Step 1 Complicated Concepts Thread

[TheSeanieB]

ASK AND ANSWER TOUGH QUESTIONS RELATED TO STEP 1.

Starting with me:
physiologic chloride shift - When CO2 diffuses into a RBC, it quickly converts with H2O to H+ and HCO3- so that CO2 will continue to passively diffuse into the RBC. The HCO3- is then excreted into the plasma by a Cl-/HCO3- exchanger. When the RBC enters the pulmonary capillaries, the process reverses. HCO3- is taken up by exchange for a Cl-. It combines with H+ to creates CO2 +H2O. The CO2 then diffuses out of the RBC and ultimately into the alveoli. This process allows for maximal CO2 excretion by a RBC.

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[JP2740]

me too, I have never seen this before, it is legit awesome. I hated memorizing this stuff during my neuroscience block....

Is this a fair thing to say for blood supply?

medial medulla - ASA
lateral medulla - PICA
lateral pons - AICA

What does basilar get? medial pons + midbrain?

Could you explain what exactly you're doing here? lol it looks interesting

 

[bangarang]

I got this question on UWorld, and I think it might be a typo. Maybe someone can help me out.

Hemochromatosis: "The crucial site for HFE expression is on the basolateral surface of the epithelial cell," and then it goes on to discuss how iron dissociates inside the enterocytes and determines the intensity of uptake on the apical surface.

Is this not reversed? I thought the apical surface always referred to the lumen of any tube. It took me about 3 reads of the explanation to realize they might've reversed it, unless I'm mistaken. It also mentions iron uptake into the enterocytes by transferrin/iron complex endocytosis on the basolateral surface in the question stem.

 

[tiedyeddog]

Could you explain what exactly you're doing here? lol it looks interesting

trying to relate specific arteries in the brainstem to localizing the lesions.

 

[bangarang]

me too, I have never seen this before, it is legit awesome. I hated memorizing this stuff during my neuroscience block....

Is this a fair thing to say for blood supply?

medial medulla - ASA
lateral medulla - PICA
lateral pons - AICA

What does basilar get? medial pons + midbrain?

Medial pons - Paramedian branches of the basilar artery
Midbrain - PCA

 

[JP2740]

I got this question on UWorld, and I think it might be a typo. Maybe someone can help me out.

Hemochromatosis: "The crucial site for HFE expression is on the basolateral surface of the epithelial cell," and then it goes on to discuss how iron dissociates inside the enterocytes and determines the intensity of uptake on the apical surface.

Is this not reversed? I thought the apical surface always referred to the lumen of any tube. It took me about 3 reads of the explanation to realize they might've reversed it, unless I'm mistaken. It also mentions iron uptake into the enterocytes by transferrin/iron complex endocytosis on the basolateral surface in the question stem.

Transferrin is a blood protein transporter for iron. I don't really know too much about Hfe, but I think anything involving the blood will be basolateral for the intestine. From the explanation I read of that question I thought maybe Hfe samples the blood iron levels to regulate how much iron the enterocyte absorbs. If Hfe can't interact with the transferrin/iron in the blood, then the enterocyte thinks there's a deficiency in iron, so freely absorbs as much as it wants causing iron overload.

 

[JP2740]

Can 70% in ~6 uworld question sets be correlated to anything? I just started doing my dedicated studying. Previously I've read the pathophys sections of first aid and listened to goljian during the school year.

 

[bangarang]

Transferrin is a blood protein transporter for iron. I don't really know too much about Hfe, but I think anything involving the blood will be basolateral for the intestine. From the explanation I read of that question I thought maybe Hfe samples the blood iron levels to regulate how much iron the enterocyte absorbs. If Hfe can't interact with the transferrin/iron in the blood, then the enterocyte thinks there's a deficiency in iron, so freely absorbs as much as it wants causing iron overload.

Thanks, dude. This makes so much sense now.

 

[bangarang]

Can 70% in ~6 uworld question sets be correlated to anything? I just started doing my dedicated studying. Previously I've read the pathophys sections of first aid and listened to goljian during the school year.

That's pretty good actually. I hit 45-50% on UWorld when I first started, and I took a practice NBME at that time which put me at around a 190. Then I buckled down and studied hard. Started getting around 70%. I'm at a 235-240 level currently, per recent NBMEs and CBSEs. Taking a practice NBME will tell you more accurately where you're at than UWorld percentages.

 

[step1april2013]

Does Cystic Fibrosis end in acidosis or alkalosis?

