Nbme 6

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combat

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A 35 year old woman comes to physician because of 2 week history of fever and headaches that see, to occur everyday. She recently returned from 1 month camping expedition in Cambodia. Her temp is 105.1F. Physical examination shows diaphoresis and splenomegaly. A peripheral blood smear shows Plasmodium vivax, and treatment with chloroquine is started and followed with course of primaquine. which of the following is best explanation for the inclusion of primaquine in this patient's medication regimen?

a) Cerebral Involvement.
b) Hemolysis.
c) High parasite load on the blood smear.
d) Minimal Toxicity.
e) Prevention of recurrence of malaria.

I chose E and i got it wrong, i thought primaquine is added to prevent further occurence, but it was wrong. Only option i can think from above is Hemolysis but not sure. Any one
 
I would also pick E- I have annotated from UW that primiquine is added to prevent reinfection by the dormant form in the liver in both Vivax and Ovale.
 
I thought I remembered this question being written a little differently on NBME 6. Am I mistaken? I thought the answer choice was something like reinfection not recurrence, in which case that wouldn't be the best choice. I wish I could remember this question a little better, I got it right and based on the way it is written here I would pick E leading me to believe that I would get it wrong.
 
man i don't know what i am doing wong, after first week of my studying i took nbme 3 and got 520/226 and now 4 weeks after studying i did nbme form 6 and got 350/186 😱 I thought nbme 6 was easy lol, i made some stupid mistakes, exam in 4 weeks any advise, i will be taking nbme 7 next week.
 
man i don't know what i am doing wong, after first week of my studying i took nbme 3 and got 520/226 and now 4 weeks after studying i did nbme form 6 and got 350/186 😱 I thought nbme 6 was easy lol, i made some stupid mistakes, exam in 4 weeks any advise, i will be taking nbme 7 next week.


So was this a stupid mistake? Or, did they score it incorrectly? I answered E on my exam and it was correct. It would be horrible if these exams were scored incorrectly.
 
man i don't know what i am doing wong, after first week of my studying i took nbme 3 and got 520/226 and now 4 weeks after studying i did nbme form 6 and got 350/186 😱 I thought nbme 6 was easy lol, i made some stupid mistakes, exam in 4 weeks any advise, i will be taking nbme 7 next week.

Either your form 3 or form 6 score is a fluke (probably the form 6 score). Take another nbme and see how you stand. Make sure you are rested, etc.
 
So was this a stupid mistake? Or, did they score it incorrectly? I answered E on my exam and it was correct. It would be horrible if these exams were scored incorrectly.

Of course it's scored correctly. Primaquine targets the hypnozoites, preventing recurrence.
 
i did it last week.

Okay here goes:
1. Isotonic saline 2L, how much goes into the extracellular fluid, I thought it was be 1/3 x 2 but 2/3 wasn't a choice ...
2. 31 yo W with retrosternal chest pain in the last two months. ST segment elevation. what epicardial artery event causes this?
3. 35 yo M with epigastric pain not responding to meds, mass in head of pancreas ... acinar carcinoma? I put ductal adenocarcinoma.
4. A left kidney 69 yo M .. gave gross pic, what is the tissue alterations
5. sexually active 18 yo W with rash including palms/soles. weeping plaques on gentilas, dense chronic inflam rich in plasma cells, swelling of endothelial cells occluding small vessels? What organism?
6. newborn with respiratory distress. I thought it was bowels herniating above diaphram.
7. 45 yo W with scleroderma, what inflamm cell releases cytokines that causes the dermological changes?
8. 28 yo W pelvic neoplasm mature glandular and chondroid elements and cyts lined by stratified squamous epithelium, dx?
9. Autistic boy. Parents want 12 yo daughter test to determine carrier state?
10. Infant RDS and it said inadequate secretion. I can even identify pneumocyte type II ...
11. 3 day old new born with meningitis. neutrophils and gram -ve rods? E. coli or H. influenza B
12. Disc herniation pushes on what ligament that compresses on spinal roots
13. 82 yo man unconscious hit by car, gives CY, where is the bleed
14. what noradrenergic receptor is found on both pre/post synaptic
15. The probably of surviving 4+ years after being alive for 2 years
16. 24 yo W shifting towards bone net loss?
17. A 22 yo W marathon runner stress fracture. What is going to have decrease bone density. it isn't PTH excess
18. 17 yo W with headaches and episodes of fading vision?
19. fish oil vs olive oil
20. 13 yo smoker. what would you tell him
21. graph with NE plus drug X
22. bad development of cerebral hemispheres with structure in brain stem is atrophied?
23. 28 yo mother with 3 children, which healthcare plan to use
24. levodopa vs levodopa + drug x
25. 66 yo M with difficult urinating. metoprolol, thiazide, insulin, mg(oh)2, dipherhydramine ... which drug causes that
26. lung transplant ... what is the contraindication
27. neural precursors migrate into which gut organ
 
