The Official StepI "Pimp each other" thread...

[Mike59]

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Hey all,

To keep our brains well tuned for stepI in the upcoming months, who else is up for some quizzing while we're on SDN?

I'll start: (answers to follow)

1. Arthritis is characteristic of what stage of Lyme Disease?

2. Which autosomal trisomy is characterized by polydactyly, microphthalmia, umbilical hernia and cleft lip?

 

[Janders]

34 y/o healthy AAF presents to your clinic with concerns of constipation, hoarse voice, cold intolerance. She also mentions that occasionally she will have dizziness, HA, tremors, and feel woozy. On PE, she is afebrile, BP 114/68, HR 52, RR 16. You notice scant and corase hair. When asked about her periods, she reports excessive bleeding. She also mentions that bother her mother and sister have had similar symptoms and are now controlled with Levothyroxine. You suspect hypothyroidism and check T4 and TSH levels. To your surprise, both come abck normal. Which is the best diagnosis for this patient?

A. Subacute thyoiditis
B. Hashimotos thyroiditis
C. Cretinism
D. Pappilary
E. Inhibition of 5' monodeiodinase

E? 5' monodeiodinase converts t4 to t3. T3 is the active compound. Without it you would present with hypothyroid symptoms, but your tsh and t4 could be normal. A is a hyperthyroid state, so these are the wrong symptoms. B, Hashimotos, usually presents with increased tsh, and pain. C and D I would expect to have different sets of symptoms.

 

[me454555]

Isn't Wolf-Chaikoff effect the inhibition of the organification of iodide? I thought it was totally different from answer choice D but closer to E. That is unless I'm confused about organification of iodide, which is probably the case. Any budding endocrinologists want to help us out?

You're completely right about that. Stupid mistake by me, missed that whole folliculare part and though he was tling about the other one. Thanx for the correction

 

[HiddenTruth]

E? 5' monodeiodinase converts t4 to t3. T3 is the active compound. Without it you would present with hypothyroid symptoms, but your tsh and t4 could be normal. A is a hyperthyroid state, so these are the wrong symptoms. B, Hashimotos, usually presents with increased tsh, and pain. C and D I would expect to have different sets of symptoms.

correct! A big hint in the question is familial disposition. Majority of the circulating thyroid hormone is in the form of T4. At peripheral sites, local action of 5'monodeiodinase convert T4--> active T3. However, keep in mind that in the BLOOD, T4 is the major factor that controls TSH secretion from the ant pit., soinhibition if this enzyme maintains normal T4 and thus, you are likely to see normal feedback to TSH. Also, keep in mind that in the thyrotrophs, it is T3 that controls TSH secretion. So T4 gets taken up into the cells, and gets converted, and thus T3 acts to secrete TSH in the ant pit.

Oh, and sorry, I was trying to write papillary carcinoma (I couldn't think of any other crazy choices)

Stay tuned for more--i gotta go study to come up with baller questions

 

[Long Dong]

Dum question here but what exactly is rocker-bottom feet, since the boards are moving away from buzz words anyway?

 

[HiddenTruth]

Dum question here but what exactly is rocker-bottom feet, since the boards are moving away from buzz words anyway?

Normally the underside of your feet are concave in the middle: the bones of the foot are arranged in such a way that there is an arch-like shape in the mid-part of the foot. In rocker-bottom feet the bones are arranged in a different way and this makes the underside of the foot convex in the middle. Thus, the foot appears to bend in the opposite direction to normal and in so doing, it resembles the shape of the bottom of a rocking chair. Whoever came up with that should get a nobel prize 🙄

 

[Shah_Patel_PT]

Bam! Nice job 🙂

Here's some more, anyone else wanna play? 😉

- describe 2 enzyme abnormailities that contribute to hyperuricemia...
- A suspicious skin lesion is biopsied and sent to pathology. Histology shows "keratin pearls", what's the diagnosis?

Those questions are way too easy for the current step one. Maybe a decade ago the Q were that easy.

 

[Idiopathic]

Those questions are way too easy for the current step one. Maybe a decade ago the Q were that easy.

