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

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Mike59

Sweatshop FP in Ontario
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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?

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Pox in a box said:
How do you see venous pulsations in the eye?


look at the veins on the retina-they pulsate normally, when they don't its because of increased ICP
 
macman said:
look at the veins on the retina-they pulsate normally, when they don't its because of increased ICP


Honestly, I haven't seen a vein pulsate. I haven't even looked. But in my lil Physical Exam secrets book, it suggests that 20% of normals do NOT have pulsations. Thus it isn't a good sign of increased ICP (unless you know the patient normally has them). It is a good rule out though! And you are very right, lack of pulsations can occur in seconds with increased ICP.
 
Janders said:
Honestly, I haven't seen a vein pulsate. I haven't even looked. But in my lil Physical Exam secrets book, it suggests that 20% of normals do NOT have pulsations. Thus it isn't a good sign of increased ICP (unless you know the patient normally has them). It is a good rule out though! And you are very right, lack of pulsations can occur in seconds with increased ICP.

There is a zero percent chance you will have to know this for Step 1.
 
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this assumes tofu has glucogenic aa's, which it probably does but still

HiddenTruth said:
Yea, and how are you going to take up that sugar you just made? Thus, BOTH insulin and glucagon go up.

However, if it was all carbs, only insulin would go up 30 mins later.
 
caribsun said:
this assumes tofu has glucogenic aa's, which it probably does but still

sure, but look at the question more globally. And, just for the record, I made sure to address that it was "all protein intake", regardless of tofu. But, anyways, you get the point.
 
Pox in a box said:
He said Step 2 and neuro rounds.

Really? How did you hear his voice?

A Step 2 question on an "official step 1 pimp each other thread"..........makes perfect sense to me. :clap:
 
p53 said:
Really? How did you hear his voice?

A Step 2 question on an "official step 1 pimp each other thread"..........makes perfect sense to me. :clap:


Please refer to my post where I apologize when I realized it was not a good question for this thread.....or continue to act like a total a**, your choice
 
Pox in a box said:
With my ears, genius.

Auditory hallucination is likely since there was no way you would have been able to "hear" macman's post with you "ears".
 
p53 said:
Auditory hallucination is likely since there was no way you would have been able to "hear" macman's post with you "ears".

Good ASSumption, p53. Have you ever heard of verbal communication? It involves someone speaking and another person listening. By the way, you are reading (probably aloud) my "typing." Lastly, the period goes inside the quotation mark. :barf:
 
Aw Gentlemen (or ladies),
Can't we have a civil discussion on Step 1 here. I mean, we've already self-selected for extra-Type A megalomanical med students by posting on this board, but I would expect us to be a bit more mature than this thread. Or not. We can just use the posts as teaching points!

Assignment: Diagnose the personality disorder each poster has. Bonus points for correctly identifying the defense mechanisms he or she is using.
 
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Janders said:
Aw Gentlemen (or ladies),
Can't we have a civil discussion on Step 1 here. I mean, we've already self-selected for extra-Type A megalomanical med students by posting on this board, but I would expect us to be a bit more mature than this thread. Or not. We can just use the posts as teaching points!

Assignment: Diagnose the personality disorder each poster has. Bonus points for correctly identifying the defense mechanisms he or she is using.

Intellectualization.
 
p53 said:
Intellectualization.


excellent! Bonus points for the first response!


How about a heart murmer question! Which two murmers INCREASE in intensity when standing, or when performing a valsalva?
 
Janders said:
excellent! Bonus points for the first response!


How about a heart murmer question! Which two murmers INCREASE in intensity when standing, or when performing a valsalva?

MVP and hypertrophic cardiomyopathy (watch out for a young athlete that dies suddenly in a game).
 
bigfrank said:
I'd do at least some questions before you review, that way, you can see which subject(s) you are weakest in. good luck to you

Altruism (secondary to low self esteem).
 
tricuspid regurg. systolic and aortic stenosis

Janders said:
excellent! Bonus points for the first response!


