Step 1 Complicated Concepts Thread

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.

TheSeanieB

Full Member
10+ Year Member
Joined
Dec 17, 2010
Messages
263
Reaction score
1
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.

Members don't see this ad.
 
Last edited:
  • Like
Reactions: 1 user
All right... collagen synthesis. SO annoying

Preprocollagen = translated chain
Pro alpha collagen = hydroxylated chains
Procollagen = triple helix formation after glycosylation
Tropocollagen = insoluble version after extracellular cleavage
Collagen Fibrils = crosslinked tropocollagen

Is this right??

I don't think pro-alpha chains are formed necessarily after hydroxylation. Pro-alpha chains are formed by removal of the hydrophobic signal sequence from prepro-alpha chain by signal peptidases. So the sequence should be Prepro-alpha --> Signal sequence removed --> Pro-alpha --> Hydroxylation --> Glycosylation --> Triple helix formation (procollagen) --> Golgi (further glycosylation & packaging) --> Secreted outside the cell --> Propeptides are removed by procollagen peptidase --> Tropocollagen is formed --> Cross-linking of tropocollagen by lysyl oxidase --> Formation of collagen fibrils --> Polymerization of collagen fibrils to form collagen fibers.
 
This is unrelated to this thread, but anyone go over their incorrects from a long time ago? I took NBME7 about a month and a half ago and made a 214, but now that I'm going back over my incorrects, 95% of the things that I missed were things that I would never miss today... sort of makes me feel better about tomorrow.
 
This is unrelated to this thread, but anyone go over their incorrects from a long time ago? I took NBME7 about a month and a half ago and made a 214, but now that I'm going back over my incorrects, 95% of the things that I missed were things that I would never miss today... sort of makes me feel better about tomorrow.

Good luck! Go set that curve!
 
Members don't see this ad :)
Do you get sideroblastic anemia with failure in every step of heme synthesis?

I know you can get it with lead poisoning (so ferrochelatase), B6 and x-linked deficiency of ALA synthase... so it seems like only the steps that take place in the mitochondria give you sideroblastic anemia.

But why does a defect in the other steps not cause an excess amount of Fe in the mitochondria?
 
Do you get sideroblastic anemia with failure in every step of heme synthesis?

I know you can get it with lead poisoning (so ferrochelatase), B6 and x-linked deficiency of ALA synthase... so it seems like only the steps that take place in the mitochondria give you sideroblastic anemia.

But why does a defect in the other steps not cause an excess amount of Fe in the mitochondria?

Because they happen in the cytosol?
 
Because they happen in the cytosol?

Yeah but what exactly stops the iron from building up in the mitochondria still?

I understand ferrochelatase deficiency, since that is the step right before the iron would be added.

But why would ALA synthase deficiency cause iron to build up in the mitochondria? Iron is not at all involved in that step.
 
Isn't it because of the same reason though? You have fewer functional porphyrin rings to complex with the iron so it just accumulates I think.
 
Isn't it because of the same reason though? You have fewer functional porphyrin rings to complex with the iron so it just accumulates I think.

Yeah but you also have fewer functional porphyrin rings with all of the other porphyrias, but you don't get sideroblastic anemia with them, right?
 
Yeah but you also have fewer functional porphyrin rings with all of the other porphyrias, but you don't get sideroblastic anemia with them, right?

I came up with this exact question early on in my study and I still haven't found an explanation. Why is it that patients with acute intermittent porphyria / PCT don't show signs of anemia?

EDIT: Nvm, I think it might have to do with some enzymes being present in liver vs erythrocytes
 
How do you distinguish between fibrocystic change and a fibroadenoma? i guess if the patient is above 35, it would be fibrocystic change, but what about the 25-35 range?
 
Members don't see this ad :)
How do you distinguish between fibrocystic change and a fibroadenoma? i guess if the patient is above 35, it would be fibrocystic change, but what about the 25-35 range?

