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Dream-2-Reality

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Dream-2-Reality said:
Why not A? View attachment 182660
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Keep in mind that Auto-regulation is key in maintaining constant blood flow at a certain level. As you can see in D there is a flat line right in the middle which is indicative of auto-regulation.

Answer A is not maintaining a constant blood flow it's just increasing the blood flow which would be the action of pressure on flow without auto-regulation.
 
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For this one I was between A or B, but the answer is B. I need explanation about what's going on with this patient.
 

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rodmichael82 said:
Keep in mind that Auto-regulation is key in maintaining constant blood flow at a certain level. Answer A is not maintaining a constant blood flow it's just increasing the blood flow which would be the action of pressure on flow without auto-regulation.
Click to expand...

Thank you it makes sense now.
 
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Dream-2-Reality said:
For this one I was between A or B, but the answer is B. I need explanation about what's going on with this patient.
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I think you should read Pathoma for Red blood cell disorders and it will be extremely helpful.
There is a systematic way of approaching heme/onc problems.
The first thing you need to do is look at MCV. You're looking for Microcytic (LOW MCV), Normocytic and Macrocytic (Large MCV) and then you can divide it based on that category.

Since MCV is LOW you know it can be certain things which includes Blood loss. The other options are NOT usually LOW MCV so that would be a huge hint.
To explain it a little better though I'm going to state what Dr. Sattar taught.
Hemoglobin is made of Heme + Globin and Heme is made of Iron and Protoporphyrin. Any time you have a deficiency in any of those then the stem cell has to do an extra division to maintain constant levels. Also anytime an extra division occurs the red blood cells get smaller. MCV is kind of an indication of red blood cells (not exactly but I'm using lay terms here). So when you bleed you have less Hemoglobin and initially the stem cell is able to maintain the MCV but with chronic blood loss you lose Iron, so you also lose hemoglobin then you have to do an extra division to maintain a proper level of hemoglobin. That extra division causes the MCV to decrease.
From what I recall hemolytic anemia on the other hand is more normocytic anemia because yeah you lose RBC in the hemolysis but you still have the Heme+ Globin supply to form new hemoglobin without the necessity of making that extra division which causes Microcytic anemia.
 
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rodmichael82 said:
I think you should read Pathoma for Red blood cell disorders and it will be extremely helpful.
There is a systematic way of approaching heme/onc problems.
The first thing you need to do is look at MCV. You're looking for Microcytic (LOW MCV), Normocytic and Macrocytic (Large MCV) and then you can divide it based on that category.

Since MCV is LOW you know it can be certain things which includes Blood loss. The other options are NOT usually LOW MCV so that would be a huge hint.
To explain it a little better though I'm going to state what Dr. Sattar taught.
Hemoglobin is made of Heme + Globin and Heme is made of Iron and Protoporphyrin. Any time you have a deficiency in any of those then the stem cell has to do an extra division to maintain constant levels. Also anytime an extra division occurs the red blood cells get smaller. MCV is kind of an indication of red blood cells (not exactly but I'm using lay terms here). So when you bleed you have less Hemoglobin and initially the stem cell is able to maintain the MCV but with chronic blood loss you lose Iron, so you also lose hemoglobin that you have to do an extra division to maintain a proper level of hemoglobin. That extra division causes the MCV to decrease.
From what I recall hemolytic anemia on the other hand is more normocytic anemia because yeah you lose RBC in the hemolysis but you still have the Heme+ Globin supply to form new hemoglobin without the necessity of making that extra division which causes Microcytic anemia.
Click to expand...

Thank you. Very good explanation. I forgot hemolytic anemia is normocytic anemia. Yeah, I think I should go over heme lecture one more time from Pathoma/FA.
 
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For this one, I was thinking CD8+T cells are the ones responsible for fighting viruses, and neoplastic cells, donar graft cells. So I chose A, but the answer is D.

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Dream-2-Reality said:
By releasing perforins and granzyme causing apoptosis.
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What's the stimulus for that release? I'm talking about big picture, not details.

