The Question Thread

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blkkd

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Alright so basically i had an idea that i thought would be interesting. One person asks a medical question and then the person who posts after them has to answer that question and then post their own. You can't post a question until you answer the one before your post. I'll start it off

What is the underlying cause of Von Gierke's?
 
I like this game! I can procrastinate and still pretend like I'm studying - yay!

blkkd said:
....What is the underlying cause of Von Gierke's?

Von Gierke's is an autosomal recessive disease that causes a Type I glycogen storage disease. Hepatic glucose-6-phosphatase is deficient, leading to hypoglycemia, enlarged liver and kidney due to trapping of glycogen, and also hyperlipidemia and hyperuricemia.



How do patients with strep throat typically present and what is the appropriate test to diagnose?
 
dante201 said:
I like this game! I can procrastinate and still pretend like I'm studying - yay!



Von Gierke's is an autosomal recessive disease that causes a Type I glycogen storage disease. Hepatic glucose-6-phosphatase is deficient, leading to hypoglycemia, enlarged liver and kidney due to trapping of glycogen, and also hyperlipidemia and hyperuricemia.



How do patients with strep throat typically present and what is the appropriate test to diagnose?


Remove the tonsils and send the specimen to path, right?



Which is more irritating to deal with, a munchausen's patient or a malingerer?
 
-Febrile
-Erythetamous pharynx with purulent exudate
-Anterior cervical lymphadenopathy
-Lack of cough

Do a rapid strep test on throat swabs to check for group A carbohydrates

Hmmmm, my question: What is Kuru, identify the infectious agent, and what kind of lifestyle do you need to live to acquire the condition?
 
felipe5 said:
-Febrile
-Erythetamous pharynx with purulent exudate
-Anterior cervical lymphadenopathy
-Lack of cough

Do a rapid strep test on throat swabs to check for group A carbohydrates

Hmmmm, my question: What is Kuru, identify the infectious agent, and what kind of lifestyle do you need to live to acquire the condition?

Kuru! my favorite of all the prion ailments. To acquire the infamous Kuru, it helps to live in an african tribe where cannibalism is the way to honor your dead.

Q: What bug is the most common cause of pneumonia in alcoholics?
 
renox9 said:
Kuru! my favorite of all the prion ailments. To acquire the infamous Kuru, it helps to live in an african tribe where cannibalism is the way to honor your dead.

Q: What bug is the most common cause of pneumonia in alcoholics?

Sorry to break the flow of the thread. But I couldn't resist correcting. Kuru was discovered in the Fore people of New Guinea. Not Africa.
 
renox9 said:
Kuru! my favorite of all the prion ailments. To acquire the infamous Kuru, it helps to live in an african tribe where cannibalism is the way to honor your dead.

Q: What bug is the most common cause of pneumonia in alcoholics?

Klebsiella pneumoniae is the most common bug in pneumonia of alcoholics.

Q: What is the treatment of choice for Plasmodium vivax and ovale malaria and what evaluation must be done before administering the drug?
 
trudub said:
Klebsiella pneumoniae is the most common bug in pneumonia of alcoholics.

Q: What is the treatment of choice for Plasmodium vivax and ovale malaria and what evaluation must be done before administering the drug?

Im pretty sure its still strep actually.
 
dynx said:
Im pretty sure its still strep actually.

Actually Klebsiella is the most common for Alcoholics although Step pneumo is the most common for the general population (I think it has something to do with increased aspiration risk in alcoholics).

The preferred treatment for Plasmodium vivax would be Chlproroquine followed by primaquine (according to my Pharm class at least) and for both of these drugs you need to test for Glucose 6 Phosphate Deficiency.


What antiviral drug is useful for both HIV and Hep B?
 
hakksar said:
Actually Klebsiella is the most common for Alcoholics although Step pneumo is the most common for the general population (I think it has something to do with increased aspiration risk in alcoholics).

The preferred treatment for Plasmodium vivax would be Chlproroquine followed by primaquine (according to my Pharm class at least) and for both of these drugs you need to test for Glucose 6 Phosphate Deficiency.


What antiviral drug is useful for both HIV and Hep B?

My bad, I stated it like it was a suggestion. Strep. P is still the most common cause of pneumonia in alcoholics.
 
dynx said:
My bad, I stated it like it was a suggestion. Strep. P is still the most common cause of pneumonia in alcoholics.

