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 +1  (nbme24#22)
  • Adductor muscles and gracilis are innervated by the obturator nerve
  • External oblique is innervated by the iliohypogastric nerve
  • obturator internus is innervated by the obturator internus nerve (L5–S2)
  • Piriformis is innervated by the sciatic nerve (L5-S3)

 +0  (nbme24#20)

These sclerotome cells differentiate into chondroblasts that form the cartilaginous precursors of the axial skeleton and bones of the cranial base (form netter embrio)



 +0  (nbme23#28)

why not decrease CA activity in the proximal tubule? this also could lead to metabolic acidosis.

ergogenic22  carbonic anhydrase inhibitors can cause Type 2 RTA but it is not the cause here (cystinosis)

 +0  (nbme22#4)

The other answers are wrong because: (if I am wrong please correct me)

A) This would be true in a patient with liver or nephrotic syndrome

C) This would be correct if the we increase capillary permeability (example sepsis)

D) This is left heart failure

E) This could be ARDS (not sure though)

F) Malignancy


 +1  (nbme22#6)

hope this image help to understand it, the pumps don't work because lack of ATP





Subcomments ...

Just because he’s having (unprotected) sex doesn’t mean he doesn’t have simple infectious mononucleosis. The sex implies he’s also kissing someone! Pharyngitis + lymph nodes + fatigue = mono.

titanesxvi  The triad of classic symptoms for infectious mononucleosis is lymphadenopathy (swollen glands), splenomegaly (large spleen), and exudative pharyngitis accompanied by high fever, malaise, and often hepatosplenomegaly (large liver and spleen) +  


submitted by fahmed14(14),

Histamine plays a major role in the cardinal signs of inflammation. It helps mediate vasodilation and vascular permeability (via endothelial cell contraction). These two functions are already contrary to A, B, C, and D. By increasing fluid in the interstitial space, you can reason that there will be increased lymph flow.

youssefa  If more transudates are leaking into the interstitium wont this dilute the interstitial proteins and cause a decrease in oncotic pressure and increase in interstitial hydrostatic pressure? +3  
titanesxvi  @youssefa I think because it is an exudate from increased permeability of venules, the oncotic pressure in the interstitium is not going to decrease +  


submitted by vshummy(58),

So the best i could find was in First Aid 2019 pg 346 under Diabetic Ketoacidosis. The hyperglycemia and hyperkalemia cause an osmotic diuresis so the entire body gets depleted of fluids. Hence why part of the treatment for DKA is IV fluids. You might even rely on that piece of information alone to answer this question, that DKA is treated with IV fluids.

fulminant_life  I just dont understand how that is the cause of his altered state of consciousness. Why wouldnt altered affinity of oxygen from HbA1c be correct? A1C has a higher affinity for oxygen so wouldnt that be a better reason for him being unconscious? +3  
toupvote  HbA1c is more of a chronic process. It is a snapshot of three months. Also, people can have elevated A1c without much impact on their mental status. Other organs are affected sooner and to a greater degree than the brain. DKA is an acute issue. +1  
snafull  Can somebody please explain why 'Inability of neurons to perform glycolysis' is wrong? +1  
johnson  Probably because they're sustained on ketones. +1  
doodimoodi  @snafull glucose is very high in the blood, why would neurons not be able to use it? +1  
soph  @snafull maybe u are confusing bc DK tissues are unable to use the high glucose as it is unable to enter cells but I dont think thats the case in the neurons? +  
drmomo  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2909073/ states its primarily due to acidosis along wth hyperosmolarity. so most relevant answer here would be dehydration +  
drmohandes  I thought the high amount of glucose in the blood (osmotic pressure), sucks out the water from the cells. But you also pee out all that glucose and water goes with it. That's why you have to drink and pee a lot.. +1  
titanesxvi  Neurons are not dependent on insulin, so they are not affected by utilization of glucose (only GLUT4 receptors in the muscle and adipose tissue are insulin dependent) +  


Why is it that the pulmonary capillary wedge preesssuree is increased? on pg. 307 of FA 2019 it says it can be increased or decreased :/

giggidy  Depends on where the infarct is I guess? Crackles in lung base means increased left sided pressure and therefore PCWP. At least that's how I thought of it. +1  
titanesxvi  Because think the circulation as a closed circuit, in this case the heart isn't pumping well and the pressure is going to backup. that is why the PCWP is increased +  


submitted by krewfoo99(10),

Can someone explain what the picture is supposed to show? Is it supposed to be segmented neutrophils?

