A few damn tricky questions

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ChoroidPlexus

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What effect would an uncoupling agent have on carbon dioxide and ATP expenditure?

A pregnant woman with an uncpmplicated pregnancy has the appearance of paradoxical hypertension 6 weeks after her pregnancy. What lab test would you use to diagnose the cause of the hypertension?

An old man collapses in a restaurant and goes into V-fib, but then is stabilized with a BP of 90/60. No murmurs or S1, 2, or 4 heard. What is the cause of his ventricular fibrillation?

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For the uncoupling agent, wouldn't that decrease ATP synthesis since electron transport continues but is "short circuited." I would think CO2 increases since it is produced by the citric acid cycle.
 
1) ATP down (no ox. phosph.), CO2 up, since the Kreb's cycle is still running.
2) Yeah, I'm not sure about this one. She could still have pre-eclempsia (I think it can occur from like mid-pregnancy till 6 weeks post-partum)...wouldn't you do like renal study, i.e. urine protein dipstick?
Or she could have post-partum dilated cardiomyopathy (does that cause HT?)...then it'd be cardiac echo.
3) I remember being forced to learn the "shocking fact" that 50% of all ischemic heart disease cases present with sudden death, i.e. V-fib. So the pt most likely just has ischemic heart disease. (note: if he was young, I'd say he has hypertrophic cardimyopathy)
 
is there any link between pheochromocytoma and pregnancy? I mean, it says paradoxical hypertension.

What about low K+, can that cause V-fib with no murmurs and low BP?
 
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Not sure about the post-partum complications...

Anyway, re. the v-fib pt, hypokalemia can cause arrythmias, esp. if the pt is on digoxin. But again, if IHD was an option, I'd absolutly choose that, just b/c any other abnormality would prob. present with a more florid history. Not sure if hypoK causes some other Sx, but I'd guess you'd be "sick," before you got a major arrythmia.
 
Yeah IHD wasnt an option, options included stuff like aortic aneurysm,aortic dissection, and valvular problems. You don't think you would hear an S4 with IHD??
 
old man. Maybe it is cardiac tamponade. It can cause rapid heart failure and faint (perhaps imperceptible?) heart sounds.
 
Yeah, you're right, it's prob cardiac tamponade...the absent heart sounds seem to be point to that end. I misread the q...didn't realize he had no S1 or 2 (I just read "no murmurs"...that's called "selective reading" that I developed after reading hundreds of qbank questions :)).
Re IHD, sure, you could get S4 if your heart is hypertrophying, but I thought IHD, per se, does not necessarily imply that the heart is remodelling (altho that's a very common consequence). Anyway, absent S1/S2 argue strongly against IHD. Sorry for the confusion.
 
Here's another tricky question. What happens when you lesion the reticular formation? Do you get insomnia or loss of consciousness?

Vaginal delivery was complicated by depression of right shoulder damaging one root of the brachial plexus, which spinal nerve is most likely to be damaged? (C7???)
 
But I thought the reticular formation is also involved with the sleep-wake cycle?
 
will v-fib cause absence of S1 or S2 since the heart is not pumping?
 
i definitely know that it results in coma/loss of consciosness, i believe sleep wake cycle is in the hypothalamus or pons
 
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Will decreasing the half life of a drug change its volume of distribution at all??

Also, is digoxin first line for atrial flutter?
 
Isn't half life equal to (0.693)Vd/Cl? Vd = amount of drug in body/[drug in plasma]. So I guess mathematically there is a relationship. But as Vd is the amount of body at a given time then my guess if I had this on a test would be that changing the half life would not affect the initial Vd unless significant metabolism occurs before the drug is completely absorbed.

I would also put on the test that digoxin is the choice for Afib (and also CHF)

But you may want to check this out with the many SDNers who are smarter than me!
 
lealf-ye said:
will v-fib cause absence of S1 or S2 since the heart is not pumping?
if you have vfib you wont have systole... there is a pulse pressure in the patient.
 
ChoroidPlexus said:
Will decreasing the half life of a drug change its volume of distribution at all??

Also, is digoxin first line for atrial flutter?

I believe CCBs are first line
 
Here is another question:

61 y/o woman with chronic HTN has excruciating anterior upper sternal pain radiating to neck and back. BP: 210/110 on admission, then 15 min later 110/64. Echo: Aortic insufficiency, double lumen of ascending aorta and a pericardial effusion. She dies suddenly on the way to the OR. Cause of death:

a) Acute hemopericardium
b) Acute MI
c) Cerebral infarct
d) CHF
e) Massive retroperitoneal hemorrhage.

I am thinking it is e, but the stem seems to indicate that the dissection is in the upper aorta, so I'm also thinking it's A. Does anyone have an idea about this??
 