Yeah, I was about to post this correction also. Even though Klebsiella is often the answer to the the classic "alcoholic with pneumonia" board question, the most common cause of pneumonia in alcoholics is still the same for the general population - Strep pneumo.
 
dynx said:
My bad, I stated it like it was a suggestion. Strep. P is still the most common cause of pneumonia in alcoholics.

You are right, I misremembered (not sure if that is a word) my notes. Strep pneumo is the most common but Klebsiella has the highest mortality rate (40%!!!!). I need to be more careful. My question still stands though, what antiviral is used for both HIV and Hep B?
 
hakksar said:
You are right, I misremembered (not sure if that is a word) my notes. Strep pneumo is the most common but Klebsiella has the highest mortality rate (40%!!!!). I need to be more careful. My question still stands though, what antiviral is used for both HIV and Hep B?

Interferon-Alpha

I think most people get the whole Strep/kleb mixed up just from confusing the fact that kleb P. is MOST OFTEN seen in alcoholics due to aspiration but Strep P. is still the most common type of pneumonia.


How does liver cirrhois cause ascites?
 
Cpt.Hook Hamate said:
Interferon-Alpha

I think most people get the whole Strep/kleb mixed up just from confusing the fact that kleb P. is MOST OFTEN seen in alcoholics due to aspiration but Strep P. is still the most common type of pneumonia.


How does liver cirrhois cause ascites?

Never actually heard of anyone actually using Ifn-alpha for HIV . . . the answer I am looking for is a particular nucleoside Reverse Transcriptase Inhibitor (remember that even though Hep B is not a retrovirus it uses a reverse transcriptase for part of its replication cycle).
 
hakksar said:
Never actually heard of anyone actually using Ifn-alpha for HIV . . . the answer I am looking for is a particular nucleoside Reverse Transcriptase Inhibitor (remember that even though Hep B is not a retrovirus it uses a reverse transcriptase for part of its replication cycle).

It is used in Aids-related Kaposi Sarcoma. I guess you wasn't specific enough so my question is still live. 🙂

Now, answer it!
 
Lamivudine....I think...

Doesn't cirrhosis just cause portal hypertension due to the fibrosis thus resulting in ascites?

What condition is a delta wave on an EKG associated with?
 
twinklz said:
Lamivudine....I think...

Doesn't cirrhosis just cause portal hypertension due to the fibrosis thus resulting in ascites?

What condition is a delta wave on an EKG associated with?

The rules were specifically stated as "You can't post a question until you answer the one before your post. I'll start it off."

You answered a question with a question and then illegally asked another question therefore disqualifying your latter question so my question is still live.
 
twinklz said:
Lamivudine....I think...

Doesn't cirrhosis just cause portal hypertension due to the fibrosis thus resulting in ascites?

What condition is a delta wave on an EKG associated with?


Delta waves are associated with Wolff-Parkinson-White Syndrome or other diseases with a bypass tract.

When looking at a Wigger diagram what causes the loss of the dichrotic notch on the aortic pressure tracing?
 
Cpt.Hook Hamate said:
Interferon-Alpha

I think most people get the whole Strep/kleb mixed up just from confusing the fact that kleb P. is MOST OFTEN seen in alcoholics due to aspiration but Strep P. is still the most common type of pneumonia.


How does liver cirrhois cause ascites?

Doesn't it have to do with a decrease in albumin (and other proteins) production, thus decreasing the oncotic pressure of the blood, leading to fluid build up extravascularly causing edema/ascitis?

What is the most common cause of nephrotic syndrome in adults?
 
YoungFaithful said:
Doesn't it have to do with a decrease in albumin (and other proteins) production, thus decreasing the oncotic pressure of the blood, leading to fluid build up extravascularly causing edema/ascitis?

What is the most common cause of nephrotic syndrome in adults?

Membranous Glomerulonephritis (Membranous Nephropathy)

What does the Mesonephric Duct turn into in males and females?
 
Vanime said:
Membranous Glomerulonephritis (Membranous Nephropathy)

What does the Mesonephric Duct turn into in males and females?

They degenerate in females and become reproductive tubing in males (epididymis, seminal vesicles, ejaculatory duct, vas deferens).


