NBME 12 discussion

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titan25

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1 v max 1 enzyme is 300 and 2 nd 30 compare the Km values

km1 is 10 times km 2
km1 is 1/10 km2
we cant compare


2 upregulation of which protects from ARDS is IL 10

3 which anti hypertensive restores back potassium other k sparing

4 a 14 years old brougt to physian because mostly sleeping withdrawn and complaining of abdomen pain 3 weeks , what history will u take first...should we recretion drug history....options school history , devlopmental, family history

5 a drug given in two patients obese and normal given same doses graph ploted with conc on y axis and time on x , slope of normal person is greater
compared to normal person drug x in obese has

greater VD/ lower bioavailability / higher clearance/ shorter absorption

6 pedigree given four genrations AD 1st genration gene seq 4 5 6 changes to 156 cause...is it recombination

7 cytoplasmic enzyme mutated at 127 alanine replaced by serine why reduction of enzyme activity
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Thanks, i dont know why I thought the mode was the "highest" number, instead of the most frequent one, so i marked one of the choices that included "decreases mode".
 
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in section 1, the 3 year old boy with sunburns...I've seen the answer posted as formation of thymidine dimers, but alternatively, double strand breaks are a sign of ataxia telangiectasia...

EDIT: nevermind, i'm an idiot. no ataxia present.
Xeroderma after all
 
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fleshwound said:
in section 1, the 3 year old boy with sunburns...I've seen the answer posted as formation of thymidine dimers, but alternatively, double strand breaks are a sign of ataxia telangiectasia...

EDIT: nevermind, i'm an idiot. no ataxia present.
Xeroderma after all
Click to expand...

lol. Yep.
 
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Hey folks, I just took my first NBME (12). I have a little over 3 weeks left before test day. I got a 203 and I am shooting for somewhere between 230 and 245. Am I in trouble?
 
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You might have just enough time to boost your score over there. Have you done DIT already? I would suggest that
 
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medpack87 said:
You might have just enough time to boost your score over there. Have you done DIT already? I would suggest that
Click to expand...
I haven't but I was thinking of watching the videos on my third exposure to FA. Currently halfway through my 2nd exposure. I know they say DIT takes about 30 days so I might need to cut stuff out -- what're the "higher yield" sections? Or should I really try to do the entire thing?
 
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dewgong said:
I haven't but I was thinking of watching the videos on my third exposure to FA. Currently halfway through my 2nd exposure. I know they say DIT takes about 30 days so I might need to cut stuff out -- what're the "higher yield" sections? Or should I really try to do the entire thing?
Click to expand...

You can do DIT in less than 30 days if you need to. But do not skip anything, everything discussed there is high yield or at least "fair game" as they say. Basically they will read and explain through FA and select high yield from there, so its already cropped out for you.
 
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Regarding the question with a kid presenting with respiratory distress and wheezing, where the answer is asthma... Why cant it be bronchitis? especially since he has a URI and acute bronchitis also causes obstruction leading to wheezes right?

Thanks in advance.
 
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soccerboy2288 said:
Regarding the question with a kid presenting with respiratory distress and wheezing, where the answer is asthma... Why cant it be bronchitis? especially since he has a URI and acute bronchitis also causes obstruction leading to wheezes right?

Thanks in advance.
Click to expand...

This was the question that I could not find an answer to, but I think I finally found it via a response from Phloston on the UW forums.

Definitely not atelectasis. Do you not see in the question that the wheezing is bilateral? Atelectasis is unilateral.

Pneumonia is out because fremitus would be increased.

Heart failure is out because the kid is too young and the Sx are too acute.

Bronchitis is out because that's more chronic, not something induced after a 2-day URI. And even if it was induced by the URI, you'd be expecting an RSV bronchiolitis, not bronchitis.

