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?

---

Members don't see this ad.

 

[Depakote]

I'm making the numbers in the following question up, go with it...


Prostate Specific Antigen is being re-evaluated as a marker for Prostate cancer. It is proposed that a level of 50 indicates the presence of prostate cancer.

The following data are obtained:

____________ Biopsy Proven Prostate Cancer _____|___Biopsy Negative for Prostate Cancer
PSA above 50_________100_____________________|________25
PSA below 50__________20_____________________|________90


What is the Sensitivity of the PSA for the data collected?
What is the Specificity of the PSA for the data collected?
What is the Positive Predictive Value for the data collected?
What is the Negative Predictive Value for the data collected?

(p. 61 of the 2009 First Aid if you need the equations)

The answers are posted in White (highlight to see them)

What is the Sensitivity of the PSA for the data collected? (.833 or 83.3%)
What is the Specificity of the PSA for the data collected? (.783 or 78.3%)
What is the Positive Predictive Value for the data collected? (.8 or 80%)
What is the Negative Predictive Value for the data collected? (.818 or 81.8%)

 

[SomeDoc]

That appears to be a pseudomembrane, which would be caused by diptheria. The fact that this is occuring in a 20yo suggests that she has waning immunity from her original TDaP vaccination and didn't get an appropriate booster. The diptheria toxin blocks Elongation Factor-2, much like clostridium difficile toxin (which also causes pseudomembrane formation).

I was going for exotoxin A of p. aeruginosa, but c. dif works too.

Regarding the 1st Q, can you think of what is unique about the exotoxin of c. diptheriae regarding it's ultimate source?

 

[SomeDoc]

I'm making the numbers in the following question up, go with it...


Prostate Specific Antigen is being re-evaluated as a marker for Prostate cancer. It is proposed that a level of 50 indicates the presence of prostate cancer.

The following data are obtained:

____________ Biopsy Proven Prostate Cancer _____|___Biopsy Negative for Prostate Cancer
PSA above 50_________100_____________________|________25
PSA below 50__________20_____________________|________90


What is the Sensitivity of the PSA for the data collected?
What is the Specificity of the PSA for the data collected?
What is the Positive Predictive Value for the data collected?
What is the Negative Predictive Value for the data collected?

(p. 61 of the 2009 First Aid if you need the equations)

Sens: 100/100+20
Spec: 90/90+25
PPV: 100/100+25
NPV: 90/90+20

P.S. very creative table!

 

[THE armada]

Just wanted to say how much I've enjoyed this thread and appreciate you folks putting the vignettes together. One of these days I'll contribute.

 

[Depakote]

I was going for exotoxin A of p. aeruginosa, but c. dif works too.

Regarding the 1st Q, can you think of what is unique about the exotoxin of c. diptheriae regarding it's ultimate source?

isn't that a phage encoded exotoxin? meaning you could get a c dipth infx but the strain could be non-toxin producing if it hadn't been infected by the phage that confers toxin production.

 

[SomeDoc]

isn't that a phage encoded exotoxin? meaning you could get a c dipth infx but the strain could be non-toxin producing if it hadn't been infected by the phage that confers toxin production.

 

[SomeDoc]

Just wanted to say how much I've enjoyed this thread and appreciate you folks putting the vignettes together. One of these days I'll contribute.

Hey Armada, glad you enjoy it! We have as much fun putting vignettes together as we do answering them.

 

[SomeDoc]

A patient with jaundice and RUQ pain presents with the following blood test:

HBSAg+
AntiHBcAg+
AntiHBSAg-

What clinical stage of infection is the patient in?

Additional tests indicate that the patient is HBeAg+. What does this indicate?

 

[Instatewaiter]

HbS= has been exposed/has infection

antiHbC is the firs antibody to develop. Since the person is negative for AntiS it means he/she is in the window period.