holy **** haha. gimme a bit i will get back to you though.

actually i just read 1. isotonic so there's no redistribution between the body compartments. IV = directly into ECF, isotonic so there's no equilibration of fluid = 2L

2. ST elevation = transmural infart of the endocardium (as opposed to ST depressions = subendo infart)

3. i'm not 100% sure what the question is, what meds was he not responding too? i'm guessing adenocarcinoma of pancreas (MCC) so acinar would be correct. ductal cells wouldn't be an adenocarcinoma, right?

4. was that the cortical atrophy? i think the guy had BPH or some post-renal obstruction-->increased back pressure is transferred up the ureter-->eventually the calyces dilate to the point compression atrophy occurs to the poor little renal cortex = hydronephrosis.

5. t. pallidum -->give away is small vessel occlusion, syphilis has a predilection for the small aa. like vaso vasorum; also rash on palms/soles of feet in a young + presumably sexually active person (genital lesion, which is i guess tertiary syphilis gumma) = syph. the only other things i know causing hand/foot involvement is 1. RMSF (hiking/camping/something outdoors) 2. Cox virus infection (lots of tips there, pretty nondescript). 3. in kids, kawasaki vasculitis can have a desquamating rash, but they'll have other vascular issues, usually asking about increased risk of aneurysm formation in the coronaries.

6. yea i got this one wrong too, i was thinking diaphragmatic (congenital) hernia, but apparently thats wrong. i'm not sure really.

7. scleroderma = excess/inappropriate collagen deposition and vasculitis -->i think of the choices fibroblasts was there, so i chose that. you'd think t cells and crap are involved also but i guess they just wanted fibros

8. sounded like a mature teratoma in the kidney. glandular + chondroid +epi = different germ layers, so i just assumed they were getting at that.

9. it's not up to them to see her carrier state status because it bares no immediate benefit, as in she's not dying/in danger from being a carrier; i think the kaplan stuff suggests just let her choose for herself when she's old enough and can make the decision for herself. tricky/stupid question though

10. it's def the type 2 pneumo. you're saying you picked it and it was wrong?

11. this was a lame question that i spent 5 minutes on at the end of the block. GNR = E. Coli; look for K1 capsule Ag. H.I is a coccobacillus.

12. post. longitudinal lig

13. i don't know/remember what CY stands for?

14. alpha 2 is found on both pre/post. -FB/inhibitory fx

15. yea i got this wrong too. i haven't looked that up yet, i have it in my notes though.

16. i got this wrong and was stumped. i thought space travel would put you in net bone loss?

17. marathoner = NMBE way of saying female athlete with low BF% = depresses the GnRH pulse (at such low BF% assumes you're starving...don't want to have a baby if starving) = decreased LH/FSH decreases E2 = low E2 = low inhibition of osteoclasts-->osteoporosis

18. got this wrong. was that the question about the teacher staring at a screen? i still don't know. the lights/colors make it an aura so maybe its a migraine?

19. fish oil is super rich in omega-3 FA-->diet high in this modifies the FA your body can produce to favor less of the inflammatory ones. what was the question again?

20. i told that punk to stop smoking. well in my head. i got this wrong, and i chose "smoking will cause long term health problems." i think the first choice was an open ended question, like when will it becme a problem. probably that choice.

21. don't really remember the graph, sorry.

22. arnold chiari?

23. HMO = cheapest copays

24. ldopa + carbidopa

25. anti-Ach effects: antihistamines are a biggie-->diphen

26. if he's still smoking/lying, can't transplant because unsure of compliance post-transplant

27. i'm not sure about the question? can you reword it?


i'll go through these in a little those two i just looked at really quickly, hope they help and i'm not saying they're 100% just my logic. i got 22 wrong on it so take it for what it's worth.
 
