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Comments ...

 +0  (nbme15#29)

How do you know for sure that this is incomplete penetrance and not gonadal mosaicism? Dont both allow an AD disease to be transmitted by a phenotypically non-expressing carrier?

nissimhazkour1  my line of thinking is that gonadal mosaicism is much less likely considering there is a family history of the disease. If there was no family history then a gonadal mutation causing mosaicism is possible, but taking into consideration how there is a clear AD inheritance, it must be that the person inherited the disorder but is not expressing the phenotype. hope this helps! +
mittelschmerz  Yes thanks! That feels like it should have been so obvious in retrospect, ugh. +




Subcomments ...

submitted by liltr(22),
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I cehsoo VMP ot,o tub sthi asenttpi’ imna pmymtos is oucgh noly ngruid eesxc.ier Tihs si omre vateidcini fo secreiexd aetscsdaoi ta.samh Yuo olucd ees sshroetns of harteb in VMP udrgni cse,irxee tbu cosonihg MVP lveeas teh chguo ucuedoctnna fo.r

.ooo.   I agree! Also, At the end of the stem, the question is which of the following best explain the patients symptoms? Not physical exam findings. Since this patient is coming in with a chief complaint of SOB while playing sports exercise induced asthma is the best choice. Hopefully that helps. +12  
uslme123  I mean... couldn't increased BP during exercise worsen his MVP and give him SOB? +  
uslme123  (by causing slight regurg) +1  
yotsubato  "Lungs are clear to auscultation" +6  
sahusema  But wouldn't choosing exercise-induced asthma leave the murmur unaccounted for? +  
cienfuegos  I incorrectly chose malingering and am wondering if the fact that he presented (although it doesn't state who brought him in/confirmed his symptoms while exercising) makes this less likely despite the fact that he clearly states "I don't want to play anymore" which could be interpreted as a secondary gain? Also, regarding the MVP, I'm wondering if the fact that these are usually benign should have factored into our decision to rule it out? Thoughts? +2  
cienfuegos  Just noticed that he has FHx, game changer. +1  
kimcharito  clear lungs, they try to say no cardiogenic Pulm. edema, means is not due to MVP shortness of breath while doing sports and no shortness at rest makes me to think more asthma induced by exercise) +1  
pg32  Isn't exercise induced asthma usually found in people running outside, especially in cold weather? I feel like that is how it is always presented in NBME questions, so this threw me off. Not to mention the MVP. +  
happyhib_  it took me a little; the FHx really pushed me to exercise induced. I was also looking at malingering but there wasnt a real reason to push me to this (as a doctor it would be sad to be like hes faking it becasue he doesnt want to play sports with out being sure first; led me away because there wasnt enough pointing there). Also MVP could be slightly benign and is very common and usually no Sx and his lungs were clear as was rest of exam. All pushed to Asthma +  
mittelschmerz  I think MVP on its own shouldnt cause SoB with cough (in a question, I'm sure it could in the real world). In the world of NBME questions where you need to follow the physiology perfectly, you would need some degree of MR that lead to LV dysfunction/vol overload, and theres no pulmonary edema nor an S3 that point us towards that. Malingering would have to be faked for gain, and theres no external gain here or evidence that he's faking symptoms. You would also need to r/o physical illness before diagnosing malingering, which hasnt been done. Cold weather is certainly known for exacerbating EIA and are the exam buzzwords, but any exercise can absolutely be a trigger +2  


submitted by euphoria(1),

i have answered this question right, but why there is mid systolic murmur in the stem?

mittelschmerz  He also has MVP, but asthma is more likely to cause this symptomatology and he has a family hx. +1  
euphoria  Thank you very much bro :-) +1  


submitted by cassdawg(586),

Aminoglycosides (like gentamycin) are bactericidal via irreversible inhibition of the initiation comblex by binding the 30S subunit [FA2020 p191]

  • Amoxicillin is a beta-lactam antibiotic which works by binding and inhibiting penicillin-binding proteins (transpeptidases) and block cross-linking in the cell wall [p187]
  • Ciprofloxacin is a bactericidal fluoroquinolone which acts by inhibiting DNA gyrase (topoisomerase II) and topoisomerase IV [p195]
  • Erythromycin is a macrolide (the macrolides are ACE - azithromycin, clarithromycin, and erythromycin) which acts by inhibiting protein synthesis via bindind to the 50S subunit and preventing translocation (macroslides) [p193]
  • Sulfamethoxazole is a sulfonamide which acts by inhibiting dihydropteroate synthase therfore inhibiting folate synthesis [p194]
mittelschmerz  Buy AT 30, CCEL at 50 got me through this one +  


submitted by cassdawg(586),

Spironolactone has a special use in hepatic ascites (FA2020 p609).

