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 AcetylCoA 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! USMLE Step 1 Radiology buzzwords Apple Core lesion signifies annular carcinomas of the colonlooks like an apple core or napkin ring(see below) due to circumferential narrowing of the lumen, noted on contrast studies.

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Bamboo Spine fused spinal segments with their syndesmophytes look, on radiographs, similar to bamboo stalksclassically associated with ankylosing spondylitis.

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Bird's Beak noted on Upper GI with contrast, a dilated upper/middle esophagus with an abrupt taper to exceptionally narrowed lumen, typical of achalasia.

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Boot-shaped Heart due to RVH, the LV is lifted above the edge of the diaphragm, forming the toe of the boot. Classic for Tetralogy of Fallot.

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Bat's Wing/Butterfly this appearance on CXR is classically associated with CHF and resultant pulmonary edema. Cobblestone appearance this sign is produced on barium studies due to ulcerative pockets, usually in the terminal ileum, indicative of Crohn's.

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Codman's Triangle a triangle on plain film of extremities that signifies reactive bone, classically associated with osteosarcoma, or other infectious/hemorrhagic process that causes periosteal elevation.

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Coin lesion solitary pulmonary nodule; may be cancer or granuloma. Cutter lesions metastatic lesions to bone cortex, or Paget's.

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Crescent sign classic sign of avascular necrosis, femoral head.

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Egg-on-a-string a large, ovoid-shaped heart on newborn CXR, classically signifying complete transposition of the great vessels with intact ventricular septum.

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Ground glass a white-out on CXR, usually PCP pneumonia or ARDS.

Hampton's Hump a peripheral triangle, usually near pleural edges, classically PE.

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Honeycomb lung used to describe any pathologic process that causes radiographic appearance of multiple small, thick-walled cystic spaces; e.g. pulmonary fibrosis. Lead pipe sign classic narrowing of bowel lumen, with loss of haustraUC.

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Napkin Ring sign see Apple core lesion above; pathology identical, but lumen more narrowed. Onion-skinning layered look of periosteum in Ewing's Sarcoma.

Rachitic Rosary this is a string of beads appearance on x-ray, a thickening of costochondral margins that is noted in Ricketts(Vit. D Deficiency).

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Sail sign (elbow) fat pad noted on plain film, indicative of elbow disclocation.

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Sail Sign (Chest X ray) Thymic shadow in children seen in chest X ray.

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Scotty dog(collar) on posterior oblique, the lumbar vertebrae look like a Scottish terrier. The neck is the pars interarticularis, and a break(a collar) noted there indicates spondylolysis.

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String sign thin, slightly irregular shadow in narrowed lumen of ileum, suggestive of Crohn's.

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Silhouette sign obliteration of cardiovascular silhouette due to adjacent disease, ie pneumonia, TB, etc.

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Stepladder appearance distended bowel loops, often indicative of obstruction, usually SBO.

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Sunburst appearance clouds, clumps, and consolidated rays of tissue emanating from bone cortex, or within bony structures, indicative of osteosarcoma.

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Thumb(print) sign on lateral c-spine, an enlarged epiglottis appears as a thumb epiglottitis.

Westermark's sign abrupt end to a pulmonary vessel, signifying oligemia or PE.

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Thanx to Myeng If you know any more, please add to the list