No, I disagree. Knowing the physiology of uric acid production and the pathophysiology of hyperuricemia is exactly the typr of thing you should be studying. Understanding concepts is the most important thing you can do, and basic ones are just as valuable to know cold.

 

[Long Dong]

Normally the underside of your feet are concave in the middle: the bones of the foot are arranged in such a way that there is an arch-like shape in the mid-part of the foot. In rocker-bottom feet the bones are arranged in a different way and this makes the underside of the foot convex in the middle. Thus, the foot appears to bend in the opposite direction to normal and in so doing, it resembles the shape of the bottom of a rocking chair. Whoever came up with that should get a nobel prize 🙄

Thanks Hidden.

Some more dum questions. What is the difference between RFLP and VNTR? Also the difference from DNA fingerprinting vs DNA footprinting? How many high energy bonds needed to make a 100 amino acid polypeptide from mRNA (I'm thinking 399, 2 atp + 1 gtp for the met, and 2 atp + 2 gtp for each aa after)? Someone correct me on this or confirm the book keeping on this. Omega 3 vs omega 6 which is good and which is bad and why? Thanks in advance.

 

[Janders]

Omega 3 vs omega 6 which is good and which is bad and why? Thanks in advance.

I'll take this one! (personal interest of mine).

Omega 3 is the "good" one. You actually want some of each, but most diets have an adundance of 6 and little 3. The reason why Omega 3's are good for you are multiple. One big one is that certain Omega 3's replace arachidonic acid in the leukotriene cascade, and when they do the end result molecules are less potent (due to that weirdly positioned double bond). This leads to an anti-inflammitory effect! Anyway, they do lots of other cool things. If you want to read more, I think this article has a great overview.

 

[Janders]

T

What is the difference between RFLP and VNTR?

I'll try to answer this one too...

RFLPs are Restriction Fragment Length Polymorphisms. Basically, if you know the concept of running a DNA Gel, these are easy to understand. Lets say we take your DNA in one lane, and Mine in another. If we simply run the uncut (just image that it will work with such a large hunk of DNA) we'll get two bands side-by-side, because our DNA is of basically even length. Now lets say we cut both samples with EcoRI, a restriction enzyme. You might get 2 bands, one that goes to the bottom of the gel, and one that stays near the top. I also get two bands, but they are both near the middle of the gel.

These are RFLPs. We used a Restriction enzyme to make Fragments. By measuring the Length of the two fragments, we realize that there is Polymorhpism! (just due to the difference in our actual coding sequence, you have an EcoRI cutting site where I don't, and I have one where you don't)

Now VNTRs are a bit more interesting. They are Variable Number Tandem Repeats. Basically, they are a section of your DNA where the same code-sequence is repeated over and over. For example, say the code is CAGCAGCAGCAGCAGCAGCAG...x10...CAGCAG. We have a CAG being repeated, tandemly (back to back). The variable part is the cool thing. While in my DNA it might repeat 100 times, in yours it might repeat 800 times. Now imagine if we combine this information with the RFLP concept.

Say we cut for RFLPs using one enzyme. We each have the cutting site twice in our DNA, in the same spots. So we each get one small hunk of DNA cut out. However, you have 800 repeats inside that hunk, while I only have 100. When we run them out on the gel, mine will go farther than yours. In this way, VNTRs have allowed us to differintiate you from me. Or OJ from the killer... oooops....

Websites for further reading:
VNTR
RFLP

 

[caribsun]

why will it run farther in the variable number tandem repeats...both samples have the same length DNA so they should run the same ont eh gel? thanks

I'll try to answer this one too...

RFLPs are Restriction Fragment Length Polymorphisms. Basically, if you know the concept of running a DNA Gel, these are easy to understand. Lets say we take your DNA in one lane, and Mine in another. If we simply run the uncut (just image that it will work with such a large hunk of DNA) we'll get two bands side-by-side, because our DNA is of basically even length. Now lets say we cut both samples with EcoRI, a restriction enzyme. You might get 2 bands, one that goes to the bottom of the gel, and one that stays near the top. I also get two bands, but they are both near the middle of the gel.

