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?

 

[lasek]

Was reviewing physio, and here's a question for you guys and girls.

Several months after being involved in an accident, your patient has trouble shrugging his right shoulder. He has a diminished gag reflex, decresed sensation on the posterior region of the tongue, and the uvula deviates to the left. The rest of the physical is WNL. Which of the following may most likely be seen on an EKG of this patient?

A) Normal sinus rhythm
B) Sinus tachycardia
C) Second degree AV block
D) Shortened PQ interval
E) Presence of U waves

How would (or would) the EKG change if the patient's symptoms were lateraized to the other side? (ie trouble with Lt shoulder shrugging, uvula deviates to right)

 

[CaNEM]

What's the lining of the mainstem bronchus, please? What's the lining of the mainstem bronchus, please?

 

[HiddenTruth]

Was reviewing physio, and here's a question for you guys and girls.

Several months after being involved in an accident, your patient has trouble shrugging his right shoulder. He has a diminished gag reflex, decresed sensation on the posterior region of the tongue, and the uvula deviates to the left. The rest of the physical is WNL. Which of the following may most likely be seen on an EKG of this patient?

A) Normal sinus rhythm
B) Sinus tachycardia
C) Second degree AV block
D) Shortened PQ interval
E) Presence of U waves

How would (or would) the EKG change if the patient's symptoms were lateraized to the other side? (ie trouble with Lt shoulder shrugging, uvula deviates to right)

Well, seems like there is an injury of IX, X, and XI. CN IX and X take afferents back from the carotid and aortic arch, respectively, so I imagine that if you sever your GP n, then you decrease your afferent firing, thus an increase in symp. activity--> so choice B makes the most sense. Vagus nerve carries firing from the aortic arch to the VM center in the medulla, but is dependent only on increases in BP, so it doesn't do a whole lot in this scenario.

As far as a lesion on the other side, I am not sure which side of CN the baroreceptors use, or if it's both.

 

[lasek]

Well, CN IX and X take afferents back from the carotid and aortic arch, respectively, so I imagine that if you sever your GP n, then you decrease your afferent firing, thus an increase in symp. activity--> so choice B makes the most sense. Vagus nerve firign from the aortic arch to the VM center in the medulla is dependent only on increases in BP.

Correct answer, but not the reason i was trying to get at. Thats partially my fault though.

The point I was going for: The patient has a right jugular foramen syndrome. The right CNX preferentially inhibits the SA node decreasing the intrinsic firing rate. Absence of the right CNX inhibition would cause sinus tach by disinhibition of the SA node.

Follow up (if other side was affected): Left vagus preferentially affects AV node, decreasing the conduction through it. If left CNX was affected, there may be a shortening of PQ interval

 

[HiddenTruth]

Correct answer, but not the reason i was trying to get at. Thats partially my fault though.

The point I was going for: The patient has a right jugular foramen syndrome. The right CNX preferentially inhibits the SA node decreasing the intrinsic firing rate. Absence of the right CNX inhibition would cause sinus tach by disinhibition of the SA node.

Follow up (if other side was affected): Left vagus preferentially affects AV node, decreasing the conduction through it. If left CNX was affected, there may be a shortening of PQ interval

o ok, wasn't aware of the selective AV and SA activity of the respective sides. For the record, it's PR interval (nomenclature).

 

[Janders]

Correct answer, but not the reason i was trying to get at. Thats partially my fault though.

The point I was going for: The patient has a right jugular foramen syndrome. The right CNX preferentially inhibits the SA node decreasing the intrinsic firing rate. Absence of the right CNX inhibition would cause sinus tach by disinhibition of the SA node.

Follow up (if other side was affected): Left vagus preferentially affects AV node, decreasing the conduction through it. If left CNX was affected, there may be a shortening of PQ interval

Nice tidbit!

 

[Bounty]

Hi everyone - i had a couple of questions that I couldn't quite figure out:

1) Why do you have increased alkaline phosphatase in von Recklinghausen dz of bone (hyperparathyroidism)? Isnt alkaline phosphatase a measure of bone formation?

2) why does hyperthyroidism cause osteoporosis? Is it due to a general catabolic state?

Thanks! I tried looking it up but couldnt find any good explanations... i figured one of you SDN smarties probably knew...🙂

 

[lasek]

Hi everyone - i had a couple of questions that I couldn't quite figure out:

1) Why do you have increased alkaline phosphatase in von Recklinghausen dz of bone (hyperparathyroidism)? Isnt alkaline phosphatase a measure of bone formation?