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Okay here goes:
1. Isotonic saline 2L, how much goes into the extracellular fluid, I thought it was be 1/3 x 2 but 2/3 wasn't a choice ...
2. 31 yo W with retrosternal chest pain in the last two months. ST segment elevation. what epicardial artery event causes this?
3. 35 yo M with epigastric pain not responding to meds, mass in head of pancreas ... acinar carcinoma? I put ductal adenocarcinoma.
4. A left kidney 69 yo M .. gave gross pic, what is the tissue alterations
5. sexually active 18 yo W with rash including palms/soles. weeping plaques on gentilas, dense chronic inflam rich in plasma cells, swelling of endothelial cells occluding small vessels? What organism?
6. newborn with respiratory distress. I thought it was bowels herniating above diaphram.
7. 45 yo W with scleroderma, what inflamm cell releases cytokines that causes the dermological changes?
8. 28 yo W pelvic neoplasm mature glandular and chondroid elements and cyts lined by stratified squamous epithelium, dx?
9. Autistic boy. Parents want 12 yo daughter test to determine carrier state?
10. Infant RDS and it said inadequate secretion. I can even identify pneumocyte type II ...
11. 3 day old new born with meningitis. neutrophils and gram -ve rods? E. coli or H. influenza B
12. Disc herniation pushes on what ligament that compresses on spinal roots
13. 82 yo man unconscious hit by car, gives CY, where is the bleed
14. what noradrenergic receptor is found on both pre/post synaptic
15. The probably of surviving 4+ years after being alive for 2 years
16. 24 yo W shifting towards bone net loss?
17. A 22 yo W marathon runner stress fracture. What is going to have decrease bone density. it isn't PTH excess
18. 17 yo W with headaches and episodes of fading vision?
19. fish oil vs olive oil
20. 13 yo smoker. what would you tell him
21. graph with NE plus drug X
22. bad development of cerebral hemispheres with structure in brain stem is atrophied?
23. 28 yo mother with 3 children, which healthcare plan to use
24. levodopa vs levodopa + drug x
25. 66 yo M with difficult urinating. metoprolol, thiazide, insulin, mg(oh)2, dipherhydramine ... which drug causes that
26. lung transplant ... what is the contraindication
27. neural precursors migrate into which gut organ


I took this offline so no promises

1. what he/she said ^^

2. endothelial dysfunction, aka spasm. Prinzmetal's angina - recurring (said in the question). its not an MI so no enzyme elevation despite ST elevations

3. Gastinoma - it started being CONSTANT (not just w/ meals)

4. its either hydronephrosis due to urethral obstruction or calyx blunting due to chronic pyelonephritis not sure, i'm bad at distinguishing these w/ no associated history - anybody else?

5. Syphilis

6. me too

7. dunno

8. teratoma? dont remember

9. wait till she's older/more mature/can understand more

10. showed RBCs in a capillary. Endothelium around air space. Then 2 cells 1 with inlusions, and one more 'lumpy bumpy' boardered one. The one w/ inclusions = lamellar bodies of surfactant. Lumpy bumpy boarder i guess is an alveolar macrophage.

11. E coli

12. anterior intraspinal or something? I forget

13. dont understand you here

14. a2

15. surviving the 2-3 interval x surviving the 3-4 interval

16. living in space

17. Low E

18. image shows papilledema

19. controlled trial (it randomized 2 treatments and looked at outcome)

20. When will it become a problem? (long term stuff irrelevant to "immortal" teen)

21. I said cocaine. Not sure tho; it blocks re-uptake so it will definitley be permissive; but I dont know if it increase the contraction on its own before NE administration.

22. corticospinal tracts/pyramids? Not sure on this one, i missed it

23. HMO = least choice, but cheapest

24. levodopa + carbidopa (periperal decarboxylase inhibitor)

25. Diphenhydramine, H1 blocker- but anit-muscarinic = reduced bladder emptying.

26. Continued smoking - waste

27. Pancreas is only gut derivative listed
 
Are you saying that the answer isn't space travel? I got this wrong but assumed that the right answer was in fact space travel.

just rechecked - i did NOT put space travel and got it wrong, so if you put space travel and got it right...we have a winner!

im like 99% the kidney question is hydronephrosis. if you google image dilated calyces i think that's the picture you're talking about.
 
just rechecked - i did NOT put space travel and got it wrong, so if you put space travel and got it right...we have a winner!

im like 99% the kidney question is hydronephrosis. if you google image dilated calyces i think that's the picture you're talking about.