Also for the question about the 75 year old woman, if you narrow it down between A and B, you're comparing the likeliness of acquired hemolytic anemia vs chronic blood loss. Basically it's autoimmune or drug induced disorders vs an occult gi bleed, probably due to cancer. There's nothing about drugs so you're basically thinking autoimmune vs gi bleed. Autoimmune is a younger woman's game, probably around 30s-40s while someone over 65 is more likely to have cancer in these questions.
 
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J DUB said:
Hep A vaccination is an inactivated one so it mounts a humoral response.
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Oh man... I know this. Inactivated killed vaccines require epitope for response and are for Cholera, Salk Polio, HAV HBV, Influenza B, and Rabies. It has killed antigen to produce antibodies.

So CD4+ T cells activate B cells to produce antibodies and will be the one to vigorously respond to HAV vaccine immunization. Right?
 
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Psai said:
What's the stimulus for that release? I'm talking about big picture, not details.

Also for the question about the 75 year old woman, if you narrow it down between A and B, you're comparing the likeliness of acquired hemolytic anemia vs chronic blood loss. Basically it's autoimmune or drug induced disorders vs an occult gi bleed, probably due to cancer. There's nothing about drugs so you're basically thinking autoimmune vs gi bleed. Autoimmune is a younger woman's game, probably around 30s-40s while someone over 65 is more likely to have cancer in these questions.
Click to expand...

About the 75 yo, that makes so much sense. Thank you

I think I answered your question on the last post.
 
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Dream-2-Reality said:
Oh man... I know this. Inactivated killed vaccines require epitope for response and are for Cholera, Salk Polio, HAV HBV, Influenza B, and Rabies. It has killed antigen to produce antibodies.

So CD4+ T cells activate B cells to produce antibodies and will be the one to vigorously respond to HAV vaccine immunization. Right?
Click to expand...

:nod:
 
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You didn't answer my question, your thinking is superficial. You think about the HAV vaccine, it's a killed virus. What do cd8 cells attack and why? Which receptors do they bind to? How do those receptors work compared to the other kind? Why would there be a humoral response modulated by cd4 to a HAV vaccine but a cd8 response to an actual infection?

The questions you're posting are relatively easy and your inability to answer them shows a deficiency in your understanding of basic principles. You know some of the facts but you're not putting the pieces together.

Petechiae, low platelet count, MATURE megakaryocytic hyperplasia on the marrow smear and everything else is normal. That question is relatively simple.

Instead of asking us to explain these questions, you need to go watch pathoma or something because your foundation is very shaky.
 
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Psai, post:

You didn't answer my question, your thinking is superficial. You think about the HAV vaccine, it's a killed virus.


What do cd8 cells attack and why? Which receptors do they bind to? How do those receptors work compared to the other kind?
CD 8 receptors use TCR to bind to MHC 1 on the virus infected cells, donor graft cells, neoplastic ells.
CD4 use TCR to bind MHC 2 with antigen on B cells and ligand 40 to bind CD40 on B cells. CD4 doesn't directly work it uses B cells to stimulate the antibody production (Humoral response).

Why would there be a humoral response modulated by cd4 to a HAV vaccine but a cd8 response to an actual infection?

CD 4 activating B cells to produce antibodies whiles CD8 cells work directly causing apoptosis.


The questions you're posting are relatively easy and your inability to answer them shows a deficiency in your understanding of basic principles. You know some of the facts but you're not putting the pieces together.

I agree with you. I'm depressed cuz of it and on the verge of emotional break down these days :(. I promise I'm working everyday to improve on it.
 
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The whole point of the question is to understand that viruses infect cells. Viruses take over the cell's machinery to produce their own proteins for replication. The cell normally cuts up endogenous proteins by the proteasome and puts it on MHC1 receptors so that CD8 cells can look at it. If there's a viral infection, then the CD8 cell will see the abnormal protein and destroy the cell.

A killed virus like in the HAV vaccine won't infect a cell because it's killed. It lost its replicative ability so it floats around, is phagocytosed and fragments are presented to cd4 cells by the mhc2 receptor on antigen presenting cells. These CD4 cells activate B cells and you get a humoral response. So there's no CD8 response.

