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Welcome to mannanโ€™s page.
Contributor score: 18


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 +0  visit this page (nbme23#8)
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Why is medullary thyroid cancer on the lateral side of the neck???

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username  I think it is referring to like not in the midline but lateral to it. Not completely lateral but like center lateral +

 +0  visit this page (nbme19#25)
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This patient has osteoporosis from hyperparathyroidism.

Hyperparathyroidism osteoporosis leads to hypercalcemia from CORTICAL SUBPERIOSTEAL EROSIONS

whereas osteoporosis from age/menopause affects trabecular bone. The latter has normal bone mineralization and normal lab values (normal Ca and PO43-)

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 +3  visit this page (nbme19#0)
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Why would it not be answer C) Lutenizing hormone?

My thought process was this:

Leydig cells make testosterone (internal genitalia) that also gets converted to DHT (external genitalia)

Without the leydig cells working you don't have internal genitalia (patient in stem) and you dont have male external (patient in stem)

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solidshake  Androgen insensitivity is the better answer because it is more specific for the findings given. A deficiency of LH secretion would point to a problem with Gonadotropic cells in the anterior pituitary which would present with problems with LH and FSH, but the sertoli cells are working here. If you say its because of LH insensitivity, i suppose this is plausible, but Androgen insensitivity is a well known condition that gives this presentation. +1

 +2  visit this page (nbme15#3)
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You could give pralidoxime but you have to give it second (after atropine) because it temporarily worsens the cholinergic toxidrome (wet picture)

Pra li dox ime an tag M+N

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 +3  visit this page (nbme15#6)
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The vaccine is against Hemagglutinin that is important for binding and entry

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 +0  visit this page (nbme15#33)
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ATP is hydrolyzed before the power stroke (contraction). It allows the power stroke to happen

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 +1  visit this page (nbme15#24)
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Defective cross linking of elastic fibers is Ehlers Danlos syndrome

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Subcomments ...

submitted by bwdc(697), visit this page
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They have described what you assume is a classic case of pneumonia. But, PNA isnโ€™t an answer choice. What the next best thing? The cause! Old frail people (and alcoholics) love to get aspiration pneumonia. RLL is the most common site, which they have provided (thank you, big vertical bronchus). They even gave you the hint that the patient has โ€œdifficulty swallowing,โ€ which is code for โ€œaspirates when swallowing.โ€

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mannan  wrong answers: Smoking and emphysema are obstructive and more importantly air trapping disease processes and wouldn't really cause the dysphagia. The main vasculitis with lung involvement is We-C-ner granulomatosis that would also have nose and kidney problems - from SATTAR +1


submitted by jp1003(12), visit this page
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FA pg614

tight junctions between adjacent sertoli cells form blood-testis barrier--> isolate gametes from autoimmune attacks

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mannan  FA2020 pg 628 +1


submitted by imgdoc(183), visit this page
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I think alot of people might have over emphasized how important ANP and BNP really are, yes it is important to know these peptides get secreted by the atrial/ventricular myocardium during heart failure. However their overall effectiveness in treating heart failure is zilch, a preceptor told me that if ANP and BNP were so useful in natriuresis then why do we give diuretics? It's because RAAS overpowers this system hence causing negative effects and the endless loop of heart failure. AKA why we give ACE inhibitors.

Knowing that ANP gets neutralized by the RAAS system, we can shift our focus back to heart failure in this patient, where cardiac output is decreased, leading to ADH secretion and finally dilutional hyponatremia.

