We should have a thread like this. Anybody up for starting one?

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A new mother is worried about her 1.5 month old infant because he isn't feeding and has high fever and neck stiffness (upon physical examination). Culture reveals an organism with tumbling motility.

1) What organism is responsible for the neonatal meningitis?
2) This organism shares a certain characteristic with gram negative bacteria--what is it?
 
A new mother is worried about her 1.5 month old infant because he isn't feeding and has high fever and neck stiffness (upon physical examination). Culture reveals an organism with tumbling motility.

1) What organism is responsible for the neonatal meningitis?
2) This organism shares a certain characteristic with gram negative bacteria--what is it?

Listeria monocytogenes. Only gram positive known to have LPS endotoxin.
 
A 20 year old man experiences sudden tearing sensation in upper back that goes away after 4 hours. He has long fingers and pectus excavatum.

1. What is the cause of his sudden tearing pain? Where is this pathology typically located?
2. What is a common gene mutation likely present in this patient?
 
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A 20 year old man experiences sudden tearing sensation in upper back that goes away after 4 hours. He has long fingers and pectus excavatum.

1. What is the cause of his sudden tearing pain? Where is this pathology typically located?
2. What is a common gene mutation likely present in this patient?

1) Aortic dissection--ascending part of arch of the aorta (?)
2) Fibrillin-1
 
28 y/o IV drug abuser presents to the ER with fever and fatigue and is found to have a new murmur on physical exam.

1) What is the most likely organism?
2) What valve is most likely affected?
 
38 y/o female presents to her PCP complaining of neck pain. Upon taking a thorough history, the physician learns that she recently recovered from an upper respiratory infection.

1) Diagnose this patient's "neck pain".
2) If there had been no neck pain but a "woody" thyroid was discovered instead, what would be your diagnosis?
 
28 y/o IV drug abuser presents to the ER with fever and fatigue and is found to have a new murmur on physical exam.

1) What is the most likely organism?
2) What valve is most likely affected?

1. Staph aureus
2. Tricuspid

?
 
38 y/o female presents to her PCP complaining of neck pain. Upon taking a thorough history, the physician learns that she recently recovered from an upper respiratory infection.

1) Diagnose this patient's "neck pain".
2) If there had been no neck pain but a "woody" thyroid was discovered instead, what would be your diagnosis?

1. it sounds like DeQuervain's thyroiditis, but I'm only thinking about the thyroid at all here because I read part 2 already
2. Reidel thyroiditis
 
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Nice to see the thread take off.

John Doe comes in and you realize that he's a solider that has several blast/burn wounds on his lower legs. Doing a patient history you find that he's allergic to certain beta-lactam drugs.

1. What's the mechanism of action of the drug, which you can give to the patient, to prevent formation of green-tinged cellulitis?
2. What does this pathogen cause in a normal healthy individual?
 
1) Aortic dissection--ascending part of arch of the aorta (?)
2) Fibrillin-1

Can you refresh my memory? Marfan's leads to this, there was an uworld question. It's primarily due to "cystic medial degeneration", correct? For instance, tertiary syphilis is due to decreased luminal caliber of the vasa vasorum.
 
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Nice to see the thread take off.

John Doe comes in and you realize that he's a solider that has several blast/burn wounds on his lower legs. Doing a patient history you find that he's allergic to certain beta-lactam drugs.

1. What's the mechanism of action of the drug, which you can give to the patient, to prevent formation of green-tinged cellulitis?
2. What does this pathogen cause in a normal healthy individual?

P. aeruginosa

1. Aztreonam (since he's allergic to beta-lactams) -- works by inhibiting cell wall synthesis only in Gram negative bacteria.

2. In healthy individuals? Hmm, burn and skin infections, osteomyelitis (d/t puncture wounds of the foot), and otitis externa are all I can think of at the moment. Endocarditis in drug abusers as well as sepsis if introduced into bloodstream.
 
