Test your might!

[Depakote]

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

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

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

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[Depakote]

They gave us this case in class and I liked it so passing it along (slight modifications):

A 28 year old female is admitted for evaluation of headache, abdominal pain, and nausea with vomiting. The headaches are bitemporal and frontal in location and increasing in severity throughout the week prior to admission. There was no history of trauma. She denied fevers, seizure, visual impairment. The abdominal pain was crampy and mid-epigastric and without radiation to the back. There was no relationship to food intake or relief with antacids. She had experience several episodes of clear to yellow emesis over the preceding three days. There was no hematemesis, change in stool, food intolerances, or jaundice. The emesis was never described as projectile. The patient complains of generalized fatigue and easy irritability. Some cold intolerance is also noted. OB history is significant for a spontaneous abortion 2 months ago, the abortion was incomplete and the patient required multiple blood transfusions. The patient had two previous full-term deliveries without complication. She has not had a return of menses since the abortion.

Lab Data:
Hbg/Hct - 11.7/33
WBC - 3.9 with 42 segs, 47 lymphs, 6 monos, 3 eos
Platelets - normal
Na - 132 meq/L (136-145)
K - 4.1 meq/L (3.5-5)
Cl - 96 meq/L (95-105)
HC03 - 28 meq/L (22-28)
T4 - 4.1 ug/dL, (T4 normal - 4.5-11.5 ug/dl)
T3U - 33% (T3U normal = 35-45%)
a.m. Cortisol - 2.0 (normal a.m. 4-24 ug/dL, p.m.- 50-70% of a.m.)
Chest x-ray and abdominal flat plate and upright films were within normal limits.


What is the likely cause of this patients complaints?
Can you explain the abnormal lab values?

 

[SomeDoc]

They gave us this case in class and I liked it so passing it along (slight modifications):

A 28 year old female is admitted for evaluation of headache, abdominal pain, and nausea with vomiting. The headaches are bitemporal and frontal in location and increasing in severity throughout the week prior to admission. There was no history of trauma. She denied fevers, seizure, visual impairment. The abdominal pain was crampy and mid-epigastric and without radiation to the back. There was no relationship to food intake or relief with antacids. She had experience several episodes of clear to yellow emesis over the preceding three days. There was no hematemesis, change in stool, food intolerances, or jaundice. The emesis was never described as projectile. The patient complains of generalized fatigue and easy irritability. Some cold intolerance is also noted. OB history is significant for a spontaneous abortion 2 months ago, the abortion was incomplete and the patient required multiple blood transfusions. The patient had two previous full-term deliveries without complication. She has not had a return of menses since the abortion.

Lab Data:
Hbg/Hct - 11.7/33
WBC - 3.9 with 42 segs, 47 lymphs, 6 monos, 3 eos
Platelets - normal
Na - 132 meq/L (136-145)
K - 4.1 meq/L (3.5-5)
Cl - 96 meq/L (95-105)
HC03 - 28 meq/L (22-28)
T4 - 4.1 ug/dL, (T4 normal - 4.5-11.5 ug/dl)
T3U - 33% (T3U normal = 35-45%)
a.m. Cortisol - 2.0 (normal a.m. 4-24 ug/dL, p.m.- 50-70% of a.m.)
Chest x-ray and abdominal flat plate and upright films were within normal limits.


What is the likely cause of this patients complaints?
Can you explain the abnormal lab values?

1-Sheehans syndrome.
2-Anterior pituitary during pregnancy gets hypervascularized. Hemorrhage during pregnancy leads to pituitary insufficiency.
Abnormal lab values=see #2

 

[Depakote]

1-Sheehans syndrome.
2-Anterior pituitary during pregnancy gets hypervascularized. Hemorrhage during pregnancy leads to pituitary insufficiency.
Abnormal lab values=see #2

Guess I made it too easy.

 

[Slide]

A patient comes with complaints of tremor, heat intolerance, palpitations, and hyperactivity. On physical exam a bulging mass in the anterior portion of the neck is visible and palpable, and proptosis is noted. Fearing surgical treatment, the patient opts for medical treatment and you put her on a drug for her condition. On follow-up 3 months later her previous complaints have lessened, but she now has a low grade fever and has noticed that she has gotten more sick often. Fearing the worst, you automatically discontinue her drug and prescribe other medication for new problems.

1) What does she have?
2) What drug(s) were initially prescribed, and how do they work?
3) What now happening to this patient?
4) What is the mechanism of this new drug you've prescribed?