2) why does hyperthyroidism cause osteoporosis? Is it due to a general catabolic state?

Thanks! I tried looking it up but couldnt find any good explanations... i figured one of you SDN smarties probably knew...🙂

1) Alkaline phosphotase is a marker found on osteoblasts, so its more a factor of osteoblast activity than bone formation. PTH doesnt activate osteclasts directly, but rather activates osteoblasts. They in turn activate osteoclasts via the RANK ligand. Thats the only reason I can think of.

2) No idea.

 

[Doc Ivy]

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.

You're right that it's a menigioma--- they tend to be very progesterone sensitive, more common in women, and can occur anywhere in the neuraxis. Meningiomas are homogenously enhancing on CT and they also tend to recur after resection. GBMs are aggressive and have a poor prognosis of less than 1 year survivial. HIV lymphomas or toxpoplasmosis are ring enhancing lesions not homogenously enhancing, and this isn't a fungus which would be more likely in an immune compromised patient so you would not treat with fluconazole.

 

[Pox in a box]

You're right that it's a menigioma--- they tend to be very progesterone sensitive, more common in women, and can occur anywhere in the neuraxis. Meningiomas are homogenously enhancing on CT and they also tend to recur after resection. GBMs are aggressive and have a poor prognosis of less than 1 year survivial. HIV lymphomas or toxpoplasmosis are ring enhancing lesions not homogenously enhancing, and this isn't a fungus which would be more likely in an immune compromised patient so you would not treat with fluconazole.

So what's the answer?

 

[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?

Bumping again for p53...help us out.

 

[chitown82]

Bumping again for p53...help us out.

I'm not in med school (yet), but I read a paper on p53 recently. From what I gathered, dysfunctional telomeres, oncogenes, or ROS signals induce DNA damage which upregulate p53. p53 then targets the gene transcription (via upregulation of p21) to cause reversibe senescence growth arrest in cells -hence preventing cancer. p53 is known as a gatekeeper tumor suppressor - it helps to prevent cancer by acting on mitotic cells that are at risk for neoplastic transformation. Loss of p53 function delays senescence in cells. It has recently been shown that constitutive hyperactive p53 accelerates aging. Cells that overexpress p53 are more susceptible to p53-related apoptosis and thus decreasing the availability of mitotic cells to renew tissue. Sorry if this is all obvious and of no help....

 

[patamulu]

here are some more qs... sorry i couldn't answer quite a few of the qs asked here i'm dead 😱
1. A healthy 30 year old man is participating in a study of the effects of a competitive inhibitor of endothelial nitric oxide synthase. After intravenous injection of the inhibitor, blood pressure immediately increases. Supplementation with which of the following amino acids is most appropriate to reverse this increase?

a. arginine, b. aspartic acid, c. glutamic acid, d. leucine, e. lysine, f. methionine, g. tyrosine

2. In gout, hyperuricemia resulting from overproduction of urate is most likely to result from a lack of feedback inhibition by ADP or GDP at which enzyme?

a. adenosine deaminase, b.dihydrofolate reductase, c. glucose 6phosphate dehydrogenase, d. necleotide phosphorylase, e. phosphoribosylpyrophosphate synthetase

3. A 45 year old woman has an acute coronary occlusion. within seconds the ischemic region shows mitochondrial swelling and depletion of glycogen granules. which of the following metabolic events is the most likely cause of these cellular changes?

a. accumulation of free fatty acids, b. ATP depletion, c. degradation of membrane phospholipid, d. efflux of K+. e. infflux of Na+

4. A sexually active 18year old woman comes to the physician's office because of fever, lower abdominal pain, and a purulent vaginal discharge for the last 3 weeks. A tender mass is palpated in the right lower quadrant on bimanual examination. wihich fo the following is the most likely site of the mass?

a. ovary, b. fallopian tube, c. uterine fundus, d. uterine body, e. vagina, f. bladder,

g. rectum

 

[Doc Ivy]

So what's the answer?

It will most likely recur.