titanesxvi  yes do to B12 deficiency +  


submitted by wired-in(31),

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 +21  
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 +4  
ht3  this is why you never waste 7 minutes on a question.... because of shit like this +5  
yotsubato  Why the FUCK did they not just give us a clearance of 0.1 if they're going to fuckin round it anyways... +6  
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! +  
jean_young2019  OMG, I've got the 25.92 mg/kg/day, which isn't any of the answer choices listed. So I chose the D 51.8, because 51.8 is double of 25.9......I thought I must have make a mistake during the calculation ...... +  
atbangura  They purposely did that so if you made a mistake with your conversion like I did, you might end up with 2.5 which was one of the answer choices. SMH +  
titanesxvi  I did well, but I thought that my mistake was something to do with the conversion and end up choosing 2.5 because it is similar to 25.92 +  


submitted by hello(80),

which letter is CN IX in this diagram?

titanesxvi  A think is D, but it is not very clear +  
usmlecharserssss  A WHAT anatomical structure is this ???????? +  


submitted by lfsuarez(68),

First heart sound (S1) is generated by two heart valves: the mitral valve and tricuspid valve. Nearly simultaneous closing of these valves normally generates a single S1 sound. Splitting of the S1 sound is heard when mitral and tricuspid valves close at slightly different times, with usually the mitral closing before tricuspid

yotsubato  Then why the fuck is it describing a mitral valve sound in the tricuspid area +4  
dr.xx  it's describing a splitting S1 — consisting of mitral and tricuspid valve closure — that is best heard at the tricuspid (left lower sternal border) and mitral (cardiac apex) listening posts. +2  
titanesxvi  tricky question, I though what sound it is in the left sternal border, so I chose tricuspid valve, but what they where asking was, what is the first component of the S1 sound +  
titanesxvi  tricky question, I though what sound it is in the left sternal border, so I chose tricuspid valve, but what they where asking was, what is the first component of the S1 sound +  


submitted by lfsuarez(68),

First heart sound (S1) is generated by two heart valves: the mitral valve and tricuspid valve. Nearly simultaneous closing of these valves normally generates a single S1 sound. Splitting of the S1 sound is heard when mitral and tricuspid valves close at slightly different times, with usually the mitral closing before tricuspid

yotsubato  Then why the fuck is it describing a mitral valve sound in the tricuspid area +4  
dr.xx  it's describing a splitting S1 — consisting of mitral and tricuspid valve closure — that is best heard at the tricuspid (left lower sternal border) and mitral (cardiac apex) listening posts. +2  
titanesxvi  tricky question, I though what sound it is in the left sternal border, so I chose tricuspid valve, but what they where asking was, what is the first component of the S1 sound +  
titanesxvi  tricky question, I though what sound it is in the left sternal border, so I chose tricuspid valve, but what they where asking was, what is the first component of the S1 sound +  


submitted by keycompany(127),

Type I Diabetes is characterized as the destruction of pancreatic islets (specifically beta cells) by T-cells. The most likely cause for hypoglycemia following insulin administration, therefore, is the destruction of alpha cells that surround the beta cells. This would cause decreased levels of circulating glucagon.

titanesxvi  I think rather that high insulin is going to block the release of glucagon +2  


submitted by yotsubato(311),

p53 is mutated and cant bind the TATA box, so what happens to transcription of inhibitory proteins?

Is basically what this question is trying to ask...

So no TATA box promoter => Decreased binding of RNA polymerase

link981  You said it, they are "trying" to ask. Should use better grammar. +1  
titanesxvi  This is on first aid, and says that the promoter region is where RNApolymerase binds +  


submitted by enbeemee(5),

sketchy says that kaposi's has infiltrating lymphocytes, so why would large aggregates of atypical lymphocytes be incorrect?

titanesxvi  Bcz I think vascular is the key thing here, whereas atypical lynphocytes would be more of EBV +  


submitted by g8427(0),

If some one can help me understand bc im a bit confused. I understand the thought process and I realized that this was an AR disease and I also got the 1/4 affected, 1/2 carrier and 1/4 unaffected. But I chose 0% bc I figured if it was an AR disease the 1 child already diseased was homozygous affected (1/4 affected). Which lead me to think that the other sister was either a carrier or not affected at all. Am I just over thinking this or am I not fully understanding whats going on?

rush  you have to think about each child individually, doesn't matter what the siblings have. The question states what are the odds of the child getting the disease. So regardless of the other siblings it still is Mom (1/2) dad (1/2) which makes it 1/4 AR +  
titanesxvi  But how do we know that the parents are heterozygous for the mutation +  
need_answers  we know that the parents have to be heterozygous Aa X Aa because on a 2x2 table, the only way the daughter could be homozygous for an AR is by having both parents be carriers (Aa) so the question was asking what are the chances the sister has the same alleles (aa) and there is only a 25% of having the same alleles. +  


submitted by usmleuser007(135),

Just note why other answers are not correct:

  1. Egophony is an increased resonance of voice sounds heard when auscultating the lungs, often caused by lung consolidation and fibrosis.

