Questions...

[DrPak]

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1. In Goljan's lectures, he says that the gold standard for diagnosing an MI is the CK-MB, but in his rapid review book, he writes that it's troponins. So has it changed then to troponin since the time he lectured and the time the Rapid Review book came out?

2. Goljan says that the dating of an MI using the gross and microscopic finding (eg, by 4-7 days you have red granulation tissue) is all "bullcrap" because there is no consensus in the books about the accurate dating of an MI. However dating an MI is there in his Rapid Review book and also in First Aid. So it's not "bullcrap" after all? We have to know it?

3. Typical and atypical pneumonia have different clinical features that easily tell the two apart. However, how does nosocomial pneumonia and pneumonia in immunocompromised people present? These are not classified as typical or atypical. So what are the clinical features there?

 

[missbonnie]

1. & 2 go with what everyone else says. Troponins. Know that between day 4-7ish, you're likely to die from rupture.

 

[Idiopathic]

Agreed with above, just remember timing for MI markers and that troponins are not recognized as an early marker, whereas CK is elevated within 30 minutes and CK-MB seen sometime before 3 hours. Troponins are the gold standard however in the first 24 hours. But if you have a guy clutching his chest having had chest pain for "45 minutes" dont go looking for cardiac troponins as the "marker most likely to be elevated"

More than likely the Goljan stuff is old, circa 1999 or so.

As for 3, you shouldnt look at the scenario just as typical v. atypical, even though both have distinct hallmarks. When you start talking about nosocomial or pneumocystic (or some variation thereof) then you wont be given the classic sx/sy of an outpatient pneumonia (i.e. patient is ventilated, low CD4+ count, IV drug user, homeless alcoholic) and the bug will be simple memorization.

 

[DrPak]

As for 3, you shouldnt look at the scenario just as typical v. atypical, even though both have distinct hallmarks. When you start talking about nosocomial or pneumocystic (or some variation thereof) then you wont be given the classic sx/sy of an outpatient pneumonia (i.e. patient is ventilated, low CD4+ count, IV drug user, homeless alcoholic) and the bug will be simple memorization.

But what will the signs and symptoms be? Cough? Fever? A nosocomial or immunocompromised patient can get lots of infections. There's no mention of any symptoms at all in such patients in the text. So how do we know it's the lungs that must be infected? And will we see exduation\consolidation in such patients or the more diffuse infiltrate of atypical pneumonia?

What I mean is, if we get an immunocompromised\hospitalized patient with pneumonia, what clinical features will that patient have to make us think it's pneumonia?

 

[Idiopathic]

There will be characteristics of respiratory involvement. You will not be given a hospitalized patient who just 'gets sick' and then be asked to determine the nature of the infection.

1) White out/consolidation on CXR

2) Decreasing SaO2/increased peak airway pressures on vent

3) physical signs of consolidation

Remember, its pneumonia. If there is no mention of respiratory involvement, look elsewhere.

 

[DrPak]

What is the mechanism of Dupuytren's contracture in cirrhosis? I know it's a fibromatosis, but why does that occur? Is it related to hyperestrinism?

 

[Idiopathic]

Unknown. Maybe due to poor metabolism of circulating fibrous compounds? Maybe too much collagen? I guess indirectly it could be due to hyperestrinism but i dont think the mechanism is known.

 

[DrPak]

What is the mechanism of respiratory acidosis in pregnancy. In Goljan's HY it says something about the CNS effect of estrogen/progesterone causing an increased clearance of CO2 per breath. How does that work?

 

[Idiopathic]

Progesterone increases tidal volume with minimal increase in RR. Results in slight but maintained resp. alkalosis (not acidosis) as excess CO2 is breathed off.

 

[DrPak]

double post

 

[DrPak]

Why does Gilbert's disease manifest (i.e.,as jaundice) only after 24 hrs of fasting? I mean how does fasting result in jaundice in these people?