This test is not about "what". You have to know "why". Of course you need to know the facts to understand the underlying processes but they assume that you already know the facts. Anyone can memorize details and regurgitate. They test you on the application of those facts and that's what makes it so difficult.
 
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Next level stuff.......I would recommend something like DIT to help you get the basics down if you have the time. It helped me get the basics. But, nothing like pouring over FA, Pathoma, and UW. At this point, you can't go back and learn all of the first 2 yrs. And, I am not a 250+ guy....more 220-230.
 
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Thank you guys for helping.

Psai said:
Instead of asking us to explain these questions, you need to go watch pathoma or something because your foundation is very shaky.
Click to expand...

So, I should stop going over the wrong FRED questions and just go do Pathoma again/DIT? I was thinking about finishing gong over the wrong ones and then go do DIT/Pathoma.
 
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J DUB said:
Yeah, you need to do some heavy content review if you did all that and still working on connecting that many dots. I mean I did not know one of them right away but still.
Click to expand...

I'm planning to do that after going over these. Can you please explain this one?
 

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F Histone acetylation happens on histones. I don't think the nucleotide sequence plays a role in that. Here you have a problem with transcription and those sequences look like the tata box and the caat box.
 
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Psai said:
F Histone acetylation happens on histones. I don't think the nucleotide sequence plays a role in that. Here you have a problem with transcription and those sequences look like the tata box and the caat box.
Click to expand...

That was the first thing that came up when I googled it. I agree. The bottom 2 look more like the tata and such problems.
I would have guessed F based on my non-internet search since most of DNA and such is negative and positive would bind it. But, I found all this histone stuff. I find I sometimes do better with my reasoning than looking stuff up. Hope that holds true. One reason my UW avg so far is in the 70s. I guess several right I do not know. Now, I am pissed I did not go with my own thoughts....:mad:
 
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My impression is that you get that intuition after you've been through about half the qbank and seen most of the questions. When I was first starting, I was pretty lost and scoring maybe 50%. You get a feel for the question style and understand that they're testing second year medical students for knowledge they should have picked up in the pre-clinical years. But I get what you're saying, I remember a question where I had no idea what was going on but I looked at the answer choices and it suddenly dawned on me that they were asking about cyp-450 inhibitors. You're basically trying to figure out what concept they're testing and eventually it comes second nature. There were a bunch of autoclicks on step 1 where I knew what they were asking for and just went for the answer without reading the question thoroughly.
 
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Do you guys agree with this explanation?

Jamiu22 said: ↑
I believe the answer is (A) Metabolic Acidosis - you can't get rid of potassium since the kidney is damaged... so you tend to retain a lot more H+, while getting rid of HCO3... over time though you would get (D) Respitatory Alkalosis as a compensatory mechanism... but it's still primarily (A).


http://forums.studentdoctor.net/threads/prerenal-azotemia-question.1002991/
 
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tiedyeddog said:
yeah, totally agree. I think with these questions where the pH and pCO2 aren't given you have to look at two things:

1. What is the bicarb?
2. What is the respiration rate?
3. What is the anion gap?

Bicarb is low (normal is 24). Respiratory rate is normal (under 24). Anion gap is normal.

Because of the low bicarb this could either be: metabolic acidosis(bicarb is eaten up trying to buffer the blood back to 7.4) or this could be respiratory alkalosis ( too much CO2 blown off, so bicarb over a long time period decreases reabsorption of bicarb).

Given that spironlactone use causes normal anion gap metabolic acidosis, (remember the HARDASS pnemonic) I would go with that. It doesn't seem like the patient is hyperpneic, meaning too much CO2 is blown off.

This is basically a type 4 renal tubular acidosis. See article on it here. Patient is hyperkalemic, which reinforces that diagnosis. http://www.turner-white.com/pdf/hp_nov01_renal.pdf

Now, watch OP come back and prove me totally wrong. ;)
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I agree more with this one.
 
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Can anyone show their elimination process for this one? Why it can't be C or D or other choices?
 

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