It was definitely hydronephrosis...

I did NOT put space travel, I think I put something about non-impact exercise, but I don't remember exactly. But it sounds like the right answer was in fact space travel. Something we should all be aware of for all of our astronaut patients right?
 
thanks a bunch guys! For the scleroderma there wasn't fibroblasts or else I would put that tho... also it was 13. CT there was a CT image of bleed sorry for typo! Sorry where are the neural precursors for the pancreas which cells? Thanks again!
 
I got 22 wrong, but I hadn't studied embryo and holoprosencephaly by that point. Not sure if my reasoning is right, but if it's a fusion of cerebral hemispheres, it might be holoprosencephaly which means that your corticospinal tracts would be funked up with large motor deficits?
 
Pt with hypothyroidism is given thyroxine. What can she develop in the next month? Angina, asthma, exopthlamos, goiter, jaundice

Answer is angina, right? But why not exopthalamos? I thought that hyperthyroidism can cause exopthalamos?
 
Pt with hypothyroidism is given thyroxine. What can she develop in the next month? Angina, asthma, exopthlamos, goiter, jaundice

Answer is angina, right? But why not exopthalamos? I thought that hyperthyroidism can cause exopthalamos?

only graves can cause exophthalmos, just hyperthy causes a kinda wide eyed stare due to overstimulation of the levator palpebrae. the infiltrative ophthalmopathy and dematopathy are both unique to graves. you're correct about the angina.
 
1. Snake venom is a vasoD, unaltered by B-blockade, exacerbated w/ captopril. What does venom induce release of? (adenosine, bradykinin, histamine, PAF, and serotonin)

2. 31 y/o AIDs pt on HAART, given hematopo-GF, gets dyspnea, muscle pain, vomiting, tachyC and hypoT. Which growth factor caused this? (EPO, filgrastim, PDGF, sargramostim, and thrombopoeitin)

3. Study about surgeon Y vs X, found out surgeon Y has a lower 30-day mortality rate than surgeon X, what are you most concerned about? (lock of complexity, lack of cholesterol data, lack of pt follow-up, lack of pt recuperation, unequal sample sizes)

4. Study of brain tumors and cell phones. Odd ratio of 4.3 w/ 95% CI of 0.9-8.2. Assume a 99% CI was computed instead. What describes a 99% CI compared to the 95% CI? (larger, smaller, the same, can't be determined)

5. This one im pretty upset at. What intracellular signal molecule regulates phosphorylation of F-6-P. I put cAMP, was thinking F-2,6-bisP but didn't think that was a intracellular signaler. And in FA p. 98 (2010 ed.) it shows increased cAMP --> increased FBPase2 which will decrease phosphorylation of F-6-P. Someone please explain this one to me 🙂

6. Why are proteins synthed in RER and secreted from eukaryotic cells shorter in length than woudl be predicted by their mRNA? I know im missing something stupid here...

These aren't the only ones i got wrong, just ones i can't figure out. Thx for any help 🙂
 
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1. Snake venom is a vasoD, unaltered by B-blockade, exacerbated w/ captopril. What does venom induce release of? (adenosine, bradykinin, histamine, PAF, and serotonin)

2. 31 y/o AIDs pt on HAART, given hematopo-GF, gets dyspnea, muscle pain, vomiting, tachyC and hypoT. Which growth factor caused this? (EPO, filgrastim, PDGF, sargramostim, and thrombopoeitin)

not sure about this one ... can anyone say for sure

3. Study about surgeon Y vs X, found out surgeon Y has a lower 30-day mortality rate than surgeon X, what are you most concerned about? (lock of complexity, lack of cholesterol data, lack of pt follow-up, lack of pt recuperation, unequal sample sizes)

4. Difference between a CI of 99% and 95%? what was the question

5. This one im pretty upset at. What intracellular signal molecule regulates phosphorylation of F-6-P. I put cAMP, was thinking F-2,6-bisP but didn't think that was a intracellular signaler. And in FA p. 98 (2010 ed.) it shows increased cAMP --> increased FBPase2 which will decrease phosphorylation of F-6-P. Someone please explain this one to me 🙂

6. Why are proteins synthed in RER shorter than mRNA? I know im missing something stupid here... introns/splicing ? What was the question?