I'm under the impression that it causes acidosis. Anyone know?

 

[dbeast]

I got one for you guys-

Is there a good way to tell the difference between cilostazol/dipyridamole vs. clopidogrel/ticlopidine for stroke/TIA/limb claudication prophylaxis?

I've gotten 2 questions so far with random combinations of the above drugs and symptoms and am so far 0 for 2. One was from an NBME (no explanation) and another from Uworld gave no meaningful clarification either. Yuck.

 

[tiedyeddog]

I got one for you guys-

Is there a good way to tell the difference between cilostazol/dipyridamole vs. clopidogrel/ticlopidine for stroke/TIA/limb claudication prophylaxis?

I've gotten 2 questions so far with random combinations of the above drugs and symptoms and am so far 0 for 2. One was from an NBME (no explanation) and another from Uworld gave no meaningful clarification either. Yuck.

I dunno, maybe you only use cilostazol/dipyridamole for claudication?

 

[tiedyeddog]

Does Cystic Fibrosis end in acidosis or alkalosis?

I'm under the impression that it causes acidosis. Anyone know?

I would guess acidosis due to the long-term restriction.

 

[tiedyeddog]

Can 70% in ~6 uworld question sets be correlated to anything? I just started doing my dedicated studying. Previously I've read the pathophys sections of first aid and listened to goljian during the school year.

I think that means you have a pretty great base.

 

[JP2740]

Does Cystic Fibrosis end in acidosis or alkalosis?

I'm under the impression that it causes acidosis. Anyone know?

Quickly checks first aid for the answer....

......................................

Not there?

 

[dbeast]

Oh I got another one! Can anybody explain gram negative bacilli versus gram negative coccobacilli? I got a question that called Haemophilus species bacilli and that was literally the clue that was supposed to give it away. Then, I got a question about a mystery bacillus where we were expected to specifically exclude Haemophilus based on the fact that it said "bacillus" rather than "coccobacillus".

I feel like so much of this test is having to know the question writer's intentions as much as the actual information

 

[Zzmed]

Does Cystic Fibrosis end in acidosis or alkalosis?

I'm under the impression that it causes acidosis. Anyone know?

I would guess acidosis due to the long-term restriction.

It's chronic metabolic alkalosis.
But, actually I can't give a complete explanation why..

 

[Zzmed]

Oh I got another one! Can anybody explain gram negative bacilli versus gram negative coccobacilli? I got a question that called Haemophilus species bacilli and that was literally the clue that was supposed to give it away. Then, I got a question about a mystery bacillus where we were expected to specifically exclude Haemophilus based on the fact that it said "bacillus" rather than "coccobacillus".

I feel like so much of this test is having to know the question writer's intentions as much as the actual information

Actually, gram negative coccobacilli are pleomorphic bacteria. (Just think of something between coccus and bacillus). These are H. influenza, L. pneumophilia, B. pertussis, Brucella, F. tularensis, P. multocida.

I agree with you than there is a mix up of the nomenclature though..

 

[bangarang]

It's chronic metabolic alkalosis.
But, actually I can't give a complete explanation why..

I think the metabolic alkalosis might be related to excessive sodium chloride loss from the skin. Heat > sweating > excessive sodium chloride loss (and thus water) > RAAS system activated > potassium wasting (and also H+) via aldosterone > contraction alkalosis.

http://www.ncbi.nlm.nih.gov/pubmed/9048354

 

[docnotsopc]

Here you go.

This looks like Pathoma

 

[tiedyeddog]

It's chronic metabolic alkalosis.
But, actually I can't give a complete explanation why..

OK, makes sense I guess.

Sent from my SAMSUNG-SGH-I997 using SDN Mobile

 

[step1april2013]

It's chronic metabolic alkalosis.
But, actually I can't give a complete explanation why..

I think the metabolic alkalosis might be related to excessive sodium chloride loss from the skin. Heat > sweating > excessive sodium chloride loss (and thus water) > RAAS system activated > potassium wasting (and also H+) via aldosterone > contraction alkalosis.

http://www.ncbi.nlm.nih.gov/pubmed/9048354

Makes sense thx and to add, in Usmle Rx it says that bicarbonate is low in the sweat of CF patients leading to alkalosis. I remember seeing a CFTR transporter picture in Uworld but I can't remember it.


Anyone know the Tx for V.cholera in specific order. Can't find it.