Asthma is right because the kid is afebrile, the wheezing is bilateral, fremitus is decreased (indicating air trapping) and he's in SNS overdrive with the increased HR/RR, which occurs with asthma. It's possible that the mother gave him aspirin for the URI, thereby causing his asthma.
Click to expand...
This is definitely the right answer. I picked atelectasis because I didn't pay attention to the bilateral wheezing thing.
 
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What was the answer for the 48 year old woman with 2 week history of lower left quadrant colicky abdominal pain, with leukocytosis, anemia, and fever?
I didnt get feedback, so I dont know if I got it wrong. I was thinking its diverticulosis, so I chose initiate high fiber diet. Any idea if that was correct?
 
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addo said:
What was the answer for the 48 year old woman with 2 week history of lower left quadrant colicky abdominal pain, with leukocytosis, anemia, and fever?
I didnt get feedback, so I dont know if I got it wrong. I was thinking its diverticulosis, so I chose initiate high fiber diet. Any idea if that was correct?
Click to expand...

That is correct.
 
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startswithb said:
That is correct.
Click to expand...

Thanks...
What about the guy who has premature ejaculation? People on this thread were saying take SSRI, but I disagree, I think it is trazodone. Actually answer choice didnt broadly say SSRI, i think it said sertraline or paroxetine or something like that.
 
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addo said:
Thanks...
What about the guy who has premature ejaculation? People on this thread were saying take SSRI, but I disagree, I think it is trazodone. Actually answer choice didnt broadly say SSRI, i think it said sertraline or paroxetine or something like that.
Click to expand...

It was paroxetine. It didn't show up on my extended feedback. I swear I saw something about SSRIs and premature ejaculation in FA, but I can't find it now.
 
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coolforschool said:
It was paroxetine. It didn't show up on my extended feedback. I swear I saw something about SSRIs and premature ejaculation in FA, but I can't find it now.
Click to expand...

oh ok... well i believe you. I googled trazodone for premature ejaculation and theres a lot of sources that say it does the trick as well. I went with it during the test because its the one that can cause priapism....lol I if I had premie ejaculation, which I of course dont, I guess I wouldnt want priapism to be the cure though... lol
 
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coolforschool said:
It was paroxetine. It didn't show up on my extended feedback. I swear I saw something about SSRIs and premature ejaculation in FA, but I can't find it now.
Click to expand...

The reason why you use SSRI's for premature ejaculation is because one of its most common adverse effects is sexual dysfunction. So normal patients on SSRI's would have low compliance because they are not going to ejaculate, they are not going to enjoy sex.

On the other hand, you have premature ejaculators, you give them SSRI's, and they can last longer because they are not going to be "over stimulated" during sex.

Giving them trazadone would cause them priapism.
 
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Can you guys help me with these questions, please?

27. Girl basically has DKA. Her bp is 92/48, fruity odor to her breath, and poor skin turgor. Question asks which of the following is most likely to be decreased?

a. PaCO2
b. PaO2 -> chose this
c. serum aceton
d. serum potassium
e. serum triglycerides
f. serum urea

31. question about influenza virus, asking about genetic alterations...
a. point mutations involving genes encoding either HA --> chose this
b. PM with matrix protein
c. PM with ribonucleoprotein
d. reassortment involving genes encoding HA
e. " " " " matrix protein
f. " " " " ribonucleoprotein

3. patient with chronic peripheral neuropathy..staining shows fiber grouping. explanation?
a. altered expression of muscle enzymes due to damaged nerve fibers?
b. altered tropic substance from innervating neurons
c. regen of muscle fibs
d. reinnervation of muscle fibers by regenerating axons
e. selective loss of nerve fibers to type 2 muscle fibers --> chose this
 
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no idea why i chose this, but for ehrlichiosis...inhibition of protein synthesis, correct?

8. what about comparing the two Km values for enzyme 1 and 2...chose Km for 1st is 10x than Km for enzyme 2, but that was wrong.

Isn't the equation (1/2)Vmax = Km

enzyme 1 = 300
enzyme 2 = 30
 
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Jonari said:
Can you guys help me with these questions, please?