Spironolactone is the drug of choice for initial treatment of ascites due to cirrhosis

cheesetouch  FA2018 P591 +  
mittelschmerz  In portal HTN, the splanchnic vasodilation results in a drop in systemic BP and renal hypoperfusion. That leads to RAAS activation that increases SBP enough to maintain renal perfusion, but the aldosterone-mediated Na/H2O retention leads to edematous states (ascites here). Treating with spironolactone allows you to treat the the fluid component without disrupting the vasoconstrictive effects of AngII that is the only thing maintaining renal perfusion, which is why spironolactone is correct here, but also why prescribing an ACEi or ARB in a hepatic patient like this is v v bad. +1  


submitted by bingcentipede(120),

https://imgur.com/RQGrWLw

G represents the primary somatosensory area of the parietal lobe. The stem describes a 69 (nice) year old woman with sensory issues on the left side. She presents w/ a Babinski sign on the left, decreased somatic sensation in the left foot, agraphesthesia (when you "draw" a number on someone's skin and they can't interpret it) on the plantar surfaces of the toes, decreased position sense in the toes. The question says there is an edematous area in the cerebral cortex of the right hemisphere.

I had trouble with this, but I think it's describing somatosensory because of the sensory problems. Don't understand the UMN lesion (Babinski). Here's what Wikipedia says: "Lesions affecting the primary somatosensory cortex produce characteristic symptoms including: agraphesthesia, astereognosia, hemihypesthesia, and loss of vibration, proprioception and fine touch (because the third-order neuron of the medial-lemniscal pathway cannot synapse in the cortex). It can also produce hemineglect, if it affects the non-dominant hemisphere. Destruction of brodmann area 3, 1, and 2 results in contralateral hemihypesthesia and astereognosis."

mittelschmerz  The Babinski tripped me up too, here's what I found: "Sixty percent of the CST fibers originate from the primary motor cortex, premotor areas, and supplementary motor areas. The remainder originates from primary sensory areas, the parietal cortex, and the operculum. Damage anywhere along the CST can result in the presence of a Babinski sign." from https://www.ncbi.nlm.nih.gov/books/NBK519009/ +5  
yourmomsbartholincyst  I think this question is more simply about the topographical arrangement of the homunculus (which I once again somehow managed to flip backwards during the exam). Lower extremity is topographically mapped to more medial portions of the somatosensory cortex, hence letter G and why ACA strokes tend to affect the LE more. Homunculus, our favorite hunk, FA2020 pg 502 +1  


Inhalant intoxication= slurred speech, disturbed gait, drowsiness

Inhalant withdrawal= headaches and irritability

usually will present with rash around nose and mouth too

FA2020 pg 570

mittelschmerz  So mad I second-guessed myself on this. Its always PCP or huffing glue smh +  
bingcentipede  Think I had UWorld question on this. Apparently in this age group (teens), inhalants like glue are the first drugs they try. Only ever seen this on It's Always Sunny but w/e +  


submitted by cassdawg(586),

I don't like how they are asking this, but I think what they are getting at is that after the stent placement ("subsequent to the stent placement") there will be reperfusion injury to the myocardial tissue which occurs through free radical injury and therefore membrane lipid peroxidation is the best answer (FA2020 p210 mentions membrane lipid peroxidation as a mechansism of free radical damage and lists reperfusion injury after thrombolytic therapy as a type). Elevations in the cardiac enzymes I assume are because of the injury to the cells.

zalzale96  Created an account just to up vote this answer +1  
cheesetouch  1998 journal via google " Myocardial injury after cardiac surgery with cardiopulmonary bypass may be related to free oxygen radical-induced lipid peroxidation" +  
peteandplop  "Evidence suggests that reactive oxygen species (ROS) may play important roles in the pathogenesis in myocardial infarction [2]. Following ischemia, ROS are produced during reperfusion phase [3, 4]. ROS are capable of reacting with unsaturated lipids and of initiating the self-perpetuating chain reactions of lipid peroxidation in the membranes" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2274989/) +1  
mittelschmerz  Honestly the wording got me on this one. Great answer +  
acerj  Also, you can rule out a few of the options to help justify this. Post MI you expect necrosis, not apoptosis. Remember, apoptosis is suicide, and necrosis is MURDER! Cell swelling is a sign of cellular injury, not cell shrinkage. The heart will undergo coagulative necrosis, not liquefactive necrosis. Also, protease inactivation by cytoplasmic free calcium is kind of nonsensical to me. Free calcium is more likely to cause cell injury via caspases (a form of proteases amongst other things), which is why calcium is usually bound up inside healthy cells. +  


submitted by brise(31),

I thought that a child with down syndrome under the age of 5, had a chance of getting acute megakaryoblastic leukemia? and over 5, acute lymphoblastic leukemia?

mittelschmerz  I was stuck between those as well. My thought process was that megakaryocytosis would be mature megakaryocytes though, which would not happen in a megakaryoblastic leukemia since they are stuck in the blast stage. That left only lymphoblasts, and I presume while one may be MORE likely age 5, a patient with Down Syndrome is still at higher risk for both. +1  
cassdawg  "Megaloblastosis" as in the answer choices refers to megaloblastic anemia in B12 and folate deficiency, so it is not associated with megakaryocytes or megakaryoblastic anemia! Hope this helps! +3  


How do you know for sure that this is incomplete penetrance and not gonadal mosaicism? Dont both allow an AD disease to be transmitted by a phenotypically non-expressing carrier?

nissimhazkour1  my line of thinking is that gonadal mosaicism is much less likely considering there is a family history of the disease. If there was no family history then a gonadal mutation causing mosaicism is possible, but taking into consideration how there is a clear AD inheritance, it must be that the person inherited the disorder but is not expressing the phenotype. hope this helps! +  
mittelschmerz  Yes thanks! That feels like it should have been so obvious in retrospect, ugh. +