 

[SomeDoc]

A patient comes with complaints of tremor, heat intolerance, palpitations, and hyperactivity. On physical exam a bulging mass in the anterior portion of the neck is visible and palpable, and proptosis is noted. Fearing surgical treatment, the patient opts for medical treatment and you put her on a drug for her condition. On follow-up 3 months later her previous complaints have lessened, but she now has a low grade fever and has noticed that she has gotten more sick often. Fearing the worst, you automatically discontinue her drug and prescribe other medication for new problems.

1) What does she have?
2) What drug(s) were initially prescribed, and how do they work?
3) What now happening to this patient?
4) What is the mechanism of this new drug you've prescribed?

1) Graves ds (but cannot R/O neoplasm, but is less likely given classic proptosis findings)
2) propthiouracil (for graves)- prevents organification of iodide, peripheral conversion of T4 to T3
Oncologic Rx (too many to list) if neoplasm
3) Myelosuppression? (thyroid hormone mediates bone growth)
4) Filgrastrim/sargramostrim- stimulates bone marrow (all cell types)

 

[mlw47]

A patient comes with complaints of tremor, heat intolerance, palpitations, and hyperactivity. On physical exam a bulging mass in the anterior portion of the neck is visible and palpable, and proptosis is noted. Fearing surgical treatment, the patient opts for medical treatment and you put her on a drug for her condition. On follow-up 3 months later her previous complaints have lessened, but she now has a low grade fever and has noticed that she has gotten more sick often. Fearing the worst, you automatically discontinue her drug and prescribe other medication for new problems.

1) What does she have?
2) What drug(s) were initially prescribed, and how do they work?
3) What now happening to this patient?
4) What is the mechanism of this new drug you've prescribed?

I'll play:

1) Graves' Disease
2) Corticosteroids for the opthalmopathy, propanalol for the symptoms and decreased peripheral conversion of T4, and some anti-thyroid like PTU or methimazole.
3) Sounds like she has an infection. Infection + steroids = bad. PTU and methimazole are also known to cause agranulocytosis. That is also bad.
4) Maybe you put her on I-131 for ablation, although radiotherapy is relatively contraindicated in pts with opthalmopathy.

 

[Slide]

1) Graves ds (but cannot R/O neoplasm, but is less likely given classic proptosis findings)
2) propthiouracil (for graves)- prevents organification of iodide, peripheral conversion of T4 to T3
Oncologic Rx (too many to list) if neoplasm
3) Myelosuppression? (thyroid hormone mediates bone growth)
4) Filgrastrim/sargramostrim- stimulates bone marrow (all cell types)

Pretty much correct, but for #2 you could also include methimazole. For #3 the buzzword is agranulocytosis, but it's more or less the same effect I'm lookig for. And for #4, just anything that stimulates G-CSF.

I'll play:

1) Graves' Disease
2) Corticosteroids for the opthalmopathy, propanalol for the symptoms and decreased peripheral conversion of T4, and some anti-thyroid like PTU or methimazole.
3) Sounds like she has an infection. Infection + steroids = bad. PTU and methimazole are also known to cause agranulocytosis. That is also bad.
4) Maybe you put her on I-131 for ablation, although radiotherapy is relatively contraindicated in pts with opthalmopathy.

See above. The only one is #4, I was looking more for SomeDoc's answer, but yes, the Graves' disease still needs to be addressed when taking the patient off PTU/methimazole. Radioactive iodide is relatively CI'ed, but other choices you could use would be ionic inhibitors that inhibit the Na/I symport (perchlorate, thiocyanate), and other drugs that could manage some of the symptoms like beta blockers and calcium channel blockers.

 

[SomeDoc]

A 30 year old caucasian male presents to the emergency department (ED) with complaints of diarrhea, a high fever, and problems breathing. He states that this has been going on for several months. He lacks health insurance and access to preventive healthcare facilities, and thus has allowed the condition to progress to the point that he is now presenting to the ED. He denies any illicit drug use, and states that he is not on any medications.

Physical examination reveals bilateral wheezes; warm, flushed skin, a high fever, and excessive salivation. WBC and hematocrit labs are normal.

Cardiac auscultation reveals a specific abnormal finding.
What is the auscultative finding? What is the pathophysiology of this finding?

 

[Redrox]

Carcinoid tumor that has metastasized to the liver, causing serotonin syndrome.
The heart has a tricuspid regurgitation and pulmonary valve stenosis.

?