I can't explain them well because female repro pathology was poorly covered in FA but here are some pictures to distinguish them on gross exam http://rojosonmedicalclinic.wordpre...a-of-the-breast-on-operation-and-palpation-2/

Fibroadenoma:

Painful OR painless
Discrete movable mass
Size fluctuates with hormones

Fibrocystic Change

Multiple lumps and bumps, often bilateral
midcycle tenderness
upper outer quadrant usually
 
Probably has to do with the regulation of iron transport to the active site of Ferrochelatase.
Not 100% clear how this is regulated. But its an intriguing question.
One paper states that "ferrous iron reaches the active site of ferrochelatase directly after its passage across the inner membrane without transient movement through the matrix." and "Iron import into isolated mitochondria was dependent on a membrane potential as an energy source. A similar requirement for energized mitochondria was observed in vivo. This appears to be the only driving force, because iron import occurred independently of adenine nucleotides both inside and outside of mitochondria. It is therefore unlikely that the transport of iron is mediated by a transport ATPase."

Basically no body knows.
 
All of you are very kind. I'm an IMG, I registered here back when I started to have an interest to take USMLE. Unfortunately, work was too busy to study for the exam. Now that I'm done with work, I'm studying full time and hope to take the exam within the next three months.

Out of curiosity, are you just finished with your preclinical years or have you done more (i.e. clinical years or entered practice)?
 
I think I just had an a-ha moment (which is probably really basic for all of you guys) but can someone confirm/deny this? I asked a similar question earlier in this thread, but now ****'s getting real. Ok here goes:

Any non-conjugated polysaccharide vaccine only generates IgM immunity. This happens from circulating antigen from the vaccine directly running into/activating membrane-bound IgM on a B-cell that fits it. This is why it's "T-cell independent".

Here's what I don't get: what if somebody gets the vaccine, but they coincidentally don't have any B-cells with receptors that fit the antigen? I assume this is why it doesn't work in babies, but isn't there a chance that some adults just never made the right receptor also? I don't know, I'm probably overthinking this.
 
sharklasers said:
How do you distinguish between fibrocystic change and a fibroadenoma? i guess if the patient is above 35, it would be fibrocystic change, but what about the 25-35 range?

Pvtbacon has listed the important clinical points: Age >35 (FC) vs. age <25 (FA), tender (FC) vs. non-tender (FA), multiple & bilateral (FC) vs. solitary (FA). Unfortunately, none of them are definitive enough to separate fibrocystic changes from fibroadenoma. So we turn to pathology:

Epithelial lesions of the breast can be malignant (carcinoma of the breast) or benign. Benign epithelial lesions of the breast (given the umbrella term "fibrocystic changes") can be non-proliferative or proliferative. Fibroadenoma, on the other hand, is a benign stromal tumor. So what we are comparing is a benign epithelial "condition" (fibrocystic changes) vs. a benign stromal tumor (fibroadenoma). Morphologically, fibrocystic changes show: (1) Cysts -as the name suggests- (which can be lined by atrophic or metaplastic apocrine cells, giving the "blue dome appearance", (2) fibrosis, and (3) adenosis (increase in # of acini). Fibroadenoma, on the other hand, has a cellular, myxoid stroma -not surprising, since it is a tumor derived from stroma-, which can compress the epithelium (giving the slit-like appearance) or become hyalinized. Epithelial cells found in fibroadenoma are not neoplastic; stromal cells are.

Summary: Fibrocystic changes: Benign epithelial lesion; fibroadenoma: benign stromal tumor. Now based on this, think about this question:

A 37 year old woman presents to the outpatient clinic with a self-discovered mass in her right breast. Physical examination reveals a non-tender but "lumpy-bumpy" right breast. Upon further radiological investigation and biopsy, the sample is assessed for a G6PD isoenzyme analysis. What would you think if the analysis showed the epithelial cells sharing the same G6PD isoenzyme? What if stromal cells shared the same G6PD isoenzyme?

Out of curiosity, are you just finished with your preclinical years or have you done more (i.e. clinical years or entered practice)?

I'm a graduate and I had to perform a mandatory service. But I'm glad I'm done.

Any non-conjugated polysaccharide vaccine only generates IgM immunity. This happens from circulating antigen from the vaccine directly running into/activating membrane-bound IgM on a B-cell that fits it. This is why it's "T-cell independent".

Here's what I don't get: what if somebody gets the vaccine, but they coincidentally don't have any B-cells with receptors that fit the antigen? I assume this is why it doesn't work in babies, but isn't there a chance that some adults just never made the right receptor also? I don't know, I'm probably overthinking this.