How about a heart murmer question! Which two murmers INCREASE in intensity when standing, or when performing a valsalva?
 
Janders said:
excellent! Bonus points for the first response!


How about a heart murmer question! Which two murmers INCREASE in intensity when standing, or when performing a valsalva?

Left sided heart murmur (mitral and aortic).
 
caribsun said:
tricuspid regurg. systolic and aortic stenosis

p53 said:
Left sided heart murmur (mitral and aortic).

Doesn't aortic stenosis actually DECREASE with Valsalva? p53, you get half-credit, though the exam is multiple choice so I believe that's still going to be scored incorrect.

If he would have asked which murmurs DECREASE with Valsalva maneuver, you would all be right.
 
Pox in a box said:
Doesn't aortic stenosis actually DECREASE with Valsalva? p53, you get half-credit, though the exam is multiple choice so I believe that's still going to be scored incorrect.

If he would have asked which murmurs DECREASE with Valsalva maneuver, you would all be right.

Thanks Charlatan for your 2 cent response. This is what happens when you walk in to the Step 1 exam with just memory skills (you become uncertain about what was or wasn't in first aid). IF YOU UNDERSTOOD THE CONCEPT YOU WOULD BE ABLE TO REASON THE RIGHT ANSWER.

Valsalva decreases preload on the right side, and increases preload on the left side of the heart.

Similarly, there is a decrease in preload on the right side when one is standing up. Majority of the blood in the systemic side is below heart level (against gravity), and majority of the blood in the pulmonary circuit is above heart level (helped by gravity). Murmurs are caused by turbulence of blood across a valve, when there is less fluid in the circuit (due to gravity) there is less blood available for turbulence.
 
p53 said:
Thanks Charlatan for your 2 cent response.

IF YOU UNDERSTOOD THE CONCEPT YOU WOULD BE ABLE TO REASON THE RIGHT ANSWER.

*cough*

So um, speaking of the reasoning behind this question.

MOST murmers increase in sound with increased Flow. There are two exceptions to this rule of thumb. MVP and HCM. Both actually increase in intensity with decreased flow (up to a point). Standing (and Valsalva) decreases left and right heart filling, vis-a-vis sitting. So, they both increase in intensity when you stand. Its a good way to try and tell the sound of a HCM murmer from an Aortic Stenosis murmer, which would become more quiet when you stand.

Sooo.... Pox wins. Now kiss and make up.
 
Janders said:
*cough*

So um, speaking of the reasoning behind this question.

MOST murmers increase in sound with increased Flow. There are two exceptions to this rule of thumb. MVP and HCM. Both actually increase in intensity with decreased flow (up to a point). Standing (and Valsalva) decreases left and right heart filling, vis-a-vis sitting. So, they both increase in intensity when you stand. Its a good way to try and tell the sound of a HCM murmer from an Aortic Stenosis murmer, which would become more quiet when you stand.

Sooo.... Pox wins. Now kiss and make up.

Janders, valsalva increases intrathroacic pressure and thus more blood is introduced into the left atrium, and less blood is introduced into the right atrium. If you think about gravity this would make logical sense. You might want to look this up in a physiology book. By saying increasing intrathoraic pressure decreases preload in BOTH left and right atrium is idiotic. Is blood stuck in the lungs if there is an increase in intrathoracic pressure with the help of gravity? Whatever!

Plus, if you stand up you mentioned that it decreases blood flow. How can a decrease in blood flow INCREASE intensity. You are confused. Does less fluid increase turbulence to a greater degree than more fluid? Feed me another one, Pal.

Explain the mechanism of the exceptions. If you can't it is essentially your word against mine, but my response has a VALID mechanism behind it. JUST SAYING it is an exception adds nothing to the table. EXPLAIN the basis of it.
 
I'll give you another example for the Goljan followers out there, this is physiologically the opposite condition.