27. Girl basically has DKA. Her bp is 92/48, fruity odor to her breath, and poor skin turgor. Question asks which of the following is most likely to be decreased?

a. PaCO2
b. PaO2 -> chose this
c. serum aceton
d. serum potassium
e. serum triglycerides
f. serum urea

31. question about influenza virus, asking about genetic alterations...
a. point mutations involving genes encoding either HA --> chose this
b. PM with matrix protein
c. PM with ribonucleoprotein
d. reassortment involving genes encoding HA
e. " " " " matrix protein
f. " " " " ribonucleoprotein

3. patient with chronic peripheral neuropathy..staining shows fiber grouping. explanation?
a. altered expression of muscle enzymes due to damaged nerve fibers?
b. altered tropic substance from innervating neurons
c. regen of muscle fibs
d. reinnervation of muscle fibers by regenerating axons
e. selective loss of nerve fibers to type 2 muscle fibers --> chose this
Click to expand...

27 - a - patients with DKA hyperventilate, so PaCO2 will decrease
31 - d - since it's a segmented virus - reassortment can occur
3 - i didn't get that question at all...

someone correct me if I'm wrong...
 
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Jonari said:
Can you guys help me with these questions, please?

27. Girl basically has DKA. Her bp is 92/48, fruity odor to her breath, and poor skin turgor. Question asks which of the following is most likely to be decreased?

a. PaCO2
b. PaO2 -> chose this
c. serum aceton
d. serum potassium
e. serum triglycerides
f. serum urea

31. question about influenza virus, asking about genetic alterations...
a. point mutations involving genes encoding either HA --> chose this
b. PM with matrix protein
c. PM with ribonucleoprotein
d. reassortment involving genes encoding HA
e. " " " " matrix protein
f. " " " " ribonucleoprotein

3. patient with chronic peripheral neuropathy..staining shows fiber grouping. explanation?
a. altered expression of muscle enzymes due to damaged nerve fibers?
b. altered tropic substance from innervating neurons
c. regen of muscle fibs
d. reinnervation of muscle fibers by regenerating axons
e. selective loss of nerve fibers to type 2 muscle fibers --> chose this
Click to expand...

Jonari said:
no idea why i chose this, but for ehrlichiosis...inhibition of protein synthesis, correct?

8. what about comparing the two Km values for enzyme 1 and 2...chose Km for 1st is 10x than Km for enzyme 2, but that was wrong.

Isn't the equation (1/2)Vmax = Km

enzyme 1 = 300
enzyme 2 = 30
Click to expand...

For the girl with DKA, it is decreased PCO2- Metabolic acidosis, so shell be hyperventilating and blowing off a lot of CO2

For influenza question, I answered reassortment of HA. HA is what binds to cells

For chronic peripheral neuropathy, I put reinnervation of muscle fibers.

Tetracycline or doxycycline for ehrlichiosis, so yes protein synthesis.

You cant figure out Km from vmax. Youre right Km=1/2 vmax, but vmax by itself doesnt tell you how fast the rate of rise to 1/2 vmax was. An enzyme can have a really high Vmax but it could take ages to get there and therefore have a high Km (low affinity). Consider hexokinse which has low vmax but high affinity (low km) vs glucokinase which has low affinity (high Km) and high vmax. Affinity or Km is a property that is related to vmax, but it is independent of it.
 
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addo said:
For the girl with DKA, it is decreased PCO2- Metabolic acidosis, so shell be hyperventilating and blowing off a lot of CO2

For influenza question, I answered reassortment of HA. HA is what binds to cells

For chronic peripheral neuropathy, I put reinnervation of muscle fibers.

Tetracycline or doxycycline for ehrlichiosis, so yes protein synthesis.