What causes Ehler-Danlos syndrome?
 
UCLAstudent said:
They degenerate in females and become reproductive tubing in males (epididymis, seminal vesicles, ejaculatory duct, vas deferens).


What causes Ehler-Danlos syndrome?

just to add to the first answer.
aside from non-functional female remnants: (not sure i ever saw this in anatomy) appendix vesiculosa, duct of epoophoron, duct of garner,
mesonephric ducts also turn into kidney-connected structures in both sexes (after hits the metanephric mass): ureter, pelvis, calices, and collecting tubules. my embryo book's still kinda fuzzy on what point it's still considered mesonephric duct and when itthe name changes to metanephric duct.
 
UCLAstudent said:
They degenerate in females and become reproductive tubing in males (epididymis, seminal vesicles, ejaculatory duct, vas deferens).


What causes Ehler-Danlos syndrome?

Ehlers Danlos is a connective tissue disorder that involves defects in collagen. The various forms of EDS are characterized by actual defects in collagen itself to defects in processing enzymes such as lysyl oxidase. The end result is joint hyperflexibility, fragile skin, and hyperextensibility. It can also cause defects in connective tissues of blood vessels and increase the risk of dissection and/or aneurysm.

Q: When looking at a Wigger diagram of the cardiac cycle, what causes loss of the dichrotic notch on the aortic pressure tracing?
 
YoungFaithful said:
Doesn't it have to do with a decrease in albumin (and other proteins) production, thus decreasing the oncotic pressure of the blood, leading to fluid build up extravascularly causing edema/ascitis?

What is the most common cause of nephrotic syndrome in adults?

There you go but this is still a question but at least it is the correct question to ask. Shame on those who proceeded without properly answering the question or "questioning" the question in your case. 😀 Good and detailed too.
 
UCLAstudent said:
They degenerate in females and become reproductive tubing in males (epididymis, seminal vesicles, ejaculatory duct, vas deferens).


What causes Ehler-Danlos syndrome?

I will repeat this so we can keep the thread on track:

Ehlers Danlos is a connective tissue disorder that involves defects in collagen. The various forms of EDS are characterized by actual defects in collagen itself to defects in processing enzymes such as lysyl oxidase. The end result is joint hyperflexibility, fragile skin, and hyperextensibility. It can also cause defects in connective tissues of blood vessels and increase the risk of dissection and/or aneurysm.

Q: When looking at a Wigger diagram of the cardiac cycle, what causes loss of the dichrotic notch on the aortic pressure tracing?
 
trudub said:
I will repeat this so we can keep the thread on track:

Ehlers Danlos is a connective tissue disorder that involves defects in collagen. The various forms of EDS are characterized by actual defects in collagen itself to defects in processing enzymes such as lysyl oxidase. The end result is joint hyperflexibility, fragile skin, and hyperextensibility. It can also cause defects in connective tissues of blood vessels and increase the risk of dissection and/or aneurysm.

Q: When looking at a Wigger diagram of the cardiac cycle, what causes loss of the dichrotic notch on the aortic pressure tracing?
Damn - I'm not 100% sure this is right. But, here's a stab at it...

When the pressure in the aorta > pressure in the ventricle, the aortic valve closes and causes the dicrotic notch (or incisura). Dicrotic notch can be absent with aging, due to stiffening of the aorta (I think). But, I think the question is asking for pathology - so I'm going to say aortic regurgitation due to valvular insufficiency?

(if that's wrong - excuse me, and ignore my question)

What are the components of the CREST syndrome, and what is the disease is it associated with?
 
dante201 said:
Damn - I'm not 100% sure this is right. But, here's a stab at it...

When the pressure in the aorta > pressure in the ventricle, the aortic valve closes and causes the dicrotic notch (or incisura). Dicrotic notch can be absent with aging, due to stiffening of the aorta (I think). But, I think the question is asking for pathology - so I'm going to say aortic regurgitation due to valvular insufficiency?

(if that's wrong - excuse me, and ignore my question)

What are the components of the CREST syndrome, and what is the disease is it associated with?

Hmmmm....
C - calcinosis
R - raynaud's
E - esophageal dysmotility
S - sclerodactyly
T - telangirctasias

The disease associated with it is limited cutaneous systemic sclerosis (LcSSc), right?