Inspiration decreases intrathoracic pressure thus there is an increase in venous return on the right side of the heart, BUT a decrease in venous return on the left side of the heart due to an increase in pulmonary compliance. Guess how someone can distinguish an aortic stenosis (left side) from a pulmonary valve stenosis (right side)?

If inspiration increases the murmur than it is on the right side of the heart due to increased venous return on that side. Ask any cardiologist my friend, if the intensity of a murmur increases during inspiration it is on the right side. Using the same logic, you can figure out the effect of the valsava on the left side and on the right side of the heart.

Mechanisms! Memorization will serve you well in anatomy, pharm, and pathology. However, physiology and pathophysiology will bite you in the butt. If you think first aid is enough for physiology and pathophysiology, you are in DEEP, DEEP trouble.
 
yep, according to the old guy on the tapes, right sided murmurs increase on inspiration and left sided murmurs increase on expiration.

new topic please.
 
Hey p53,

I'm wondering if you have swapped your toilet bowl for a potted plant yet?

;)
 
p53 said:
I'll give you another example for the Goljan followers out there, this is physiologically the opposite condition.

Inspiration decreases intrathoracic pressure thus there is an increase in venous return on the right side of the heart, BUT a decrease in venous return on the left side of the heart due to an increase in pulmonary compliance. Guess how someone can distinguish an aortic stenosis (left side) from a pulmonary valve stenosis (right side)?

If inspiration increases the murmur than it is on the right side of the heart due to increased venous return on that side. Ask any cardiologist my friend, if the intensity of a murmur increases during inspiration it is on the right side. Using the same logic, you can figure out the effect of the valsava on the left side and on the right side of the heart.

Mechanisms! Memorization will serve you well in anatomy, pharm, and pathology. However, physiology and pathophysiology will bite you in the butt. If you think first aid is enough for physiology and pathophysiology, you are in DEEP, DEEP trouble.

Goljan's a pretty decent tool for learning, but he's not a source. He makes mistakes just like you did on the question. Don't count on Goljan to solidify a great score.
 
p53 said:
Thanks Charlatan for your 2 cent response. This is what happens when you walk in to the Step 1 exam with just memory skills (you become uncertain about what was or wasn't in first aid). IF YOU UNDERSTOOD THE CONCEPT YOU WOULD BE ABLE TO REASON THE RIGHT ANSWER.

It's okay if you didn't understand the concept now. This is a learning experience for you and I'm sure you'll get it right now if it appears on your exam. By the way, I don't learn by First Aid. It's a review tool. If you want to learn, try sources that are solid such as Robbins Pathologic Basis of Disease, Harrison's Internal Medicine Textbook, Cecil's, etc. By the way, I did reason the right answer. I even reasoned why you were wrong. I don't know why you are being such a punk to everyone on this board. Half of what you say has no credibility because every time you post you are negative. Either way, I'll accept your attitude as a challenge and move on...let's get a new question.
 
p53 said:
Janders, valsalva increases intrathroacic pressure and thus more blood is introduced into the left atrium, and less blood is introduced into the right atrium. If you think about gravity this would make logical sense. You might want to look this up in a physiology book. By saying increasing intrathoraic pressure decreases preload in BOTH left and right atrium is idiotic. Is blood stuck in the lungs if there is an increase in intrathoracic pressure with the help of gravity? Whatever!

Plus, if you stand up you mentioned that it decreases blood flow. How can a decrease in blood flow INCREASE intensity. You are confused. Does less fluid increase turbulence to a greater degree than more fluid? Feed me another one, Pal.

Explain the mechanism of the exceptions. If you can't it is essentially your word against mine, but my response has a VALID mechanism behind it. JUST SAYING it is an exception adds nothing to the table. EXPLAIN the basis of it.

Dx: Narcissistic Personality Disorder
 
p53 said:
I'll give you another example for the Goljan followers out there, this is physiologically the opposite condition.

Inspiration decreases intrathoracic pressure thus there is an increase in venous return on the right side of the heart, BUT a decrease in venous return on the left side of the heart due to an increase in pulmonary compliance. Guess how someone can distinguish an aortic stenosis (left side) from a pulmonary valve stenosis (right side)?

