Pimping Thread for Step 1

TY06 said:

I thought it would be nice to start a thread where we can test eachother and talk about the material (instead of just asking eachother what book is good, because a lot of us learn better in group settings/testing eachother)...

So let it begin...

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(Comes out swinging). I love this kind of stuff. Here goes:

1) Pretend you're a GI specialist. A middle-aged woman presents with generalized pruritis and hypercholestrolemia. What's at the top of your differential?

2) 60 y/o female presents with unilateral visual loss, jaw claudication, and elevated ESR. What's the diagnosis? Whats the gold standard for Dx? What's the Tx?

3) Triad: Micronodular cirrohosis, DM, and increased skin pigmentation. What's the Dx?

DOCTORSAIB said:

(Comes out swinging). I love this kind of stuff. Here goes:

1) Pretend you're a GI specialist. A middle-aged woman presents with generalized pruritis and hypercholestrolemia. What's at the top of your differential?

2) 60 y/o female presents with unilateral visual loss, jaw claudication, and elevated ESR. What's the diagnosis? Whats the gold standard for Dx? What's the Tx?

3) Triad: Micronodular cirrohosis, DM, and increased skin pigmentation. What's the Dx?

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1) primary biliary cirrhosis, seen in middle-aged women (anti-mitochondrial antibodies), sometimes associated with other autoimmune diseases

2) diagosis is giant cell arteritis, gold standard is biopsy of temporal artery? tx is corticosteroids?

3) hereditary hemochromatosis (bronze diabetes)

BC ?
2: temp arteritis , dx with sed rate tx with steroids
3: hemochromotosis

damn you and your GI, why couldnt we couldnt we do endo?

surrender903 said:

BC ?
2: temp arteritis , dx with sed rate tx with steroids
3: hemochromotosis

damn you and your GI, why couldnt we couldnt we do endo?

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Lets see if you know this about endo. Hyperthyroid patients are treated w/ beta blockers because they have increased sympathetic tone, palpitations, tachycardia, and all that other good stuff you get with high sympathetic tone. Why is there no increased alpha tone in these patients?

selectivity of pharmalogical action?

alpha receptors have different actions then betas?

surrender903 said:

selectivity of pharmalogical action?

alpha receptors have different actions then betas?

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thats true. they have different actions. but that doesnt answer why they arent affected in hyper-t. (this is a combined endo/autonimcs question)


i'll give you a hint. dont read below if you dont want it








think about the action of T-hormone on the cellular level. what does it do to a cell? what 2nd messengers are increased/decreased?

ahhh.. i think i see

thyroid homormones have similar actions of beta 1 agonists (NE, epi) so beta blockers would block the action of those the excess TH.

someone come up with a list of all rashes that are diagnostic for bugs

someone write a thorough rash list that easily identifies bugs

forum is acting very strange...doesnt show replies in main window and keeps coming with error when posting....

surrender903 said:

ahhh.. i think i see

thyroid homormones have similar actions of beta 1 agonists (NE, epi) so beta blockers would block the action of those the excess TH.

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I think you got it, but aren't saying the 'buzzwords.' last chance to think of the answer on your own. the answer is a few lines down, so dont scroll down juat yet if you want to think for a moment.








answer: T-hormone increases intracellular cAMP levels (and some nitrous oxide levels). of the sympathtic receptors, only betas work by cAMP (Gs protein). alphas use IP3 (Gq protein). no cAMP, no sensitization, and normal alpha responce to epi/ne.

Name the syndrome associated with:

--Familial Adenomatous Polyposis
--Multiple osteomas
--Aggressive, intra-abdominal fibromatosis

turcots syndrome

It's Gardner's Syndrome.

Turcot's is associated with FAP and
--medulloblastomas (2/3)
--glioblastomas (1/3)

(And, yes, I had to look that up. 7th ed Big Robbins, p. 862.)

By the way, whomever came up with this thread is a friggin genius.

Should be a sticky. (Hint, hint, mods!)

A 35 year-old male presents with early satiety and epigastric tenderness. Bloodwork reveals hypoalbuminemia. An endoscopy is performed and reveals grossly enlarged rugal folds. Histologically, what would a biopsy most likely reveal?

GuP said:

someone come up with a list of all rashes that are diagnostic for bugs

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Come up with your own list you Lazy a$$!

Also,

I don't know the stomach question but - list three infectious causes of rashes on the soles of the feet and palms of the hands.

THP said:

Come up with your own list you Lazy a$$!

Also,

I don't know the stomach question but - list three infectious causes of rashes on the soles of the feet and palms of the hands.