 

[SomeDoc]

Carcinoid tumor that has metastasized to the liver, causing serotonin syndrome.
The heart has a tricuspid regurgitation and pulmonary valve stenosis.

?

Re: the pathophysiology; why is the right side of the heart (selectively) affected?

 

[Redrox]

Hematogenous spread from the liver.

 

[SomeDoc]

Hematogenous spread from the liver.

Nope. The valvular insufficiency is due to the secondary effects of serotonin (a secretory product of the tumor) on the endocardium and valves, not due to the direct effect of a metastasized tumor on host tissue.

With that being said, let's ask the question in the following manner:

Why isn't the left side of the heart affected?

 

[Slide]

Nope. The valvular insufficiency is due to the secondary effects of serotonin (a secretory product of the tumor) on the endocardium and valves, not due to the direct effect of a metastasized tumor on host tissue.

With that being said, let's ask the question in the following manner:

Why isn't the left side of the heart affected?

Gonna take a shot by reasoning it out...
The valvular insufficiency isn't due to spread of tumor, it's because the right cardiac valves are being damaged by the actual serotonin and other crap being released from the tumor (venous circulation goes to the right side first). How it damages it, I don't know. Since it doesn't damage the left side, it probably means that the lung metabolizes the drug somehow. I'm basing this because I know some drugs and chemicals are excreted or metabolized via lungs.

However, I do think it is possible for the left side to get hit by serotonin effects as well, like a endocardial cushion defect.

 

[SomeDoc]

Gonna take a shot by reasoning it out...
The valvular insufficiency isn't due to spread of tumor, it's because the right cardiac valves are being damaged by the actual serotonin and other crap being released from the tumor (venous circulation goes to the right side first). How it damages it, I don't know. Since it doesn't damage the left side, it probably means that the lung metabolizes the drug somehow. I'm basing this because I know some drugs and chemicals are excreted or metabolized via lungs.

However, I do think it is possible for the left side to get hit by serotonin effects as well, like a endocardial cushion defect.

That's it- 5HT is metabolized by the lung, thus the left side of the heart is mostly unaffected in extra-GI carcinoid syndromes

 

[ENThopeful]

That's it- 5HT is metabolized by the lung, thus the left side of the heart is mostly unaffected in extra-GI carcinoid syndromes

Goljan level explanation


I got one:

Tall patient with long arms and a systolic murmur presents with blurry vision.
What does the patient chronically have,
what are you does the patient acutely have,
what may the acute disease cause,
and what would you use to treat in emergent situations as such?

 

[BoneNibbler]

Goljan level explanation


I got one:

Tall patient with long arms and a systolic murmur presents with blurry vision.
What does the patient chronically have,
what are you does the patient acutely have,
what may the acute disease cause,
and what would you use to treat in emergent situations as such?

1. marfans
2. subluxation of his lens/ mitral valve prolapse
3.heart failure/arrhythmias
4.meds

Am eye at least close?

 

[SomeDoc]

Goljan level explanation

thanks

I got one:

Tall patient with long arms and a systolic murmur presents with blurry vision.
What does the patient chronically have,
what are you does the patient acutely have,
what may the acute disease cause,
and what would you use to treat in emergent situations as such?

1) Marfans disease
2) Collagen defect- leads to "floppy" mitral valve (versus mitral valve "prolapse" in adult polycystic kidney disease), berry aneurysm @ circle of willis (most often @ anterior communicating branch)=visual field defects [optic chiasm impingement]
3)aortic dissection, berry aneurysm rupture
4) Stent mesh aortic arch prophylactic reinforcement

 

[Slide]

A 60 year old man comes into your ER with nausea, vomiting, excruciating abdominal pain, and eye pain. He recollects this episode occurred when he walked into a movie theater, with the pain occurring shortly afterwards. History is significant for depression, and on examination you discover he has hyperopia.

1) What's most likely going on?
2) Why?
3) What other causes should be included in your differential?

 

[FutureInternist]

A 60 year old man comes into your ER with nausea, vomiting, excruciating abdominal pain, and eye pain. He recollects this episode occurred when he walked into a movie theater, with the pain occurring shortly afterwards. History is significant for depression, and on examination you discover he has hyperopia.

1) What's most likely going on?
2) Why?
3) What other causes should be included in your differential?