If inspiration increases the murmur than it is on the right side of the heart due to increased venous return on that side. Ask any cardiologist my friend, if the intensity of a murmur increases during inspiration it is on the right side. Using the same logic, you can figure out the effect of the valsava on the left side and on the right side of the heart.

Mechanisms! Memorization will serve you well in anatomy, pharm, and pathology. However, physiology and pathophysiology will bite you in the butt. If you think first aid is enough for physiology and pathophysiology, you are in DEEP, DEEP trouble.


Frankly-I do not know who is wrong or right on that question--lets move on or have multiple sources quoted with a consistent answer.

p53-If it wasn't for that fact that you appear to have some medical knowledge I'd swear you were a troll. Can't you contribute without being rude, demeaning, and sarcastic? We are all here to learn and part of that process must involve errors, whether real or perceived. Are you related to Bill O'Reilly???? Sorry that was sarcastic and probably a little rude. :luck:
 
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20 yr old college student presents to the clinic with a complaint of diarrhea for the past 3 days. The patient also states that he has had difficuty with memory and concentration which is interfering with his studies in college. On physical examination the physician notes a "flaky paint" rash over the trunk and upper extremities. The patient states that he does not use any drugs, lives on a proper diet, and exercises. After the physical examination, the physician diagnoses the patient with Hartnup disease. Which of the following describes the phathophysiology of the clinical presentation in this patient.

A. Deficiency of Vit B3 (Niacin)
B. Abnormality in Zinc Metabolism
C. Deficiency of alpha-glucosidase in the brush border
D. Defect in proximal renal tubular reabsorbtion of tryptophan
E. Failure to synthesize tryptophan from serotonin
F. Deficiency of Vit B2 (Riboflavin)
G. Deficinecy of Vit B1 (Thymine)
 
45 yr old male with atherosclerosis and a positive family history of hyperlipidimia presents to his cardiologist. The cardiologist suspects that the patient's atherosclerosis may be due to his genetic predisposition to hyperlipidimia. Lab tests are ordered and the following results are obtained. Serum IDL levels are elevated and a defect in the synthesis of Apolipoprotein E is suspected. The patient is started on Nicotinic Acid and Gemfibrozil. Which of the following hyperlipidimias is present in this patient's family history.

A. Exogenous Hyperlipidimia
B. Combined Hyperlipoproteinimia
C. Familial Dysbetalipoproteinimia
D. Familial Hypercholestorelimia
E. Familial Hypertryglisaridimia
 
kcumbDO said:
20 yr old college student presents to the clinic with a complaint of diarrhea for the past 3 days. The patient also states that he has had difficuty with memory and concentration which is interfering with his studies in college. On physical examination the physician notes a "flaky paint" rash over the trunk and upper extremities. The patient states that he does not use any drugs, lives on a proper diet, and exercises. After the physical examination, the physician diagnoses the patient with Hartnup disease. Which of the following describes the phathophysiology of the clinical presentation in this patient.

A. Deficiency of Vit B3 (Niacin)
B. Abnormality in Zinc Metabolism
C. Deficiency of alpha-glucosidase in the brush border
D. Defect in proximal renal tubular reabsorbtion of tryptophan
E. Failure to synthesize tryptophan from serotonin
F. Deficiency of Vit B2 (Riboflavin)
G. Deficinecy of Vit B1 (Thymine)



classic-the 3 D's of pellegra diarrhea, dementia, dermatitis

nice case

answer: A
 
kcumbDO said:
45 yr old male with atherosclerosis and a positive family history of hyperlipidimia presents to his cardiologist. The cardiologist suspects that the patient's atherosclerosis may be due to his genetic predisposition to hyperlipidimia. Lab tests are ordered and the following results are obtained. Serum IDL levels are elevated and a defect in the synthesis of Apolipoprotein E is suspected. The patient is started on Nicotinic Acid and Gemfibrozil. Which of the following hyperlipidimias is present in this patient's family history.