Can you refresh my memory? Marfan's leads to this, there was an uworld question. It's primarily due to "cystic medial degeneration", correct? For instance, tertiary syphilis is due to decreased luminal caliber of the vasa vasorum.

Yea, it's due to cystic medial degeneration. And tertiary syphilis is due to inflammation (and subsequent narrowing) of the vasa vasorum supplying the proximal aorta.
 
I'll write one up too -- hopefully, it's not botched too badly! :)

3 y/o M patient comes in with a 4-day history of constitutional symptoms such as fever, fatigue, conjunctivitis, enlarged lymph nodes, etc. Parents also noted a red rash on his palms the other day. Earlier today, the patient was complaining of crushing chest pain as well, so the parents got worried and brought him into the ER.

1) What is the diagnosis? And what complication occurred in this patient? Also, is it reversible?
2) What is the treatment of choice for this disease (don't worry about the complication)?
3) In what other (general) conditions is one of the treatments for this disease contraindicated? And why is it contraindicated?
 
P. aeruginosa

1. Aztreonam (since he's allergic to beta-lactams) -- works by inhibiting cell wall synthesis only in Gram negative bacteria.

2. In healthy individuals? Hmm, burn and skin infections, osteomyelitis (d/t puncture wounds of the foot), and otitis externa are all I can think of at the moment. Endocarditis in drug abusers as well as sepsis if introduced into bloodstream.

Healthy individuals according to Kaplan Micro.

Don't forget Aztreonam only works on Gram negative rods

1. Hot tub folliculitis - but not the mcc, as S. Aureus is.
2. Eye ulceration - due to prolonged contact wearing, trauma
 
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I'll write one up too -- hopefully, it's not botched too badly! :)

3 y/o M patient comes in with a 4-day history of constitutional symptoms such as fever, fatigue, conjunctivitis, enlarged lymph nodes, etc. Parents also noted a red rash on his palms the other day. Earlier today, the patient was complaining of crushing chest pain as well, so the parents got worried and brought him into the ER.

1) What is the diagnosis? And what complication occurred in this patient? Also, is it reversible?
2) What is the treatment of choice for this disease (don't worry about the complication)?
3) In what other (general) conditions is one of the treatments for this disease contraindicated? And why is it contraindicated?

I got this question wrong on Kaplan, so I think I know what it is...

1. Kawasaki's Disease/Vasculitis. Complication should be the blockage of one of the coronary arteries, LAD since it's the mc. Not sure what you mean by is it reversible? if you're asking about the damage - then no. x > 20 minutes of ischemia would cause swelling and then eventual flow of cellular enzymes out which is the hallmark of irreversible injury.

2. Aspirin &/or IVIG.

3. When is aspirin c/i'd? I guess if patient has had recent surgery, low platelet count. Not sure which disease, just know that aspirin reduces mitochondria's ability to do beta-oxidation since it irreversibly inhibits the enzymes.
 
Had this question on my Micro shelf.

John Doe, a 15 year old male patient comes into your office complaining of constant fatigue, even with sleeping for eight hours, and intolerable throat pain. Workout shows enlarged lymph nodes. Blood work shows agglutination of the blood when mixed with sheep agar.

1. What is most commonly found on the surface of the cells, where this pathogen binds to?
2. If the agglutination test came back negative, what are the reasons? **HINT: 2 answers to this question**
3. You decide to treat John Doe with a beta-lactam, what will John Doe come back, presenting with? **HINT: Also 2 answers, but the second one is not as obvious as the first**
 
I got this question wrong on Kaplan, so I think I know what it is...

1. Kawasaki's Disease/Vasculitis. Complication should be the blockage of one of the coronary arteries, LAD since it's the mc. Not sure what you mean by is it reversible? if you're asking about the damage - then no. x > 20 minutes of ischemia would cause swelling and then eventual flow of cellular enzymes out which is the hallmark of irreversible injury.