I thought CCBs were prophylactic for nodal arrhythmias??
 
What would a superior sagital sinus thrombosis look like on a scan? Would it be white in the posterior section of the brain?
 
ChoroidPlexus said:
CCBs, are you sure?? I thought they weren;t first line for anything

I could be wrong. but ccb's primary action is at AV node if you want to decrease the rate going through there. As for converting the atrial flutter, it isnt CCB for sure.

edit: and b-block to decease av nodal conduction as well.
 
02115 said:
Here is another question:

61 y/o woman with chronic HTN has excruciating anterior upper sternal pain radiating to neck and back. BP: 210/110 on admission, then 15 min later 110/64. Echo: Aortic insufficiency, double lumen of ascending aorta and a pericardial effusion. She dies suddenly on the way to the OR. Cause of death:

a) Acute hemopericardium
b) Acute MI
c) Cerebral infarct
d) CHF
e) Massive retroperitoneal hemorrhage.

I am thinking it is e, but the stem seems to indicate that the dissection is in the upper aorta, so I'm also thinking it's A. Does anyone have an idea about this??

agree
 
lealf-ye said:

It is E, most aortic aneurysms will occur in the abdominal aortic section due to atherosclerosis, only syphilitic aneurysms will occur at the arch and cause tamponade.
 
ChoroidPlexus said:
It is E, most aortic aneurysms will occur in the abdominal aortic section due to atherosclerosis, only syphilitic aneurysms will occur at the arch and cause tamponade.
So why is the aorta starting to dissect in the arch??
 
02115 said:
So why is the aorta starting to dissect in the arch??

Oh im sorry, I didnt read the question carefully, if its in the ascending aorta, then its hemopericardium i believe
 
ChoroidPlexus said:
Oh im sorry, I didnt read the question carefully, if its in the ascending aorta, then its hemopericardium i believe

Pain radiating to the back is almost synonymous w/dissection/AAA. not enough history. Hemopericardium would present with stabbing pain to the chest. radiating to the left if anything.
 
Here is another one, a newborn infant has hydrocephalus (high volume of CSF) in the lateral and third ventricles , what is the most likely diagnosis, a choroid plexus papilloma or obstruction?
 
I was thinking hemopericardium secondary to aortic arch rupture??? I agree that all other signs point to AAA, but the ascending aortic dissection is really throwing me towards hemop.
 
ChoroidPlexus said:
Here is another one, a newborn infant has hydrocephalus (high volume of CSF) in the lateral and third ventricles , what is the most likely diagnosis, a choroid plexus papilloma or obstruction?
I would go with obstruction. There is something blocking the flow between the third and fourth ventricle, which suggests a problem with the cerebral aqeduct. According to HY Neuroanatomy p23: "The cerebral aqueduct connects the third and 4th ventricles. It has no choroid plexus. Blockage results in hydrocephalus." So if there isn't any choroid plexus in the cerebral aqueduct there couldn't be a tumor causing obstruction. But I could be wrong!
 
Would an immunoglobulin deficiency (all classes) with a normal number of leukocytes and lymphocytes w/differential be associated with a complement deficiency in any way?
 
02115 said:
I was thinking hemopericardium secondary to aortic arch rupture??? I agree that all other signs point to AAA, but the ascending aortic dissection is really throwing me towards hemop.

you've convinced me. she probably died from tamponade.
 
ChoroidPlexus said:
Would an immunoglobulin deficiency (all classes) with a normal number of leukocytes and lymphocytes w/differential be associated with a complement deficiency in any way?

sounds like common variable immunodeficiency. I dont see how they would have reduced complement.
 
so then normal B lymphs, but probably reduced CD4 lymphocytes correct? Due to inability to stimulate them.
 
ChoroidPlexus said:
so then normal B lymphs, but probably reduced CD4 lymphocytes correct? Due to inability to stimulate them.

not sure about the t-cells. could be b-cell unresponsiveness to activation. I'm pretty sure tcell count is normal.
 
Is it topical tretinoin? If so I would go with that!
 
A 45 y/o F has a left flank mass. 2 months ago she had a hysterectomy for cervical CA that invaded beyond the serosa of the uterus. The mass is largely comprised of dilated renal pelvic and calyceal system. DX is:

a) Hydronephrosis
b) Hypernephroma
c) Nephrosclerosis
d) Pyelonephrosis
e) Vesicoureteral reflux

It's hydronephrosis, right, and not vesicoureteral reflux b/c we have no evidence of backwards urine flow??
 
ChoroidPlexus said:
doesnt specify, is 19-nortestosternone progesterone or androgen?
Isn't nortesosterone an anabolic steroid that would worsen acne? I know that my girlfriend uses topical tretinoin, although the systemic one has all kinds of nasty side effects.
 
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