A. Exogenous Hyperlipidimia
B. Combined Hyperlipoproteinimia
C. Familial Dysbetalipoproteinimia
D. Familial Hypercholestorelimia
E. Familial Hypertryglisaridimia


are most of those answers real words??? I'd go with D only b/c I think the other answers (other than a and d) look like made up words. :)

one of our professors used to do that-until they fired him!
 
Janders said:
*cough*

So um, speaking of the reasoning behind this question.

MOST murmers increase in sound with increased Flow. There are two exceptions to this rule of thumb. MVP and HCM. Both actually increase in intensity with decreased flow (up to a point). Standing (and Valsalva) decreases left and right heart filling, vis-a-vis sitting. So, they both increase in intensity when you stand. Its a good way to try and tell the sound of a HCM murmer from an Aortic Stenosis murmer, which would become more quiet when you stand.

Sooo.... Pox wins. Now kiss and make up.

Wow. This is quite a pissing contest.
HCM murmurs are from LVOFT obstruction and hence act like aortic stenosis...so you are both right on that one.
MVP - Valsalva will increase the duration of the murmur since the prolapse will occur earlier during the contraction but I am entirely unsure that it increases the intensity...I can't think of a way that would work. Maybe the increased duration is what you were thinking of.
MS - I am pretty sure valsalva increases the intensity of MS.
 
A. B3 Niacin deficiency. The patient has the 3 D's diarrhea dementia dermatitis of pellagra. Hartnup disease is an autosomal recessive disorder with decreased absorption of tryptophan and other amino acids. Tryptophan can be converted to niacin. Niacin is important in NAD reactions.
 
isnt gemfibrozil used for hypertriglyceridemia? i think its E even though its spelled wrong

kcumbDO said:
45 yr old male with atherosclerosis and a positive family history of hyperlipidimia presents to his cardiologist. The cardiologist suspects that the patient's atherosclerosis may be due to his genetic predisposition to hyperlipidimia. Lab tests are ordered and the following results are obtained. Serum IDL levels are elevated and a defect in the synthesis of Apolipoprotein E is suspected. The patient is started on Nicotinic Acid and Gemfibrozil. Which of the following hyperlipidimias is present in this patient's family history.

A. Exogenous Hyperlipidimia
B. Combined Hyperlipoproteinimia
C. Familial Dysbetalipoproteinimia
D. Familial Hypercholestorelimia
E. Familial Hypertryglisaridimia
 
Sorry to beat a dead and rotting horse everyone, but I figured we should all agree on the right answer... its clinically kinda useful (sports physicals and all), and is a fun 'lil testable point. If you don't care to read the explanation, here is the gist of it:
Standing and Valsalva both increase the intensity of HOCM and MVP... almost all other murmers become quieter with these manuvers.

Now for the long version...

p53 said:
*random insults*
Explain the mechanism of the exceptions. If you can't it is essentially your word against mine, but my response has a VALID mechanism behind it. JUST SAYING it is an exception adds nothing to the table. EXPLAIN the basis of it.

Wow big guy, take a chill pill. Or whatever the cool kids are saying these days. You are right, most murmers Increase in sound with increased flow. HOCM is a big exception to that rule. Apparently you didn't know that (I didn't til I had an exam on it about 2 days ago.. trust me I'm no genius med-student).

Just so you know where I was pulling that info, it was straight out of my lecture notes... not the ones I wrote down, but the ones Dr. Cardiologist typed up for us. Now I agree this might not be a perfect source, but let me see the others I can find with a bit of googling:

[url said:
http://www.mcevoy.demon.co.uk/Medicine/Medicine/ClinExamn/Murmurs.html][/url]

Performing the Valsalva manoeuvre (get patient to strain silently)

* amplifies the murmurs of mitral valve prolapse and hypertrophic obstructive cardiomyopathy
* softens the murmurs of mitral regurgitation and aortic stenosis

Many other easily google-able sites agree!
http://www.postgradmed.com/issues/2000/06_00/deluca.htm
one from my home hospital: http://www.shands.org/health/information/article/000180.htm
etc.