These are RFLPs. We used a Restriction enzyme to make Fragments. By measuring the Length of the two fragments, we realize that there is Polymorhpism! (just due to the difference in our actual coding sequence, you have an EcoRI cutting site where I don't, and I have one where you don't)

Now VNTRs are a bit more interesting. They are Variable Number Tandem Repeats. Basically, they are a section of your DNA where the same code-sequence is repeated over and over. For example, say the code is CAGCAGCAGCAGCAGCAGCAG...x10...CAGCAG. We have a CAG being repeated, tandemly (back to back). The variable part is the cool thing. While in my DNA it might repeat 100 times, in yours it might repeat 800 times. Now imagine if we combine this information with the RFLP concept.

Say we cut for RFLPs using one enzyme. We each have the cutting site twice in our DNA, in the same spots. So we each get one small hunk of DNA cut out. However, you have 800 repeats inside that hunk, while I only have 100. When we run them out on the gel, mine will go farther than yours. In this way, VNTRs have allowed us to differintiate you from me. Or OJ from the killer... oooops....

Websites for further reading:
VNTR
RFLP

 

[HiddenTruth]

why will it run farther in the variable number tandem repeats...both samples have the same length DNA so they should run the same ont eh gel? thanks

no, i don't think both samples have the same length. The restriction enzyme site was at the same "spot" per say, but whatever in between was variable.

e.g

ACTGTCGTCGTCGTCGTCGTCGTC...x800...GTCGTCATG
ACTGTCGTCGTCGTCGTC...x100...GTCGTCATG

somwhere along the lines of this, i believe. Someone correct me if i am wrong. Thanks.

 

[HiddenTruth]

ok, so i got this question on qbank with a classic SIADH presentation, and it asked which drug. And, the correct answer was amitryptilline. what? I have never been taught or have read that TCA's and SSRI's (according to qbank) can cause SIADH. I selected hydrocodone, as that was the best choice present. i know opioids can rarely cause increased ADH secr. Is SIADH common with tca/ssri, or am i just a dumdum?

Btw, they did not have the classic drugs of siadh that we all know of (CBZ, sulfonylureas, etc.)

 

[Long Dong]

ok, so i got this question on qbank with a classic SIADH presentation, and it asked which drug. And, the correct answer was amitryptilline. what? I have never been taught or have read that TCA's and SSRI's (according to qbank) can cause SIADH. I selected hydrocodone, as that was the best choice present. i know opioids can rarely cause increased ADH secr. Is SIADH common with tca/ssri, or am i just a dumdum?

Btw, they did not have the classic drugs of siadh that we all know of (CBZ, sulfonylureas, etc.)

Hey I got that same question wrong yesterday, and yeah I was looking for the classic drugs. So I just wrote it into my FA as another cause.

Also got a Qbank question about pANCA in polyart nodosa and Hep B (also in goljan path review says same thing), but my 2005 FA says pn is not associated with ANCA and I think I remember a question from robbins review saying the same thing. Anyone no what the deal is with this.

 

[Pox in a box]

Hey I got that same question wrong yesterday, and yeah I was looking for the classic drugs. So I just wrote it into my FA as another cause.

Also got a Qbank question about pANCA in polyart nodosa and Hep B (also in goljan path review says same thing), but my 2005 FA says pn is not associated with ANCA and I think I remember a question from robbins review saying the same thing. Anyone no what the deal is with this.

Almost every source has this wrong (including Goljan and even First Aid until last year). P-ANCA is NOT associated with Polyarteritis Nodosa. The newest version of Robbins does NOT include it either.

 

[HiddenTruth]

so how much do we have to know about cephalosporins? I am getting bogged down with all the distinctions that certain 2nd and 3rd generations have activity against. Plus, its damn hard to memorize the various ones in each generation (there are of course the classis ones). But, for e.g., it say's, 3rd generations no activ against anaerobes, but then there is one (moxalaxtam, and this other one, which i forgot already). Likewise, the general theme is, that they are not good for psuedomonas, but then cefaperazone (sp?) has activ against psuedomonas.

any insight as to the detail of this that i should know? Thanks.