2. Aspirin &/or IVIG.

3. When is aspirin c/i'd? I guess if patient has had recent surgery, low platelet count. Not sure which disease, just know that aspirin reduces mitochondria's ability to do beta-oxidation since it irreversibly inhibits the enzymes.

I'm okay with this answer. I think part 3 was aiming at that you should never use Aspirin to treat any other cause of pediatric fevers except Kawasaki's due to the potential to cause Reye's.
 
I'm okay with this answer. I think part 3 was aiming at that you should never use Aspirin to treat any other cause of pediatric fevers except Kawasaki's due to the potential to cause Reye's.

:thumbup:

answer my question above &/or ask a question of your own. :)
 
A 19-year-old previously healthy woman has had a mild pharyngitis followed by a high fever, neck pain, and fatigue. After 24 hours, her skin now shows extensive areas of petechial, purpuric rash. She is hypotensive, hyponatremic, hyperkalemic.

1. What organism?
2. What syndrome did it cause?
 
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A 19-year-old previously healthy woman has had a mild pharyngitis followed by a high fever, neck pain, and fatigue. After 24 hours, her skin now shows extensive areas of petechial, purpuric rash. She is hypotensive, hyponatremic, hyperkalemic.

1. What organism?
2. What syndrome did it cause?

Nice input of the mild pharyngitis.

1. N. meningitidis, however keep in mind that n. gonorrhea is actually the mcc of pharyngitis in sexually active individuals.
2. The petechia, purpuric rash indicates the toxin/bacteria has gone systemic. Death was due to Waterhouse-Friedrichsen Syndrome aka collapse of the adrenal glands.


I guess I'm back up again...

1. What is the general clinical picture of somebody you'd expect to have the symptoms you described?
2. How can you prevent it from people in close contact, and what is the major side effect of this drug?
3. Lastly, if there's a vaccine, what're the serotypes used and which serotype isn't used? What's the significance of the serotype not used? **HINT 3 ANSWERS TO THE LAST PART**
 
Is the last question serotype B isn't used even though it's the most prevalent because there is really no vaccine available for the serotype?
 
Is the last question serotype B isn't used even though it's the most prevalent because there is really no vaccine available for the serotype?

Correct, serotype B isn't used. It's used primarily for:

1. Identification
2. Serotyping
3. Identification of N.M. on the latex particle agglutination

You didn't answer the other questions.
 
Is the last question serotype B isn't used even though it's the most prevalent because there is really no vaccine available for the serotype?

There is a vaccine for group B. It is being approved for use in the European Union right now. But since this is the USMLE you can delete it from your brain. Maybe we'll see it in a few years once data on its efficacy has been studied on a widespread scale.
 
A 45-year-old man has a history of drinking 1 liter of whisky per day for the past 18 years. He has experienced many instances of N/V in the past 5 years. Today he experienced vomiting and massive hematemesis. Vitals are: Cardio--afebrile, tachycardic regular rhythm no murmurs no gallops; Resp--tachypnic, clear; BP--hypotensive sitting and supine, normal JVD; GI--normal bowel sounds in frequency and tone, no fluid wave, no tenderness, no occult blood in stool.

1. Diagnosis?
2. If fluid wave and increased JVD were present, what pathophysiological process/diagnosis must be added to the differential? Bonus point for naming the indicated confirmatory imaging test.
3. If subcutaneous crepitations/crackles/emphysema/pneumomediastinum were present instead of hematemesis, what syndrome has occurred? Bonus point for naming the indicated confirmatory imaging test.
 
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A 45-year-old man has a history of drinking 1 liter of whisky per day for the past 18 years. He has experienced many instances of N/V in the past 5 years. Today he experienced vomiting and massive hematemesis. Vitals are: Cardio--afebrile, tachycardic regular rhythm no murmurs no gallops; Resp--tachypnic, clear; BP--hypotensive sitting and supine, normal JVD; GI--normal bowel sounds in frequency and tone, no fluid wave, no tenderness, no occult blood in stool.