And for the explanation of WHY, I turn to Physical Diagnosis Secrets, by Dr. S. Mangione.

Re: Valsalva
"The held (or strain phase) is carried out by asking the patient to bear down as if having a bowel movement... leads to an increase in intrathoracic pressure, a decrease in venous return, and a smaller left ventricular volume. The strain phase, therefore, increases the left ventricular gradient in hypertrophic obstructive cardiomyopathy and makes its systolic murmer much louder. This is clinically useful because it is the opposite of how left ventricular outflow murmers typically act. The strain phase also favors the prolapse of a floppy mitral valve, making its murmer longer and its click earlier. Finally, straining fixes a widely split normal s2, but has no effect on the split s2 of an ASD. p243
Pearl. Conversely, most heart sounds and murmers will become softer during the strain phase, especially in patients with aortic stenosis and pulmonary stenosis (because of the decreased venous return to both ventricles) "

"from p257 of same text, re: HOCM:
Conversely, factors that decrease the diameter of the left ventricular cavity... are associated with an increase in the intenstity of the murmer (for obvious reasons)... Similarly, the Valsalva maneuver also causes a reduction in the diameter of the left ventricular cavity because of the decrease in venous return and leads an increase in intensity"

OK, now for mitral prolapse:

"p262 of same text... one must remember that in mitral regurg the left ventricle has two outlets for discharge: a high resistance one (aorta) and a low resistance one (left atrium). There for, by manipulating the resistance of the aorta one may influence the amount of blood flowing into the atria. Manuvers that increase PVR (say a Valsalva) thus lead to a more severe regurg and a louder murmer.... If mitral regurg is due to mitral prolapse, a smaller left ventricle (as seen during standing) causes more prolapse. Thus stnading may accentuate the intensity and prolong the length of the mitral valve prolapse."

Hopefully that satisfies the burden of proof. Can we be a bit mroe civil next time we disagree about an answer? :)
 
caribsun said:
yep, according to the old guy on the tapes, right sided murmurs increase on inspiration and left sided murmurs increase on expiration.

I forgot to add, the above is totally correct. Its a great way to tell aortic and pulmonic stenosis apart, like p53 said. HOCM and MVP are just exceptions to this rule.
 
Mad props to whoever started this thread. At first I thought it was a dumb idea but it has really helped solidify some concepts and has incited some very nice discussion. :horns:
 
macman said:
are most of those answers real words??? I'd go with D only b/c I think the other answers (other than a and d) look like made up words. :)

one of our professors used to do that-until they fired him!

It's not familial hypercholesterolemia. That disease is best treated with ezetimibe (cholesterol absorption inhibitor at the small intestine brush border) alone or in combination with an HMG-CoA reductase inhibitor (the combination of ezetimibe and simvastatin has the trade name Vytorin).

Let'd dissect the question a bit further:

kcumbDO said:
45 yr old male with atherosclerosis and a positive family history of hyperlipidimia presents to his cardiologist. The cardiologist suspects that the patient's atherosclerosis may be due to his genetic predisposition to hyperlipidimia. Lab tests are ordered and the following results are obtained. Serum IDL levels are elevated and a defect in the synthesis of Apolipoprotein E is suspected. The patient is started on Nicotinic Acid and Gemfibrozil. Which of the following hyperlipidimias is present in this patient's family history.