Welcome to the world of antigen diversity :) How does the immune system respond against millions and millions of different types of antigens? A large section of immunology is devoted to answering that very question. What happens is our bodies generate a very large repertoire of B-cells through recombination of Ig genes (and various other mechanisms). Now, once these cells are generated, they don't sit idly by and wait for an antigen to come to themselves. They circulate throughout the body and they're drained into the lymphatic system where they can interact with antigens within the lymph node. They complete a whole tour of the body approximately within 24 hours. So it is very unlikely that the B-cell somehow misses encountering an antigen.

As for the babies, the issue here is about polysaccharide vs. protein antigen. T-cell independent activation is certainly possible by certain polysaccharide antigens like you've mentioned, but it is not a very effective method. Without T-cell interaction, there won't be isotype switching, affinity maturation, memory cell production, etc., which all aid in mounting an effective response. Neonatal immune system is not yet mature, so an immature system using an ineffective method doesn't really work. They can, however, respond to protein antigens: This is why hepatitis B vaccination can be effective in neonates.
 
Myxedema said:
I'm a graduate and I had to perform a mandatory service. But I'm glad I'm done.

Ah! Your understanding of topics and presentations seemed really deep, thought that might be the case. Thanks for taking the time to make the helpful explanations you have. I'm sure you're going to murder step
 
Friends,

Could someone please explain what the mood symptoms are in schizoaffective disorder(maybe how they would present in a question stem?) and more importantly how to differentiate between the mood symptoms in schizoaffective disorder from disorders such as pure bipolar/major depression?
 
Friends,

Could someone please explain what the mood symptoms are in schizoaffective disorder(maybe how they would present in a question stem?) and more importantly how to differentiate between the mood symptoms in schizoaffective disorder from disorders such as pure bipolar/major depression?

Shizoaffective is like schizophrenia added with some bipolar like qualities, with that in mind. Schizophrenia will have qualities of: disorganized speech (speaking sentences that make no sense), paranoia (delusions that make little sense and are not delusional disorder), or can have varying other positive or negative symptoms.

The real difference between schizoaffective and schizophrenic is the manic stages. This is like gross grandiosity, patterns of not sleeping for days, irritability, and fast speech, etc.

To sum it up for you:
Schizophrenic: mostly a thought disorder
bipolar: mostly a mood disorder
schizoaffective: qualities of both
 
Shizoaffective is like schizophrenia added with some bipolar like qualities, with that in mind. Schizophrenia will have qualities of: disorganized speech (speaking sentences that make no sense), paranoia (delusions that make little sense and are not delusional disorder), or can have varying other positive or negative symptoms.

The real difference between schizoaffective and schizophrenic is the manic stages. This is like gross grandiosity, patterns of not sleeping for days, irritability, and fast speech, etc.

To sum it up for you:
Schizophrenic: mostly a thought disorder
bipolar: mostly a mood disorder
schizoaffective: qualities of both

I wouldn't say this is a great explanation. Manic episode is not necessary to make the diagnosis of schizoaffective disorder. If the patient has symptoms that qualify for both a mood disorder (MDD, bipolar) and schizophrenia, then it's schizoaffective disorder. Think of it as a mood disorder superimposed on schizophrenia (these patients are very sick).

Probably the trickiest part is to distinguish it from MDD with psychosis. Schizoaffective will have a history of periods where the patient has mood symptoms independently from psychotic symptoms, whereas MDD with psychosis never has psychotic features without also satisfying the criteria for a MDE at the same time.
 
I got another one- studying antivirals and I ran into some stuff I wrote that no longer makes sense (happens way more often than I'd like to admit). Can anybody differentiate between RNA-dependent RNA polymerase vs. RNA-dependent DNA polymerase?

I think I may have actually written them down in the wrong order too (might be DNA-dependent RNA pol or something like that).
 
I got another one- studying antivirals and I ran into some stuff I wrote that no longer makes sense (happens way more often than I'd like to admit). Can anybody differentiate between RNA-dependent RNA polymerase vs. RNA-dependent DNA polymerase?

I think I may have actually written them down in the wrong order too (might be DNA-dependent RNA pol or something like that).

Hmm I'm not really sure exactly what you are asking, but if this helps, RNA dependent DNA polymerase is only relevant in HIV and HBV (I guess HTLV/other retroviruses as well, but these are not as imp for Step 1 purposes)

And RNA dependent RNA polymerases is what all most RNA viruses use for replication.

I know this isn't very helpful, or really that clear either lol, but maybe if you have specific questions regarding the above I can try my best at those too!
 