 

[Doc Ivy]

Patamulu,
1) arginine-- L arginine is the first step in the NOS pathway. Knowing that you can look up the specifics
2) not sure, sorry 🙁
3) my guess is ATP depletion which is the first thing that happens with ischemia, you can only generate so much ATP anaerobically, that messes with Na/KATPase and then you get the electrolyte disturbances that cause the cell to swell and die
4) probably the fallopian tube, my guess is that she either has gonorrhea or chlamydia that has spread and caused a salpingitis-- very painful and in the right spot based on the physical exam

here are some more qs... sorry i couldn't answer quite a few of the qs asked here i'm dead 😱
1. A healthy 30 year old man is participating in a study of the effects of a competitive inhibitor of endothelial nitric oxide synthase. After intravenous injection of the inhibitor, blood pressure immediately increases. Supplementation with which of the following amino acids is most appropriate to reverse this increase?

a. arginine, b. aspartic acid, c. glutamic acid, d. leucine, e. lysine, f. methionine, g. tyrosine

2. In gout, hyperuricemia resulting from overproduction of urate is most likely to result from a lack of feedback inhibition by ADP or GDP at which enzyme?

a. adenosine deaminase, b.dihydrofolate reductase, c. glucose 6phosphate dehydrogenase, d. necleotide phosphorylase, e. phosphoribosylpyrophosphate synthetase

3. A 45 year old woman has an acute coronary occlusion. within seconds the ischemic region shows mitochondrial swelling and depletion of glycogen granules. which of the following metabolic events is the most likely cause of these cellular changes?

a. accumulation of free fatty acids, b. ATP depletion, c. degradation of membrane phospholipid, d. efflux of K+. e. infflux of Na+

4. A sexually active 18year old woman comes to the physician's office because of fever, lower abdominal pain, and a purulent vaginal discharge for the last 3 weeks. A tender mass is palpated in the right lower quadrant on bimanual examination. wihich fo the following is the most likely site of the mass?

a. ovary, b. fallopian tube, c. uterine fundus, d. uterine body, e. vagina, f. bladder,

g. rectum

 

[HiddenTruth]

can someone please explain to me, why is it that u get lactic acidosis with Von gierke's (type 1) ds? I understand you're not making enough glc--> decrs ATP (from decrs substrates??, but O2 is normal), NADH/FADH2 accum-> inhibit TCA--> shift pyr into lactate? I don't know--any thoughts?

 

[Pox in a box]

Here's something to bump this thread back up top...

Describe a patient that has:

A) Broca's area damaged

B) Wernicke's area damaged

C) Bonus: Name the Brodmann's numbers associated (please don't be on the exam!!!)

 

[Janders]

Here's something to bump this thread back up top...

Describe a patient that has:

A) Broca's area damaged

B) Wernicke's area damaged

C) Bonus: Name the Brodmann's numbers associated (please don't be on the exam!!!)

yay, i'm studying neurosci today 🙂

Broca's is the motor area of speech and writing. without it patients can understand what you say, and even think of things to say, but they can't say (or write them), at least not well. An "Expressive" Aphasia

A problem to Weirnicke's area creates a "wordy" patient. So they are fluent (they speak) but they don't make much sense, nor do they understand you.... "word salad" comes up as term to describe this

Broca's is 44/45
Wernike's is normally 22
post central (sensory) is 1, 2, 3
pre central (motor) is 4
pre-motor is 6....
I dont know any others off my head.

 

[lasek]

yay, i'm studying neurosci today 🙂

Broca's is the motor area of speech and writing. without it patients can understand what you say, and even think of things to say, but they can't say (or write them), at least not well. An "Expressive" Aphasia

A problem to Weirnicke's area creates a "wordy" patient. So they are fluent (they speak) but they don't make much sense, nor do they understand you.... "word salad" comes up as term to describe this

Broca's is 44/45
Wernike's is normally 22
post central (sensory) is 1, 2, 3
pre central (motor) is 4
pre-motor is 6....
I dont know any others off my head.

Also keep in mind that patients with Broca's aphasia know they have a problem and may be frustrated by it, unlike most of the Wernicke's patietns who dont realize it and are not too bothered by it.

 

[Doc Ivy]

Also remember conduction aphasia which is a lesion in the arcuate fasciculis area 39 that connect the Broca motor and Wernicke sensory areas. These patients are articulate and can generate meaningful speech, and can they can comprehend when you speak. But if you ask them a question or to repeat something they can't receive it in the sensory and CONDUCT it to the motor area, therefore they can't answer you.