A. Exogenous Hyperlipidimia
B. Combined Hyperlipoproteinimia
C. Familial Dysbetalipoproteinimia
D. Familial Hypercholestorelimia
E. Familial Hypertryglisaridimia

If there's a defect in ApoE synthesis, you have major effects on what? ApoE participates in all three known pathways involved in lipoprotein metabolism: transport of dietary lipid from the intestine to the liver (the exogenous pathway), transport of lipid from the liver to extra-hepatic cells (the endogenous pathway), and transport of cholesterol from extra-hepatic cells to the liver (the reverse cholesterol transport pathway). There is a genetic polymorphism of the ApoE gene that's called Type III (famial dysbetalipoproteinemia) dyslipidemia. You get increased IDL and VLDL and elevated blood levels of triglycerides and cholesterol. So, why is the patient on nicotinic acid and a fibrate? The nicotinic acid is broad spectrum and will lower LDL and triglycerides while raising HDL. Interestingly, nicotinic acid will also lower Lp(a), which is a modified lipoprotein that is a harbinger of advanced atherosclerosis. The fibric acid derivative will also decreased triglycerides and raise HDL while providing a modest LDL reduction.

Therefore, I believe the answer is (C), familial dysbetalipoproteinemia for the reason stated. On a side note, GREAT QUESTION, kcumbDO! This is the most intellectually challenging question I've read on this thread thus far. It was probably a 5-jump question!
 
47 y/o female with a history of long standing hypertension that is poorly controlled presents to the ER with a BP of 222/118. She complains of dizziness, headaches, and blurry vision. On exam, she is afebrile, tachy, 310 pounds, and papilloedema is noted. She reports no changes in diet and continues to eat McDonaalds several times a day. She is admitted for hypertensive emergency and continous IV Nitroprusside drip is started. Her BP remains elevated and IV Nitroprusside is continued over the next 3 days. On hospital day 3, her BP has reduced to 140/92, however, she reports of blurry vision, tinnitus, cold insensitivity, and nausea. On exam, she is afebrile, HR 52, there is puffyness of her eyelids and face, flushed skin, some mental slowing, and is having trouble with her memory. Lab reveals serum glucose 90mg/dl, serum T4 1.2 (decreased), serum TSH elevated. Which pathophysiological mechanism best accounts for this patient's hypothyroidism?

A. NO mediated inhibiton of Iodide uptake
B. Antibodies against TSH receptor
C. Wolf Chaikoff sydrome
D. Inhibiton of Iodide pump in follicular membrane
E. Inhibiton of peroxidase
 
HiddenTruth said:
47 y/o female with a history of long standing hypertension that is poorly controlled presents to the ER with a BP of 222/118. She complains of dizziness, headaches, and blurry vision. On exam, she is afebrile, tachy, 310 pounds, and papilloedema is noted. She reports no changes in diet and continues to eat McDonaalds several times a day. She is admitted for hypertensive emergency and continous IV Nitroprusside drip is started. Her BP remains elevated and IV Nitroprusside is continued over the next 3 days. On hospital day 3, her BP has reduced to 140/92, however, she reports of blurry vision, tinnitus, cold insensitivity, and nausea. On exam, she is afebrile, HR 52, there is puffyness of her eyelids and face, flushed skin, some mental slowing, and is having trouble with her memory. Lab reveals serum glucose 90mg/dl, serum T4 1.2 (decreased), serum TSH elevated. Which pathophysiological mechanism best accounts for this patient's hypothyroidism?

A. NO mediated inhibiton of Iodide uptake
B. Antibodies against TSH receptor
C. Wolf Chaikoff sydrome
D. Inhibiton of Iodide pump in follicular membrane
E. Inhibiton of peroxidase

Lets see if I can finally get one right

I can rule out choices C and D b/c they are essentially the same thing. Wolf Chaikoff syndrome is the inhibition of the Iodide pump by too much iodine so they would probobly present the same way. No mediated inhibition of Iodide uptake would cause you to have hyperthyroidism so I can eliminate A. Choice B is referring to Hashimoto's disease which takes a long time to cause full blown hypothyroidism. That leaves choice E so thats what I'm choosing.
 