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almondbreeze  a concept continuously emphasized by uw, but I get always wrong :'( +4
almondbreeze  good work done! +1
raffff  why does the body make anp at all since its so useless +4
makinallkindzofgainz  @raffff - at least BNP gives us a good marker for heart failure exacerbations :) thanks body! +1
mannan  Yeah it's important clinically because it has a high sensitivity (if negative, rule out) for Heart failure. +1
alimd  At the same time ANP inhibits renin release? +1
freemanpeng  If it is High RAAS, Aldo must be High as well(AngII induce Aldo more than ADH). Then that would be SALT-WATER retention rather than PURE WATER retention. NO hyponatremia +
plaguedbyspleen  This patient is third-spacing and therefore has low effective circulating volume. I like to think that given his CV history, he is probably on an ACE inhibitor or something similar. So that leaves ADH to do its thing. Also high aldosterone saving salt isn't something we need to consider given the stem and answer choices. +


submitted by atstillisafraud(217), visit this page
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Weight loss - think cancer Hyponatremia - SIADH from small cell lung cancer Edema + JVD - SVC syndrome

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peridot  I was thinking lung cancer secreting SIADH, resulting in hyponatremia. But because the question asked specifically about the cause of the facial edema, I put hyponatremia (answer choice C). I was wondering how you guys were able to differentiate between C. hyponatremia and E. lung cancer? Thank you! +2
mannan  The first thing that crossed my mind was SVC syndrome from the cancer obstructing the R brachiocephalic vein preventing venous blood from returning to the heart (and staying in the facial area). Also I assume Hyponatremia would be equivalent to decreased body volume so there wouldn't be edema. FA Renal physiology section has a good chart on what happens during electrolyte imbalances (hypo and hyper) +2
mannan  @peridot +2
peridot  I was thinking that hyponatremia would be more loss of osmotic pressure --> edema, but I definitely see the argument for a mass that's simply blocking blood flow. Thank you! +1
jaramaiha  only thing affecting osmotic pressure is albumin, which would be more towards liver cirrhosis. The body will attempt to maintain a Na+ of 140 with various mechanisms, but doesn't contribute to osmotic pressure. +1


submitted by atstillisafraud(217), visit this page
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Weight loss - think cancer Hyponatremia - SIADH from small cell lung cancer Edema + JVD - SVC syndrome

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peridot  I was thinking lung cancer secreting SIADH, resulting in hyponatremia. But because the question asked specifically about the cause of the facial edema, I put hyponatremia (answer choice C). I was wondering how you guys were able to differentiate between C. hyponatremia and E. lung cancer? Thank you! +2
mannan  The first thing that crossed my mind was SVC syndrome from the cancer obstructing the R brachiocephalic vein preventing venous blood from returning to the heart (and staying in the facial area). Also I assume Hyponatremia would be equivalent to decreased body volume so there wouldn't be edema. FA Renal physiology section has a good chart on what happens during electrolyte imbalances (hypo and hyper) +2
mannan  @peridot +2
peridot  I was thinking that hyponatremia would be more loss of osmotic pressure --> edema, but I definitely see the argument for a mass that's simply blocking blood flow. Thank you! +1
jaramaiha  only thing affecting osmotic pressure is albumin, which would be more towards liver cirrhosis. The body will attempt to maintain a Na+ of 140 with various mechanisms, but doesn't contribute to osmotic pressure. +1


submitted by peridot(115), visit this page
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While I understand why it's hyperplastic arteriosclerosis and how it classically occurs with HTN, I was wondering why it couldn't be berry aneurysm? Is it because the question is asking which is "most likely", making C the better answer? Thank you.

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mannan  Berry Aneurysm is not CAUSED by HTN. It's caused by weakening of the arterial wall (at bifurcations). Hypertensive disease exacerbates them and causes the clinical picture of SAH (worst headache of life) when they rupture. Hope that helps -- Reference: FA CNS pathology, aneurysms. +2
usmleboy  Actually according to Goljan this is incorrect. Berry aneurysms are caused by hypertension. The weakening of the wall (no tunica media) at bifurcations is inherent in human anatomy. Basically you have to have elevated BP to cause the dilation, outside of the inherited connective tissue disorders. Hence why PKD has the berry association. However, these aneurysms present with extremely prolonged HTN, whereas our guy in this Q only has a 1 year history. The key to answering this question is recognizing that this is MALIGNANT hypertension that is relatively acute in onset. Malignant HTN = hyperplastic arteriolosclerosis (onion rings). +3


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