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1. Syphillis
2. Rocky Mounted Spotted Fever
3. CoxSackie Virus

Vriesea said:

A 35 year-old male presents with early satiety and epigastric tenderness. Bloodwork reveals hypoalbuminemia. An endoscopy is performed and reveals grossly enlarged rugal folds. Histologically, what would a biopsy most likely reveal?

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is this menetriers? i know albumin leaks out and u get edema...maybe u do get hypoalbumin also...if so then you will see foveolar cell hyperplasia and decrease in parietal (mainly) and chief cells. increased gastrin. late complication = descrease b12.

THP said:

Come up with your own list you Lazy a$$!

Also,

I don't know the stomach question but - list three infectious causes of rashes on the soles of the feet and palms of the hands.

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thanks your help is greatly associated

anyways, the previous list you can staph to it...causes desquamation of the plams and soles.


heres a couple of questions:

whats the highest risk factor for developing type 1 dm?

pt. was noted with extensive pseudopolyps throughout his colon. now the pt comes with an increase in bilirubin. what is the dx? what is the pt at risk for developing?

a diabetic mother birthed a child in whom the pressure in the left ventricle was 11mm/hg and the right ventricle was 85 mm/hg. what is the diagnosis? what is the pathology?

A 5 yr old boy is rushed to the emergency room with a fever of 105F and a diffuse petechial rash over his body. The ER physician orders lab work which shows the following. Glc=30mg/dl, ketones=elevated, ACTH=elevated, Na=120mEq, K=5.7mEq, urinary 17-ketosteroids=low, PT=elevated, PTT=elevated, platelets=50,000. The blood pressure is 90/60 and dropping. The patient does not survive and a pathology report is requested by the ER physician. Which of the following findings would be noted on the pathology report?

A. Necrotic cells in the pituitary
B. Hamartoma in the hypothalamus
C. Red blood cells in the zona glomerulosa
D. Lymphocytes in the CSF
E. Warthin-Finkeldy cells in sample skin tissue

40 yr old male with a significant sexual history, presents to the internist with the complaint that he has recently been having trouble walking. A careful history reveals that the patient is a fisherman with a very ravenous appetite for seafood. The internist performs the physical exam and notices that the patient has bilateral loss of proprioception, 2-point-tactile discrimination, and vibratory sensation. Further examination reveals that the patient has bilateral spastic paralysis with hyperreflexia, hypertonia, and a positive Babinski sign. A positive Romberg test was also noted. With respect to the general appearance of the patient, the physician noted that the patient was in slight distress and appeared pale. There were no other remarkable physical findings. The physician ordered lab work which included: CBC, blood cultures, and urinalysis. The CBC revealed an RBC=2.5billion, WBC=11,000, MCV=110, HCT=45%. The urinalysis revealed presence of excess amounts of methylmalonic acid. The blood cultures were negative. Imagine that you are this patient’s physician, based on the above, what is a reasonable working diagnosis for this case?

A. Tabes Dorsalis
B. Thrombosis of Anterior Spinal Artery
C. Subacute Sclerosing Panencephalitis
D. Friedrich’s Ataxia
E. Subacute Combined Degeneration
F. Schwanoma

6 yr old male presents to his pediatrician with weakness in the arms and legs of 3 day duration. The boy's mother states that he recently recovered from an upper respiratory tract infection 1 week ago. History of present illness reveals that the weakness started in the lower extremities and then spread to the upper extremities. The physician orders a spinal tap and the CSF profile returns with the following finding: “Albuminocytologic dissociation”. What is the diagnosis?

A. Poliomyelitis
B. Multiple Sclerosis
C. Duchene-Muscular Dystrophy
D. Guillain-Barre Syndrome
E. Polymyositis

A 6 mo. old male presents to the clinic with recurrent pulmonary infections. The mother states that the boy had had an uncomplicated delivery, but had difficulty passing stool for weeks after birth. When the child was able to move his bowels the mother noted that the stool was greasy in appearance. The mother also states that the child has recently started coughing up large amounts of sputum. On physical exam the physician notes dullness to percussion in both lung fields and several petechiae on the lower limbs. Which of the following medications are used to treat the organism that most commonly affects patients with this presentation?