HiddenTruth said:
47 y/o female with a history of long standing hypertension that is poorly controlled presents to the ER with a BP of 222/118. She complains of dizziness, headaches, and blurry vision. On exam, she is afebrile, tachy, 310 pounds, and papilloedema is noted. She reports no changes in diet and continues to eat McDonaalds several times a day. She is admitted for hypertensive emergency and continous IV Nitroprusside drip is started. Her BP remains elevated and IV Nitroprusside is continued over the next 3 days. On hospital day 3, her BP has reduced to 140/92, however, she reports of blurry vision, tinnitus, cold insensitivity, and nausea. On exam, she is afebrile, HR 52, there is puffyness of her eyelids and face, flushed skin, some mental slowing, and is having trouble with her memory. Lab reveals serum glucose 90mg/dl, serum T4 1.2 (decreased), serum TSH elevated. Which pathophysiological mechanism best accounts for this patient's hypothyroidism?

A. NO mediated inhibiton of Iodide uptake
B. Antibodies against TSH receptor
C. Wolf Chaikoff sydrome
D. Inhibiton of Iodide pump in follicular membrane
E. Inhibiton of peroxidase


I think the answer is D (Inhibition of iodide pump in follicular membrane). Activity of this pump is stimulated by TSH, which is elevated in the case history. Unless she has Hashimoto's (unlikely) or received postablative surgery while our backs were turned, she must have a problem at the level of the thyroid related to iodine deficiency. Nitroprusside has a very RARE adverse effect of causing hyperthyroidism but I am not sure of the mechanism. Hopefully you'll supply us with it. Choice E is the only other possible answer and I eliminated this by saying that inhibiting peroxidase is the same mechanism of PTU, which is the therapy for hyperthyroidism. You can get hypothyroidism with radioactive iodine and /or PTU but I believe this would not be immediate as in the case history.

Side note: In my wanderings, I picked up this tidbit of Jeopardy trivia. Nitrates are goitrogenic. They stimulate goiter formation. Nitrates can be found in hot dogs, sausages, luncheon meats, and variously prepared meat products. Nitrates are also found in well water and from fertilizer runoff.
 
me454555 said:
Lets see if I can finally get one right

I can rule out choices C and D b/c they are essentially the same thing. Wolf Chaikoff syndrome is the inhibition of the Iodide pump by too much iodine so they would probobly present the same way. No mediated inhibition of Iodide uptake would cause you to have hyperthyroidism so I can eliminate A. Choice B is referring to Hashimoto's disease which takes a long time to cause full blown hypothyroidism. That leaves choice E so thats what I'm choosing.

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?
 
Pox in a box said:
I think the answer is D (Inhibition of iodide pump in follicular membrane). Activity of this pump is stimulated by TSH, which is elevated in the case history. Unless she has Hashimoto's (unlikely) or received postablative surgery while our backs were turned, she must have a problem at the level of the thyroid related to iodine deficiency. Nitroprusside has a very RARE adverse effect of causing hyperthyroidism but I am not sure of the mechanism. Hopefully you'll supply us with it. Choice E is the only other possible answer and I eliminated this by saying that inhibiting peroxidase is the same mechanism of PTU, which is the therapy for hyperthyroidism. You can get hypothyroidism with radioactive iodine and /or PTU but I believe this would not be immediate as in the case history.

Side note: In my wanderings, I picked up this tidbit of Jeopardy trivia. Nitrates are goitrogenic. They stimulate goiter formation. Nitrates can be found in hot dogs, sausages, luncheon meats, and variously prepared meat products. Nitrates are also found in well water and from fertilizer runoff.

correct! Good reasoning. This was kind of a tricky question. First off, Wolf Chaikoff syndrome inhibiton of iodide pump or uptake secondary to increased levels. However, in Nitroprusside poisoning, or overuse, thiocyanate, a metabolite produced, can inhibit iodide pump and decrease uptake. Infact, other anions, such as perchlorate can do that as well. Therefore, you present with hypothyroidism. To be honest, I just made that up based on the mechanism--I really don't know whether that can occur with excess Nitroprusside use, or whether it has been reported. Infact, you mention, HYPERthyr, so I don't know.

Here is another one.

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
 
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