Test your might!

[Depakote]

In the same vein as Allo's Name that Pathogen thread, let's get some good review going here. Anything on Step I is fair game.

A 37 year old male presents with a BP of 80/?. PT and PTT are elevated. Fibrinogen and Platelet count are decreased. D-Dimers are present. Peripheral blood smear reveals schistocytes as well as the following pathologic abnormality:

What is this patient's acute illness?
What is this patient's underlying illness?
Is there a specific abnormality associated with the underlying illness?
What must be done to treat this patient's underlying illness as not to aggravate the acute disease?

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[bluntdissector]

The only thing about the B12 deficiency case is that I would expect there to be more severe anemia. i would guess that a hemoglobin of 12 is kinda high to see neurological sequellae but i couldnt find anything online that said the level of anemia where cord degeneration occurs. Anyone know for sure?

Her doctor could have screwed up and given her folate, which can correct the hematological abnormalities caused by B12 deficiency but will obviously not correct the other problems.

 

[SouthernSurgeon]

keep in mind that menigococcus, step pneumo, and h. flu are all much more likely, as are viral causes like HSV. he needs an LP following empiric treatment for meningitis.

USMLE seems big on the amoeba for some reason - if the clue involves anything about a freshwater lake/pond, that's pretty much a giveaway

 

[Sublimelvc]

Apologies if this has been asked already, but on the USMLE Free 150 I can't figure out this basic pharm question. Could some please explain it to me? The part I am having trouble with is defining the Median Effective Dose (Same as ED50 right??? --> then what is the "X" for???) Thanks a bunch.

Four drugs produce the same therapeutic effect
by the same mechanism, but each has a unique
toxicity. When used at a maximally effective
therapeutic dose, the drug with which of the
following sets of characteristics is most likely to
have the highest incidence of toxicity?

Median Effective Dose------------- Effective Dose1/Toxic Dose99
(A) 0.5x --------------------------------- 2.8
(B) 1x ---------------------------------- 2.1
(C) 5x ------------------------------------ 4.0
(D) 33x ----------------------------------- 3.0

 

[Richspiders07]

... maybe because the effective and toxic dose are so close together in value... so theres not much wiggle room between.

 

[bluntdissector]

Isnt simply the smallest second value, since that implies the largest toxic dose relative to the effective dose, hence the greatest theraputic window and hence the lowest risk?

 

[FutureInternist]

These are more like pimping Qs rather than the long vignettes that people have posted, but hope these help.

1. Kid has apical displacement of tricuspid valve w/ increased R ventricular vol.
a) Name of Dz
b) Cause

2. Kid is practicing for a swim meet when he loses consciousness. EKG in ER reveals that he has an elongated QT interval.

a) What are the 2 possibilities for what this kid has?
b) What is the inheritance pattern for each?
c) What is the cause of death in each?
d) What question could you ask parents to determine which of the 2 he has?

3. A patient w/ PMH of hyperchol, DM & gout was recently started on niacin. What changes need to be made to his DM & gout drugs?

4. What is the one kids' disease where giving aspirin is recommended? What is the most worrisome sequela of this dz?

5. What are the 4 things that every comatose patient in the ER gets? Is there a sequence to these things & if so, why?

 

[Slide]

These are more like pimping Qs rather than the long vignettes that people have posted, but hope these help.

1. Kid has apical displacement of tricuspid valve w/ increased R ventricular vol.
a) Name of Dz
b) Cause

4. What is the one kids' disease where giving aspirin is recommended? What is the most worrisome sequela of this dz?

1) Ebstein's anomaly, lithium usage in mother during preggers or WPW

4) Kawasaki's Dz (if the kid doesn't have influenza), MI in children or some other event relating to coronary arteries like aneurysms.

For #2 the only thing that comes to my mind is Hypertrophic cardiomyopathy, Auto Dominant, defect in beta-mysosin gene. The other one could possibly be dilated cardiomyopathy or some rare congenital QT syndrome disease that I only have heard about by chance. Have no clue for/don't wanna think for #3 and #5 right now, but I kinda have a hunch for #5 (glucose, naloxone, thiamine, don't know the other one).