Hbe means they are actively shedding virus b/c it is replicating

 

[bola]

I thought the HBsAg was negative in the window period and only antiHBc Ab is positive - this would put the pt at early infection but before the window period?

and they are definitely shedding virus since HBe Ag is positive (HBVDNA will also be positive)

 

[SomeDoc]

I thought the HBsAg was negative in the window period and only antiHBc Ab is positive - this would put the pt at early infection but before the window period?

This patient is in the "prodrome" phase of Hepatitis B infection, the stage that proceeds the "incubation" stage.
Stages go from incubation->prodrome->early convalescence(window phase) ->late convalescence.

and they are definitely shedding virus since HBe Ag is positive (HBVDNA will also be positive)

A positive HBeAG indicates a high risk of transmission.

 

[SomeDoc]

A physiologist studying cardiovascular hemodynamic properties injects an unspecified amount of norepinephrine (NE) into an animal subject. As expected, pulse pressure increases from an increase in both systolic and diastolic pressures. Heart rate also increases. However, she notes that within a few minutes, the increased heart rate is replaced with a significantly decreased heart rate, which is well below the normal resting physiological level.

The study protocol calls for an increased pulse pressure through the use of NE, an increased heart rate, and skeletal muscle neuro-excitability. What prototypical pharmacological agent can the physiologist administer in addition to NE, to the animal subject, in order to achieve these parameters?

 

[ENThopeful]

60 y/o male comes into your clinic with for a physical exam. You discover mitral regurgitation that wasn't there a month ago. History is insignificant except for an ER visit due to epigastric pain for which he was discharged on omeprazole for.

Diagnosis?

 

[FutureInternist]

60 y/o male comes into your clinic with for a physical exam. You discover mitral regurgitation that wasn't there a month ago. History is insignificant except for an ER visit due to epigastric pain for which he was discharged on omeprazole for.

Diagnosis?

So the anti-acid led to increase chances of infection. Old guy w/ regurg so you may have a guy w/ Strep Bovis endocarditis & colon cancer

 

[FutureInternist]

A 17 yr old male is brought to your office by his parents who say that he has not yet achieved puberty. His older brother & neighborhood friends all progressed on a normal time table. When asked for any other complaints, patient claims to have a decreased sense of smell.

1. What does the kid have?
2. What is the cause of this?
3. What would his LH, FSH & testosterone be (high, normal, low)?
4. What other developmental defects are associated with this disease?

 

[Saladin MD]

I'm making the numbers in the following question up, go with it...


Prostate Specific Antigen is being re-evaluated as a marker for Prostate cancer. It is proposed that a level of 50 indicates the presence of prostate cancer.

The following data are obtained:

____________ Biopsy Proven Prostate Cancer _____|___Biopsy Negative for Prostate Cancer
PSA above 50_________100_____________________|________25
PSA below 50__________20_____________________|________90


What is the Sensitivity of the PSA for the data collected?
What is the Specificity of the PSA for the data collected?
What is the Positive Predictive Value for the data collected?
What is the Negative Predictive Value for the data collected?

(p. 61 of the 2009 First Aid if you need the equations)

Sensitivity = 100/120
Specificity = 90/115
PPV = 100/125
NPV = 90/110

Hope I did that right!

EDIT : Hmmmm, seems my browser messed up...I thought this was the most recent question.

 

[Saladin MD]

A 17 yr old male is brought to your office by his parents who say that he has not yet achieved puberty. His older brother & neighborhood friends all progressed on a normal time table. When asked for any other complaints, patient claims to have a decreased sense of smell.

1. What does the kid have?
2. What is the cause of this?
3. What would his LH, FSH & testosterone be (high, normal, low)?
4. What other developmental defects are associated with this disease?

1. Kallman's Syndrome
2. Something to do with an empty Sella or something or the other?
3. everything would be low
4. ?

 

[FutureInternist]

1. Kallman's Syndrome
2. Something to do with an empty Sella or something or the other?
3. everything would be low
4. ?

2. (Failure of GnRH cells to migrate from olfactory lobes to hypothalamus, hence the associated hearing loss)

4. Midline facial defects (cleft lips/palate)

That was quick Saladin......looks like someone just took Step 1

 

[Richspiders07]

60 y/o male comes into your clinic with for a physical exam. You discover mitral regurgitation that wasn't there a month ago. History is insignificant except for an ER visit due to epigastric pain for which he was discharged on omeprazole for.