 

[Idiopathic]

Its mainly stress induced, but fasting can increase the plasma unconjugated bilirubin level. Again, stress can also induce the hyperbilirubinemia, as can menses, fasting, etc.

These px have diminished UGT levels.

 

[DrPak]

How exactly does stress (fasting, menses, etc...) cause bilirubin levels to go up? Mebbe the liver become "less efficient" thereby tipping the bilirubin levels over the edge??

 

[Idiopathic]

Im not sure, I just know that it does. I dont think that part of the mechanism is too important, but rather the enzyme deficiency and the presentation.

 

[DrPak]

Hey idiopathic, I can't send you a PM cuz your inbox is full...

 

[DrPak]

In cystic fibrosis, the defiency of the CFTR prevents the secretion of Cl ions into the mucus. This prevents sodium and water from following the Cl- and as a result, the secretion is too thick and viscous.

However, when it comes to the sweat glands, the text says that CFTR's job is actually to reabsorb Na+ back into the sweat gland. That is why in CF, where CFTR is missing, the patient has really salty sweat.

Are these two different mechanisms here? In the production of mucus/bile/pancreatic fluid, the CFTR puts Na/Cl/water INTO the secretion, where as in the sweat glands, it moves the same ions OUT of the secretion.

It just seems counter-intuitive that the same CFTR would do opposite things with the same set of ions in different places. So am I understanding this right?

 

[OSUdoc08]

In cystic fibrosis, the defiency of the CFTR prevents the secretion of Cl ions into the mucus. This prevents sodium and water from following the Cl- and as a result, the secretion is too thick and viscous.

However, when it comes to the sweat glands, the text says that CFTR's job is actually to reabsorb Na+ back into the sweat gland. That is why in CF, where CFTR is missing, the patient has really salty sweat.

Are these two different mechanisms here? In the production of mucus/bile/pancreatic fluid, the CFTR puts Na/Cl/water INTO the secretion, where as in the sweat glands, it moves the same ions OUT of the secretion.

It just seems counter-intuitive that the same CFTR would do opposite things with the same set of ions in different places. So am I understanding this right?

Yes, they are completely different mechanisms. Salt is normally added to mucus, and salt is normally taken away from sweat. In CF, salt does not enter the mucus, so it becomes solidified. Sweat contains large amounts of salt, and a way that it can be initially detected is when a mother kisses her baby and it tastes salty.

This is also the basis of the "sweat test."

 

[surgwannabe]

In cystic fibrosis, the defiency of the CFTR prevents the secretion of Cl ions into the mucus. This prevents sodium and water from following the Cl- and as a result, the secretion is too thick and viscous.

However, when it comes to the sweat glands, the text says that CFTR's job is actually to reabsorb Na+ back into the sweat gland. That is why in CF, where CFTR is missing, the patient has really salty sweat.

Are these two different mechanisms here? In the production of mucus/bile/pancreatic fluid, the CFTR puts Na/Cl/water INTO the secretion, where as in the sweat glands, it moves the same ions OUT of the secretion.

It just seems counter-intuitive that the same CFTR would do opposite things with the same set of ions in different places. So am I understanding this right?

One gene, one transporter, different mechanisms, and different systems, it's called the pleiotropy!

 

[BlackNDecker]

However, when it comes to the sweat glands, the text says that CFTR's job is actually to reabsorb Na+ back into the sweat gland. That is why in CF, where CFTR is missing, the patient has really salty sweat.

Remember that the CFTR protein is merely a channel for Cl- transport. It simply opens and allows Cl- to passively flow down its concentration gradient.

When we sweat, ions(Cl, Na, K, HCO3-) are secreted into the acinar portion of the sweat gland. The composition of the sweat is then adjusted in the ductal portion of the sweat gland before being secreted onto the surface of the skin.

At slow flow rates(light sweating), alternative modes of Cl- transfer are operating (natural leakiness of the membrane, other Cl channels, etc.)....so the Cl and the Na (for electrical neutrality) along with the water (for Osmotic equilibrium) are adjusted appropriately within the ductal cells of the sweat gland before the secretion ends up on the skin.