 

[FutureInternist]

1) Ebstein's anomaly, lithium usage in mother during preggers or WPW (although I did not you could use Li for WPW)

4) Kawasaki's Dz (if the kid doesn't have influenza), MI in children or some other event relating to coronary arteries like aneurysms.

For #2 the only thing that comes to my mind is Hypertrophic cardiomyopathy, Auto Dominant, defect in beta-mysosin gene. The other one could possibly be dilated cardiomyopathy or some rare congenital QT syndrome disease that I only have heard about by chance. Have no clue for/don't wanna think for #3 and #5 right now, but I kinda have a hunch for #5 (glucose, naloxone, thiamine, don't know the other one).

For # 2 I guess HOCM is a viable option but remember that the presenting sign for this is "death". . You are on the right track w/ "rare congenital QT syndrome", anyone else?

For # 5 - O2 is the 4th thing. Any thoughts about the order in which 2 of these must be given?

 

[arroser]

For # 5 - O2 is the 4th thing. Any thoughts about the order in which 2 of these must be given?

I'd give the thiamine before the glucose to avoid thiamine deficiency brought on by the rush of glucose through TCA. Always nice to be able to use that fuel...

I'd also give the naloxone before the O2 in case the patient is in respiratory distress due to narcotic-induced reduced respiratory drive and lack of O2 is the only thing driving respiration.

 

[FutureInternist]

I'd give the thiamine before the glucose to avoid thiamine deficiency brought on by the rush of glucose through TCA. Always nice to be able to use that fuel...

I'd also give the naloxone before the O2 in case the patient is in respiratory distress due to narcotic-induced reduced respiratory drive and lack of O2 is the only thing driving respiration.

Yet again something that I had not remembered...although I definitely remember learning it at some point. Thanks for the refresher.

 

[Sublimelvc]

Isnt simply the smallest second value, since that implies the largest toxic dose relative to the effective dose, hence the greatest theraputic window and hence the lowest risk?

I would agree with you, except they are asking for the highest incidence of toxicity....

As such, I am confused.

 

[Natatiap]

Finding the apical impulse on the opposite side of what is considered normal (dextrorotation?), in addition to the possibility of male factor infertility (perhaps congenital bilateral absence of the vas deferens) and recurrent respiratory infections, brings to mind mucoviscidosis. I wonder if the patient has a mutation in the Cystic Fibrosis Transmembrane Conductance Regulator gene. Mutations in exon 509 are most common in CF, but this patient may have a milder mutation, resulting in less severe disease than full blown CF.

Great questions. Karatenger with situs inversus. Cilia dyskinesia disorder or something like that haha.

 

[bluntdissector]

I would agree with you, except they are asking for the highest incidence of toxicity....

As such, I am confused.

Sorry, I didn't read properly!

I think that if you look at the range of dosages you can plot them like:

ED1......ED50......ED99 and LD1......LD50......LD99

The degree of overlap will obv determine the TI and the safety....so the closer you push ED1 and LD99 to one another, the more the overlap, the less safe (and hence more toxic) the drug becomes, and the lower the ED1/LD99 ratio will be...

 

[Sublimelvc]

Thanks dissector, I think I am getting somewhere near wrapping my head around this....

I guess the curveball is the 1 and 99 percentiles. I understand normal TI and how you want the two values to be as far apart as possible when using ED50 and LD50.

 

[bluntdissector]

Thanks dissector, I think I am getting somewhere near wrapping my head around this....

I guess the curveball is the 1 and 99 percentiles. I understand normal TI and how you want the two values to be as far apart as possible when using ED50 and LD50.

Pleasure!

That might also help...see that to get the lowest ED1/TD99, you move the purple to the left, or blue to the right, meaning higher incidence of toxicity at theraputic levels...and thats the answer...

Edit: Uhm sorry, I just realised that the ED1/TD99 ration is >1 in the question, which means ED1>TD99, which doesn't seem to make a lot of sense...So probably just ignore everything I've been going on about, cause I'm not really sure wtf they mean with a ED1/TD99 of more than one...