Diagnosis?

So.. PT actually had an MI... survived... then ruptured a papillary muscle and now has mitral regurg.

 

[FutureInternist]

So.. PT actually had an MI... survived... then ruptured a papillary muscle and now has mitral regurg.

OK....I vote for this one as well

 

[Saladin MD]

That was quick Saladin......looks like someone just took Step 1

Haha, yeah studying for step 2 now.

 

[McSnubbs]

A physiologist studying cardiovascular hemodynamic properties injects an unspecified amount of norepinephrine (NE) into an animal subject. As expected, pulse pressure increases from an increase in both systolic and diastolic pressures. Heart rate also increases. However, she notes that within a few minutes, the increased heart rate is replaced with a significantly decreased heart rate, which is well below the normal resting physiological level.

The study protocol calls for an increased pulse pressure through the use of NE, an increased heart rate, and skeletal muscle neuro-excitability. What prototypical pharmacological agent can the physiologist administer in addition to NE, to the animal subject, in order to achieve these parameters?

Sounds like they are looking for something to block the reflexive bradycardia which occurs after high pressures are sensed at the carotid bodies/aortic arch. The reflex would be mediated through and increase in vagal tone, thus a muscarinic antagonist like atropine should do the job.

Let me know if Im wrong here - I havent seen some of this material for a while. Cheers

 

[SomeDoc]

Sounds like they are looking for something to block the reflexive bradycardia which occurs after high pressures are sensed at the carotid bodies/aortic arch. The reflex would be mediated through and increase in vagal tone, thus a muscarinic antagonist like atropine should do the job.

Let me know if Im wrong here - I havent seen some of this material for a while. Cheers

A muscarinic antagonist will most definitely work.

There is, however, a prototypical drug that is used in research settings to specifically block NE-induced reflexive bradycardia.

P.S. This drug is a ganglionic nicotinic receptor antagonist.

Edit: this drug appears in BRS Physiology, and FA for the USMLE.

 

[Slide]

A muscarinic antagonist will most definitely work.

There is, however, a prototypical drug that is used in research settings to specifically block NE-induced reflexive bradycardia.

P.S. This drug is a ganglionic nicotinic receptor antagonist.

Edit: this drug appears in BRS Physiology, and FA for the USMLE.

Hexamethonium?

 

[SomeDoc]

Hexamethonium?

 

[Mortal_Lessons]

A 30-year old female presents to your clinic with a chief complaint of intolerance to cold items as her hands spasm and become painful and white. She has also noticed a recent onset of pyrosis soon after eating heavy meals. She drinks 2 cups of coffee daily. Nail-fold exam reveals dilated capillary loops that blanch on diascopic examination. What is your leading diagnosis? Are there any laboratory data that can prognosticate this woman's course?

 

[Re3iRtH]

A 30-year old female presents to your clinic with a chief complaint of intolerance to cold items as her hands spasm and become painful and white. She has also noticed a recent onset of pyrosis soon after eating heavy meals. She drinks 2 cups of coffee daily. Nail-fold exam reveals dilated capillary loops that blanch on diascopic examination. What is your leading diagnosis? Are there any laboratory data that can prognosticate this woman's course?

CREST, with limited features.
Anti-centromere Abs. Just guessing though.

 

[Mortal_Lessons]

CREST, with limited features.
Anti-centromere Abs. Just guessing though.

Definitely. You obtain a titer for ANA which is positive, but you get a negative anti-centromere titer. However, you begin treatment with calcium channel blockade for her Raynaud's and omeprazole for her heartburn. At a follow-up two weeks later, you take her blood pressure and it's sky high. You also notice that she has skin tightening proximal to her elbows. Has your diagnosis changed? Which drug do you need to institute immediately, and which serology are you going to obtain for further prognostication?