You cant figure out Km from vmax. Youre right Km=1/2 vmax, but vmax by itself doesnt tell you how fast the rate of rise to 1/2 vmax was. An enzyme can have a really high Vmax but it could take ages to get there and therefore have a high Km (low affinity). Consider hexokinse which has low vmax but high affinity (low km) vs glucokinase which has low affinity (high Km) and high vmax. Affinity or Km is a property that is related to vmax, but it is independent of it.
Click to expand...

F.M.L

i shouldnt have gotten that DKA answer wrong...or the silly mistake about ehrlichiosis...

i keep missing questions pertaining to that concept: PO2, PCO2, A-a gradient, O2 saturation, etc etc...any good suggestions on how to fix this?

did you take 15?
 
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Jamiu22 said:
27 - a - patients with DKA hyperventilate, so PaCO2 will decrease
31 - d - since it's a segmented virus - reassortment can occur
3 - i didn't get that question at all...

someone correct me if I'm wrong...
Click to expand...

thanks! crap...i knew it was segmented...damn it...worse feeling like Goljan says in his audio "you get to 3 quarters of the way to solving it...but it's the last quarter the USMLE wants to know if you can put together"
 
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Jonari said:
F.M.L

i shouldnt have gotten that DKA answer wrong...or the silly mistake about ehrlichiosis...

i keep missing questions pertaining to that concept: PO2, PCO2, A-a gradient, O2 saturation, etc etc...any good suggestions on how to fix this?

did you take 15?
Click to expand...

Yea I took 15, and I agree those relationship questions can be tricky. PCO2 and acid/base balance are like :xf: so you always got to know whats going on in that regard... Keep resp compensations in mind when dealing with metabolic imbalances and vice versa. I dont really got much for the other parameters, except to know exactly what they are measuring and factors that affect them.
 
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Jonari said:
Can you guys help me with these questions, please?


3. patient with chronic peripheral neuropathy..staining shows fiber grouping. explanation?
a. altered expression of muscle enzymes due to damaged nerve fibers?
b. altered tropic substance from innervating neurons
c. regen of muscle fibs
d. reinnervation of muscle fibers by regenerating axons
e. selective loss of nerve fibers to type 2 muscle fibers --> chose this
Click to expand...

It's reinnervation, which is grouped, whereas denervation is usually not grouped.
 
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startswithb said:
It's reinnervation, which is grouped, whereas denervation is usually not grouped.
Click to expand...

do you know where i can find info to read about this...i chose the type II answer because i remember reading about it in FA regarding the fast twitch fibers...but yeah, obviously that was wrong...:oops:
 
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Jonari said:
do you know where i can find info to read about this...i chose the type II answer because i remember reading about it in FA regarding the fast twitch fibers...but yeah, obviously that was wrong...:oops:
Click to expand...

I'm with you on this... I had never heard of this before... or it's just buried too deep within my brain that I can't retrieve it anymore - it's as good as gone.
 
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Jonari said:
do you know where i can find info to read about this...i chose the type II answer because i remember reading about it in FA regarding the fast twitch fibers...but yeah, obviously that was wrong...:oops:
Click to expand...

Jamiu22 said:
I'm with you on this... I had never heard of this before... or it's just buried too deep within my brain that I can't retrieve it anymore - it's as good as gone.
Click to expand...

The only reason I got that question right was because I dug deep into the recesses of my mind from first year and remembered a picture that one of our lecturers showed us. It was something like: when the nerve fibers get damaged, they can often times reinnervate muscles in groups that may change all of the muscles that they innervate into the same fiber type.

This website: http://missinglink.ucsf.edu/lm/ids_104_musclenerve_path/student_musclenerve/musclepath.html explains it pretty well. Skip down to the paragraph above Figure 3 if you wanna get to the meat of the explanations.

The picture that I remembered looked like this: http://neuromuscular.wustl.edu/pathol/grouping.htm. Notice how it goes from checkerboard (different fiber types) to a huge group of the same muscle fiber type.
 