 

[Janders]

Just for fun, another neuro question:

A 48 year old alcoholic complains of unsteady gait. You suspect a possible cerebellar problem. Which of the following accounts for the outflow of this part of the brain?
a) Excitatory Granule Cells of the Vermis
b) Inhibitory Outer Layer Purkinje cells
C) GABA-Releasing middle layer purkinje cells
d) Inhibitory climbing fibers
e) excitatory Purkinje cells found in the cerebellar hemispheres

 

[caribsun]

Patamulu,
1) arginine-- L arginine is the first step in the NOS pathway. Knowing that you can look up the specifics
2) not sure, sorry 🙁
3) my guess is ATP depletion which is the first thing that happens with ischemia, you can only generate so much ATP anaerobically, that messes with Na/KATPase and then you get the electrolyte disturbances that cause the cell to swell and die
4) probably the fallopian tube, my guess is that she either has gonorrhea or chlamydia that has spread and caused a salpingitis-- very painful and in the right spot based on the physical exam

2 is PRPP synthetase AMP, GMP inhibit PRPP decreaseing 5 phosphoribosyl 1 pyrophosphate

 

[Doc Ivy]

Just for fun, another neuro question:

A 48 year old alcoholic complains of unsteady gait. You suspect a possible cerebellar problem. Which of the following accounts for the outflow of this part of the brain?
a) Excitatory Granule Cells of the Vermis
b) Inhibitory Outer Layer Purkinje cells
C) GABA-Releasing middle layer purkinje cells
d) Inhibitory climbing fibers
e) excitatory Purkinje cells found in the cerebellar hemispheres

c? aren't purkinje always inhibitory?

 

[Janders]

c? aren't purkinje always inhibitory?

Precisely. Also always in the middle layer. And the only outflow neurons. Good job.

 

[HiddenTruth]

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:


Quote:
Originally Posted by kcumbDO
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.
!

I thought the function of apo E is to mediate uptake of IDL and chylomicrons in the liver, but no primary fxn extrahepatically. I know type 3 is familial dysbetalipoproteinemia (which is due to a defective apo E isoform), but most of the TG are removed by the time you form IDL and chylo remnant, and all the cholesterol is still there, which is very little to begin with in these lipoproteins. So, I guess I don't really understand why first off, there is a greater increase in TG than LDL (according to some chart i have from class), and secondly, why there is such an increase in TG, because the function of apoE is to mediate uptake of the remnants, which already have very little TG in them. Unless of course, it's just the obvious, that that very little over time accumulates.

 

[Pox in a box]

Bumping up for Dr. Pak and the rest of the 2006 Step 1 Club...

 

[GuP]

wow thanks pox! i would have never known about this if it werent for u 👍

 

[coolmavs]

Hey Pox, thanks a lot mate for reviving this thread! A great method of keeping oneself going!

 

[Pox in a box]

This was my favorite thread last year. I learned a lot from it and it really kept me thinking critically, even when I was dead tired at the end of the night from studying.

 

[DrPak]

Toxic doses of apirin causes depression of the respiratory center leading to respiratory acidosis. In addition, interference with the Kreb's cycle and uncoupling of oxidative phosphorylation causes metabolic acidosis and hyperthermia (which I get due to Goljan). However it also leads to hypokalemia - why does that happen? I don't get it.

Also, chronic use of aspirin can cause hypoglycemia. Why is that?

I'm not testing anyone here... I don't know myself.

 

[wam_256]

thanks Pox!!!! 👍

 

[eripearson]

If I remember correctly salicylates uncouple oxidative phosphorylation which increased tissue demand for glucose ultimately resulting in the hypoglycemia. By a similar mechanism if glycogen stores are adequate aspirin can induce a hyperglycaemic state by catecholamine production with glycogenolysis. Recently i came across a paper that demonstrates aspirin's use in Type II diabetes as it ameliorates insulin resisitance (Hundal et al, 2002 JCI).

 

[GuP]

can someone expand on the concept of radial traction in lungs? from what i know (at least i think i know) is that radial traction bascially is the force that pushes the alveoli against the lung parenchyma, hence keeping the alveoli open longer. this is the reason it is increased in restrictive diseases and is inversely related to elasticity? is that it?

 

[GuP]

57 y/o female who has been on dialysis for the past 15 years now appears at the ER in distress. Pt has tachycardia, tachypnea but a rise in the systemic venous pressure upon inspiration is not seen. Upon catheterization, a prominent x-descent of the jvp is noted. Ecg shows electrical alternans and lowered voltage. what is the likely diagnosis?

 

[Columbia22]

57 y/o female who has been on dialysis for the past 15 years now appears at the ER in distress. Pt has tachycardia, tachypnea but a rise in the systemic venous pressure upon inspiration is not seen. Upon catheterization, a prominent x-descent of the jvp is noted. Ecg shows electrical alternans and lowered voltage. what is the likely diagnosis?