 

[Slide]

Definitely. You obtain a titer for ANA which is positive, but you get a negative anti-centromere titer. However, you begin treatment with calcium channel blockade for her Raynaud's and omeprazole for her heartburn. At a follow-up two weeks later, you take her blood pressure and it's sky high. You also notice that she has skin tightening proximal to her elbows. Has your diagnosis changed? Which drug do you need to institute immediately, and which serology are you going to obtain for further prognostication?

Looks like this patient has blown up into systemic scleroderma. Malignant hypertension/sky high BP probably caused by kidney damage, and the skin tightening at the elbows means collagen is starting to form in more places, indicating systemic progression may be to come. Get Anti-scl70 titers to confirm, treat patient with limited steroids and immunosuppresive drugs and hope for the best. Give ACE inhibitor to protect kidneys as well.

 

[Mortal_Lessons]

Looks like this patient has blown up into systemic scleroderma. Malignant hypertension/sky high BP probably caused by kidney damage, and the skin tightening at the elbows means collagen is starting to form in more places, indicating systemic progression may be to come. Get Anti-scl70 titers to confirm, treat patient with limited steroids and immunosuppresive drugs and hope for the best. Give ACE inhibitor to protect kidneys as well.

Nice -

I just wanted to add that idiopathic pulmonary fibrosis is something you're going to want to follow with this patient. A baseline X-ray might be useful. You're going to want to look for bibasilar markings (unlike emphysematous change which takes place apically). Make sure to ask about dyspnea at follow-up visits. Regular echocardiograms will help assess right heart function. Should IPF occur, long-term cyclophosphamide is indicated to slow the progression of the lung disease.

 

[ENThopeful]

So the anti-acid led to increase chances of infection. Old guy w/ regurg so you may have a guy w/ Strep Bovis endocarditis & colon cancer

RCA infarction

 

[ENThopeful]

So.. PT actually had an MI... survived... then ruptured a papillary muscle and now has mitral regurg.

boom

 

[Mortal_Lessons]

A 67-year old tan male presents to your rheumatology clinic with painful hands. He explains that in the morning his hands are stiff for about 30 minutes, after which they become more comfortable to him. However, he notes that by the end of the day his joints are painful and limited in their range of motion. On physical examination, bony prominences are found bilaterally in the DIP and PIP joints. You also find bony changes in his MCP joints. X-rays of both hands reveal subchondral sclerosis and decreased articular space at the aforementioned joints.

What are the eponymous findings in his DIP and PIP joints?
What is the underlying process leading to his MCP findings?

 

[SomeDoc]

A 67-year old tan male presents to your rheumatology clinic with painful hands. He explains that in the morning his hands are stiff for about 30 minutes, after which they become more comfortable to him. However, he notes that by the end of the day his joints are painful and limited in their range of motion. On physical examination, bony prominences are found bilaterally in the DIP and PIP joints. You also find bony changes in his MCP joints. X-rays of both hands reveal subchondral sclerosis and decreased articular space at the aforementioned joints.

What are the eponymous findings in his DIP and PIP joints?
What is the underlying process leading to his MCP findings?

Heberden's (DIP) and Bouchard's (PIP) nodes
Eburnation (or alternatively, osteophyte formation)

While I was initially thinking RA due to the presentation of initial ROM increases with time of day- subchondral sclerosis, and eventual pain and limited motion at the end of the day are more descriptive of OA.

 

[Mortal_Lessons]

Heberden's (DIP) and Bouchard's (PIP) nodes
Eburnation.

Nice. The DIP and PIP joints are most often affected in this patient's disease, primary osteoarthritis.

However, MCP joint involvement is quite uncommon, unless there was previous trauma to this joint (leading to secondary osteoarthritis), which the patient denies.

What other pathophysiological process might lead to MCP osteoarthritis (hint: the patient is tan and you're practicing in Alaska)?