But at High flow rates, the rate of flow is too much for the alternative transport processes to compensate for the lack of CFTR function, and the sweat composition can't be adjusted...excessive NaCl ends up on the epithelial surface. I have never seen CFTR to be directly involved in Na+ reabsorption...only indirectly via Cl- reabsorption.

In CF, salt does not enter the mucus, so it becomes dissipated.

I think you mean the mucus becomes very thick like concrete correct? N-acetylcysteine causes dissipation of the mucus, which is the rationale for its use.

Normally, the secretion of Na+ and Cl- pull water into the bronchioles. If Cl- transport is defective, very little Na+ and water can be added to secretions due to the positive lumenal potential that develops.

 

[Idiopathic]

Hey idiopathic, I can't send you a PM cuz your inbox is full...

solved

 

[DrPak]

Just want to confirm this point...

Alcohol is a P450 inducer and causes an increased expression of gamma-glutamyltransferase (GGT). Other drugs are inducers as well and also cause an increase in GGT. Alcohol is different however, because hepatocytes can also die from it as alcohol is a mitochondrial poison. This create the unique situation where we end up having GGT in the blood that is there not only because alcohol has increased it's production, but thereafter also killed the cell that produced it. That is why GGT is an excellent enzyme marker for alcoholic liver disease.

Is this correct?

Is there anything else that would cause GGT to show up in the blood like alcoholic liver disease?

 

[Idiopathic]

Is there anything else that would cause GGT to show up in the blood like alcoholic liver disease?

I dont think so, since it needs to be induced. AST and ALT are good nonspecific markers of liver disease because their presence signifies cellular necrosis, but GGT needs to be stimulated (i.e. it isnt just hanging around in the cell like AST/ALT)

 

[BlackNDecker]

I dont think so, since it needs to be induced. AST and ALT are good nonspecific markers of liver disease because their presence signifies cellular necrosis, but GGT needs to be stimulated (i.e. it isnt just hanging around in the cell like AST/ALT)

GGT is elevated along with Alk Phos in obstruction of the bile ducts...the cells of the bile canaliculi produce these enzymes, whereas the hepatocytes produce AST/ALT.

 

[DrPak]

GGT is elevated along with Alk Phos in obstruction of the bile ducts...the cells of the bile canaliculi produce these enzymes, whereas the hepatocytes produce AST/ALT.

Yeah, that's right, I looked it up. So GGT isn't all that great an enzyme marker of alcholic hep, is it? Mebbe GGT is increased in far greater amounts in alcoholic hep than in cholestatis?

 

[BlackNDecker]

Yeah, that's right, I looked it up. So GGT isn't all that great an enzyme marker of alcholic hep, is it? Mebbe GGT is increased in far greater amounts in alcoholic hep than in cholestatis?

GGT is most useful as a marker of RECENT relapse...or "falling off the wagon"...in pts who abuse alcohol. It is the first enzyme to rise due to excessive alcohol intake (not sure how much it rises in moderate consumption). The AST/ALT ratio is a better indicator of alholic hepatitis.

GGT isn't necessary for cholestasis because the direct/indirect bilirubin ratio is a much better indicator of obstruction.

 

[surgwannabe]

Yeah, that's right, I looked it up. So GGT isn't all that great an enzyme marker of alcholic hep, is it? Mebbe GGT is increased in far greater amounts in alcoholic hep than in cholestatis?

GGT is good for confirmation since it's expensive. Once you get your alk phos result, you can use GGT to determine whether the alk phos elevation is related to bone or GI.

 

[DrPak]

Would the mode of delivery in an HIV+ patient have an impact on maternal-neonatal transmission? Does it make a difference if the delivery is NVD or C-section?

 

[DrPak]

Why does serotonin in carcinoid syndrome cause valvular damage?