    • a. It is due to enhanced transmission of high-frequency sound across fluid, such as in abnormal lung tissue, with lower frequencies filtered out.
  2. Whispered pectoriloquy refers to an increased loudness of whispering noted during auscultation with a stethoscope on the lung fields on a patient’s torso.

    • a. Usually spoken sounds of a whispered volume by the patient would not be heard by the clinician auscultating a lung field with a stethoscope.

    • b. However, in areas of the lung where there is lung consolidation, these whispered spoken sounds by the patient (such as saying ‘ninety-nine’) will be clearly heard through the stethoscope.

    • c. This increase in sound exists because sound travels faster and thus with lower loss of intensity through liquid or solid (“fluid mass” or “solid mass,” respectively, in the lung) versus gaseous (air in the lung) media.

    • d. Whispered pectoriloquy is a clinical test typically performed during a medical physical examination to evaluate for the presence of lung consolidation, which could be caused by cancer (solid mass) or pneumonia (fluid mass).

titanesxvi  why not wheezing? +  


submitted by marbledoc(0),

Why would you ask the patient to identify the pros and cons? I don’t get the approach here!

someduck3  There was a question about this in Uworld. for *stubborn* patients who are "not ready to quit" just yet you use the motivational approach. The technique acronym is OARS: Open ended questions, Affirmation, Reflect, Summarize. +3  
yotsubato  Additionally the guy himself says "I know smoking is bad for me" Like he knows its bad, he doesnt care, but give him nicotine replacement and maybe he'll quit... +1  
usmleuser007  I didn't think nicotine replacement was a good answer choice b/c if he isn't ready to quit then why would he agree to use alternatives. +  
usmleuser007  People who smoke and are addicted like the feel of the cigs and environmental ques. Using replacements would be more challenging. The second best answer choice would have been Rx. +  
titanesxvi  why not detail the long-therm health effects of smoking? +  
seracen  @ titanesxvi: I assume because they always like the most "open ended" response. If you start detailing the long term effects, the patient might interpret that as attempting to convince, and might resist or feel pressured. By having the patient elucidate what they consider pros and cons, you allow it to be an open discussion. +  


submitted by bobson150(4),

The wording of this question confused me. This is asking "which of these vessels is the high pressure system" right? So the high pressure superior rectal is causing increased pressure into the inferior rectal?

welpdedelp  Superior rectal comes from the inferior mesenteric vein which comes from the splenic vein --> portal veins Thus, this dude had cirrhosis so it would "back-up" into the superior rectal vein. FA 2018: p360 +5  
nc1992  Superior rectal not superior mesenteric. Took me a minute +  
hyperfukus  ugh am i ever gonna get these right EVER +2  
titanesxvi  why not the inferior mesenteric, since the superior rectal drains there +  
thomasburton  @titanesxvi think it is because question says direct which is why superior rectal +1  
lilyo  thomasburton, so are they asking what vessels do internal hemorrhoids directly drain into? The order is Superior rectal vein--> Inferior mesenteric vein--> portal vein. +  
thomasburton  Yes exactly, so they do eventually reach IMV but not 'directly' +  


submitted by sklawpirt(14),

I think the idea here is simply that one should think about where vesicles are coming from on their way to the golgi complex.

"Two steps forward and one step back." Specfically the question may be referring to a rare craniofacial disorder. an awarenesss of that disease is not necessary. What is necessary is understanding the origin from where vesicles are traficked to the Golgi apparatus.

COPI protein is needed to coat vescles from the RER to send to golgi. Thus, with a mutation in that protein, the packaged proteins that should bleb off and be sent to the golgi, instead accumulate in the RER and dilate it. Thus the answer.

https://www.cell.com/ajhg/pdf/S0002-9297(16)30214-2.pdf

hayayah  pg. 47 on FA got the good visuals! +2  
notadoctor  COPII* proteins are needed to coat vesicles from the RER to Golgi. "Two(COPII) steps forward; one(COPI) step back." Anterograde goes RER -> Golgi -> Lysosomes/Secretory Vesicles -> Plasma membrane +7  
titanesxvi  why not small lysosomes? +  
varunmehru  and I thought large lysosomes due to lack of enzymes to degrade +