Edit: I made the question trickier by including early morning gelling that is characteristic of inflammatory arthritis. However, this patient's morning stiffness only lasted for 30 minutes which is much shorter (~ 2 hours) than that seen in inflammatory joint disease. And as you noted, the patient's progressive pain with day-time use, physical exam and X-ray findings favor osteoarthritis over rheumatoid arthritis.

 

[SomeDoc]

A 23 year old caucasian male is brought into the emergency department in a strait-jacket, along with the escort of two police officers. The officers first confronted the patient when they received a call from the patients neighbor, with the complaint that the patient was yelling on his rooftop, and making violent threats to his neighbors and pedestrians.

The officers state that the patient appeared to be talking to imaginary people, and went into a violent rage when confronted by the officers. The officers were told by the patient's neighbor that the patient had had this violent fit a few hours ago, which then recurred spontaneously at the time of the confrontation with police.

Ophthalmologic examination reveals horizontal and vertical nystagmus. Pupillary examination reveals neither miosis nor mydriasis. What agent is the cause of this patient's symptoms? What is the etiology of the recurrent episode of the second spontaneous episode?

 

[Mortal_Lessons]

A 23 year old caucasian male is brought into the emergency department in a strait-jacket, along with the escort of two police officers. The officers first confronted the patient when they received a call from the patients neighbor, with the complaint that the patient was yelling on his rooftop, and making violent threats to his neighbors and pedestrians.

The officers state that the patient appeared to be talking to imaginary people, and went into a violent rage when confronted by the officers. The officers were told by the patient's neighbor that the patient had had this violent fit a few hours ago, which then recurred spontaneously at the time of the confrontation with police.

Ophthalmologic examination reveals horizontal and vertical nystagmus. Pupillary examination reveals neither miosis nor mydriasis. What agent is the cause of this patient's symptoms? What is the etiology of the recurrent episode of the second spontaneous episode?

Phencyclidine, also known as angel dust on the street?
I'm not entirely sure about the second spontaneous episode...

 

[SomeDoc]

What other pathophysiological process might lead to MCP osteoarthritis (hint: the patient is tan and you're practicing in Alaska)?

I'm stumped on this one... I'm looking forward to what the responses are (and the ultimate confirmation from the author )

 

[SomeDoc]

Phencyclidine, also known as angel dust on the street?
I'm not entirely sure about the second spontaneous episode...

PCP use can be characterized by a second, unpredictable emergence in violent tendencies and hallucinations, due to reabsorption of the agent in the GI tract.

 

[SomeDoc]

What other pathophysiological process might lead to MCP osteoarthritis (hint: the patient is tan and you're practicing in Alaska)?

Hypercalcemia from excessive vitamin D production from having ~24 hours of sunlight?

 

[Mortal_Lessons]

Hypercalcemia from excessive vitamin D production from having ~24 hours of sunlight? Not sure if I can completely rule out cushings syndrome or disease, or primary addisons from something that I may be missing.

I've never been to Alaska but I was trying to imply that there is very little sunlight in his environment, thus leading one to the conclusion that there must be something else leading him to bronze. Increased POMC and MSH in Addison's is definitely one explanation for his sun-free tan. However, the process responsible for his tan is also responsible for the preferential development of MCP osteoarthritis, thus making Addison's less likely.

A family history reveals that a parent suffered from cirrhosis, heart disease, and diabetes. He also remembers this parent covered in leeches to help treat their disease.

 

[SomeDoc]

I've never been to Alaska but I was trying to imply that there is very little sunlight in his environment, thus leading one to the conclusion that there must be something else leading him to bronze. Increased POMC and MSH in Addison's is definitely one explanation for his sun-free tan. However, the process responsible for his tan is also responsible for the preferential development of MCP osteoarthritis, thus making Addison's less likely.

A family history reveals that a parent suffered from cirrhosis, heart disease, and diabetes. He also remembers this parent covered in leeches to help treat their disease.