A. Ceftriaxone
B. Penicillin G
C. Cefotaxime
D. Azithromycin
E. Cefazolin
F. Ceftazidime

2. tabes dorsalis
3. guillain-barre

can't help ya on the other 2

good questions

1: waterhouse fredreichsen syndrome so rbcs in adrenals ? usuall associated with n. menigitidis (hence the petechial rash)
2: tabes dorsalis
3: GB
4: azithromyocin

my guesses

The last one should be ceftazidime for pseudomonas, i think (CF presentation)

i think you are right idiopathic

i thought azithromycin and toby were in the same family...
well 3/4 aint bad

the correct answers in order of appearance,

C: this pt. is presenting with bilateral hemorrhagic necrosis of adrenals, aka waterhouse friedrechsen syndrome

E: Subacute combined degeneration subsequent to infection with fish tapeworm diphilobothrium latum. vit b12 def is classically associated with increased methylmalonic acid in urine as a result of decreased enzyme activity of methylmalonyl coA mutase. pts develope degeneration of CST and dorsal columns. It is not tabes dorsalis because that is associated with degeneration of dorsal columns and roots and pt would not present with UMN symptoms.

D: Gulluiane Barre Syndrome. Usually folowing viral illness causes a peripheral demyelination associated with ascending weakness. Classic CSF finding is increased protein in relationship to cells, aka Albuminocytologic dissociation.

F: Ceftazidime. This pt has cystic fibrosis and patients with this condition have increased suceptibility to psudomonas auriginosa. Ceftazidime is a 3rd gen ceph that is given IM or IV and has rel good cov for psudomonas although i heard recently that ceftaz has lost its affect on psedomonas. Now the best tx is a double coverage with a 3rd gen cephalosporin and either imipenem cilastin or fluroquinolones, or aminoglycosides.

lasek said:

answer: T-hormone increases intracellular cAMP levels (and some nitrous oxide levels). of the sympathtic receptors, only betas work by cAMP (Gs protein). alphas use IP3 (Gq protein). no cAMP, no sensitization, and normal alpha responce to epi/ne.

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I'm pretty sure this is somewhat incorrect. TSH works with cAMP as a second messenger, but Thyroid Hormone receptors work by a completely different mechanism: they are intracellular receptors.

The beta effect is due (I believe) to upregulation of beta-receptor synthesis induced by thyroid hormone. Increased cAMP is then due to this upregulation.

To answer your original question: There is no increased alpha tone simply because those receptors are not upregulated by thyroid hormone.

This whole thing can be a little confusing because thyroid hormone receptors are also designated "alpha-1, alpha-2, beta-1, beta-2," although they have no structural or functional relation to adrenergic receptors.

Someone please correct me if I'm wrong.

lasek said:

Lets see if you know this about endo. Hyperthyroid patients are treated w/ beta blockers because they have increased sympathetic tone, palpitations, tachycardia, and all that other good stuff you get with high sympathetic tone. Why is there no increased alpha tone in these patients?

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They actually dont have increased sympathetic tone. They are in a hypermetabolic state (thyroid hormone causes more Na/K pumps to be made) and they 'idle higher', so to speak. You treat the symptoms of hyperthyroidism with B-blockers but is not due to thyroid hormones Beta-effect, rather it is a side effect of an increased metabolic rate.

BTW, thyroid hormone is a steroid like hormone, and acts intracellularly on the genome, causing the above process. One other known effet is to increase myosin synthesis, which would cause the body to react to physiologically normal levels of adrenaline with increased contractility.

lord_jeebus said:

The beta effect is due (I believe) to upregulation of beta-receptor synthesis induced by thyroid hormone. Increased cAMP is then due to this upregulation.

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As mentioned above, I believe all these effects are actually secondary to the normal physiologic mechanism of T4/T3 activity. No added effect on B-receptors from what I can tell.

Idiopathic said:

As mentioned above, I believe all these effects are actually secondary to the normal physiologic mechanism of T4/T3 activity. No added effect on B-receptors from what I can tell.

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Damnit, now I'm curious about this subject.

Here's are two old papers I found: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15999&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6247145&dopt=Citation

It doesn't answer whether this is the primary reason for increased catecholamine sensitivity but there seems to be a fair bit of literature suggesting a relationship between T3/T4 and beta-receptor expression.

I also found this on uptodate:

"In many tissues, hyperthyroidism is associated with an increased number of ß-adrenergic receptors [1]. The ensuing increase in ß-adrenergic activity is responsible for many of the symptoms associated with this disorder. It also explains the ability of ß-blockers to ameliorate rapidly many of the symptoms, including palpitations, tachycardia, tremulousness, anxiety, and heat intolerance [2]."

While I was looking this up I also learned that propranolol has an additional effect of blocking conversion of T4 to T3.

lord_jeebus said:

Damnit, now I'm curious about this subject.

Here's are two old papers I found: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15999&dopt=Abstract
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6247145&dopt=Citation

It doesn't answer whether this is the primary reason for increased catecholamine sensitivity but there seems to be a fair bit of literature suggesting a relationship between T3/T4 and beta-receptor expression.

