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Old 05-05-2011
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Arrow Alcohol: Things to know

Well, it's Cinco de Mayo and since I won't be consuming alcohol, I thought I'd study it instead. Here are some things to know about alcohol:

First of all, to understand the changes in alcohols, I think there is one major concept to know/understand: Alcohol metabolism uses up all NAD+ and converts it to NADH (by dehydrogenases)

Here we go:

1. Why do alcoholics have fasting hypoglycemia and how does this contribute to liver disease?

Buildup of NADH inhibits Gluconeogenesis, thus fasing hypoglycemia. How does it do this? Well, because there is excess NADH, Pyruvate is converted to lactate instead of Acetyl-CoA (in order to consume the NADH that is produced by alcohol metabolism). Although Acetyl-CoA is not directly a substrate for gluconeogenesis, it MUST be present for the first enzyme of gluconeogenesis to work. Since gluconeogenesis is impaired, you get fasting hypoglycemia. This hypoglyecemia then triggers the release of glucagon, which mobilizes fat stores via Hormone sensitive lipase. The fatty acids reach the liver and then cannot be sent out again because VLDL assembly is inhibited.

2. Why do alcoholics get fatty livers?

Alcohol metabolism provides the liver with calories/ATP, so the fatty acids that were released from glucagon (see above) do not need to be broken down by beta-oxidation because the liver has enough energy. Instead, they are used to make Triglycerides (TG); TG assembly into VLDL is inhibited by alcohol so the TGs buildup in the liver instead of getting released and this leads to fatty liver and eventually cirrhosis -- mediated by those crazy transforming stellate cells (NOTE: Check albumin level to determine extent of liver damage, AST/ALT are non-specific indicators of liver damage)

3. Why do alcoholics have thiamine and folate deficiencies?

Acetaldehyde Dehydrogenase consumes Thiamine and Folate

4. An alcoholic presents in with signs of hypoglycemia. You quickly administer glucose and are feeling good about yourself when all of a sudden the patient goes into a coma and dies. Why did this happen?

If an alcoholic has thiamine deficiency (and many do), then Pyruvate Dehydrogenase is not working very well. So if you administer glucose, PDH is not converting Pyruvate into Acetyl-CoA so it will be converted to lactic acid. This patient died of lactic acidosis. Always remember to give thiamine with glucose in a suspected alcoholic!

5. Why do alcoholics often get gout?

Increase in lactic acid --> competes with uric acid for excretion (because they are both weak acids), thus will have hyperuricemia and increased risk for gout. Note: Most diuretics are also weak acids and this is the same mechanism by which they increase risk for gout! Theoretically, any weak acid that is excreted in the urine can cause hyperuricemia (ex/ Aspirin -- but not acetaminophen, which is metabolized in liver). Also, to be complete, anything that leads to massive breakdown of cells (release of purines such as chemotherapy) can lead to hyperuricemia.

6. Why do alcoholics have skinny arms and legs? Why should this worry you?

Muscle wasting can occur in alcoholics because of the combined effects of glucagon and cortisol. Glucagon directs amino acids to gluconeogenesis (thus preventing them from being used in protein synthesis) and cortisol (released because of fasting hypoglycemia) leads to a breakdown of muscle proteins. The combination of these two effects leads to excess ammonia production. With a faulty liver, the urea cycle is not in the best shape so this can lead to hyperammonemia and hepatic encephalopathy (asterixis is a sign of hepatic encephalopathy; had to look this up on youtube, it's an involuntary flicking of the wrists -- like a bird flapping
)

7. What cancers are alcoholics especially at risk for?

Squamous cell cancer of Esophagus (especially if also a smoker) and Signet ring carcinoma of the stomach. Probably others too like Hepatocellular carcinoma due to cirrhosis

8. Why do chronic alcoholics get pancreatitis?

Not very well known, but alcohol is thought to alter/increase digestive enzyme activation (most importantly trypsinongen --> trypsin). These pancreatic enzymes then eat away at the pancreas. Note: Treatment for pancreatitis is almost always supportive, do NOT operate because this can actually kill the patient.