Ah...hemochromatosis.

 

[Mortal_Lessons]

Ah...hemochromatosis.

MCP osteoarthritis is a characteristic finding in hemochromatosis. However, this is probably the least of the patient's worries...

 

[neil100]

An 8 month old has a congenital heart defect. On ausculation, holosystolic mumur is detected. The infant also has severe cyanosis.
The infant also squats on occasions during shortness of breath.


1) What is the dx?

2) Why is the infant squatting during periods of shortness of breath? The mechanism!

3) If the patient survives into the 20's or 30's, what will be the most likely cause of death?

4) What shunts are "good" to have in this dx? (VSD, ASD, or Patent Ductus arterious)

 

[Slide]

An 8 month old has a congenital heart defect. On ausculation, holosystolic mumur is detected. The infant also has severe cyanosis.
The infant also squats on occasions during shortness of breath.


1) What is the dx?

2) Why is the infant squatting during periods of shortness of breath? The mechanism!

3) If the patient survives into the 20's or 30's, what will be the most likely cause of death?

4) What shunts are "good" to have in this dx? (VSD, ASD, or Patent Ductus arterious)

1) Tetralogy of Fallot
2) Squatting kinks off the iliac arteries and other arteries to the lower extremities, increasing blood flow to the upper body.
3) Heart failure, prognosis dependent on skill of surgeon and extent of deformity.
4) PDA, in order to mix oxygenated blood with the deoxygenated blood, else the patient will die of hypoxia.

 

[Slide]

A 17 year-old teenager is brought to the ER with complaints of nausea and tinnitus. On elaboration of history, the patient reports taking medication recently for a headache but cannot remember what it was or how much she took.

1) What is the most likely drug she took?
2) What is the metabolic toxic effect that could be occuring?
3) How would you treat this patient?

 

[Saladin MD]

A 17 year-old teenager is brought to the ER with complaints of nausea and tinnitus. On elaboration of history, the patient reports taking medication recently for a headache but cannot remember what it was or how much she took.

1) What is the most likely drug she took?
2) What is the metabolic toxic effect that could be occuring?
3) How would you treat this patient?

1) Aspirin
2) Metabolic Acidosis / Respiratory Alkalosis
3) Activated charcoal, IV fluids, sodirum bicarb, and if all else fails, then dialysis

 

[FutureInternist]

A 17 year-old teenager is brought to the ER with complaints of nausea and tinnitus. On elaboration of history, the patient reports taking medication recently for a headache but cannot remember what it was or how much she took.

1) What is the most likely drug she took?
2) What is the metabolic toxic effect that could be occuring?
3) How would you treat this patient?

1) Aspirin
2) ASA --> stimulation of respiratory center --> hyperventilation --> resp alkalosis (early) while the metabolism of the drug by the liver --> metabolic acidosis (late)
3) Since it's an acid, alkalanise the urine to increase excretion.

I swear I started typing before Saladin....I'm just a slow typer

 

[Slide]

1) Aspirin
2) ASA --> stimulation of respiratory center --> hyperventilation --> resp alkalosis (early) while the metabolism of the drug by the liver --> metabolic acidosis (late)
3) Since it's an acid, alkalanise the urine to increase excretion.

I swear I started typing before Saladin....I'm just a slow typer

to both of you!

 

[neil100]

1) Tetralogy of Fallot
2) Squatting kinks off the iliac arteries and other arteries to the lower extremities, increasing blood flow to the upper body.
3) Heart failure, prognosis dependent on skill of surgeon and extent of deformity.
4) PDA, in order to mix oxygenated blood with the deoxygenated blood, else the patient will die of hypoxia.

1) good.
2) good. Increasing systemic vascular resistance, so that more blood reaches the lungs.
3) I was going for Infective endocarditis. I believe goljan said that pts with congenital heart defects are likely to die of infective endocarditis. But, I can imagine heart failure too.
4) Yeah PDA and also ASD. Left to right shunting. Achieving the same effect in a way.