1) Closed angle glaucoma (d/t walking into a darkened theater)
2) Eye dilation --> blockage of Schlem ?? canal --> buildup of aqeous humor & increased IOP
3) DDx

• Eye pain so maybe TIA
• Since you mentioned he is depressed, I'm going to guess some anti-depressants can predispose to this (no idea which one)
  
• Nausea so feels bad about paying $20 for a crappy movie
  
• Vomiting so a Ben Affleck movie
  
• Abdominal pain so bad movie popcorn

 

[Argatroban]

1) Closed angle glaucoma (d/t walking into a darkened theater)
2) Eye dilation --> blockage of Schlem ?? canal --> buildup of aqeous humor & increased IOP
3) DDx

• Eye pain so maybe TIA
• Since you mentioned he is depressed, I'm going to guess some anti-depressants can predispose to this (no idea which one)
  
• Nausea so feels bad about paying $20 for a crappy movie
  
• Vomiting so a Ben Affleck movie
  
• Abdominal pain so bad movie popcorn

TCA's have anticholinergic effects.

 

[Slide]

1) Closed angle glaucoma (d/t walking into a darkened theater)
2) Eye dilation --> blockage of Schlem ?? canal --> buildup of aqeous humor & increased IOP
3) DDx

• Eye pain so maybe TIA
• Since you mentioned he is depressed, I'm going to guess some anti-depressants can predispose to this (no idea which one)
  
• Nausea so feels bad about paying $20 for a crappy movie
  
• Vomiting so a Ben Affleck movie
  
• Abdominal pain so bad movie popcorn

All spot on, even the last 3 points. Hyperopia increases the risk of closed-angle glaucoma during dilatation because the shortened eye contorts the anterior chamber in a way that normal dilation of the eye could possibly block the canal of Schlem. The other medically possible explanation for the glaucoma attack are antidepressant meds the patient is on; specifically TCA's, due to their anti-muscarinic activity. In reality this patient was probably forced to watch Jonas Brothers: The 3D Concert Experience with his grandkids.

 

[Depakote]

A patient presents to your office complaining of bouts where she gets cool skin, becomes shaky and feels faint. As she appears this way at the time of presentation you perform a finger-stick glucose and discover a level of 40mg/dL. Your patient is very interested in these results and inquires whether she may be admitted to the hospital for treatment.

You decline to admit the patient and draw supporting blood-work before providing orange juice.

Following the orange juice, blood glucose rises to reasonable levels.

The blood-work comes back:
Serum Blood Glucose: 40 mg/dL
Serum Insulin: elevated
C-Peptide: absent

What condition does this patient have?

 

[Richspiders07]

..gotta love the crazies who shoot themselves up with insulin

 

[Redrox]

Although dizzyiness relieved by OJ is classic for insulinoma, the patient is lacking c-peptide which implicates an exogenous source of insulin. She has Munchausen's syndrome most likely, and want to "assume the sick role" primary gain, etc. . .

However, I did see a guy who was trying to get workman's comp by claiming the dizzy spells were caused by chemicals on the job. Malingering, in that case.

 

[Depakote]

Although dizzyiness relieved by OJ is classic for insulinoma, the patient is lacking c-peptide which implicates an exogenous source of insulin. She has Munchausen's syndrome most likely, and want to "assume the sick role" primary gain, etc. . .

However, I did see a guy who was trying to get workman's comp by claiming the dizzy spells were caused by chemicals on the job. Malingering, in that case.

 

[McSnubbs]

Im not one to contribute very often, but I like what you guys are doing here... its a great way to connect the dots on some of the more "mysterious" questions I'm expecting to see on the step.

Cheers and thanks for the effort!!

 

[SouthernSurgeon]

A patient presents to your office complaining of bouts where she gets cool skin, becomes shaky and feels faint. As she appears this way at the time of presentation you perform a finger-stick glucose and discover a level of 40mg/dL. Your patient is very interested in these results and inquires whether she may be admitted to the hospital for treatment.

You decline to admit the patient and draw supporting blood-work before providing orange juice.

Following the orange juice, blood glucose rises to reasonable levels.

The blood-work comes back:
Serum Blood Glucose: 40 mg/dL
Serum Insulin: elevated
C-Peptide: absent

What condition does this patient have?

You forgot to include that the patient is a nurse

 

[FutureInternist]

Young female presents to ED on Friday night w/ intense abdominal pain & claiming that her friends are out to "kill her". During the physical exam, in a well-lit room, you note that her movements seem uncoordinated.

1) What enzyme def & disease does this pt have?
2) What is the accumulated product in this disease?
2) What are some of the triggering factors for this presentation? & by what mechanism?
3) Tx?