I also found this on uptodate:

"In many tissues, hyperthyroidism is associated with an increased number of ß-adrenergic receptors [1]. The ensuing increase in ß-adrenergic activity is responsible for many of the symptoms associated with this disorder. It also explains the ability of ß-blockers to ameliorate rapidly many of the symptoms, including palpitations, tachycardia, tremulousness, anxiety, and heat intolerance [2]."

While I was looking this up I also learned that propranolol has an additional effect of blocking conversion of T4 to T3.

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did not know about propranolol and T4/T3 conversion. I guess thats why its alwasy mentioned as the beta blocker for hyper T.

I talked to several endocrinologists about this, and they said that its difficult to explain because t-homone has so many functions. Idiopathic is 100% correct about T-homone acting intracellulary, and hyper-t pateints having higher basal metabolic activity. This explains the systemic effects. The beta-receptor effects are not related to the increased metabolism. The way the endocrinologists explained it was that its the cAMP increase thats important for the beta receptor hypersensitivity. beta receptor upregulation happens, but they dont think that its a major mechanism for increased sensitivity.

I did find an article that seems to contradict this though. Their conclusion seems to be that cAMP levels are increased in hypo-t. They do say that it is a controvercial issue. I can only read the abstract from home so i'll refrain from commenting any more till i read it. Maybe someone wants to read it and comment on it.

This is becoming more intersting and complicated then i thought.

http://www.ncbi.nlm.nih.gov/entrez/..._uids=10690958&query_hl=3&itool=pubmed_DocSum

Metabolism. 2000 Feb;49(2):275-9.

whats so bad about terfenidine and astemizole?

felipe5 said:

whats so bad about terfenidine and astemizole?

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Don't they give you some type of tachycardia? Sheesh, I haven't thought about antihistamines in a while.

Torsades de Pointes, I believe.

felipe5 said:

whats so bad about terfenidine and astemizole?

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I've never heard of either of those drugs and they are not in first aid.

THP said:

I've never heard of either of those drugs and they are not in first aid.

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I've heard of them -- but I wonder if drugs that have been withdrawn from the market are covered on Step I? Granted there aren't that many recent ones besides these and a couple of COX-2 inhibitors...

I agree with Idiopathic that the side effect is Torsades de Pointes, especially when taken with P450 inhibitors.

lord_jeebus said:

I've heard of them -- but I wonder if drugs that have been withdrawn from the market are covered on Step I? Granted there aren't that many recent ones besides these and a couple of COX-2 inhibitors...

I agree with Idiopathic that the side effect is Torsades de Pointes, especially when taken with P450 inhibitors.

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according to my pharm teacher, about 5 million drugs that are off market are fair game, and heavily tested on, for step 1 and shelfs. he also says that torsades is a hot topic.

Here is a question for ya:

Your pt, 25yo woman, tells you that 6 months ago she had balance problems and numbness in her right hand, but the numbness subsided after a week or so. She is a secretary and thinks that she may have carpal tunnel syndrome. Today, you note that she has decreased vibratory sense in both the right hand and right leg, decreased pinprick sensation in the right lower limb, and that both of her right limbs are weak. Analysis of CSF following lumbar tap reveals heterogenous IgG staining with oligoclonal banding. Which of the following might also be seen in the pt?
A. Bilateral ptosis
B. Blurry vision
C. Claw hand
D. Tic douloureux
E. Foot drop

Follow up to the last question - whats the drug most likely to be prescribed?

a) Amoxicillin + Clavulanate
b) Ribavirin + Interferon
c) Interferon Beta
d) Cisplatin
e) Meclizine

MS so blurry vision

rx - umm i would have to go with interferon beta based on the process of exclusion

infereron beta for MS.... alpha for hep c (with ribavirin), hep b (with lamivudine), kaposi's sarcoma, gamma for nadph oxidase deficiency

what the hell is meclizine?

Catalyst said:

infereron beta for MS.... alpha for hep c (with ribavirin), hep b (with lamivudine), kaposi's sarcoma, gamma for nadph oxidase deficiency

what the hell is meclizine?

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1st generation H1 antagonist causing mild sedation, used to treat motion sickness. (we had a big pharm test today over this stuff.)

If this is the kind of stuff we need to know for step I then I am definitely failing this test at the end of the month.

lilmo said:

1st generation H1 antagonist causing mild sedation, used to treat motion sickness. (we had a big pharm test today over this stuff.)

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See, this is the **** i'm worried about... that even though I know the mechanism/clinical use/side effects of the drugs, I might recognize a particular drug name on the exam... does first aid have the names of the drugs we need to know? I've heard it's enough for pharm... anyone can care to comment who's taken the exam?

You guys went right to the money for the Dx of MS and treatment