 

[bluntdissector]

Ah...I found the problem...in your question you have it as ED1/TD99, but it should be TD1/ED99, in which case the answer is quite obvious...


Edit: BTW - those questions seem really easy...obviously the ones in the exam are much harder, right?

 

[Sublimelvc]

Yep, yor're right, it was TD1 over ED99. That makes it easier. This question sucks anyway.
FYI, it is directly from the NBME Free 150, which I have read are a little easier than Step 1. I got an 82% and there is a calculator where you can enter that score and project your Step 1 3-digit score, although I'm sure there are better methods of score prediction. I'm just not too keen on shelling out $45 bucks a test for the NBME's when my school already gave us the CBSSE and this Free 150 in addition to all the work I am doing on USMLEworld. Anyway....thanks again.

 

[bluntdissector]

Yep, yor're right, it was TD1 over ED99. That makes it easier. This question sucks anyway.
FYI, it is directly from the NBME Free 150, which I have read are a little easier than Step 1. I got an 82% and there is a calculator where you can enter that score and project your Step 1 3-digit score, although I'm sure there are better methods of score prediction. I'm just not too keen on shelling out $45 bucks a test for the NBME's when my school already gave us the CBSSE and this Free 150 in addition to all the work I am doing on USMLEworld. Anyway....thanks again.

It's all good...sorry, I wasn't suggesting that this particular question was necessarily all that easy, but some of the other ones in that free 150 pack seemed very simple (I just grabbed the 2007 pdf). If I were you I'd still do World and the NBME's though. I assume you were gonna do World anyway? I am under the impression that the NBME's and CBSSE's taken together are fairly accurate at predicting your score...just a thought! Good luck

 

[SomeDoc]

Alright, getting the thread back on track. May I suggest that with each vignette posted, that questions be kept to board relevance (sans non-standardized red-herring findings), and questions be kept at a reasonable number to maximize yield and to facilitate the flow of new concepts.


A 16 year old male is brought into the clinic, with complaints of joint stiffness. Initial impression reveals that the child has coarse facial features. An aspiration of synovial fluid of the right knee was carried out, and revealed high levels of free hexoseaminidase, galactosidase, aryl sulfatase, and sphingomyelinase. What cellular process is deficient in the patient, and what is the disease?

 

[bluntdissector]

coarse facial features...sphingomyelinase

When I see that I think Hurler's Sd...can't remember what exactly would be rhe cellular process! If it is Hurler's - I had no idea they can get that old! For some reason I thought these kids will die by like 8y...

 

[SomeDoc]

When I see that I think Hurler's Sd...can't remember what exactly would be rhe cellular process! If it is Hurler's - I had no idea they can get that old! For some reason I thought these kids will die by like 8y...

Good correlation. Hurlers= "gargoylism" (buzzword). However, hurlers is due to a deficiency/dysfunction of a-L-iduronidase.

Can you think about what is unique about the grouping of enzymes identified (a-L-iduronidase can be included as well) and the location in which they are seen?

 

[DonkeyD]

Can you think about what is unique about the grouping of enzymes identified (a-L-iduronidase can be included as well) and the location in which they are seen?

M1 here so this might be wayyyy off base, but aren't those all lysosomal enzymes? I seem to remember some disease where you don't put the right sugar somewhere in the Golgi and enzymes destined for lysosomes are secreted instead...mannose-6-phosphate maybe?

 

[bluntdissector]

Good correlation. Hurlers= "gargoylism" (buzzword). However, hurlers is due to a deficiency/dysfunction of a-L-iduronidase.

Can you think about what is unique about the grouping of enzymes identified (a-L-iduronidase can be included as well) and the location in which they are seen?

Argh...that much is true...no gargoyles then! Was such a reflex!