These aren't the only ones i got wrong, just ones i can't figure out. Thx for any help 🙂

see above
 
1. Snake venom is a vasoD, unaltered by B-blockade, exacerbated w/ captopril. What does venom induce release of? (adenosine, bradykinin, histamine, PAF, and serotonin)

i can't remember this question, but looking at what you wrote i would say they either wanted bradykinin or histamine. histamine would mediate anything in the acute phase of inflam./HSR (except pain, that's bradykinin).


2. 31 y/o AIDs pt on HAART, given hematopo-GF, gets dyspnea, muscle pain, vomiting, tachyC and hypoT. Which growth factor caused this? (EPO, filgrastim, PDGF, sargramostim, and thrombopoeitin)

i got this wrong too (and have yet to look it up), sorry amigo.


3. Study about surgeon Y vs X, found out surgeon Y has a lower 30-day mortality rate than surgeon X, what are you most concerned about? (lock of complexity, lack of cholesterol data, lack of pt follow-up, lack of pt recuperation, unequal sample sizes)

difference in complexity of cases i believe


4. Difference between a CI of 99% and 95%?

1 standard dev. +/-1SD = 68%; +/-2SD = 95%; +/-3SD = 99% (approximately). they love asking this (or at least the qbanks do)

5. This one im pretty upset at. What intracellular signal molecule regulates phosphorylation of F-6-P. I put cAMP, was thinking F-2,6-bisP but didn't think that was a intracellular signaler. And in FA p. 98 (2010 ed.) it shows increased cAMP --> increased FBPase2 which will decrease phosphorylation of F-6-P. Someone please explain this one to me 🙂

ill try, i'm not 100%, so bare with me:
they're asking phosphorylation of F6P-->F16BP which is further down the path of glycolysis, so you want an action of insulin:

insulin-->dephosphorylates through decreased cAMP and less PKA activity
glucagon-->phosphorylates through increased cAMP and more PKA

insulin increases PFK2-->increases F26BP-->allosteric activation


6. Why are proteins synthed in RER shorter than mRNA? I know im missing something stupid here...

RER = destined to be secreted so they have a secretory sequence that is cleaved prior to leaving the cell, which makes them a little bit shorter than their mRNA

These aren't the only ones i got wrong, just ones i can't figure out. Thx for any help 🙂

i'll try. hope that helps.
 
2 weeks later, a healing incision has a pink, shiny granular appearance. Which of the findings is most likely on tissue examination?
angiogenesis, epitheloid cells, fibrinoid necrosis, granulomatous inflammation, ischemic injury
 
2 weeks later, a healing incision has a pink, shiny granular appearance. Which of the findings is most likely on tissue examination?
angiogenesis, epitheloid cells, fibrinoid necrosis, granulomatous inflammation, ischemic injury

i thought this was weird, usually they ask about granulation tissue or keloid formation from this kind of topic. i put angiogenesis (involved in granulation process) by process of elimination. epitheloid is giant cell formation in chronic inflammation, but it says healing and doesn't give any hint of inflam (red/hot/swollen/painful); fibrinoid nec is seen in vessels, i think mostly during autoimmune vasculitis type disease; granulomatous i just crossed off, no evidence; ischemic i just crossed off, i'm not even sure how an ischemic process would occur as a result of scar formation. that was just my thought process...hope it makes sense.
 
i thought this was weird, usually they ask about granulation tissue or keloid formation from this kind of topic. i put angiogenesis (involved in granulation process) by process of elimination. epitheloid is giant cell formation in chronic inflammation, but it says healing and doesn't give any hint of inflam (red/hot/swollen/painful); fibrinoid nec is seen in vessels, i think mostly during autoimmune vasculitis type disease; granulomatous i just crossed off, no evidence; ischemic i just crossed off, i'm not even sure how an ischemic process would occur as a result of scar formation. that was just my thought process...hope it makes sense.
Thanks again...that helps! That's how I approached it (process of elimination and what makes sense)...I would have been a lot more comfortable with the answer "granulation tissue" but I guess angiogenesis is true too.
 