 

[Pox in a box]

so how much do we have to know about cephalosporins? I am getting bogged down with all the distinctions that certain 2nd and 3rd generations have activity against. Plus, its damn hard to memorize the various ones in each generation (there are of course the classis ones). But, for e.g., it say's, 3rd generations no activ against anaerobes, but then there is one (moxalaxtam, and this other one, which i forgot already). Likewise, the general theme is, that they are not good for psuedomonas, but then cefaperazone (sp?) has activ against psuedomonas.

any insight as to the detail of this that i should know? Thanks.

You're speaking Greek to me. I hope we just need the basics (first and second generations have intrinsic staphylococcus activity and that later generations have better activity against Beta-lactamase producing strains).

 

[Row Jimmy]

You're speaking Greek to me. I hope we just need the basics (first and second generations have intrinsic staphylococcus activity and that later generations have better activity against Beta-lactamase producing strains).

"fam" "fot" and "fop" have an anabuse like reaction with alcohol.

 

[Pox in a box]

"fam" "fot" and "fop" have an anabuse like reaction with alcohol.

I forgot to mention that aspect. Cephalosporin side chains can cause a disulfuram-like reaction so encourage your patients to drink O'Doul's when everybody else in the club's gettin' tipsy.

Name 3 other drugs (I can think of at least 3 off the top of my head) that cause a disulfuride-like reaction...

1.
2.
3.

 

[HiddenTruth]

I forgot to mention that aspect. Cephalosporin side chains can cause a disulfuram-like reaction so encourage your patients to drink O'Doul's when everybody else in the club's gettin' tipsy.

Name 3 other drugs (I can think of at least 3 off the top of my head) that cause a disulfuride-like reaction....

1.chlorpropramide (sulfonylureas)
2.metranidazole
3. procarbazine

1. while we're at it with antiobiotics. Give me 3 antiobiotics that are ok to use in pregnancy (one of them is a class)

2. Only cell wall inhibitor with NO activity against gram pos?

3. 2 differences between imipenem and meropenem? (they both have same MOA--this may be kinda' tricky)

4. 2 cephalosporins that are ok to give to a pt with CRI? (bonus points for naming 4 other drugs, of which 2 are from same class, that can be given in CRI--[meaning no renal elimination]...well there may be more, but these are the most important i think).

5. Name 3-4 big/impt bugs that Imipenem will not cover.

6. antiobiotic that prolongs QT?

7. drug that can be antagonized by flmazenil, that is not a BZD.

8. what do u give to treat drug induced EPS? (bonus points for naming one other drug that is not in the same class, and tripple bonus points for naming a treatment option that is not a drug [hint: can be used specifically to treat acute dystonias, it's also a big fashion trend these days, esp. for our friends in hollywood ).

ok that's all for now--

 

[HiddenTruth]

You're speaking Greek to me. I hope we just need the basics (first and second generations have intrinsic staphylococcus activity and that later generations have better activity against Beta-lactamase producing strains).

ok this is what i came up with after looking through my notes from pharm and kaplan and FA. don't know if this is too much detail--but eh, it won't hurt ya.

1. 3rd gen mostly cross CNS except "peraz" -- cefaperazone
2. "taz" and "peraz" are buddies--cefaperazone and ceftazidime are selective TGC for psuedomonas
3. "peraz" and ceftriaxone - eliminated in bile--thus, can be used in CRI (well there's an answer for one og my questions above).
4. "fix" the vagina - cefixime (po) and ceftriaxone (IV--everyone knows this one) for gonorrhea (don't confuse with cefiPime--which is 4th gen)
5. "foto" graphic MEMORY - cefotaxime -active against most bacteria causign meningitis (im sure the other TGC can be used, but i guess this is a big one for meningitis).
6. the 3 cephalosporins that cause disulf like rxn that a previous poster mentioned.