 

[tiedyeddog]

Makes sense thx and to add, in Usmle Rx it says that bicarbonate is low in the sweat of CF patients leading to alkalosis. I remember seeing a CFTR transporter picture in Uworld but I can't remember it.


Anyone know the Tx for V.cholera in specific order. Can't find it.

I thought the treatment was just oral rehydration solution unless they are in hypovolemic shock. If they are in shock give if fluids and counteract nonion gap acidosis.

 

[step1april2013]

I thought the treatment was just oral rehydration solution unless they are in hypovolemic shock. If they are in shock give if fluids and counteract nonion gap acidosis.

Nice. Have you ever seen a question where you had to choose a line up of sequential treatments (i.e. fluids, antitoxin, ampillicin)? I think it would be a good idea to make a list in this thread.

I remember having a question on a school NBME where you had to choose which treatment was best for rhabies infection. Its very vague to me now, but some of the choices included antitoxin, vaccine, etc. Anyway do you know what the treatment for rhabies would be?

 

[MLT2MT2DO]

Nice. Have you ever seen a question where you had to choose a line up of sequential treatments (i.e. fluids, antitoxin, ampillicin)? I think it would be a good idea to make a list in this thread.

I remember having a question on a school NBME where you had to choose which treatment was best for rhabies infection. Its very vague to me now, but some of the choices included antitoxin, vaccine, etc. Anyway do you know what the treatment for rhabies would be?

Antitoxin followed by x# of vaccinations, I believe the # is 3.

 

[tiedyeddog]

Quickly checks first aid for the answer....

......................................

Not there?

rofl, sums up my reaction every time I check FA and don't see the answer

or every time USMLErx gives an explanation not referencing FA.

 

[step1april2013]

Antitoxin followed by x# of vaccinations, I believe the # is 3.

When a person has been bitten or an open wound licked by a possibly rabid animal, the wound should be aggressively cleaned with soap and water. Washing alone will significantly lower the risk of infection.
3) The animal should be captured or destroyed. Captured animals are confined, and if no symptoms develop in the animal within 10 days, the animal does not have rabies. If destroyed, the dead animal's brain can be examined for Negri bodies or tested for uptake of fluorescently labeled antibodies to rabies virus.
4) If the animal cannot be captured or the above tests are positive, the bitten individual should receive human rabies immune globulin (passive immunization), followed
by 5 injections of the killed rabies virus vaccine (active immunization). The idea is to develop immunity while the virus is still in the prolonged (variable length) incubation period.

Source is Micro made simple. Thx MLT you were right

I'M adding in tetanus below

In the emergency room you will encounter 3 types of patients with skin wounds: 1) Patients who were immunized as a child and received periodic boosters but the last shot was more
than 10 years ago. These patients are given another booster. 2) Patients who have never been immunized. Not only do these patients need a booster, but they should also receive preformed antibodies to the tetanus toxin
called human tetanus immune globulins. 3) Patients who come to the hospital having already developed tetanus. The big picture is to clear the toxin and the toxin-producing bacteria and to keep the patient alive until the toxin has cleared. This is accomplished in the following 5 steps of therapy: a) Neutralize circulating toxin with human tetanus immune globulins. b) Give an immunization booster to stimulate the patient's own immune system to develop antitetanus
toxin antibodies.c) Clean the wound, excising any devitalized tissue, to remove any remaining source of Clostridium
tetani. d) Antibiotics (penicillin) may help to clear the remaining toxin-producing bacteria. e) Provide intensive supportive therapy until the toxin is cleared. Muscle relaxants may have to be administered, and the patient may have to be placed on a ventilator].

 

[MLT2MT2DO]

When a person has been bitten or an open wound licked by a possibly rabid animal, the wound should be aggressively cleaned with soap and water. Washing alone will significantly lower the risk of infection.
3) The animal should be captured or destroyed. Captured animals are confined, and if no symptoms develop in the animal within 10 days, the animal does not have rabies. If destroyed, the dead animal's brain can be examined for Negri bodies or tested for uptake of fluorescently labeled antibodies to rabies virus.
4) If the animal cannot be captured or the above tests are positive, the bitten individual should receive human rabies immune globulin (passive immunization), followed
by 5 injections of the killed rabies virus vaccine (active immunization). The idea is to develop immunity while the virus is still in the prolonged (variable length) incubation period.

Source is Micro made simple. Thx MLT you were right

Looked it up looks like 3 doses is a pre-exposure amount with 5 being the post.

