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Old 03-07-2012
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Arrow NBME 2 Block 2 Discussion

#8: i've never heard of a lung tumor that projects into the lumen of the bronchus. is that characteristic for a carcinoid tumor?
#10: Explanation please
#11: I don't think the answer key is right. Looks like B is the answer to me.
#17: Explanation please
#18: Really? I thought it was either C or D. I figured the rectus abdomanis muscle is responsible for flexion.
#20: I think i read somewhere that you can give a dopamine agonist because that will decrease Ach in the enteric system, no? Seems kind of backwards to give an Ach-esterase inhibitor and then give Atropine. It would have widespread cancellation of the pyridostigmine therapy, no?
#21: Explanation please
#27: How can you tell its RCC?
#35: doesn't RT make DNA from RNA? here, we're making RNA from DNA, so shouldn't it be E?
#46: Explanation please
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Old 03-10-2012
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@avash.nrs : "block2:1,6,9,10,16,18,21,25,26,27,33,34,35,36,39, 40"

1: habituation is when you are exposed to a stimulus so much that you become desensitized to it and it fails to elicit the behaviour it once did.

6: meckel's diverticula always contains gastric tissue. its a remnant of its embryological development. so whenever you get a question about what kind of tissue could be seen in a meckel's diverticula, the answer is gastric tissue.

9: i put B because its the only one that made sense. none of the others would give the clinical presentation explained in the question.

10: its a blister, which i guess can also be described as a vacuolated lesion in the epidermis, which the overlying epidermis being thick.

16: She has that Kartageners syndrome thing, which theres a defect in dynein arms. We know this because it says she has messed up cilia. Cilia, flaggellum and that sort of stuff have dynein. So we know its a motility issue. so the answer is D.

18: i thought it was C but they say B :/

21: yea i dont know this one.

25: its G because the mutation is basically tricking the body into thinking you have hypercalcemia, so your body A) wont release PTH (so decreased PTH, and therefore hypocalcemia) and B) wont reabsorb Ca2+ in the kidney (therefore, increased urinary excretion of calcium)

26: answer is A; CMV pneoumonitis. which is a condition we see in transplant patients. The photo shows "Owl's eye inclusion".

27: im not sure how the photo shows you its RCC. but the presentation says she has brain problems, so to me the only way you can have both a kidney tumor and a brain problem is if you have RCC, which we know can cause Berry Aneurysms in the brain.

33: B. just something you need to know. type 1 collagen made by chondrocytes.

34: in this situation you want to give an ACEI. i dont think a loop diuretic would help, or atleast ive never heard of giving one in this situation. and E is the correct choice for when we give an ACEI.

35: i dont know this one. i thought it was E.

36: D. he panicks when he's at work. panic disorder.

39: i just went with which sounded most correct to me and it was right. E. i feel like that would be the most drastic change and therefore have the most drastic effect on its metabolism.

40: easy question. classic O2 dissociation curve. I recommend you look over it if you have any trouble. Basically an increase in anything (except pH, because its like the inverse of H+ ions) will cause O2 to be unloaded.
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Default Familial Hypocalciuric hypercalcemia

[QUOTE=Dr.NickRiviera;101048]@avash.nrs : "block2:1,6,9,10,16,18,21,25,26,27,33,34,35,36,39, 40"

25: its G because the mutation is basically tricking the body into thinking you have hypercalcemia, so your body A) wont release PTH (so decreased PTH, and therefore hypocalcemia) and B) wont reabsorb Ca2+ in the kidney (therefore, increased urinary excretion of calcium)


25. B. I think this is a case of familial hypocalciuric hypercalcemia.

Normally the Calcium sensing receptors (CaSR) of parathyroid gland and kidneys should detect hypercalcemia, that would normally lead to a decrease in PTH.

Since the receptors are defective, even in the state of hypercalcemia, the mutation of the CaSr loses its feedback inhibition of high calcium levels to decrease the levels of PTH. In other words, the parathyroid gland thinks that the body is in the state of hypocalcemia and thus will continue to release PTH. Increase in PTH will lead to increase in urinary calcium absorption and phosphate excretion. Leading to hypercalcemia, increase PTH and decrease urine calcium.
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