 

[HiddenTruth]

have a question about clindamycin.
In FA it says that the MOA involves a block in peptide bond formation. I thought that it was the same MOA as macrolides, in which there is a block in translocation of peptidyl tRNA from acceptor site (A) to donor site (p). Has FA jus' simplified the MOA?

 

[Pox in a box]

"fam" "fot" and "fop" have an anabuse like reaction with alcohol.

Can you explain these terms you are using?

 

[HiddenTruth]

Can you explain these terms you are using?

ceFAMondole, ceFOTetan, ceFOPerazone

 

[Janders]

Hey Hidden,
I've been studying for my pharm test on tuesday that covers Abx. I can't answer a single one of your questions. This is after looking though my notes. Heh. I'm afraid its not because your questions are too hard, rather my pharm education borders on weak. Oh well, i'm trying to catch up!

be looking forward to the answers and explanations.

 

[bigfrank]

Hey Hidden,
I've been studying for my pharm test on tuesday that covers Abx. I can't answer a single one of your questions. This is after looking though my notes. Heh. I'm afraid its not because your questions are too hard, rather my pharm education borders on weak. Oh well, i'm trying to catch up!

be looking forward to the answers and explanations.

don't worry; pharm questions tend to be the easiest questions on the step I. I couldn't answer any of hidden's ?s either. 😉

 

[Janders]

don't worry; pharm questions tend to be the easiest questions on the step I. I couldn't answer any of hidden's ?s either. 😉

*whew* I'm hoping that holds true for my exam.

 

[Pox in a box]

don't worry; pharm questions tend to be the easiest questions on the step I. I couldn't answer any of hidden's ?s either. 😉

What do you mean bigfrank?

 

[HiddenTruth]

well i didn't think too many of them wern't from FA. oh well--


1. while we're at it with antiobiotics. Give me 3 antiobiotics that are ok to use in pregnancy (one of them is a class)
pcn, cephalosporin, azithromycin
One's that you should not use: EM estolate, fluoroquin, TCN, clarithromycin, sulfonamides

2. Only cell wall inhibitor with NO activity against gram pos?
Aztreonam- remember, this is often reserved for those that have pcn allergy or CRI pts who cannot tolerate aminoglycosides. This ONLY has gram neg. activity. So, a good substitue in pcn allergy are macrolides (to cover gram pos), and aztreonam (to cover the gram negs).

3. 2 differences between imipenem and meropenem? (they both have same MOA--this may be kinda' tricky)
Imipenem requires cilastatin and can cause seizures while meropenem requires/causes neither.

4. 2 cephalosporins that are ok to give to a pt with CRI? (bonus points for naming 4 other drugs, of which 2 are from same class, that can be given in CRI--[meaning no renal elimination]...well there may be more, but these are the most important i think).

Ok, this may have been poorly asked. Potentially, you should be able to give most of the drugs with CRI--but would have to renally dose them. Better way of asking this would, drugs that are not renally eliminated and are probably more safer in CRI patients.

1. ceftriaxone and ceFAPerazone
2. EM (elim. in bile)
3. doxycycline (feces)
4. nafcillin and oxacillin

5. Name 3-4 big/impt bugs that Imipenem will not cover.
i don't know, i thought this was kinda' important. Everyone knows this is the king of all antiobiotics, but i figured it may be useful to know some of the big bugs that this guy doesn't cover, at least by itself.

1. MRSA
2. Enterococcus
3. C. dif

Also, for additional uselss knowledge, it doesn't cover non areuginosa psuedomonas, and ofcourse, it wouldn't cover those atypical's (chl, mycplasma, etc).

6. antiobiotic that prolongs QT? EM and fluroquin (sparfloxacin)

7. drug that can be antagonized by flmazenil, that is not a BZD.
zolpidem and zoleplan--bind at BZ1 site, but are NON-BZD's, used for insomnia, can be reversed by flumazenil

8. what do u give to treat drug induced EPS? (bonus points for naming one other drug that is not in the same class, and tripple bonus points for naming a treatment option that is not a drug [hint: can be used specifically to treat acute dystonias, it's also a big fashion trend these days, esp. for our friends in hollywood ).
1. musc blockers- benztropine and trihexyphenidyl
2. diphenhydramine (used specifially to reverse acute dystonias)
3. Botulinum toxin ("....)