General rule: If something is producing a toxin you treat with an anti toxin first (acute issue) then vaccination/antibiotics second (depending on the organism)

 

[Pinkleton]

A UW question I did recently said that B12 deficiencies do not occur with alcoholism. I understand that the liver has ample reserve, but alcoholism can last a long time. I have written in FA (presumably from UW) that cirrhosis decreases the transcobalamin 2 receptor, leading to megaloblastic anemia...anyone care to clear this up?

 

[Jonari]

A UW question I did recently said that B12 deficiencies do not occur with alcoholism. I understand that the liver has ample reserve, but alcoholism can last a long time. I have written in FA (presumably from UW) that cirrhosis decreases the transcobalamin 2 receptor, leading to megaloblastic anemia...anyone care to clear this up?

could you post the question up, please?

 

[Pinkleton]

could you post the question up, please?

Pretty basic stem: Alcoholic with hypersegmented PMNs on peripheral smear. Cause?

Folate deficiency was the answer, B12 was another choice. Explanation said B12 def is not common in alcoholics

 

[step1april2013]

Pretty basic stem: Alcoholic with hypersegmented PMNs on peripheral smear. Cause?

Folate deficiency was the answer, B12 was another choice. Explanation said B12 def is not common in alcoholics

I think I remember this question. I'm not sure about the receptor aspect of it, but I can say that alcoholics are asso. with nutritional def. and so Vit B12 stores are much greater than that of folate. The person was probably homeless too.

 

[Jonari]

Pretty basic stem: Alcoholic with hypersegmented PMNs on peripheral smear. Cause?

Folate deficiency was the answer, B12 was another choice. Explanation said B12 def is not common in alcoholics

yeah that can't be right, alcohol does cause deficiency of vb12. the probably mean relative to folate deficiency, alcohol is more commonly associated with folate...i mean whenever i think of vb12 deficiency the reasons that come to mind are:

- pernicious anemia
- d. latum
- vegans
- crohn's
- pancreatic insufficiency

reasons that come to mind when i hear folate deficiency:

- etoh
- phenytoin
- liver damage
- etc
- etc

i've noticed that at times uworld does makes mistakes with their explanations.

 

[bangarang]

yeah that can't be right, alcohol does cause deficiency of vb12. the probably mean relative to folate deficiency, alcohol is more commonly associated with folate...i mean whenever i think of vb12 deficiency the reasons that come to mind are:

- pernicious anemia
- d. latum
- vegans
- crohn's
- pancreatic insufficiency

reasons that come to mind when i hear folate deficiency:

- etoh
- phenytoin
- liver damage
- etc
- etc

i've noticed that at times uworld does makes mistakes with their explanations.

Yeah, folate stores last a few months whereas vitB12 stores last a few years, so in a nutritional deficiency of both vitamins, symptoms of folate deficiency would show up first.

 

[Pinkleton]

Thanks guys. I guess a possible exception would be an alcoholic who drinks beers, since most beers are rich in folate

 

[SLC]

Pretty basic stem: Alcoholic with hypersegmented PMNs on peripheral smear. Cause?

Folate deficiency was the answer, B12 was another choice. Explanation said B12 def is not common in alcoholics

Also remember, that both B12 and Folate deficiency can cause hypersegmented PMN's and macrocytic anemia.

But B12 question stems have to mention neurologic symptoms (peripheral neuropathy, Dementia, posterior column disease etc), because that's the main way to differentiate between the two.

you can also differentiate with a methylmalonic acid level (normal in folate def. high in B12 deficiency)

That and Folate deficiency is commonly asked using an alcoholic as the patient.

 

[tiedyeddog]

Also remember, that both B12 and Folate deficiency can cause hypersegmented PMN's and macrocytic anemia.

But B12 question stems have to mention neurologic symptoms (peripheral neuropathy, Dementia, posterior column disease etc), because that's the main way to differentiate between the two.

you can also differentiate with a methylmalonic acid level (normal in folate def. high in B12 deficiency)

That and Folate deficiency is commonly asked using an alcoholic as the patient.

this is a good point.

 

[step1april2013]

Is megaloblastic anemia hyperchromic, macrocytic or hypochromic, microcytic? I remember seeing this question on a school path nbme and i never found out the answer

 

[bangarang]

Is megaloblastic anemia hyperchromic, macrocytic or hypochromic, microcytic? I remember seeing this question on a school path nbme and i never found out the answer

Megaloblastic anemia is a type of macrocytic anemia. I think megaloblastic refers specifically to vitB12/folate deficiency.