9. Why do alcoholics get ascites? What are some complications of the portal hypertension?

Liver damage leads to portal hypertension. This increases hydrostatic pressure in capillaries due to back up of blood and thus more fluid leaves the blood and enters the interstitum --> Note: Do not drain fluid from belly of a patient with ascites because this will cause even more fluid to leave circulation (leads to greater difference in hydrostatic pressure) and can lead to hypotension or even circulatory shock. For other complications, you gotta think back to anatomy and some of the portal-caval anastamoses: this includes internal hemorrhoids via superior rectal vein, esophageal varicies via the left gastric vein (all these anastomoses are easily testable), and caput medusa via paraumbilical veins. The esophageal varices often lead to heavy bleeding and hematemisis --> are often fatal.

10. Why is it a bad idea to drink alcohol after extreme physical activity?

Alcohol metabolism will consume all of the NAD+ available and convert it to NADH. In order for Lactic acid to be converted to Pyruvate, you need NAD+. If this is not available, then lactic acid will build up and can lead to severe lactic acidosis

11. What's up with those spider looking spots on the skin of alcoholics?

Spider angiomas come from increased estrogen. Unfortunately for male alcoholics, Estrogen is broken down in the liver so if the liver is not working then there is increased estrogen (can also see spider angiomas in pregnancy with increased estrogen levels)

12. Well, that was a mouthful. Anything else?

One last thing to consider is that the liver synthesizes a whole lot of our proteins, most importantly clotting factors (increased tendency to bleed), Steroid hormone binding proteins/other binding glubulins (can affect levels of hormones/ions), Urea (hyperammonia), Albumin (edema), and probably some others. Also, on histo if you are given a picture of hepatocytes in an alcoholic with a bunch of pink stuff in them (eosinophilic inclusions-Mallory bodies) they might as what those represent and it's keratin intermediate filaments of the cytoskeleton that are damaged.


Phew, hope that was useful to some of you and good luck studying. Please let me know if I made a mistake somewhere in there and please add anything else that might be important to know!

Last edited by apx85; 05-06-2011 at 03:42 PM.
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Old 05-05-2011
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That's an awesome post.

You should write a USMLE book, it would be as famous as FA
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This is some real help, I was looking for these yesterday and was really confused.. I m surprised how u gathered the things .. Thanks for such an awesome post
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Old 05-05-2011
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why does streptococcus pneumoniae is the leading cause of pneumonia in an alcoholic patient?
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Old 05-05-2011
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hey this information is awesome, its shows ur true dedication towards studies
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Old 05-05-2011
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Quote:
Originally Posted by cadaver View Post
why does streptococcus pneumoniae is the leading cause of pneumonia in an alcoholic patient?
I'm not sure if there is really much of a mechanism to be concerned with because Strep pneumonia is the most common cause of pneumonia in normal patients as well. Review books might make it seem like it's a unique thing but I doubt it.

In alcoholics, you might consider the possibility of Spontaneous bacterial peritonitis which can be caused by strep pneumonia, but most commonly gram negative enterics like E. coli. Somehow cirrhosis can lead to increased permeability in the small intestine, or at least that is what is proposed (See attached image for possible mechanism)
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Alcohol: Things to know-pathogenesis_of_sbp.gif  
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Not sure why I can't edit my post above but I am studying endocrine right now and wanted to clarify a point about glucagon.

Glucagon, GH, and cortisol all have the effect of increased glucose and increased lipolysis but they have different effects on proteins

Cortisol leads to breakdown of proteins (catabolism)
GH leads to synthesis of proteins (anabolism)
Glucagon takes amino acids that could be used to make proteins and directs them to gluconeogenesis

Basically what I said about glucagon breaking down muscle is not really true. It prevents proteins from being synthesized thus over time can lead to decreased muscle mass. It does not directly break down muscles (only cortisol does this)
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I am bookmarking it .. it sure will help me when I come to this topic
Thanks a ton
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Old 05-07-2011
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You forgot Dehydration in alcoholics. The reasons behind which are explained nicely over here:
http://www.healthy-water-best-filter...hydration.html
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Old 05-08-2011
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Very nice post. thanks for sharing.