I just know they are all enzymes involved in lysosomal function...the fact that they are all high in the aspiration...hmmm... Maybe they are being shipped off to the extracellular space instead of being kept in the cell...now what is that called again? (This sounds like a cute joke but I really can't remember...or the process...damn...sorry )

Edit - Too late I see...damn...lol

or

 

[Slide]

A 16 year old male is brought into the clinic, with complaints of joint stiffness. Initial impression reveals that the child has coarse facial features. An aspiration of synovial fluid of the right knee was carried out, and revealed high levels of free hexoseaminidase, galactosidase, aryl sulfatase, and sphingomyelinase. What cellular process is deficient in the patient, and what is the disease?

This sounds like a lysosomal disease where a certain part of a protein chain isn't being modified by the golgi apparatus to get to its appropriate compartment, namely the lysosome. I was going to say I-cell disease, but the fact that the patient is 16 and still alive kinda crosses that out, so I'm gonna go on a hunch on mucolipidosis type IV, assuming there's no cherry red macula.

 

[SomeDoc]

I just know they are all enzymes involved in lysosomal function...the fact that they are all high in the aspiration...hmmm... Maybe they are being shipped off to the extracellular space instead of being kept in the cell...now what is that called again? (This sounds like a cute joke but I really can't remember...or the process...damn...sorry )

Edit - Too late I see...damn...lol

or

This sounds like a lysosomal disease where a certain part of a protein chain isn't being modified by the golgi apparatus to get to its appropriate compartment, namely the lysosome. I was going to say I-cell disease, but the fact that the patient is 16 and still alive kinda crosses that out, so I'm gonna go on a hunch on mucolipidosis type IV, assuming there's no cherry red macula.

You got it.

The cellular process deficient in this patient is mannose-6-phosphate tagging of proteins by the golgi apparatus- proteins which would normally be destined for the lysosome. As a consequence, these proteins (and enzymes) which lack this tag are secreted from the cell, as was seen freely floating in synovium in the patient.

 

[bluntdissector]

A very lame one, just to take a breather! Not board style, but at least it's kinda funny...

So it's November 1879, and the Einstein family has brought their baby boy, Albert, to you for evaluation. They think he is mentally ******ed, since he's not doing what other kids of his age are - for example, he cannot sit or roll over! Being in a rush, and somewhat inexperienced, you jump straight to a fundoscopic exam and viola - a cherry red spot.

What's the Dx?
What is the basic defect? (shortage, excess, malfunction, whatever)
What's the mechanism underlying the cherry red spot?
How does this mechanism differ from the one causing a cherry red spot in, say, a 48year old obese diabetic woman?

The parents ask you whether there eldest child, the birth of which they have hidden from all the historians, could have the same disease, as the first time they took him out on a summer day he developed a severe facial rash. Furthermore he is just too short to be seen with them in public, so they hide him in the basement.
Is this caused by the same disease? If not, what does the eldest son have?
What is the defect?

 

[FutureInternist]

A very lame one, just to take a breather! Not board style, but at least it's kinda funny...

So it's November 1879, and the Einstein family has brought their baby boy, Albert, to you for evaluation. They think he is mentally ******ed, since he's not doing what other kids of his age are - for example, he cannot sit or roll over! Being in a rush, and somewhat inexperienced, you jump straight to a fundoscopic exam and viola - a cherry red spot.

What's the Dx?
What is the basic defect? (shortage, excess, malfunction, whatever)
What's the mechanism underlying the cherry red spot?
How does this mechanism differ from the one causing a cherry red spot in, say, a 48year old obese diabetic woman?

The parents ask you whether there eldest child, the birth of which they have hidden from all the historians, could have the same disease, as the first time they took him out on a summer day he developed a severe facial rash. Furthermore he is just too short to be seen with them in public, so they hide him in the basement.
Is this caused by the same disease? If not, what does the eldest son have?
What is the defect?

Ok..so he's Jewish & has a LSD w/ a cherry red spot. That is b/w Niemann-Pick & Tay-Sach's....I think both are found in high freq in Jews although TS may be higher. Also w/ NP you have what UW called "loss of previously acquired milestones" so he would have been doing fine & then regressed vs TS that's just plain developmental delays.
Defect is lack of hexoaminidase
Underlying cherry red spot d/t ??? deposition of the accumulated product ???
DMers can get cherry red spots d/t central retinal aretry occlusion.