 

[SLC]

Is megaloblastic anemia hyperchromic, macrocytic or hypochromic, microcytic? I remember seeing this question on a school path nbme and i never found out the answer

Macrocytic-hyperchromic.

Think of it this way, the folate/Cobalamin deficiency delays DNA replication which causes a delay in RBC maturation. But there's nothing wrong with protein synthesis. So basically the RBC's just sit there and kick out a TON of extra hemoglobin while they are waiting to mature.

You end up with huge cells packed with extra hemoglobin, but a lot fewer cells overall so you still end up anemic.

That's the rough and dirty (free of detail) version, but it's good enough to get a grip on what type of RBC morphology you can expect.

 

[tiedyeddog]

Megaloblastic anemia is a type of macrocytic anemia. I think megaloblastic refers specifically to vitB12/folate deficiency.

Also orotic aciduria, which can't be fixed by B12/folate administration.

 

[bangarang]

Also orotic aciduria, which can't be fixed by B12/folate administration.

Dang, I completely forgot about that pathway. Thanks.

 

[tiedyeddog]

I have always been confused by lung V/Q. I got a question in USMLErx I don't really understand.

So in the apex, V/Q is about 3 meaning there is wasted ventilation, not enough blood flow.
In the base, V/Q is under 1, due to wasted perfusion.

Is this perfusion difference due gravity entirely? Blood gets pulled down into zone 3, air fills the apex and in the base, the blood squeezes capillaries?

So the question I got asked: if positive pressure (like a vent) is put on a person, how does perfusion change? answer was that zone 1 will have an even higher V/Q, so zone 1 perfusion decreases. Why doesn't zone 3 perfusion decrease, too???

 

[bangarang]

I have always been confused by lung V/Q. I got a question in USMLErx I don't really understand.

So in the apex, V/Q is about 3 meaning there is wasted ventilation, not enough blood flow.
In the base, V/Q is under 1, due to wasted perfusion.

Is this perfusion difference due gravity entirely? Blood gets pulled down into zone 3, air fills the apex and in the base, the blood squeezes capillaries?

So the question I got asked: if positive pressure (like a vent) is put on a person, how does perfusion change? answer was that zone 1 will have an even higher V/Q, so zone 1 perfusion decreases. Why doesn't zone 3 perfusion decrease, too???

I've always understood the difference to be due to gravity. For the other question, this is the way I make sense of it, but it might not be 100% correct.

In zone 1, the pressures are PA (alveolar) > Pa (arterial) > PV (vein), so if you increase the PA via positive pressure ventilation, then you will further increase V/Q because the increased PA further compresses the arteries since Pa was less than PA to begin with.

In zone 3, the pressures are Pa > PV > PA, so if you increase positive pressure in the alveoli (PA), you won't really get much compression of the arteries since the Pa is higher than the PA in that region.

 

[JP2740]

Omg I have never understood that concept... and now I do. Thank you for this thread

 

[TheSeanieB]

Can anyone explain the pathogenesis of koilocytic change cause by HPV? Why does HPV cause nuclear enlargement, irregularity of the nuclear membrane contour, a darker than normal staining pattern, a perinuclear halo, and a overall raisin-like appearance?

 

[MLT2MT2DO]

Can anyone explain the pathogenesis of koilocytic change cause by HPV? Why does HPV cause nuclear enlargement, irregularity of the nuclear membrane contour, a darker than normal staining pattern, a perinuclear halo, and a overall raisin-like appearance?

The Koilocyte is actually an immature Epi cell, hence the larger N/C ratio.

 

[TheSeanieB]

That makes sense. Any idea how HPV infection results in the production of immature epithelial cells?

 

[MLT2MT2DO]

Yeah, no idea.

 

[tiedyeddog]

That makes sense. Any idea how HPV infection results in the production of immature epithelial cells?

eh, I don't think that's testable. Maybe just guess something to do with E6 or E7?

 

[step1april2013]

Macrocytic-hyperchromic.

Think of it this way, the folate/Cobalamin deficiency delays DNA replication which causes a delay in RBC maturation. But there's nothing wrong with protein synthesis. So basically the RBC's just sit there and kick out a TON of extra hemoglobin while they are waiting to mature.

You end up with huge cells packed with extra hemoglobin, but a lot fewer cells overall so you still end up anemic.

That's the rough and dirty (free of detail) version, but it's good enough to get a grip on what type of RBC morphology you can expect.

simply amazing my friend. This thread is awesome