Hey guys,

could someone help distinguish between conus medullaris syndrome and cauda equina syndrome?

I read the UW explanation a few times but some reason am not getting it (except for the difference in lesion area)
 
Hmm I'm not really sure exactly what you are asking, but if this helps, RNA dependent DNA polymerase is only relevant in HIV and HBV (I guess HTLV/other retroviruses as well, but these are not as imp for Step 1 purposes)

And RNA dependent RNA polymerases is what all most RNA viruses use for replication.

I know this isn't very helpful, or really that clear either lol, but maybe if you have specific questions regarding the above I can try my best at those too!

Don't sell yourself short, that was helpful. I was so lost I couldn't even ask a coherent question, my fault not yours.
 
Can someone sum up different energy sources while fasting for me?

Here is a start, with what I know.

Between meals - glycogen breakdown
Fasting - GNG
>3 days no food - ketogenesis

Is this correct?
 
Hey guys,

could someone help distinguish between conus medullaris syndrome and cauda equina syndrome?

I read the UW explanation a few times but some reason am not getting it (except for the difference in lesion area)

One sure fire way is that in Cauda Equina syndrome..the patellar and ankle jerk reflexes are always absent. They are preserved in Conus
 
Summary: Fibrocystic changes: Benign epithelial lesion; fibroadenoma: benign stromal tumor. Now based on this, think about this question:

A 37 year old woman presents to the outpatient clinic with a self-discovered mass in her right breast. Physical examination reveals a non-tender but "lumpy-bumpy" right breast. Upon further radiological investigation and biopsy, the sample is assessed for a G6PD isoenzyme analysis. What would you think if the analysis showed the epithelial cells sharing the same G6PD isoenzyme? What if stromal cells shared the same G6PD isoenzyme?

Going to try and take a stab at this one. I don't promise anything:

Wouldn't we just see a monoclonal G6PD isoenzyme increased on the fibroadenoma, but normal on the fibrocystic change?


Stupid Question:

Anyone want to explain to me the difference between somatic hypermutation and affinity maturation?
 
Question: why do bile acid resins predispose a patient to cholesterol stones? Specifically, why does it seem like the body overcompensates by increasing the cholesterol content in the bile? If anything, wouldn't bile acids excreted = less cholesterol returned via enterohepatic circulation?
 
Question: why do bile acid resins predispose a patient to cholesterol stones? Specifically, why does it seem like the body overcompensates by increasing the cholesterol content in the bile? If anything, wouldn't bile acids excreted = less cholesterol returned via enterohepatic circulation?

Bile acids are surfactants-their job is to solubilize less soluble molecules. So when you bind them up with resins, the enterohepatic cycling is reduced. This is good in one way-you end up with less cholesterol in the body as the liver uses some of it up to produce more bile acid. In another way, though, it's bad; with less surfactant around to solubilize cholesterol, there is more of a chance the cholesterol will precipitate. This leads to gallstones.
 
I don't really know what I want from this, but can anyone give me a hint at how to recognize serum sickness questions?

I ALWAYS miss them on UWorld...
 
Going to try and take a stab at this one. I don't promise anything:

Wouldn't we just see a monoclonal G6PD isoenzyme increased on the fibroadenoma, but normal on the fibrocystic change?

Ah, but which cells? Would epithelial cells share monoclonal G6PD? Would stromal cells? Or both?

Stupid Question:

Anyone want to explain to me the difference between somatic hypermutation and affinity maturation?

Both of them are features of the secondary response to antigen, so they both require initial binding & recognition of the antigen.

- Somatic hypermutation: DNA coding for antigen binding site undergoes mutation --> Hypervariable region has better fit --> Stronger binding
- Affinity maturation: Plasma cells with stronger binding to the antigen(whether through somatic hypermutation or other mechanisms) get activated by antigen more frequently --> Larger population of plasma cells eventually become composed of these cells with stronger binding.

In short, plasma cells undergo somatic hypermutation and become better able to bind antigen. Those plasma cells which can bind antigen better get activated more and eventually, compose most of the plasma cells. That process is called as affinity maturation.
 
I don't really know what I want from this, but can anyone give me a hint at how to recognize serum sickness questions?

I ALWAYS miss them on UWorld...