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Jamiu22 said:
I'm with you on this... I had never heard of this before... or it's just buried too deep within my brain that I can't retrieve it anymore - it's as good as gone.
Click to expand...

defense mechanism in use...? :naughty:

coolforschool said:
The only reason I got that question right was because I dug deep into the recesses of my mind from first year and remembered a picture that one of our lecturers showed us. It was something like: when the nerve fibers get damaged, they can often times reinnervate muscles in groups that may change all of the muscles that they innervate into the same fiber type.

This website: http://missinglink.ucsf.edu/lm/ids_104_musclenerve_path/student_musclenerve/musclepath.html explains it pretty well. Skip down to the paragraph above Figure 3 if you wanna get to the meat of the explanations.

The picture that I remembered looked like this: http://neuromuscular.wustl.edu/pathol/grouping.htm. Notice how it goes from checkerboard (different fiber types) to a huge group of the same muscle fiber type.
Click to expand...

interesting...thanks for this!! i have several more questions to ask as well...especially those neuro cross sections...the one at the medulla is one of them. ill come back in a few hours and ask...need to read for a few more hours...
 
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coolforschool said:
The only reason I got that question right was because I dug deep into the recesses of my mind from first year and remembered a picture that one of our lecturers showed us. It was something like: when the nerve fibers get damaged, they can often times reinnervate muscles in groups that may change all of the muscles that they innervate into the same fiber type.

This website: http://missinglink.ucsf.edu/lm/ids_104_musclenerve_path/student_musclenerve/musclepath.html explains it pretty well. Skip down to the paragraph above Figure 3 if you wanna get to the meat of the explanations.

The picture that I remembered looked like this: http://neuromuscular.wustl.edu/pathol/grouping.htm. Notice how it goes from checkerboard (different fiber types) to a huge group of the same muscle fiber type.
Click to expand...

Ooohh.. I remember that now - after seeing the checkerboard pattern, of course transitioning to the grouped one - for the life of me I couldnt remember that! Thanks bro!.
 
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can someone help me out here...

70 year old woman wants to donate 1million$ to b/c her husband dies of sudden cardiac arrest. She wants to see a decrease in this manner of death in 1-2 years

a. create antismoking campaign
b. city wide aerobic exercise
c. put asa in the water supply
d. put AEDs throughout the city
e. provide statins to everyone over 50
f. relaxation and stress management programs for people over 50

I picked a only because i had a uworld question the other day that said decreasing smoking is the best way to reduce mortality from cardiovascular events (Uworld even put an exclamation mark and said, This is very high yield!). Any thoughts?
 
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RIPSanto said:
can someone help me out here...

70 year old woman wants to donate 1million$ to b/c her husband dies of sudden cardiac arrest. She wants to see a decrease in this manner of death in 1-2 years

a. create antismoking campaign
b. city wide aerobic exercise
c. put asa in the water supply
d. put AEDs throughout the city
e. provide statins to everyone over 50
f. relaxation and stress management programs for people over 50

I picked a only because i had a uworld question the other day that said decreasing smoking is the best way to reduce mortality from cardiovascular events (Uworld even put an exclamation mark and said, This is very high yield!). Any thoughts?
Click to expand...

Immediate impact = AEDs. I learned it in BLS class.
 
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Sweet thanks for the help

I feel tricked by UW because it even went into detail regarding how if someone quits smoking, and then has a heart attack, they are already less likely to die from the event. If this comes up on my real deal im gonna be at a crossroads
 
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RIPSanto said:
Sweet thanks for the help

I feel tricked by UW because it even went into detail regarding how if someone quits smoking, and then has a heart attack, they are already less likely to die from the event. If this comes up on my real deal im gonna be at a crossroads
Click to expand...

Sorry I can't explain it further, it's just what I learned. Quitting smoking does have profound impacts (lungs can go back to near normal function if you quit early enough), but you probably won't see it within 1-2 years with just an anti-smoking campaign, especially compared to placing AEDs around the city. Supposedly these things can significantly reduce cardiac-related deaths if you get to the person fast enough.

http://www.ncbi.nlm.nih.gov/pubmed/22007075
 
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Saw a little discussion regarding this question but i dont want to go back through and read everything to see if it was covered.