And I beleive the severe form of the disease can result in pulm fibrosis, cor pulmonale, ARF, and malignant HTN (according to my First Aid 😉 )


My question (if I got it the correct answer): What is the treatment(s) for symptomatic hyperkalemia? And what are the "symptoms" of hyperkalemia?
 
ear-ache said:
Hmmmm....
C - calcinosis
R - raynaud's
E - esophageal dysmotility
S - sclerodactyly
T - telangirctasias

The disease associated with it is limited cutaneous systemic sclerosis (LcSSc), right?

And I beleive the severe form of the disease can result in pulm fibrosis, cor pulmonale, ARF, and malignant HTN (according to my First Aid 😉 )


My question (if I got it the correct answer): What is the treatment(s) for symptomatic hyperkalemia? And what are the "symptoms" of hyperkalemia?

I think the more severe version is diffuse scleroderma.
Renal was awhile ago so I am going to completely guess. . . treat hyperkalemia with loop diuretics, I know they can cause hypokalemia. Hyperkalemia causes arrythmias. (U wave?)

Which autoantibody is the best indicator of SLE?
 
*Anti Nuclear Antibodies (anti ds dna, x reaction w/ smith antigen)

Avian flu: strain, ideas about how it came to be, and what makes it so feared around these parts
 
THP said:
I think the more severe version is diffuse scleroderma.
Renal was awhile ago so I am going to completely guess. . . treat hyperkalemia with loop diuretics, I know they can cause hypokalemia. Hyperkalemia causes arrythmias. (U wave?)

Which autoantibody is the best indicator of SLE?

I'd guess aldo blockers would be useful too?

anti-dsDNA, I think. there was another one which also had high specificity, contrasted w/ anti-nuclear antibody which is high sensitivity but low specificity? haven't covered this in several months, so someone correct me if I'm off.

What are the primary types of testicular cancer, and the main treatment methods for them?

EDIT: other antibody that was also highly specific was anti-Sm(ith)
 
Rendar5 said:
I'd guess aldo blockers would be useful too?

anti-dsDNA, I think. there was another one which also had high specificity, contrasted w/ anti-nuclear antibody which is high sensitivity but low specificity? haven't covered this in several months, so someone correct me if I'm off.

What are the primary types of testicular cancer, and the main treatment methods for them

the other one is anti-smith
 
THP said:
Renal was awhile ago so I am going to completely guess. . . treat hyperkalemia with loop diuretics, I know they can cause hypokalemia. Hyperkalemia causes arrythmias. (U wave?)
Clinical signs of hyperkalemia;
Cardiac Effects
Tall, peaked T waves in precordial leads
Widened QRS
Prolonged P-R interval/AV blocks
Decrease amplitude and disappearance of P waves
Sine wave (blending of the QRS into the T wave)
Ventricular arrhythmias
Cardiac arrest

Neuromuscular effects
Vague muscular weakness (usually the first sign)
Flaccid muscle paralysis (starts at feer and ascends)
Paresthesia of the face, tongue, feet, and hands
CNS is NOT affected. Patient often remains A&O.

GI Effects
Nausea
intermittent intestinal colic or diarrhea

Treatment
1. Block Cardiac effects of hyperkalemia (For emergent use. I.e. - if there are ECG changes, and/or >7.0)
• IV Calcium (Calcium gluconate or chloride) – DO THIS FIRST! CaCl2 5ml of 5% solution, Calcium gluconate 5ml of 10% solution. Calcium antagonizes the membrane effect of hyperkalemia (membrane stabilizer), although how this is achieved is not well understood. The onset of action is immediate, but short lived (30-60 minutes). Long enough for the insulin/dextrose/bicarbonate cocktail to take effect. CaCl2 is 3x more potent, but needs to be administered via central line.

2. Increase cellular K+ uptake (also for emergent use)
• Insulin and Dextrose -10U regular insulin & 1 ampul of D50 (50g dextrose). Onset of action in 15min, peaks in 60min, and lasts several hours.
• Sodium Bicarbonate – one 50meq ampule (or 1mEq/kg). Onset of action is 30-60min and lasts several hours. More effective when acidosis is present.
• Albuterol nebulizer. Peak effect within 30min. Beware of cardiac arrhythmias!