A 37-year-old woman develops pancytopenia after exposure to a benzene-containing agent. Tissue obtained on a bone marrow biopsy is most likely to show replacement of normal hematopoietic cells by which of the following cells?

A) Adipocytes
B) Lymphocytes
C) Monocytes
D) Osteoblasts
E) Reticuloendothelial cells

Pancytopenia makes you think adipocytes...but benzene causes leukemia (goljan fact). So is there any way the answer could be lymphocytes?
 
A 37-year-old woman develops pancytopenia after exposure to a benzene-containing agent. Tissue obtained on a bone marrow biopsy is most likely to show replacement of normal hematopoietic cells by which of the following cells?

A) Adipocytes
B) Lymphocytes
C) Monocytes
D) Osteoblasts
E) Reticuloendothelial cells

Pancytopenia makes you think adipocytes...but benzene causes leukemia (goljan fact). So is there any way the answer could be lymphocytes?

i think that's over thinking it. if they didn't have pancytopenia then yea definitely. the time frame of aplastic anemia vs a leukemia is different. when i read this i thought it was more emergent, but they really don't specify. still, the pancytopenia pretty much rules out leukemia i think this is the most i've ever posted on sdn in a day. i REALLY don't want to study neuro, ugh.
 
I'm sorry...the disk herniation question (which ligament will it hit?) is still bothering me and no atlas has made it easier for me. What's the answer and why?

Posterior longitudinal ligament. I don't know the pathophysiology behind it (just remembered that it was involved in disc herniation from Anatomy class), but I just wiki'd it, and it says:

It is broader above than below, and thicker in the thoracic than in the cervical and lumbar regions. The ligament is more narrow at the vertebral bodies and wider at the intervertebral disc space which is more pronounced than the anterior longitudinal ligament. This is significant in understanding certain pathological conditions of the spine such as the typical location for a spinal disc herniation.
 
OK thanks! I remember in the kaplan videos the guy said that the herniation is always in the posterolateral direction due to the strength of the posterior longitudinal ligament.

This patient has footdrop, so this herniation is involving the anterior ramus of the spinal nerve? So I chose the anterior longitudinal ligament?
 
Never learned much on anesthetics. Can someone explain the question on Halothane and the effect on alveolar ventilation and PaCO2?
 
only graves can cause exophthalmos, just hyperthy causes a kinda wide eyed stare due to overstimulation of the levator palpebrae. the infiltrative ophthalmopathy and dematopathy are both unique to graves. you're correct about the angina.

Really?

I thought the key to this question was the timeline of progression such that hyperthyroidism itself (regardless if it's autoimmune or due to exogenous T4) can lead to those systemic effects like exopthalamos, goiter, etc. but that those exist only in chronic conditions. I thought the 1 month mentioned in the question stem would only be sufficient time enough to see the acute manifestations of hyperthyroidism (e.g. angina, diarrhea, weight loss, etc.) but that exopthalamos etc. could still develop...

I'm confused. :scared:
 
Really?

I thought the key to this question was the timeline of progression such that hyperthyroidism itself (regardless if it's autoimmune or due to exogenous T4) can lead to those systemic effects like exopthalamos, goiter, etc. but that those exist only in chronic conditions. I thought the 1 month mentioned in the question stem would only be sufficient time enough to see the acute manifestations of hyperthyroidism (e.g. angina, diarrhea, weight loss, etc.) but that exopthalamos etc. could still develop...

I'm confused. :scared:

hyperthyroidism will cause all of those sx mentioned above, but only graves can cause infiltrative exophthalmos and pretibial myxedema. Not 100% on the pathogenesis, but requires the TSI auto-Ab to react with adipocytes and increase glycosaminoglycan deposition. i remember that from robbins and goljan, but don't have the books with me. they love asking questions about this - it's key to differentiate between some random thyrotoxicosis and then true graves dz.
 
