
tallerthanmymom  If BC > AC in BOTH ears, why does he have hearing loss in only one ear? My logic was that he probably had otosclerosis in both ears and then something extra going on in his right ear that would make it worse than the left. I still don't understand why otosclerosis is the best answer here. +1  
dul071  Finally!!!! Someone who ACTUALLY explains what the fuck bone conduction even is and teaches the whole topic. Here's the link for anyone else who struggled to find someone who takes time to explain this concept https://www.youtube.com/watch?v=cZYJL9Jg-3k +  

submitted by joker4eva76(20),

This is representative of leukoplakia, a pre-cancerous lesion of squamous cells. In order for it to spread to distant sites, it must first invade through the basement membrane/submucosa. Could be confused with oral hairy leukoplakia (which also is a white patch that classically arises on the lateral tongue). However, oral hairy leukoplakia is not pre-cancerous and is often associated with EBV infections or people that are severely immunocompromised.

hpkrazydesi  How did you know that this wasnt oral hairy leukoplakia? just from the picture? +1  
nwinkelmann  To piggyback off of @hpkrazydesi, you ruled out oral hairy leukoplakia because the patient was seeing the doctor for normal health maintenance, i.e. not immunocompromised, I'm assuming. +2  
dentist  @nwinkelmann thats correct! my time to shine. +  

Since you see vascularity that is why it is granulation tissue. Fibrous scar would be 1 month after and you wouldn't see that much blood.

dentist  The v-fib/death is an attempt to throw you off. The simple way of asking this question would have been: "18 days after an MI, you should see____?" +2  
gubernaculum  i would use pathoma for this. it says 1-3 weeks after an MI you can see granulation tissue +2  

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