Pretty sure this is wrong but unlike the SATs no point staken away for a wrong answer
The older could have xeroderma pigmentosum although I do not think it does anything to height. This is a DNA repair defect in which your body cannot fic the Thymidine dimers made d/t exposure to UV light.

 

[bluntdissector]

Ok..so he's Jewish & has a LSD w/ a cherry red spot. That is b/w Niemann-Pick & Tay-Sach's....I think both are found in high freq in Jews although TS may be higher. Also w/ NP you have what UW called "loss of previously acquired milestones" so he would have been doing fine & then regressed vs TS that's just plain developmental delays.
Defect is lack of hexoaminidase
Underlying cherry red spot d/t ??? deposition of the accumulated product ???
DMers can get cherry red spots d/t central retinal aretry occlusion.

Yup...kinda left the first one open...They have higher carrier rate for TS tho...
Red spot - the neurons swell and appear white, but the fovea will obv stay red...this is similar to CRAO, where there will also be swelling, but in addition the underlying tissue will be white a.r.o. no blood/infarcted, except the fovea has choriocapillaries nourishing it... (Strange question, I say)

Pretty sure this is wrong but unlike the SATs no point staken away for a wrong answer

The older could have xeroderma pigmentosum although I do not think it does anything to height. This is a DNA repair defect in which your body cannot fic the Thymidine dimers made d/t exposure to UV light.

Ah...try and get something that DOES explain the height...remember he's jewish...ASHKENAZI jewish...

 

[SomeDoc]

A 6-year-old caucasian female is brought to the clinic by a concerned mother who states that her child isn't growing at the normal rate for children her age, and that the child is starting to develop breasts prematurely. Physical examination of the child reveals short stature, cafe-au-lait spots characterized by irregular borders (see inset), and the onset of precocious puberty. What is the probability of the child passing this condition on to offspring, and what is the diagnosis?

 

[MD-iwish]

Does the oldest child have Achondroplasia (AD)?

 

[bluntdissector]

Obviously, I think most people see cafe-au-lait spots and normally scream NF, but the size, distribution and morphology, not to mention the rest of the Hx, doesn't fit. We actually had a pt in hospital the other day with NF, and we obviously had to go study the list of diseases associated with cafe-au-lait spots, two of which are ones everyone should now. It would be kind of cheating if I answered this, someone else can get the Dx...

Two things:
1) Nice case (Most of your cases are)
2) The Dx in my comic-relief case is Bloom Sd, which can also present with cafe-au-lait spots.

 

[Miss155]

McCune albright.
It does not have mendelian inheritance so no risk to future children.

 

[SomeDoc]

McCune albright.
It does not have mendelian inheritance so no risk to future children.

 

[Twohundred73]

Yet again something that I had not remembered...although I definitely remember learning it at some point. Thanks for the refresher.

I think goljan said it in one of his mp3s. Know them well.


Patient suffers from acute appendicitis and ascites but no hepatomegaly. How is the spleen and why?

 

[Depakote]

I think goljan said it in one of his mp3s. Know them well.


Patient suffers from acute appendicitis and ascites but no hepatomegaly. How is the spleen and why?

Splenomegally.

Appendicitis due to EBV infection. The hyperplasia of the germinal centers constrict the lumen and predisposes to abcess. Most common mode of appendicitis in children v. fecolith in adults.

 

[Twohundred73]

Splenomegally.

Appendicitis due to EBV infection. The hyperplasia of the germinal centers constrict the lumen and predisposes to abcess. Most common mode of appendicitis in children v. fecolith in adults.

Interesting theory and not impossible!

My own answer would be the appendicitis causing portal vein thrombosis, through pylephlebitis, causing ascites and splenomegaly without causing hepatomegaly.

 

[Depakote]

Interesting theory and not impossible!

My own answer would be the appendicitis causing portal vein thrombosis, through pylephlebitis, causing ascites and splenomegaly without causing hepatomegaly.