2. 31 y/o AIDs pt on HAART, given hematopo-GF, gets dyspnea, muscle pain, vomiting, tachyC and hypoT. Which growth factor caused this? (EPO, filgrastim, PDGF, sargramostim, and thrombopoeitin)
Sargramostim for sure. dunno why

4. Study of brain tumors and cell phones. Odd ratio of 4.3 w/ 95% CI of 0.9-8.2. Assume a 99% CI was computed instead. What describes a 99% CI compared to the 95% CI? (larger, smaller, the same, can't be determined)
more % of CI = larger range.. because a larger range means you are THAT much more confident the true mean lies in those values

5. This one im pretty upset at. What intracellular signal molecule regulates phosphorylation of F-6-P. I put cAMP, was thinking F-2,6-bisP but didn't think that was a intracellular signaler. And in FA p. 98 (2010 ed.) it shows increased cAMP --> increased FBPase2 which will decrease phosphorylation of F-6-P. Someone please explain this one to me 🙂
F26BP upregulates PFK1


These aren't the only ones i got wrong, just ones i can't figure out. Thx for any help 🙂

Just to clarify a few of these.. I took the test today also..
And back on someone's question about Scleroderma, cytokines are released from T lymphocytes so the answer was lymphocytes. Missed that one too and just looked it up
 
Sorry, why is it carbidopa for 24? Why can't it be selegiline?

how did the question go again? im not sure, but i think the specific results of each differs slightly.

selegiline will decrease the dose needed for levodopa and carbidopa will increase bioavailability and decrease side effects.

i dont remember the question, so i dont know exactly what they wanted, but if they wanted decreased side effects that could be why.
 
i don't remember the question, can you give me the jist? i'll give it a shot but just straight up forget this question
It was a graph of Va (on the vertical axis) and Pco2 (on the horizontal axis) and it asked how halothane would affect the normal ventilatory response to CO2 changes. The options were: it would shift to the left, it would shift to the right, or the slope would decrease.

Sorry! That's the best way I can explain it.
 
It was a graph of Va (on the vertical axis) and Pco2 (on the horizontal axis) and it asked how halothane would affect the normal ventilatory response to CO2 changes. The options were: it would shift to the left, it would shift to the right, or the slope would decrease.

Sorry! That's the best way I can explain it.
yup. I can post a screenshot of just the graph. But im not sure if thats against the rules.
 
It was a graph of Va (on the vertical axis) and Pco2 (on the horizontal axis) and it asked how halothane would affect the normal ventilatory response to CO2 changes. The options were: it would shift to the left, it would shift to the right, or the slope would decrease.

Sorry! That's the best way I can explain it.

hmm, i still don't remember, but apparently i got it right so i can't look at it. well, here's my thought process: normally vent rate increases with increasing PaCO2. the halothanes are marked resp. depressants so the CNS isn't as responsive to the changes in PaCO2 = no shift, but decreased slope. Not 100% on this, after thinking about it I don't really know much about inhaled anesthetics besides NO vs -thanes and all those stupid measurement variables, sorry if this was useless haha.
 
hmm, i still don't remember, but apparently i got it right so i can't look at it. well, here's my thought process: normally vent rate increases with increasing PaCO2. the halothanes are marked resp. depressants so the CNS isn't as responsive to the changes in PaCO2 = no shift, but decreased slope. Not 100% on this, after thinking about it I don't really know much about inhaled anesthetics besides NO vs -thanes and all those stupid measurement variables, sorry if this was useless haha.
I agree the correct answer is that it decreases the slope. This will require the graph to answer this question...but one of the choices had a line shifted to the right with a slightly decreased slope while another had a greater decrease in slope without a slight shift.

That really threw me off. And I don't remember what I ended up choosing but I got it right...so I also can't see it. :laugh:
 
hyperthyroidism will cause all of those sx mentioned above, but only graves can cause infiltrative exophthalmos and pretibial myxedema. Not 100% on the pathogenesis, but requires the TSI auto-Ab to react with adipocytes and increase glycosaminoglycan deposition. i remember that from robbins and goljan, but don't have the books with me. they love asking questions about this - it's key to differentiate between some random thyrotoxicosis and then true graves dz.

Thanks!
 
I have a couple questions...

1) acts like the autoinhibitory effects of NE? B1 B2 A1 A2
is it refereeing to reflex bradycardia?

2) patient is anemic – low hematocrit/hemoglobin – increased Reticulocytes - microspherocytes – increased unconjugated bilirubin… what is the cause? Autoimmune hemolytic/HUS/TTP/Hypersplenism
I thought it was Spherocytosis so I put Hypersplenism. I'm thinking autoimmune hemolytic now but not sure why.

any help would be great...thanks!
 
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