1. Diagnosis?
2. If fluid wave and increased JVD were present, what pathophysiological process/diagnosis must be added to the differential? Bonus point for naming the indicated confirmatory imaging test.
3. If subcutaneous crepitations/crackles/emphysema/pneumomediastinum were present instead of hematemesis, what syndrome has occurred? Bonus point for naming the indicated confirmatory imaging test.

1.Mallory Weiss
2.cardiac cirrhosis / alcohol induced cardiotoxicity - echocardiography
3. Boerhaave's syndrome
 
1. yep!
2. I was going for adding signs of liver cirrhosis --> consider ruptured esophageal varices
3. yep!

Oops i missed the original diagnoses
Screwed my brain with pathophysiology and got confirmatory test for dilated cardiomyopathy
 
Had this question on my Micro shelf.

John Doe, a 15 year old male patient comes into your office complaining of constant fatigue, even with sleeping for eight hours, and intolerable throat pain. Workout shows enlarged lymph nodes. Blood work shows agglutination of the blood when mixed with sheep agar.

1. What is most commonly found on the surface of the cells, where this pathogen binds to?
2. If the agglutination test came back negative, what are the reasons? **HINT: 2 answers to this question**
3. You decide to treat John Doe with a beta-lactam, what will John Doe come back, presenting with? **HINT: Also 2 answers, but the second one is not as obvious as the first**

Guess no one got it (me neither). Could you answer it yourself?
 
I'll post one I read from a small book of assorted questions I had.

A middle-aged woman dies suddenly. As a pathologist, you are called to look at her kidneys at autopsy. They are of normal size and surface is granular. The cortex appears pale but you see small hemorrhages! You check it under a microscope and you notice small renal arteries and arterioles all have luminal narrowing and concentric intimal thickening. What autoimmune disease could she have had and what antibody would have been positive?

If you haven't figured it out by now, use this hint: (you need to select the hidden text below to see it)
It is one of these four: DM, SLE, Scleroderma, RA.
 
John Doe, a 15 year old male patient comes into your office complaining of constant fatigue, even with sleeping for eight hours, and intolerable throat pain. Workout shows enlarged lymph nodes. Blood work shows agglutination of the blood when mixed with sheep agar.

1. What is most commonly found on the surface of the cells, where this pathogen binds to?
2. If the agglutination test came back negative, what are the reasons? **HINT: 2 answers to this question**
3. You decide to treat John Doe with a beta-lactam, what will John Doe come back, presenting with? **HINT: Also 2 answers, but the second one is not as obvious as the first**

I'll give it a quick go (could only come up with one of the answers for your dual questions). Sounds like infectious mononucleosis.

1. CD21 - EBV antigen
2. Could be CMV infectious mono
3. Ampicillin rash is associated with IM
 
I'll post one I read from a small book of assorted questions I had.

A middle-aged woman dies suddenly. As a pathologist, you are called to look at her kidneys at autopsy. They are of normal size and surface is granular. The cortex appears pale but you see small hemorrhages! You check it under a microscope and you notice small renal arteries and arterioles all have luminal narrowing and concentric intimal thickening. What autoimmune disease could she have had and what antibody would have been positive?

If you haven't figured it out by now, use this hint: (you need to select the hidden text below to see it)
It is one of these four: DM, SLE, Scleroderma, RA.

I'd guess DM. This always trips me up, because if you hadn't given us those choices, I would've thought this has something to do with malignant hypertension, where we see narrowing and intimal thickening - the onion type of appearance.
 
Guess no one got it (me neither). Could you answer it yourself?

I'll give it a quick go (could only come up with one of the answers for your dual questions). Sounds like infectious mononucleosis.