Ah, I skipped over the ascites first time through... the EBV mechanism doesn't produce that to my knowledge.

 

[ENThopeful]

Ah, I skipped over the ascites first time through... the EBV mechanism doesn't produce that to my knowledge.

out of curiosity Depakote, how are you doing on your Q bank questions? with such a huge knowledge base, you seem like you would destroy them

 

[Depakote]

out of curiosity Depakote, how are you doing on your Q bank questions? with such a huge knowledge base, you seem like you would destroy them

Glad to hear that I at least seem smart...

I'm currently using a Kaplan free trial. I do well with the newer questions, not as well with the older ones. I've got a paid UWorld subscription waiting in the wings for when I get to my last month or two of study. I'll consider that the better indicator.


Sadly, my knowledge base is really skewed towards Path (Lil bit of Micro thrown in). Get into the other major test content and I'm concerned I'll take some big hits... currently trying to reinforce those areas.

 

[SomeDoc]

A 20 year old female presents to the academic medical center outpatient clinic with generalized abdominal discomfort. She states that she has noted changes in her skin around her lips, genitals, and palmar areas develop insidiously. She is unaware for how long she has had these epidermal symptoms. Physical examination reveals the following, which was also present on the epidermis of the genital and palmar surfaces:

She is referred to gastroenterology, whereby CEA and guiac tests, and a colonoscopy are performed. Colonoscopy reveals a significant proliferation of polyps in the sigmoid, ascending, and transverse colon. CEA and guiac tests are negative. What is the diagnosis?

 

[YanCanCook]

Peutz-Jegher

 

[SomeDoc]

Peutz-Jegher

 

[ENThopeful]

Peutz-Jegher

i think goljan specifically states its in the small bowel (the polyps)

 

[ENThopeful]

Glad to hear that I at least seem smart...

I'm currently using a Kaplan free trial. I do well with the newer questions, not as well with the older ones. I've got a paid UWorld subscription waiting in the wings for when I get to my last month or two of study. I'll consider that the better indicator.


Sadly, my knowledge base is really skewed towards Path (Lil bit of Micro thrown in). Get into the other major test content and I'm concerned I'll take some big hits... currently trying to reinforce those areas.

Im rooting for you!

 

[neil100]

Here's one from a student who will be starting med school this coming fall. They might be easy though.

What is the reason for prescribing Spirinolactone AND ACE inhibitor to a patient with congestive heart failure?

A patient comes into the clinic with explosive diarrhea. He says that he went to a church congregation and ate food that was recooked several hours after it was initially prepared? What is the MAIN cause of his complaint? Be specific. What MHC type receptors are responsible for mediating the massive release of inflammatory cytokines in this patient. (Think of one of the hallmarks of this bug).


Lastly, IS the Residual volume in patients with obstructive lung dz. higher or lower? And, Why does it need to be kept at that level? (higher or lower)

 

[SomeDoc]

Here's one from a student who will be starting med school this coming fall. They might be easy though.

What is the reason for prescribing Spirinolactone AND ACE inhibitor to a patient with congestive heart failure?

A patient comes into the clinic with explosive diarrhea. He says that he went to a church congregation and ate food that was recooked several hours after it was initially prepared? What is the MAIN cause of his complaint? Be specific. What MHC type receptors are responsible for mediating the massive release of inflammatory cytokines in this patient. (Think of one of the hallmarks of this bug).


Lastly, IS the Residual volume in patients with obstructive lung dz. higher or lower? And, Why does it need to be kept at that level? (higher or lower)

ACE inhibitors lead to low levels of Angiotensin II, which normally activates the renin angiotensin aldosterone system. Hypoaldosteronism leads to hyperkalemia, and spironolactone is a K+ sparing diuretic. Hyperkalemia leads to decreased inotropy in cardiac muscle, so my guess is that the concurrent use of these drugs would be contraindicated in CHF.