Pericardial tamponade?

 

[SarahGM]

Or chronic pericarditis?

 

[Rogue_Leader]

57 y/o female who has been on dialysis for the past 15 years now appears at the ER in distress. Pt has tachycardia, tachypnea but a rise in the systemic venous pressure upon inspiration is not seen. Upon catheterization, a prominent x-descent of the jvp is noted. Ecg shows electrical alternans and lowered voltage. what is the likely diagnosis?

I vote for constrictive pericarditis.

 

[GuP]

cardiac tamponade

 

[GuP]

AIDS pt now presents with a headache. CSF: gram stain is negative, latex agglutination is positive, urease positive. most likely cause?

 

[surrender903]

just taking a guess... cryptococcus

?

aids patient

my other guess would be toxo

 

[GuP]

crypto indeed - remember crypto is the only medically significant, urease positive yeast - common in aids and cancer

 

[GuP]

digoxin administration causes:

a) decrease in systole
b) increase in diastole
c) increase in systole
d) decrease in diastole
e) decrease in systole and diastole
f) increaes in systole and diastole

 

[SarahGM]

digoxin administration causes:

a) decrease in systole
b) increase in diastole
c) increase in systole
d) decrease in diastole
e) decrease in systole and diastole
f) increaes in systole and diastole

maybe it's just early, but i'm not sure i know what you mean. increase in S and D pressure? volume? rate of filling? output?

digoxin is a positive inotrope, so it would increase the systolic output. and in patients with heart failure, it potentiates the vagal input by sensitizing the baroreceptors... so there is more time for diastolic filling.

soooo, going by that reasoning... i would say F?

 

[surrender903]

sarah i was thinking the same thing.

i knew that dig increase sys by allowing a larger diastole... but i wasnt sure how that fit into the answers provided.

 

[GuP]

ah thas a bad question indeed....the answers correspond to duration

 

[Rogue_Leader]

A 50 year old male who has undergone chemotherapy for advanced lung cancer for the past 5 months presents with a headache and stiff neck. A spinal tap reveals numerous neutrophils and gram positive rods. What is the likely organism?

 

[DrPak]

Listeria monocytogenes.

Listeriosis is not a common condition in normal folks but does occur in immunocompromised people, as this patient is likely to be as a result of his chemo.

One question though: the reason listeriosis develops is because of the immunosuppressive action of the chemo drugs. If that is the case, then shouldn't there be a less vigorous neutrophil presence in the CSF?

 

[DrPak]

A 50 year old male who has undergone chemotherapy for advanced lung cancer for the past 5 months presents with a headache and stiff neck. A spinal tap reveals numerous neutrophils and gram positive rods. What is the likely organism?

Listeria monocytogenes.

Listeriosis is not a common condition in normal folks but does occur in immunocompromised people, as this patient is likely to be as a result of his chemo.

One question though: the reason listeriosis develops is because of the immunosuppressive action of the chemo drugs. If that is the case, then shouldn't there be a less vigorous neutrophil presence in the CSF?

 

[Rogue_Leader]

One question though: the reason listeriosis develops is because of the immunosuppressive action of the chemo drugs. If that is the case, then shouldn't there be a less vigorous neutrophil presence in the CSF?

I would have thought so too, but the source I got the question from definately says there are numerous neutrophils. My guess would be that the neutrophils haven't been activated because the chemo supresses release of TNF-a and gamma intereferon.

 

[tupac_don]

I'll write the answer explanation out like before. These are fun to make up but they are taking too much time, so this is my last.

Answer: E. The patient has symptoms indicative of portal hypertension secondary to liver cirrhosis. Encephalopathic comas and esophageal varices are the most common causes of death in this population. Encephalopathy arises from a buildup of toxic metabolites, particularly ammonia compounds.

Answer choice A is a complication of congenital diaphragmatic fistulas. Choice B is a rare and serious complication of parasitic infections of the biliary tree, particularly Clonorchis sinsensis and Ascaris lumbricoides. Choice C, the coarse hand tremor associated with portal hypertension, may be present in this patient but would be an unlikely cause of mortality. Hemorroids are an important anastomotic complication of portal hypertension, however, they are unlikely to incur severe blood loss (D). The portal system does not supply the vasculature of the brain, so hepatic cirrhosis would be unlikely to cause a malignant hypertensive crisis (F).

I like the way you answer your questions.