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Answer B: Spironolactone + Furosemide

1. History of chronic ETOH abuse (pack of beers/day)
2. Alcoholic hepatitis
3. Recent weight gain and increased abdominal girth
4. LFT's: Previous AST- 363 & ALT- 199, Current AST- 120 and ALT- 65
5. Ascites and gynecomastia are noticed

These are the five things that should help you come to the dx of liver cirrhosis 2/2 chronic alcohol abuse which as a result is causing ascites.

**MCC of ascites is liver cirrhosis
**MC complication of liver cirrhosis is ascites

You can see AST > ALT. That is consistent with alcoholic hepatitis. Usually, these patients will have a 2:1 AST:ALT ration. LFT's associated with alcoholic hepatitis are much higher than liver cirrhosis. This occurs because in alcoholic hepatitis the freshly injured hepatocytes leak enzymes excessively, whereas, with liver cirrhosis the hepatocytes are permanently damaged and don't have many enzymes in its reservoir.

*This same concept is also seen with acute vs chronic pancreatitis where you will see a very significant rise in pancreatic enzymes in the acute phase, but if it keeps reoccurring then the pancreas loses it's ability to produce the appropriate enzymes and therefore we wouldn't see a significant rise in lipase...for that reason, CHRONIC PANCREATITIS can't be dx via lab values**

Initial management of ascites involves alcohol abstinence, dietary changes (restrict sodium and water intake) and combination of Spironolactone and Furosemide (dosage may vary depending on the severity of the ascites).

Systemic pressure tends to fall with liver cirrhosis and the renin-angiotensin system plays a key role in maintaining the pressure. Also, systemic arterial pressure is directly correlated with survival in liver cirrhosis and for that reason ACE-I and ARB should be avoided.

Propranolol can prevent vatical hemorrhages, but studies have shown that survival worsens especially with refractory ascites. No direct role in removing excessive fluid which is seen with ascites.