While not a cause of explosive diarrhea (TSST of s. aureus [an agent of food poisoning in some cases], since this is a question on MHC, as opposed to a direct effect of exotoxin), fixes MHC II and TCR,CD4 of T Helper cells. This leads to massive continued release of IL1(main agent of inflammation), and IL2 (polyclonal CD8 proliferation and activation), and subsequent toxic shock syndrome.

Obstructive residual volume=increased. This is so that alveoli are prevented from collapsing at lower volumes.

 

[neil100]

ACE inhibitors lead to low levels of Angiotensin II, which normally activates the renin angiotensin aldosterone system. Hypoaldosteronism leads to hyperkalemia, and spironolactone is a K+ sparing diuretic. Hyperkalemia leads to decreased inotropy in cardiac muscle, so my guess is that the concurrent use of these drugs would be contraindicated in CHF, not to mention the possibility of arrythmias.

While not a cause of explosive diarrhea (TSST of s. aureus [an agent of food poisoning in some cases], since this is a question on MHC, as opposed to a direct effect of exotoxin), fixes MHC I and TCR,CD4 of T Helper cells. This leads to massive release of IL1(main agent of inflammation), and IL2 (polyclonal CD8 proliferation and activation), and subsequent toxic shock syndrome.

Obstructive residual volume=increased. This is so that alveoli are prevented from collapsing at lower volumes.

1) I was thinking like this. Spirinolactone is an antiandrogen and antialdosterone. So, it would decrease aldosterone. This would increase renin since aldosterone has a negative feedback on renin (and there would be less kidney perfusion, which would cause kidneys to secrete renin). Then of course blocking the AgI to Ag II step with ACE inhibitor in the RAAS (Renin -> Angiotensin -> Ag I -> AgII -> Aldosterone) would lead to decrease in AgII (which is vasoconstrictive and wouldn't want that in someone with CHF). This made sense to me logically. so basically blocking aldosterone's effects and blocking activation of the RAAS.

2) Yeah... I was trying too hard to tie in the concept of superantigens with that question though. Basically, the exotoxins of staph aureus causing gastroenteritis. So the person becomes intoxicated. (heat and acid-labile exotoxins) And, I think the superantigens of staph mediate their effect through beta chains in TCR and type II MHC receptors stimulating T cell activation.

3) Right on the money with my thinking.

Edit: Btw, that I cell disease question was pretty good man. I got it right but it was tricky.

 

[SomeDoc]

A 20 year old Caucasian female is brought in to the medical center by her significant other, with a chief complaint of high fever, and problems swallowing. Physical examination reveals an intact gag reflex, and a posterior pharyx characterized by the following:

What is the ultimate source of this pathogens ability to cause the pathology depicted? What microorganism produces pathology different from that depicted in the inset via the same mechanism of the current offending pathogen?

 

[Depakote]

A 20 year old Caucasian female is brought in to the medical center by her significant other, with a chief complaint of high fever, and problems swallowing. Physical examination reveals an intact gag reflex, and a posterior pharyx characterized by the following:

What is the ultimate source of this pathogens ability to cause the pathology depicted? What microorganism produces pathology different from that depicted in the inset via the same mechanism of the current offending pathogen?

That appears to be a pseudomembrane, which would be caused by diptheria. The fact that this is occuring in a 20yo suggests that she has waning immunity from her original TDaP vaccination and didn't get an appropriate booster. The diptheria toxin blocks Elongation Factor-2, much like clostridium difficile toxin (which also causes pseudomembrane formation).

 

[Depakote]

I'm making the numbers in the following question up, go with it...


Prostate Specific Antigen is being re-evaluated as a marker for Prostate cancer. It is proposed that a level of 50 indicates the presence of prostate cancer.

The following data are obtained:

____________ Biopsy Proven Prostate Cancer _____|___Biopsy Negative for Prostate Cancer
PSA above 50_________100_____________________|________25
PSA below 50__________20_____________________|________90


What is the Sensitivity of the PSA for the data collected?
What is the Specificity of the PSA for the data collected?
What is the Positive Predictive Value for the data collected?
What is the Negative Predictive Value for the data collected?

(p. 61 of the 2009 First Aid if you need the equations)