 

[AllUpOnYoMama]

A study of the association of HL-A antigens with malignant neoplasms has indicated a predisposition to breakdown of the immune resistance mechanism and resulting malignant transformation. In carcinoma of the breast the HL-A phenotype found to be most often present is
a. HL-A7
B. HL-A5
C. HL-A1
D. HL-A3
E. all of the above
f. none of the above
g. george bush
h. girls with huge jugs

Booya!

 

[AllUpOnYoMama]

Young female presents to ED on Friday night w/ intense abdominal pain & claiming that her friends are out to "kill her". During the physical exam, in a well-lit room, you note that her movements seem uncoordinated.

1) What enzyme def & disease does this pt have?
2) What is the accumulated product in this disease?
2) What are some of the triggering factors for this presentation? & by what mechanism?
3) Tx?

I have no idea what this is... girl maybe dropped a little LSD?

 

[AllUpOnYoMama]

The intestinal bacterial flora high in the GI tract and unaltered by gastric acid
a. can deconjugate bile, impairing micelle formation
b. may convert fats to irritating substances
c. may convert carbs to short-chain fatty acids which can cause osmotic diarrhea
d. all of the above
e. none of the above
f. girls running with huge jugs

 

[SomeDoc]

Young female presents to ED on Friday night w/ intense abdominal pain & claiming that her friends are out to "kill her". During the physical exam, in a well-lit room, you note that her movements seem uncoordinated.

1) What enzyme def & disease does this pt have?
2) What is the accumulated product in this disease?
2) What are some of the triggering factors for this presentation? & by what mechanism?
3) Tx?

I have no idea what this is... girl maybe dropped a little LSD?

Sounds like it may be metachromatic leukodystrophy, with accumulation of cerebroside sulfate. Deficient/dysnfunctional enzyme would be galactosidase.

Something to do with the light might be precipitating her ataxia- there might be a connection between the activated calcarine fissure (visual cortex) and her cerebellum (a connection which I'm not aware of), which is demyelinated due to the disease, but this explanation is stretching it.

 

[FutureInternist]

Young female presents to ED on Friday night w/ intense abdominal pain & claiming that her friends are out to "kill her". During the physical exam, in a well-lit room, you note that her movements seem uncoordinated.

1) What enzyme def & disease does this pt have?
2) What is the accumulated product in this disease?
2) What are some of the triggering factors for this presentation? & by what mechanism?
3) Tx?

OK so maybe I should have been a bit more thorough....
"During the physical exam, in a well-lit room, you note that her movements seems uncoordinated. Furthermore there is no sign of any rashes on her skin"

 

[Redrox]

Porphyria of some sort?

 

[FutureInternist]

Porphyria of some sort?

Ding ding ding

Any thoughts on which one? enzyme def etc?

 

[Slide]

Ding ding ding

Any thoughts on which one? enzyme def etc?

Any photosensitivity and/or nail changes? Abdominal pain is leading me to hereditary coproporphyria but lack of skin rash also points me somewhat to acute intermittent porphyria.

 

[Mortal_Lessons]

Any photosensitivity and/or nail changes? Abdominal pain is leading me to hereditary coproporphyria but lack of skin rash also points me somewhat to acute intermittent porphyria.

This sounds like acute intermittent porphyria, an ailment the late King George III suffered.

 

[FutureInternist]

Any photosensitivity and/or nail changes? Abdominal pain is leading me to hereditary coproporphyria but lack of skin rash also points me somewhat to acute intermittent porphyria.

This sounds like acute intermittent porphyria, an ailment the late King George III suffered.

Autosomal dominant deficiency of uroporphrinogen I synthase --> accumulation of porphobilinogen & 5-ALA
Triggers = EtOH, barbiturates, hypoxia, menstruation --> activation of ALA synthase
Tx = hematin (heme analog so does negative feedback & stops further production), & glucose (inhibits ALA synthase)

Mnemonic for AIP
A - Alcohol induced Acute Abd pain, Ataxia,
I - Insensitive to light
P - Paranoia, Porphobilinogen build up

 

[mlw47]

Mnemonic for AIP
A - Alcohol induced Acute Abd pain, Ataxia,
I - Insensitive to light
P - Paranoia, Porphobilinogen build up

Great mneumonic. The porphyrias are something I've always had a hard time keeping straight.

 

[AllUpOnYoMama]

A study of the association of HL-A antigens with malignant neoplasms has indicated a predisposition to breakdown of the immune resistance mechanism and resulting malignant transformation. In carcinoma of the breast the HL-A phenotype found to be most often present is
a. HL-A7
B. HL-A5
C. HL-A1
D. HL-A3
E. all of the above
f. none of the above
g. george bush
h. girls with huge jugs

Booya!