There is a spinal cord section and a person with what seems to be LMN signs (weakness, atrophy). The reasonable answer choices are an arrow to the lateral corticospinal tract, and two different arrows to the anterior motor horn. I picked the more medial of the two anterior horns but cannot figure out what the correct answer is.
 
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RIPSanto said:
Saw a little discussion regarding this question but i dont want to go back through and read everything to see if it was covered.

There is a spinal cord section and a person with what seems to be LMN signs (weakness, atrophy). The reasonable answer choices are an arrow to the lateral corticospinal tract, and two different arrows to the anterior motor horn. I picked the more medial of the two anterior horns but cannot figure out what the correct answer is.
Click to expand...

It's the more lateral one. The anterior horns are organized somatotopically, so the more medial portion innervates the proximal muscles and the lateral portions innervate the distal muscles. I think the question was asking about intrinsic hand muscles or something like that.

http://en.wikipedia.org/wiki/Alpha_motor_neuron#Spinal_cord
 
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Question...did one of the UWorld practice exams 2 weeks ago, got around 57% correct, and it told me my 3 digit score was 206. Today, I just did NBME 12, got 75% correct, which is a 440/ 207. I was kinda bummed that there was basically no difference in the scores, despite me getting an 18% increase in percentage of correct answers. Are the UWorld tests that much harder than the NBMEs??
 
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ciruelo said:
Question...did one of the UWorld practice exams 2 weeks ago, got around 57% correct, and it told me my 3 digit score was 206. Today, I just did NBME 12, got 75% correct, which is a 440/ 207. I was kinda bummed that there was basically no difference in the scores, despite me getting an 18% increase in percentage of correct answers. Are the UWorld tests that much harder than the NBMEs??
Click to expand...

The UW curves are more generous, but the NBMEs are considered pretty accurate predictors, especially 7, 11, 12, 13, and 15 (the most recent ones).
 
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ciruelo said:
Question...did one of the UWorld practice exams 2 weeks ago, got around 57% correct, and it told me my 3 digit score was 206. Today, I just did NBME 12, got 75% correct, which is a 440/ 207. I was kinda bummed that there was basically no difference in the scores, despite me getting an 18% increase in percentage of correct answers. Are the UWorld tests that much harder than the NBMEs??
Click to expand...
The general consensus is that the Uworld exams over-predict by maybe about 10 points, so you may have actually been closer to 196 or so 2 weeks ago. Looks like you've improved about 10 points in that time. Also, the curve is definitely harsher on the NBMEs when comparing percent to correlated scores, because overall yes, the questions on Uworlds are both harder and more picky (in my own opinion atleast).
 
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thanks, didn't realize there was SUCH a high discrepancy, almost 20% (just one exam comparison, but still). I was happy because it seemed like I had done a lot better % wise, but...guess that doesn't help your overall score out too much after the curve :(
 
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Anyone have a pretty large drop from 11--->12?

This thing was a P.I.T.A. genetics literally rocked me
 
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MLT2MT2DO said:
Anyone have a pretty large drop from 11--->12?

This thing was a P.I.T.A. genetics literally rocked me
Click to expand...

I did 11 (238) about 2.5 weeks ago (after 2 fulls weeks of dedicated study time) , had to stop studying for a week and a half right after that (for graduation stuff w/family) and then started studying again Monday of last week and took 12 yesterday and got a 235.

Wasn't a huge drop but I was hoping to at least be above 240 by now but I guess the combination of not doing anything for 1.5 weeks and it being a generally harder test (from what I've heard) dropped me a little. Funny thing was most of the questions I missed were just straight recall minutia from FA...oh well. Taking UWSA-1 on the 10th so I expect that one to give me a boost of confidence.
 