@cadaver; I think that the leading cause of pneumonia in alcoholics is Klebsiella pneumoniae. correct me if i am wrong.
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why does streptococcus pneumoniae is the leading cause of pneumonia in an alcoholic patient?
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Old 05-08-2011
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Quote:
Originally Posted by dr_ram View Post
Very nice post. thanks for sharing.


@cadaver; I think that the leading cause of pneumonia in alcoholics is Klebsiella pneumoniae. correct me if i am wrong.

Klebsiella pneumonia should be associated with alcoholics but it is not the most common cause.
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Old 05-08-2011
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Why does operating on a patient with pancreatitis kill him???
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Quote:
Originally Posted by eesfee View Post
Why does operating on a patient with pancreatitis kill him???
Don't have much of an explanation but the risks associated with the surgery are very high with a high rate of complications. It is better to treat conservatively. Here is an excerpt from an article I found:

The clinical outcomes of 88 patients who underwent pancreatic necrosectomy between 1997 and 2003 were reviewed.RESULTS: The median age was 55.5 (range, 18-85) years, 54 (61%) were males, 68 (77%) had primary pancreatic infection, 71 (81%) had>50% necrosis, and the median admission Acute Physiology and Chronic Health Evaluation score was 9 (range, 1-21). Median time to surgery was 31 (range, 1-161) days; 47 patients underwent minimally invasive necrosectomy and 41 open necrosectomy; 81 (92%) of patients had complications postoperatively, and 25 (28%) died. Multiorgan failure (odds ratio = 3.4, P = .05) and hemorrhage (odds ratio = 6.1, P = .03) were the only independent predictors of mortality. During a median follow-up of 28.9 months, 39 (62%) of 63 surviving patients had one or more late complications: biliary stricture in 4 (6%), pseudocyst in 5 (8%), pancreatic fistula in 8 (13%), gastrointestinal fistula in 1 (2%), delayed collections in 3 (5%), and incisional hernia in 1 (2%); intervention was required in 10 (16%) patients. Sixteen (25%) of 63 surviving patients developed exocrine insufficiency, and 19 (33%) of 58 without prior diabetes mellitus developed endocrine insufficiency.CONCLUSIONS: Almost all patients undergoing necrosectomy developed significant early or late complications or both. Multiorgan failure and postoperative hemorrhage were independent predictors of mortality. Long-term follow-up was important because 62% developed complications, and 16% of those with complications required surgical or endoscopic intervention.

Source: PubMed

"Early and late complications after pancreatic necrosectomy."

Connor S, Alexakis N, Raraty MG, Ghaneh P, Evans J, Hughes M, Garvey CJ, Sutton R, Neoptolemos JP
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Old 06-01-2011
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awesome post!!!!
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Old 04-29-2012
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goljan and FA dont mention alcohol as a potent cause of signet ring cell gastric adenocarcinoma, can anyone make this clear?
Thanks
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Old 05-04-2012
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Why potential risk for hepatotoxicity due to acetaminophen is greater in chronic alcoholics?

Chronic use of ethanol enhances liver toxicity via induction of p450. (more N - acetylbenzoquinoneimine which is a reactive metabolite)
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Old 05-07-2012
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Excellent review!!!!!!!!!

Do not forget ETOH is toxic for mitochondria and explains the effects at the level of organs .For systems do not forget Wernicke -Korsachoff syndrome which appears in many USMLE questions
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Old 05-10-2012
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Alcohol metabolism causes ketoacidosis which increase anion gap
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Old 05-13-2012
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Thanks Mate.
I was studying environmental pathology (Alcohol Abuse) and came across this...This is awsome..Helped me get it easily.
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Old 08-16-2012
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Awesome review.....That really helped. Thanks a lot!!!!
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Good post.. Thanks..
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To view links or images in signatures your post count must be 10 or greater. You currently have 0 posts.
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Old 03-25-2013
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Hi..

I wanna know how are the increased NADH and decreased NAD levels ultimately corrected in the liver of an alcoholic after withdrawal and infusion of glucose and thiamine?
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Good review .... Easy to catch!
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awesome
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Old 12-21-2014
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Can you explain the effects of OAA to malate on ethanol hypoglycemia? can't get it right... is in FA 2013 pay 95..

Last edited by Charsmd; 12-21-2014 at 02:14 PM.
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