Answer is A in case anyone wanted to know

 

[AllUpOnYoMama]

The intestinal bacterial flora high in the GI tract and unaltered by gastric acid
a. can deconjugate bile, impairing micelle formation
b. may convert fats to irritating substances
c. may convert carbs to short-chain fatty acids which can cause osmotic diarrhea
d. all of the above
e. none of the above
f. girls running with huge jugs

answer is D

 

[FutureInternist]

I posted this before but no guesses...Don't want to think of a new Q yet.

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

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

 

[BoneNibbler]

I posted this before but no guesses...Don't want to think of a new Q yet.

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

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

Is this the type of question on step 1??

 

[Slide]

I posted this before but no guesses...Don't want to think of a new Q yet.

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

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

I tried answering this before so I'll bite with a real answer.

A) Long QT syndromes; either JLNS or Romano-Ward syndrome.
B) JLNS - AR; Romano-Ward - AD
C) JLNS - v-fib; RW - arrhythmia
D) Ask the parents if the kid has any problems hearing. If the kid's deaf, probably JLNS.

 

[Slide]

Just a quickie that I found a little grotesquely hilarious.

A farmer's hand drinks a dark liquid, believing it to be Coke. To his surprise, he soon learns that he drank paraquat instead. He turns up at the hospital later with breathing problems.

A) What is paraquat, and what is its mechanism of toxicity?
B) What can you do for this patient to treat him?

 

[BoneNibbler]

I tried answering this before so I'll bite with a real answer.

A) Long QT syndromes; either JLNS or Romano-Ward syndrome.
B) JLNS - AR; Romano-Ward - AD
C) JLNS - v-fib; RW - arrhythmia
D) Ask the parents if the kid has any problems hearing. If the kid's deaf, probably JLNS.

what review book did you learn about these>?

 

[Depakote]

Just a quickie that I found a little grotesquely hilarious.

A farmer's hand drinks a dark liquid, believing it to be Coke. To his surprise, he soon learns that he drank paraquat instead. He turns up at the hospital later with breathing problems.

A) What is paraquat, and what is its mechanism of toxicity?
B) What can you do for this patient to treat him?

I just found this in my toxicology lecture.

Paraquat is a free radical that releases superoxide ions. Gets the lungs (had to look that up elsewhere).

No clue how you treat it, but I'm going to say you need to find a new patient, this one is broken.

 

[Depakote]

Just a quickie that I found a little grotesquely hilarious.

A farmer's hand drinks a dark liquid, believing it to be Coke. To his surprise, he soon learns that he drank paraquat instead. He turns up at the hospital later with breathing problems.

A) What is paraquat, and what is its mechanism of toxicity?
B) What can you do for this patient to treat him?

I just found this in my toxicology lecture.

Paraquat is a free radical that releases superoxide ions. Gets the lungs (had to look that up elsewhere).

No clue how you treat it, but I'm going to say you need to find a new patient, this one is broken.

BTW, if this shows up on my test on tuesday, you win the internet. I never would have studied this.

 

[AllUpOnYoMama]

I tried answering this before so I'll bite with a real answer.

A) Long QT syndromes; either JLNS or Romano-Ward syndrome.
B) JLNS - AR; Romano-Ward - AD
C) JLNS - v-fib; RW - arrhythmia
D) Ask the parents if the kid has any problems hearing. If the kid's deaf, probably JLNS.

nice dude

 

[Depakote]

A 55 year old Caucasian male presents to the emergency room complaining of blurry vision and headache for the past 4 hours. He has not seen a physician in the past 25 years. He has moderate obesity and is employed as a Medical Malpractice Claims Attorney, despite this, he is calm and cooperative with your examination.

Fundoscopic examination reveals the following:

Blood pressure is found to be: 230/130
Auscultation of the lungs is clear.
Auscultation of the apex of the heart notes a S4 heart sound.
Auscultation of the abdomen reveals normal bowel sounds and no bruits.
No abnormalities are noted on auscultation of the chest or abdomen.


What is his current condition?
How should this be treated?
What is his underlying condition?
Does his underlying condition have a genetic predisposition? What is it's means of inheritance?
Explain the S4 heart sound.
If this dude checked out AMA b/c he planned to sue you, was standing on the corner minding his own business and was shot by "some dude"... What pathological observations (due to his current condition) would be visible at autopsy?