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Melkor said:
I did 11 (238) about 2.5 weeks ago (after 2 fulls weeks of dedicated study time) , had to stop studying for a week and a half right after that (for graduation stuff w/family) and then started studying again Monday of last week and took 12 yesterday and got a 235.

Wasn't a huge drop but I was hoping to at least be above 240 by now but I guess the combination of not doing anything for 1.5 weeks and it being a generally harder test (from what I've heard) dropped me a little. Funny thing was most of the questions I missed were just straight recall minutia from FA...oh well. Taking UWSA-1 on the 10th so I expect that one to give me a boost of confidence.
Click to expand...

Well don't feel bad, you probably definitely went up. At least if my n=1 is any indication.

4 days ago I had a 242 on 11, today a 231 on 12. It was the perfect storm of me getting my severely weak areas on a test and getting ~90% of the question that I could narrow down to 2 answers incorrect as well.
 
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MLT2MT2DO said:
It was the perfect storm of me getting my severely weak areas on a test and getting ~90% of the question that I could narrow down to 2 answers incorrect as well.
Click to expand...

Yeah, I felt like that same thing happened to me on many of the questions I missed. Went back and saw that of the 27 I missed, I had 16 where it was narrowed down to 2 answers and I chose the wrong ones.
 
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ijn said:
So normally you have type 1 and 2 muscles fibers evenly distributed in a muscle biopsy. Let's say you have a disease like ALS where you have death of peripheral neurons. The body tries to compensate via axonal regeneration. The regenerating axon will then innervate the muscle fibers in a given area of deinnervation. All muscle fibers will assume either type 1 or type 2 depending on what type of muscle the neuron originally innervated. On biopsy you no longer have a checkboard appearance of type 1 and 2 fibers. They'll either be pure type 1 or pure type 2.

The other test question they really like related to this topic are giant motor unit action potentials (MUAPs).
Click to expand...

Could you clarify what you mean by giant motor unit action potentials? I'm not familiar with the topic. And could you also give an example of a question. Thanks in advance!
 
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Can someone also help me with this question:

52 year old with 2 month history of difficulty attaining an erection. Normal libido and no history of erectile dsyfunction. Pysical examination and diagnostic testing show no abnormalities. A drug w/ which mechanism of action is appropriate?
a) action as synthetic version of prostaglandin E diverting blood into the penis
b) blockade of peripheral acetylcholinesterase activity, increasing parasympathetic activity in the penis (I picked this because I thought "point and shoot." He has a hard time pointing so parasympathetics. Wrong answer)
c) increasing concentrations of cGMP, relaxing smooth muscle in the penis (I though viagra is for sustaining only)
d) prevention of peripheral a-adrenergic activity, allowing increased blood flow to the penis
e) transient increase in peripheral concentration of testosterone, allowing for erection

Can anyone explain sustaining vs attaining and the drugs to use? I get we use SSRI for premature ejaculation.
Thanks for any help!
 
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epicccfail said:
Can someone also help me with this question:

52 year old with 2 month history of difficulty attaining an erection. Normal libido and no history of erectile dsyfunction. Pysical examination and diagnostic testing show no abnormalities. A drug w/ which mechanism of action is appropriate?
a) action as synthetic version of prostaglandin E diverting blood into the penis
b) blockade of peripheral acetylcholinesterase activity, increasing parasympathetic activity in the penis (I picked this because I thought "point and shoot." He has a hard time pointing so parasympathetics. Wrong answer)
c) increasing concentrations of cGMP, relaxing smooth muscle in the penis (I though viagra is for sustaining only)
d) prevention of peripheral a-adrenergic activity, allowing increased blood flow to the penis
e) transient increase in peripheral concentration of testosterone, allowing for erection

Can anyone explain sustaining vs attaining and the drugs to use? I get we use SSRI for premature ejaculation.
Thanks for any help!
Click to expand...

Sustaining/attaining viagra for both. Additionally if you chose "B" think of all the other issues you'd have throughout your body.
 
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