__________________________________

some more things, if you're interested.

1. 2 antibacterials that you should recommend your patients to NOT take with milk, antacids, divalent ions (ca, fe, mg, etc.). TCN and fluroquin (also as a side note, bisphonates ahave the same story i think).

2. bacterioCIDAL drugs: Beta lactams (pcn, cephalo,imipenem, aztreonam) quinolones, aminoglycocides, vanco, TMP/SMX combo
bacterioSTATIC: tetracycline, sulfonamides, trimethaprin, clindamycin, streptogrammins (not sure about lineazolid)

alrite, im done--

 

[Row Jimmy]

ceFAMondole, ceFOTetan, ceFOPerazone

And Anabuse is the trade name for Disulfiram.

 

[HiddenTruth]

so i got this on the cbse. what do u guys think

Pt had came in for angina. Was given pharmacotherapy, and these are the results. Decrease in preload and EDV, tachycardia, and decrs in arterial BP. WHich drug was she given?

a. Propanolol,
b.prop and nitro
c. diltiazam,
d. diltiazam and propanolol
e. nitroglycerine

i think these were teh choices (maybe nitro and diltiazam may have been one), but i just put nitro, as propanolol is only cardio selective, and diltiazam, even though has some vasc selectivity, it is primarily arterial, so it would not decrease PL, it would decrs AL. So, I figured nitro was the best choice, and u get reflexive tachy, which results in decrs EDV. Infact BB, would produce increase in EDV due to the decreaed HR. Does this seem like the right choice?

I also had another q. about a 70 year old dude who got orthostatic hypotension, and they wanted to know, what is decreased in the old dude relative to a 30 year old dude, which accounts for the orthostat

a. mm mass
b. hematocrit
c. albumin
d. ?
e. ?

 

[Row Jimmy]

so i got this on the cbse. what do u guys think

Pt had came in for angina. Was given pharmacotherapy, and these are the results. Decrease in preload and EDV, tachycardia, and decrs in arterial BP. WHich drug was she given?

a. Propanolol,
b.prop and nitro
c. diltiazam,
d. diltiazam and propanolol
e. nitroglycerine

i think these were teh choices (maybe nitro and diltiazam may have been one), but i just put nitro, as propanolol is only cardio selective, and diltiazam, even though has some vasc selectivity, it is primarily arterial, so it would not decrease PL, it would decrs AL. So, I figured nitro was the best choice, and u get reflexive tachy, which results in decrs EDV. Infact BB, would produce increase in EDV due to the decreaed HR. Does this seem like the right choice?

I also had another q. about a 70 year old dude who got orthostatic hypotension, and they wanted to know, what is decreased in the old dude relative to a 30 year old dude, which accounts for the orthostat

a. mm mass
b. hematocrit
c. albumin
d. ?
e. ?

I would have to go with Nitro on the first one as Diltiazam and Propanolol pretty have the same effects in relation to angina and combined with Nitro, we will see decreased HR and increased EDV with administration of them.

In the second one none of the answers make sense to me but I would be looking for something about decreased Beta response or decreased baroreceptor response or sensitivity.

 

[Janders]

I also had another q. about a 70 year old dude who got orthostatic hypotension, and they wanted to know, what is decreased in the old dude relative to a 30 year old dude, which accounts for the orthostat

a. mm mass
b. hematocrit
c. albumin
d. ?
e. ?

Wow, thats a tough one. I've read the number one cause of orthostatic hypotension is medications. But doesn't your hematocrit drop a bit as you age? It wouldn't help the situation.

I found this article. If you look at Table 1 they list 50+ causes of orthostatic hypotension. Whew.

 

[HiddenTruth]

Wow, thats a tough one. I've read the number one cause of orthostatic hypotension is medications. But doesn't your hematocrit drop a bit as you age? It wouldn't help the situation.