Serum sickness is a systemic type III hypersensitivity. There's an another disease with type III sensitivity which I'm sure you're all familiar with: SLE. So it is expected that signs and symptoms of serum sickness would be similar to SLE:

- Systemic: Fever; lymphadenopathy & splenomegaly
- Skin: Maculopapular rash, often with pruritus; angioedema
- MSK: Arthralgia and arthritis
- Renal: Hematuria, proteinuria, red cell casts

The disease is called as "serum sickness" because historically, it was seen in patients who received serum from animals for treatment (most common example: horse serum because of antibodies). Nowadays, it is most often due to drugs.
 
Serum sickness is a systemic type III hypersensitivity. There's an another disease with type III sensitivity which I'm sure you're all familiar with: SLE. So it is expected that signs and symptoms of serum sickness would be similar to SLE:

- Systemic: Fever; lymphadenopathy & splenomegaly
- Skin: Maculopapular rash, often with pruritus; angioedema
- MSK: Arthralgia and arthritis
- Renal: Hematuria, proteinuria, red cell casts

The disease is called as "serum sickness" because historically, it was seen in patients who received serum from animals for treatment (most common example: horse serum because of antibodies). Nowadays, it is most often due to drugs.

they used to use horse products for that?! damn, makes me wonder what we will look at at when we are 80 and say "those barbarians really did that back than?" haha
 
Serum sickness is a systemic type III hypersensitivity. There's an another disease with type III sensitivity which I'm sure you're all familiar with: SLE. So it is expected that signs and symptoms of serum sickness would be similar to SLE:

- Systemic: Fever; lymphadenopathy & splenomegaly
- Skin: Maculopapular rash, often with pruritus; angioedema
- MSK: Arthralgia and arthritis
- Renal: Hematuria, proteinuria, red cell casts

The disease is called as "serum sickness" because historically, it was seen in patients who received serum from animals for treatment (most common example: horse serum because of antibodies). Nowadays, it is most often due to drugs.

So we're talking lupus-like symptoms in response to drugs... do you guys think we'd ever have to differentiate serum sickness from drug-induced lupus? If so, how would you tell the difference? Anti-histones?
 
uworld q - basically said influenza spread across southeast asia. cause is orthomyxo transmitted from poultry.

how do i tell if this is drift or shift? is it based on how widespread it is or that it came from poultry? what's the difference between epidemic and pandemic?
 
uworld q - basically said influenza spread across southeast asia. cause is orthomyxo transmitted from poultry.

how do i tell if this is drift or shift? is it based on how widespread it is or that it came from poultry? what's the difference between epidemic and pandemic?

i think for testing purposes, any time you see influenza (or any other segmented virus), think shift aka reassortment

but to actually reason through it a bit... (i think) the revealing hint would be that it came from poultry. since drift = minor changes, it wouldn't be enough to allow an animal virus to infect AND spread among humans
 
So we're talking lupus-like symptoms in response to drugs... do you guys think we'd ever have to differentiate serum sickness from drug-induced lupus? If so, how would you tell the difference? Anti-histones?

or the actual condition probably. if the pt was described having a seizure disorder (phenytoin), hypertension (hydralazine), arrythmia (procainamide) or TB/TB prophylaxis (isoniazid)

i imagine them saying something like pt has ____ symptoms with anti-histones, what was the drug
 
Can someone sum up different energy sources while fasting for me?

Here is a start, with what I know.

Between meals - glycogen breakdown
Fasting - GNG
>3 days no food - ketogenesis

Is this correct?

anyone mind clarifying this? an NBME question regarding this topic is really bothering me...
 
Have you looked at Page 114 of FA 2013? Or do you want something a little more than that?
 
Have you looked at Page 114 of FA 2013? Or do you want something a little more than that?

I guess some more clarification, because of that NBME. I posted in that thread but it hasn't gotten much response. It is NBME 12, highlight the below area if you want to see it (I don't want to spoil the question for anyone).