3. Removal of excess K+ (emergent and insidious)
• Loop or Thiazide diuretics – 20-40mg Lasix IV.
• Cation exchange resins (Kayexalate™) administered PO or PR. Each gram of resin may bind as much as 1 meq of potassium and release 1 to 2 meq of sodium. Peak effect is in 2-4 hours.
• Hemodialysis – Used both emergently and for long-term.

PM me if anyone wants the references

BOO KU! GO MIZZOU!
 
Rendar5 said:
beat me to my look-up-and-edit. thanks 🙂 👍
sorry beat ya both 🙂 🙂 🙂


ps---Muck Fizzou
 
Rendar5 said:
I'd guess aldo blockers would be useful too?

anti-dsDNA, I think. there was another one which also had high specificity, contrasted w/ anti-nuclear antibody which is high sensitivity but low specificity? haven't covered this in several months, so someone correct me if I'm off.

What are the primary types of testicular cancer, and the main treatment methods for them?

EDIT: other antibody that was also highly specific was anti-Sm(ith)

When talking about testicular cancer, 95% of testicular cancers are germ cell tumors. Within germ cell tumors of the testicle there are two broad divisions, there are seminomas and non-seminomas. Often times, you actually find mixed germ cell tumors that have both portions of a seminoma and non-seminoma in them. Seminomas respond better to treatment and generally require only radiation after orchidectomy. However, advanced seminomas (Class IIc and Class III) do require additional chemotherapy. Non-seminomas respond poorly to radiation therapy. As a result, following orchidectomy chemotherapy is required. Non-seminomas tend to metastasize early and thus usually present in more advanced stages of the disease process. The most likely place for metastases is the retroperitoneal lymph nodes by lymphogenous spread or to the lungs by hematogenous spread. Because non-seminomas are more aggressive, all mixed tumors should be treated as non-seminomas.

Q: What disease or condition is associated with Aschoff bodies and what is the cause of the disease/condition?
 
trudub said:
When talking about testicular cancer, 95% of testicular cancers are germ cell tumors. Within germ cell tumors of the testicle there are two broad divisions, there are seminomas and non-seminomas. Often times, you actually find mixed germ cell tumors that have both portions of a seminoma and non-seminoma in them. Seminomas respond better to treatment and generally require only radiation after orchidectomy. However, advanced seminomas (Class IIc and Class III) do require additional chemotherapy. Non-seminomas respond poorly to radiation therapy. As a result, following orchidectomy chemotherapy is required. Non-seminomas tend to metastasize early and thus usually present in more advanced stages of the disease process. The most likely place for metastases is the retroperitoneal lymph nodes by lymphogenous spread or to the lungs by hematogenous spread. Because non-seminomas are more aggressive, all mixed tumors should be treated as non-seminomas.

Q: What disease or condition is associated with Aschoff bodies and what is the cause of the disease/condition?

Aschoff bodies are associated with rheumatic fever, which is caused by strep throat.

Q: What is the cause of Crocodile Tears Syndrome?
 
Antigunner said:
Aschoff bodies are associated with rheumatic fever, which is caused by strep throat.

Q: What is the cause of Crocodile Tears Syndrome?

Crocodile tears syndrome results from damage to cranial nerve VII. This obviously results in facial paralysis. The syndrome gets its name because it also causes the patient to lacrimate extensively, particularly when eating.

What family of viruses cause the histopathological findings of Downey cells, Cowdry bodies, and Owl's eye cells? What members of the family cause each finding?
 
herpes viridiae......downey=EB, Cowdry=HSV1,2, Owl's Eye= CMV

Which condition is also known as 'pulseless disease' and what are some typical findings associated w/ it?
 
accidentally duplicated my post, see below
 
felipe5 said:
herpes viridiae......downey=EB, Cowdry=HSV1,2, Owl's Eye= CMV

Which condition is also known as 'pulseless disease' and what are some typical findings associated w/ it?

We just talked about this today in class, pulseless disease is Takayasu arteritis.

Patients tend to have absent radial pulses due to the affect of the disease on the vessels as they come off the aorta. This can result in upper extremity pain due to decreased blood flow. In addition, the carotids are affected as they branch off the aorta and can cause visual disturbances and neurological findings such as dizziness and even stroke. If flow to the descending aorta is impaired significantly, poor renal perfusion can lead to hypertension and all the symptoms that accompany hypertension.