I found this article. If you look at Table 1 they list 50+ causes of orthostatic hypotension. Whew.

does your hematocrit decrs as you age? I don't know--but even if, that would increase your plasma volume. Altho, decrease in albumin, would decrease your intravascular volume; but, i don't know if albumin would be decreased in an older person.

 

[HiddenTruth]

In the second one none of the answers make sense to me but I would be looking for something about decreased Beta response or decreased baroreceptor response or sensitivity.

oh, now that u mention it, i think baroreceptor was one of them, but i didn't think that decreased in older people. hmmm

 

[Row Jimmy]

oh, now that u mention it, i think baroreceptor was one of them, but i didn't think that decreased in older people. hmmm

Yeah, baroreceptor sensitivity decreases with age and that will cause orthostatic hypotension.

 

[Row Jimmy]

Can anyone explain to me the mechanism by which hypercortsolism causes osteoporosis? I can't seem to find it anywhere.

THanks!!

 

[HiddenTruth]

Can anyone explain to me the mechanism by which hypercortsolism causes osteoporosis? I can't seem to find it anywhere.

THanks!!

cortisol increases bone resorption; this mechanism is likely facilitated by cortisol's function in protein catabolism, thus breaking down bone matrix proteins.

 

[omarsaleh66]

Can anyone explain to me the mechanism by which hypercortsolism causes osteoporosis? I can't seem to find it anywhere.

THanks!!

Glucocorticoids or cortisol can inhibit Ca+2 absorption from the GI tract, and may also inhibit osteoblasts. Speaking from memory, and not sure, can anyone confirm?

 

[Pox in a box]

This question is for the member named p53:

How does p53 guard the genome?

Bump. Can anyone else help user p53 out?

 

[HiddenTruth]

have a question about cardiac curves. I'd appreciate it if someone would touch on this.

In BRS, they have the preload cardiac curve, and it doesn't show an increase in ventricular pressure. I figured if you increased the volume, and increased stretch of the ventr (up to an optimal length of course), then the pressure INCREASES to expell the extra blood. I think it's on pg. 90 of 3rd ed, and they just simply show an increase in EDV, and as a result increased SV, but no increase in pressure. What's the story?

Also, in mild-moderate exercise in an untrained individual, the increased HR is what accounts for the increased CO. So, is there anything else going on in the curve, bsedies: decreased EDV, increased contractility (due to increased CO), and decreased ESV (2' to decrs filling to begin with)?

Thanks.

 

[Doc Ivy]

Ok, I'll try my hand at this question writing stuff:

A 37 year old healthy woman 26 weeks gestation presents to the ED complaining of new onset anosmia. She also notes that she has recently had trouble reading the newspaper and could no longer drive herself to work because of double vision. Her husband notes that she has had some trouble remembering things but he attributed to her pregnancy.

An astute neuro resident orders a CT which shows calcifications, mild edema, and a large homogenously enhancing lesion in the floor of the anterior cranial fossa. What is the most accurate statement regarding this condition?

a) it results in death between 5-12 months
b) it is best treated with fluconazole
c) she should be tested for HIV
d) it will most likely recur

 

[sapience8x]

does camphylobacter jejuni= helicobacter jejuni? i had a question on helicobacter jejuni that i got wrong i think i qbank and when i get stuff wrong i look up the topics and couldnt' find this organism anywhere. one textbook i foudn said that helicobacter pylori used to be camphylobacter pylori so i was thinking that it is possible that the same this or the reverse happend to jejuni? trivial i know but you watch it will be the first question on my test! 😱

 

[Linus2807]

H. pylori was once grouped with the Campylobacter species of bacteria, and you may still see references to its old name, Campylobacter pylori

 

[Pox in a box]

Ok, I'll try my hand at this question writing stuff:

A 37 year old healthy woman 26 weeks gestation presents to the ED complaining of new onset anosmia. She also notes that she has recently had trouble reading the newspaper and could no longer drive herself to work because of double vision. Her husband notes that she has had some trouble remembering things but he attributed to her pregnancy.