1. CD21 - EBV antigen
2. Could be CMV infectious mono
3. Ampicillin rash is associated with IM

1. Good answer. On my NBME micro exam, it had the answer choices: natural killer cells, immunoglobulins, and 2 other options. I couldn't figure out for the life of me what it was. Then it hit me that EBV --> B-cells --> B-cells have immunoglobulins on them.

2. Yup, it's either because it's due to CMV or we've done the test too early, and need to wait a bit longer.

3. Yup, amp causes the rash. The 2nd part was that it would also cause GI disturbance and allow c. difficile to become overactive. so give metronidazole to tx the psedu colitis.
 
Which cancers/lymphomas are the following associated with?

1. PNHemoglobinuria
2. IgG autoimmune hemolytic anemia
3. Hepatitis C
4. Strep bovis
5. Thoroplast exposure - 2 answers to this.
6. Tuberous Sclerosis - cardiac related
7. Hasimoto's Thyroiditis
8. Crohn's Disease
9. Minimal Change Disease aka Lipoid Nephrosis
10.Chronic TTP
 
Which cancers/lymphomas are the following associated with?

1. PNHemoglobinuria
2. IgG autoimmune hemolytic anemia
3. Hepatitis C
4. Strep bovis
5. Thoroplast exposure - 2 answers to this.
6. Tuberous Sclerosis - cardiac related
7. Hasimoto's Thyroiditis
8. Crohn's Disease
9. Minimal Change Disease aka Lipoid Nephrosis
10.Chronic TTP

1) leukaemia (unspecified)?
2) CLL/SLL (or sometimes mantle cell, as I've seen in an NBME)
3) HCC
4) CRC
5) Did you mean thorotrast? TCC is the big one. I'm not sure of the other. I would guess angiosarcoma (not necessarily intrahepatic).
6) rhabdomyosarcoma
7) NHL
8) CRC
9) Checked Google --> says a case study in 1986 found thymoma and pancreatic carcinoma in a patient with MCD, but I would think this combination to be coincidental (or reflective of a rare syndrome) rather than notably linked.
10) Since when does TTP cause cancer?
 
1) leukaemia (unspecified)?
2) CLL/SLL (or sometimes mantle cell, as I've seen in an NBME)
3) HCC
4) CRC
5) Did you mean thorotrast? TCC is the big one. I'm not sure of the other. I would guess angiosarcoma (not necessarily intrahepatic).
6) rhabdomyosarcoma
7) NHL
8) CRC
9) Checked Google --> says a case study in 1986 found thymoma and pancreatic carcinoma in a patient with MCD, but I would think this combination to be coincidental (or reflective of a rare syndrome) rather than notably linked.
10) Since when does TTP cause cancer?

5. Yes, meant to say thorotrast, no sure what I was thinking. Angiosarcoma and cholangiosarcoma.

9. For MCD/LN apparently NHL's Reed Sternberg cells release cytokines which lead to the effacement. (source: Pathoma)

10. Yeah, I was trying to get at the idea of it's association with HIV and lymphoproliferative disorders. (source: Goljan RR)
 
5. Yes, meant to say thorotrast, no sure what I was thinking. Angiosarcoma and cholangiosarcoma.

9. For MCD/LN apparently NHL's Reed Sternberg cells release cytokines which lead to the effacement. (source: Pathoma)

10. Yeah, I was trying to get at the idea of it's association with HIV and lymphoproliferative disorders. (source: Goljan RR)

5) Thorotrast is associated with TCC though. I guess cholangio would also make sense.

9) Did you mean Hodgkin's, not NHL? RS cells are Hodgkin's.
 
I'd guess DM. This always trips me up, because if you hadn't given us those choices, I would've thought this has something to do with malignant hypertension, where we see narrowing and intimal thickening - the onion type of appearance.

Quite close actually. Severe hypertension is the answer so it can occur with scleroderma.

Another one. 18 year old with WBCs in urine but no organisms on gram stain. What all do you think of?
 
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