Dude goes a week without food. What happens to fructose 2,6 bisphosphate, glucose 6 phosphatase, PEPCK, pyruvate kinase? I put they all decrease, since you would be relying on ketones... apparently PEPCK and glucse 6 phosphatase would go up is what the consensus is in that topic. Even if you still have some GNG, surely it would be less than baseline though right, since you would MOSTLY be relying on ketogenesis at that point?
 
anyone mind clarifying this? an NBME question regarding this topic is really bothering me...
Summary of my notes:
Post-Absorptive Period:
Produced -
Glucose from Liver Glycogenolysis(major), Liver GluconeogenesisStarts (4-6hrs after meal, Fully active 10-18hrs)
Fatty Acids from Adipose Tissue(minor)
Used: Muscles,Brain, and other tissues use Mainly Glucose

24hrs Starvation:
Produced: Glucose from Gluconeogenesis; Fatty acids from adipose tissue
Used: Brain uses Mainly Glucose
Muscles and other tissues use some Glucose but Mainly Fatty acids

48hrs Starvation:
Produced: Glucose from Gluconeogenesis; Fatty Acids from adipose tissue; Ketone bodies from Liver
Used: Brain uses mainly Glucose but also Some Ketone bodies
Muscles and other tissues use Mainly Fatty acids but also some Ketone bodies

5 days Starvation:

Produced: Glucose from Liver Gluconeogenesis, Fatty acids from adipose tissue, Ketone bodies from Liver
Used: Brain uses Mainly Ketone Bodies
Muscles and other tissue use Mainly Fatty acids but also Some Ketone bodies


3day vs. Overnight fast:
Over night- 90% Glucose; 5%Ketone bodies
3 Day- 60%Ketone bodies; 40% Glucose
 
Biochemically, how does alcohol consuption cause hyperlipidemia?
Hmm Page 95 of FA 2013 might clarify that for you. Its bascially increase in NADH levels caused by alcohol leads to increase Fatty acid synthesis
 
Last edited:
Hmm Page 95 of FA 2013 might clarify that for you. Its bascially increase in NADPH levels caused by alcohol leads to increase Fatty acid synthesis

This is kind of confusing...

Increased NADH (from alcohol and acetaldehyde dehydrogenases) leads to OAA --> malate, regenerating some NAD+. This enzyme is malate dehydrogenase (part of TCA cycle)

Now excess malate is present, which somehow leads to NADPH. This enzyme, according to wikipedia, is also malate dehydrogenase. I'm not exactly sure what the difference is.

Excess NADPH leads to increased FA synthesis
 
This is kind of confusing...

Increased NADH (from alcohol and acetaldehyde dehydrogenases) leads to OAA --> malate, regenerating some NAD+. This enzyme is malate dehydrogenase (part of TCA cycle)

Now excess malate is present, which somehow leads to NADPH. This enzyme, according to wikipedia, is also malate dehydrogenase. I'm not exactly sure what the difference is.

Excess NADPH leads to increased FA synthesis
So
Ethanol --->Acetaldehyde--->Acetate--->--->Acetyl COA
2 NADH is made from this rxn
Now this increased NADH/NAD+ ratio causes OAA to get converted to Malate

OAA +NADH ----> Malate

Now we have Acetyl CoA and Malate
Acetyl CoA -->Malonyl CoA -----> --->---> Palmitoyl CoA

To make FA you need NADPH for Fatty acid synthase
Malate--->Pyruvate cause release of NADPH
This NADPH is then combined with Malonyl CoA to make Palmitoyl CoA

Basically Alcohol breakdowns to Acetyl CoA and increases NADH which used to make Malate from OAA.
Acetyl CoA gets converted to Malonly CoA by Acetyl CoA carboxylase.
Malate is converted to pyruvate releasing NADPH.
This NADPH then gets combined with Malonyl CoA to make Fatty Acid
 
So
Ethanol --->Acetaldehyde--->Acetate--->--->Acetyl COA
2 NADH is made from this rxn
Now this increased NADH/NAD+ ratio causes OAA to get converted to Malate

OAA +NADH ----> Malate

Now we have Acetyl CoA and Malate
Acetyl CoA -->Malonyl CoA -----> --->---> Palmitoyl CoA

To make FA you need NADPH for Fatty acid synthase
Malate--->Pyruvate cause release of NADPH
This NADPH is then combined with Malonyl CoA to make Palmitoyl CoA

Basically Alcohol breakdowns to Acetyl CoA and increases NADH which used to make Malate from OAA.
Acetyl CoA gets converted to Malonly CoA by Acetyl CoA carboxylase.
Malate is converted to pyruvate releasing NADPH.
This NADPH then gets combined with Malonyl CoA to make Fatty Acid
http://en.wikipedia.org/wiki/Malic_enzyme

this is what confused me. 3 enzymes called malate dehydrogenase, two of them involving NAD/NADH while the third involves NADP/NADPH lol
 
Top