Cirrhosis + Liver Tumors B&B Flashcards
how does cirrhosis affect the gross appearance of the liver?
liver tissue replaced by fibrosis and nodules —> bumpy, shrunken liver
what are the symptoms of hyperammonemia caused by cirrhosis?
asterixis (hand flapping), confusion, coma
what is the treatment for hyperammonemia caused by cirrhosis? (2)
- low protein diet
- lactulose: laxative (synthetic disaccharide), broken down to fatty acids in colon —> lowers pH, favoring formation of NH4+ (over NH3) which cannot be absorbed
what hormonal abnormality is caused by cirrhosis? how does this present? (3)
elevated estrogen - liver normally removes estrogen
- gynecomastia in men
- spider angiomata (skin)
- palmar erythema
[just remember that estrogen can make your skin red]
explain the hemodynamic changes (2) that occur in cirrhosis that cause an increase in total body water (and edema, ascites, etc)
- loss of albumin —> decreased oncotic pressure causes a decrease in effective circulating volume, so RAAS/ADH are increased in response
- increased NO release —> vasodilation causes a decrease in SVR and BP, so SNS is activated to raise CO and RAAS/ADH
name 4 key locations were collaterals between the portal and systemic veins can become engorged and symptomatic in patients with portal HTN
collaterals between systemic and portal veins are normally small/collapsed because pressure is equal between systems… in portal HTN, pressure causes collaterals to open/engorge
- umbilicus —> “caput medusa”
- esophagus —> upper GI bleeding
- stomach —> upper GI bleeding
- rectum —> hemorrhoids
what is the mechanism of low platelets in patients with cirrhosis?
splenic vein drains into portal system… back pressure from portal HTN causes engorgement of the spleen —> low platelets
2 reasons why a patient could develop new or worsening ascites - how can these be differentiated?
portal HTN or malignancy (leaky vasculature)
differentiate via SAAG (Serum Ascites Albumin Gradient): take sample of fluid via paracentesis and subtract level of albumin from serum albumin:
serum albumin - ascites albumin = SAAG
high SAAG (>1.1g/dL) = portal HTN
low SAAG (<1.1g/dL) = malignancy
what is the DOC for treating ascites?
spironolactone: K+ sparing diuretic, blocks aldosterone in distal tubules
can add loop diuretics (furosemide) if extra strength is needed, can also take large volume paracentesis, can also do TIPS (surgical, connects portal vein to hepatic vein)
which 2 infectious agents most commonly cause spontaneous bacterial peritonitis (SBP)? what is the tx?
SBP = infection of ascites fluid, bacteria gain enters via gut
typically E. coli or Klebsiella (Gram neg.)
tx = cefotaxime (3rd gen. cephalosporin) - provides good gram +/- coverage
MELD Score
Model for End-stage Liver Disease: scoring system for chronic liver disease or cirrhosis, estimates 3-month mortality
takes into account bilirubin levels, creatinine, INR - these assess how well the liver is functioning [AST/ALT really only assess inflammation]
Child-Pugh classification
predicts risk/survival from cirrhosis based on 5 variables: encephalopathy, ascites, bilirubin, albumin, PT
5-6 = class A cirrhosis
7-9 = class B cirrhosis
10-15 = class C cirrhosis (bad!)
which cell type becomes activated in liver disease and is a major contributor to cirrhosis
stellate cells: perisinusoidal, storage site for retinoids (vit A metabolites) and secrete TGF-beta
proliferate and produce fibrous tissue
what is the most common primary liver tumor, and how does it typically develop?
hepatocellular carcinoma - usually a consequence of chronic liver disease
ex - hep B/C, alcoholic cirrhosis, Wilson’s Disease, hemochromatosis, alpha-1 antitrypsin
which fungus is associated with hepatocellular carcinoma? what are the risk factors?
aspergillus produces aflatoxin, which can contaminate corn, soybeans, peanuts
high rates of dietary intake are a risk factor in non-industrialized countries (no screening for aflatoxin) or those who eat a lot of locally-grown foods