An astute neuro resident orders a CT which shows calcifications, mild edema, and a large homogenously enhancing lesion in the floor of the anterior cranial fossa. What is the most accurate statement regarding this condition?

a) it results in death between 5-12 months
b) it is best treated with fluconazole
c) she should be tested for HIV
d) it will most likely recur

This is pretty tough. Is it a meningioma in the olfactory groove? I'd say that the answer is death within 5 to 12 months because I don't think surgery is a good option with these tumors. Chemo is worthless from what I've heard. It's got a lot going on to be a fungal infection (b), HIV doesn't usually produce these sequelae, and I have no idea why answer D should be removed but a hunch says no.

 

[Pox in a box]

A 46-year-old G3 P0 woman is expecting her first child, a son, after experiencing several unsuccessful attempts at parenthood with her husband over a 10 year span. At one of her prenatal visits, the physician notes in the chart that the mother has low unconjugated estriol and alpha-fetoprotein. A preliminary diagnosis is made by the physician by assessing the karyotype in fetal cell samples obtained by amniocentesis.

At the age of 43, the child is still alive. He is being treated for a malignancy. The patient has been noted by the nursing staff as wandering about the halls and never knowing how to get back to his room. He seems confused and disoriented.

1. What is the initial diagnosis?

2. What is the most common cardiac anomaly?

3. What malignancy is the patient being treated for in the hospital?

4. Why is confused and disoriented?

5. What gross anatomical features are present?

6. What chromosomal features are present?

7. Will the patient be able to have children? If not, why?

8. What pathohistological features are noted at autopsy?

9. What chromosomal abnormalities might the parents have, if any?

 

[dynx]

1. What is the initial diagnosis? Down's?

2. What is the most common cardiac anomaly Asd I think

3. What malignancy is the patient being treated for in the hospital ALL

4. Why is confused and disoriented He's ****ing ******ed...and he probably has alzheimers by now

5. What gross anatomical features are present Simian crease, epicanthal folds some facial anomalies.

6. What chromosomal features are present? Trisomy 21

7. Will the patient be able to have children? No, hard to get a chick when you're ******ed

8. What pathohistological features are noted at autopsy? ahh....hmmmmm....can't remember this one.

9. What chromosomal abnormalities might the parents have, if any? Hmmm...I think balanced translocations in parents can be passed down as trisomy.

 

[Pox in a box]

1. What is the initial diagnosis? Down's?

2. What is the most common cardiac anomaly Asd I think

3. What malignancy is the patient being treated for in the hospital ALL

4. Why is confused and disoriented He's ****ing ******ed...and he probably has alzheimers by now

5. What gross anatomical features are present Simian crease, epicanthal folds some facial anomalies.

6. What chromosomal features are present? Trisomy 21

7. Will the patient be able to have children? No, hard to get a chick when you're ******ed

8. What pathohistological features are noted at autopsy? ahh....hmmmmm....can't remember this one.

9. What chromosomal abnormalities might the parents have, if any? Hmmm...I think balanced translocations in parents can be passed down as trisomy.

Your answers are not worth discussing. If you talk like that in real life, you deserve to be kicked out of medical school. That's sick.

 

[dynx]

Your answers are not worth discussing. If you talk like that in real life, you deserve to be kicked out of medical school. That's sick.

Take a deep breath and relax a little slick.

Just to check, you don't see anything funny in a question asking why a mentally ******ed person might be confused?

 

[Pox in a box]

Take a deep breath and relax a little slick.

Just to check, you don't see anything funny in a question asking why a mentally ******ed person might be confused?

Hard to get a chick when you're ******ed? ****ing ******ed? Hey, ace, some people are born with what God gave them and they are blessed. Obviously you were not born with one ounce of humility and compassion. Are you sure you're suppose to be a doctor? Your post is indicative of the callous attitude that medical schools should be screening out. How you slipped through is a mystery. I pity you and your patients. On this, I'm done with the conversation. Back to pimping each other.

By the way, I didn't ask why a mentally ******ed person would be confused.