questions...

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Radon

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just did the 2 nbme exams and some q's are still confusing me despite spending wayyyy too much time trying to look up the answers and the other q's i just want to be sure are correct....there are 11 questions....just warning you in advance... 🙂

1. this is a real brain teaser: what drug causes vasoconstriction that is not blocked by prazosin and bradycardia that is blocked by scopolamine? choices: amphetamines, angiotensin, NE, or phenylepi.....well, i'm totally stumped by this how can something that vasoconstricts also be a muscarinic blocker a la scopolamine??


2. 52yo w/ HTN. systolic bruit over L renal a. which is stenosed. R renal a. is NML. the R kidney is bigger than L. which of the following describes the most likely response to treatment?
a. decr. plasma renin activity and decr. AT-1 following administration of a loop
b. decr. plasma renin following a ACE-i
c. incr. plasma renin and decr AT-1 following loop
d. incr plasma renin follwing a ACE-i
well i get the whole concept of the goldblatt (sp.??) kidney but have no idea what this question is asking...went w/ D...

3. why does hydrocortisone make you fat, impede your growth and cause edema?
a. it binds to glucorticoid and mineralcortic receptors
b. drug is converted to mineralcortic in liver
c. pulm prdxn of angiotensin is incr.
d. renin activity is incr b/c of stress
e. secr of ADH is incr b/c of stress.....well, C, D AND E made no sense to me and so i went w/ A even tho i cant a find a book that tells me...

4. why is inactivated polio virus good for paralysis but not enteric tract replic?
a. doesnt elicit CMI to viral capsid proteins
b. it does not neutralize ab to virulent poliovirus
c. elicits igG and not igA
d. protects against one serotype of virulent poliovirus.....went w/ C

5. MOA: methimazole
a. blocks binding of thyroxine to receptor?
b. decr. uptake of iodine
c. inhibits thyroidal peroxidase activity
d. prevents proteolysis of thyroglob
e. stim prodxn of serum thyroid-binding globulin?
hmmm NONE of the answers match the MOA in my pharm book...i went w/ c.

6 ciliogenesis in oviduct epith cells depend on: a. biogen of addnl mitoch b. chrms DNA rep c. glycosylation w/i golgi d. multiplic of centrioles e. synth of cytokeratin..

7 so you have a myasthenia gravis pt who 30 mins after taking pyridiostigmine develops nausea and abd. cramping. what will help her sx? a. atropine b. bromocriptine c. neostigmine d. phenoxybenzamine e. propranolol...so her sx are due to incr. ach but you wouldn't give atropine t oa MG pt...so i dunno....

8 a kid has mutation in Ca receptors on cell surfaces of his parathyroid gland and on the blood side of the thick asc. loop. what would you expect w/ a mutaion that lead to activation of this receptor in the absence of its ligand, Ca???? i went w/ incr. Ca , incr. PTH and low urine Ca

9. if your feet feel hot and dry what fibers are most liked screwed? i know that sympa cholinergic innervates sweat gl. so is the answer postgang sympa?

10. in a isometric pressure-flow curve at 25% of TLC, what incr. the plateau of exp. flow rate? 1. airway resistance 2. amt of surfactant in alv. space 3. ciliary beating freq 4. exp effort 5. lung vol 6. parasymp activity....hmmm went w/ lung volume...

11. in a pt taking oral hypoglycemics why would you have to incr. the dosage of ibuprofen.....my google searchs say taht pts on ibuprofen potentiates the oral hypogly...in any case, the choices:
a. anit-inflam dose is near 2 times analgesic dose
b. the drug is exr. at a faster rate b/c of renal prob in DM
c. incr. dose extends half-life
d. menapausal women met drug faster
e. oral hypogly interferes w/ protein binding of ibuprofen
i went w/ A even though when i asked a MD he had no clue....gotta love that!

well that's it....i apologize for my question overload and appreciate any help as time is running out... 😱 ...thanks so much,

ray

P.S. CONGRATS to everyone who kicked a$$ on the test!!!!
 
1) must be a B-blocker or ATII, although I dont know the mechanism of bradycardia in ATII...the others are all adrenergic agonists.

2) its correct. just asking you in a round-about way if you know the feedback loop.

3) i went with A also, because I think there is weak mineralocorticoid activity with all glucocorticoids.

4) correct

5) correct

6) i think A on this one, just because it is the only one that happens in cells that are not dividing, but are making new equipment.

7) you would giver her atropine, because she has signs of cholinesterase inhibitor toxicity. atropine is a muscarinic blocker anyway, so it shouldnt affect the MG symptoms too much. regardless, the toxicity could kill her, and will likely be uncomfortable.

8) i think all these are the opposite. it looks to me like the kid cant pull back calcium, so blood Ca is decreased, urine Ca is increased and PTH is increased, because of the feedback from low blodd Ca.

9) correct.

10) i think it is amount of surfactant, because the limiting factor for flow is collapse of the small airways, which is overcome by surfactant.

11) oral hypoglycemics will displace drugs from albumin (sulfa compounds) but I dont know if that is the case here. thats the one i would go with because it is so non-specific.
 
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