Q: What effects do potassium channel blocking agents have on the EKG and what arrhythmia do these agents and these EKG findings predispose patients to?
 
K+ blockers (Class III antiarrhythmics) act on Phase 3. By inhibiting K+ current, the effective refractory period is lengthened. But, with toxicity, you could get torsade de pointes.

What visual field defect do you get with a lesion at the optic chiasm?
 
dante201 said:
K+ blockers (Class III antiarrhythmics) act on Phase 3. By inhibiting K+ current, the effective refractory period is lengthened. But, with toxicity, you could get torsade de pointes.

What visual field defect do you get with a lesion at the optic chiasm?


A: Bitemporal hemianopsia.

Q: What portion of the brain (I'm looking for a gyrus here) decodes symbolic information like letters or numbers into the conceptual representation of the symbol (i.e. "D-O-G" = "the thing that barks and does tricks"). Give me the name or the Brodmann area.

Hope that's not too vague, but the questions were getting too "STEP I" for my taste.
 
HamOnWholeWheat said:
A: Bitemporal hemianopsia.

Q: What portion of the brain (I'm looking for a gyrus here) decodes symbolic information like letters or numbers into the conceptual representation of the symbol (i.e. "D-O-G" = "the thing that barks and does tricks"). Give me the name or the Brodmann area.

Hope that's not too vague, but the questions were getting too "STEP I" for my taste.

The angular gyrus decodes symbolic information

Q:What vascular injury is associated with posterior knee dislocations and what is the standard of care when a patient presents with a posterior knee dislocation to detect this injury?
 
trudub said:
The angular gyrus decodes symbolic information

Q:What vascular injury is associated with posterior knee dislocations and what is the standard of care when a patient presents with a posterior knee dislocation to detect this injury?

Damage to the popliteal artery; evaluate posterior tibial and dorsal pedal pulses.

What nerve injury is associated with a mid-shaft humeral fracture vs. a fracture of the medial epicondyle?



-------------------------------------
http://ipods.freepay.com/?r=21779090
 
mules05 said:
Damage to the popliteal artery; evaluate posterior tibial and dorsal pedal pulses.

What nerve injury is associated with a mid-shaft humeral fracture vs. a fracture of the medial epicondyle?



-------------------------------------
http://ipods.freepay.com/?r=21779090

radial vs. ulnar

mechanism of action of amantidine?
 
felipe5 said:
radial vs. ulnar

mechanism of action of amantidine?

Increases Dopamine output via displacement of the vesicles into the synaptic cleft, commonly used to treat parkinsons. Its also used to treat influenza type A I think (I may be talking out of my ass on that one).


So who first discovered (or I should say "is credited with the discovery") that blood circulates?
 
felipe5 said:
radial vs. ulnar

mechanism of action of amantidine?

Amantidine inhibits the M2 ion channel and is useful in the treatment of Influenza A. By inhibiting the M2 ion channel it inhibits acid mediated ribonucleoprotein dissociation and it also potentiates the acid induced conformational changes to hemagglutinin.

Q: What is used to keep a ductus arteriosus open and in what conditions might having a patent ductus arteriosus be beneficial to the neonatal patient?
 
indomethicin (prostaglandin inhibitor), used for keeping the ductus open allowing for a mixing of blood in conditions such as transposition of the great vessels.

now, this one's a bit on the molecular biology side, but we just heard about it in Path and I wanted to see if anyone knew about this.....has anyone heard about the "Tinman" gene???
 
felipe5 said:
indomethicin (prostaglandin inhibitor), used for keeping the ductus open allowing for a mixing of blood in conditions such as transposition of the great vessels.

now, this one's a bit on the molecular biology side, but we just heard about it in Path and I wanted to see if anyone knew about this.....has anyone heard about the "Tinman" gene???


I call foul! No-one answered mine yet. 😡
 
HamOnWholeWheat said:
I call foul! No-one answered mine yet. 😡

William Harvey

"tinman" gene controls heart development in Drosophila (i think?)

Q: True or False - wearing tightie-whities reduces sperm production
 
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