cirrhosis and complications Flashcards
causes of cirrhosis
HBV, HCV, HDV, alcoholic and non-alcoholic fatty liver disease, and other diseases like Wilson’s disease, alpha-1 antitrypsin disease, autoimmune disease, chronic cholestatic conditions, drugs like methotrexate, vascular/cardiac disease; cryptogenic
sequence of events leading to cirrhosis
liver damage, inflammatory mediators, destruction of hepatocytes, bile duct cells, vascular endothelium, repair through cell prolif and regeneration that forms a fibrous scar instead of normal tissue, obliteration of sinusoidal fenestrations, block of normal nutrient flow to hepatocytes and incr. vascular resistance
What cells are important in the progression to cirrhosis?
stellite cells. normally store fat. are responsible for fibrosis because the activate in resposne to injury and promote the production of fibril-forming gollagen. Kupffer cells activate stellate cells via cytokin release. fibrosis obliterases siusoidal fenestrations…. incr. vascular resistance
How does fibrosis become cirrhosis?
sustained injury from irreversible ischemic damage of nutrient deprivation. during disease progression, we see fibrotic bridges btw central veins and portal triads and regenerating nodules of hepatocytes.
what is the definition of portal HTN?
vein pressure above 5-9 mmHg or a portal-hepatic ven pressure gradient above 5 mmHg.
how does bloodflow in the liver work? What is portal venous htn, physiologically? what are the circulatory ramifications?
blood from intestines goes to liver via the splenic vein and the sumperior mesenteric vein. it flows through the portal vein, and then to the hepatic vein where it is returned to the heart. with portal venous HTN, portal ven blood flow decreases and the splenic vein and SMV dilate. with venous dilation, systemic vascular resistance goes down, and cardiac output and blood vol. increase. With worsening cirrhosis, blood pressure decreases and renal blood flow decreases.
main sites of varices from cirrhosis. how high must the HVP gradient be for bleeding to occur?
esophageal, umbilical, rectal. must be over 12 for bleed to occur (normal 5-9).
How is the serum ascites albumin gradient useful in diagnosing the cause of ascites?
gradients above 1.1 gm/dl suggest ascites related to portal HTN
How do we manage varices in pts with cirrhosis? non-acute setting
- screening endoscopy. Red whale signs (dilated red spots) suggest high risk of bleeding. If no varices, repeat screening later.
- If moderate/large varicies, add a non-selective beta blocker (propanolol or nadolol)
How do we manage varices acutely?
resuscitate, decr. portal pressure with vasopressin and abx, emergent endoscopy with rubber band ligation or sclerosing agent injection.
balloon tamponade: temorary- balloon down the esophagus that stops the bleeding with pressure buta also cuts oral access to the stomach.
transjugular intrahepatic portosystemic shunt.
Management of ascites
50% of pts; harginger of death/transplant
Low salt diet. No protein restruction.
Tx: sprionolactone for secondary hyperaldosteronism
furosemide if necessary.
NO ACE-Is, ARBs, or NSAIDs.
What is hepatic encephalopathy
encephalopathy is confusion, altered level of consciousness and coma due to liver failure from ammonia build up. Ammonia is produced by muscle and by bacteria in the gut. portal HTN allows gut blood to bypass the liver and go to the CNS. Additionally, systemic inflammation weakens the BBB. exacerbated by poor nutrition and poor renal function. poor prognostic indicator.
management of hepatic encephalopathy
lactulose: more absorption of carbs, more bacterial fermentation and an acidic pH in the gut- ammonia can’t escape. Abx also helpful (rifaximin, metronidazole, neomycin). No protein restriction.
cirrhosis dx and types (compensated vs. uncompensated)
dx: needs biopsy for definitive dx, but can usually be made with imaging, clinical findings, and labs. compensated cirrhosis: sile b/c liver can function despite structural changes.
decompensated: complications of cirrhosis.
How is cirrhosis classifed?
on the basis of nodule morphology: micronodular if nodules less than 3 mm; macronodular if greater than 3 mm, mixed
