cirrhosis Flashcards
cirrhosis common etiology
hep B (D), Hep C, Alcohol, hemochromatosis, Wilsonsn Disease, NAFLD, PBC, Primary sclerosing cholangitis, Autoimmune hepatitis, Alpha 1 anti trypsin defincy, budd chiari syndrome (clot in hepatic vein)
cirrhosis exam and lab
exam: cachexia, jaundice, ascites, spider angioma, dupuytren’s contractures they cant extend palms, edema, breast development, testiculat atrophy, palmer erythema, hair loss, encephalopathy (increased estrogens- males cannot metabolize and clear estrogens), caput medusa
Laboratory: elevated bilirubin, elevated transaminases, Elevated alk phos, decreased albumin, elevated PT/INR, thrombocyto penia, leukopenia, renal insufficiency, hyponatremia
Splenomegaly (platelets are sequestered)
Hepatic fibrosis
activated kupffer cell in sinusoids secretes TNFa (inflammation- grade, causes inflamatorry cells to) stellate cells laying down collagen and obliterating spce of disse and preventing biliary canalicular flow
Cirrhotic liver does not regenerate
child pugh scoring
albumin, bili, INR, acites, encephalopathy
A (5-6) healthy, up to 15 in C
5 yr survival = 70-75%, B and C for transplant
Model for END Stage liver disease (MELD)
looks at INR, bilirubin, creatinine, dialysis
predicts 90 day survival
MELD scores of 15+ get on the list
QMd
Portal HTN
Pre-hepatic (portal vein thrombosis)
Intra hepatic- cirrhosis
Post- hepatic- hepatic vein Thrombosis (Budd Chiari syndrome), Right heart failure, valvular heart disease
there need to be a pressure gradient
If theres a block (ie stage 4 cirrhhosis) blood gets shunted into the portal vein and goes to acessory locatins- Spleen (where platelets and white cells are located), veracies
Complications of cirrhosis
Variceal bleeding, Ascites (hyponatremia, spontaneous bacterial peritonitis (SBP), hepatorenal syndrome)
Hepatopulmonary syndrome
Hepatic encephalopathy
Esophageal varices- rupture and bleed
esophageal varices treatment
B- adrenergic blockers
non selective B-blocker- propanolol, nadolol, they decrease cardiac output by blocking B- 1 receptos, produce splanchnic vasconstriction by B 2 blocade
Decreases risk of bleeding and increases survival
treatment of ACTIVE variceal hemorrhage, pharmacologic and surgical
Octreotide aka synthetic somatostatin- compresses the portal vein from spewing out more blood.
Variceal band ligation
Ascites
bulging of flanks, drained
Portal HTN, low albumin, fluid leakage in the abddomen
pathophysiology of ascities
cirrhosis–> increased resistance to portal flow–> portal hypertension–> splanchnic arterial vasodilation–> decreased effective circulating volume–> Activation of Vasoconstrictor and antinatriuretic factors (RAAS, vasopress), sodium and water retention–> plasma volume expansion–> ascites
What happens when you dilate the hepatic/splanchnic artery and decrease the effective circulating volume
Decreased effective circulating volume–> increased vasopressin –> water retention–>
Decreased ef circ volume–> increased RAAS–> sodium Retention–>
–> water retention>sodium retention= hyponatremia via dilution
Management of ascites
low NA restricted diet
Diuretics- spironolactone inhibits aldosterone, furosemide (lasix)
signs and symptoms in patients with spontaneous bacterial peritonitis (SBP) due to ascites
All patients with cirrhosis are immunocomprimised, and the asictes fluid can become infected (SBP) –> abdominal pain and fever
Hepatorenal syndrome, a complication of ascites
Progressive renal failure associated with advanced cirrhosis and ascites
no other cause of renal failure or disease
kidneys sense a lowered peerfusion–> vasoconstrict, dont make urine to increase the volume of the blood, kidney failure
3 types of renal failure in cirrhosis
Acute tubular necrosis- damage to tubules in kidney, and kidney cant hold on to Na, cell debris in kidney (Muddy brown casts), central venous pressure is normal
Pre renal- as if you ran 20 miles without water. Urine Na is going to be very low, but the urine will be normal just dehydrated so central venous pressure is low- improves with IV fluids
Hepatorenal- severe form of pre renal, kidneys are normal, but hang on to na very tightly, no improvement with IV fluids, need to liver transplant, very bad prognosis (type 1 is the worst, they die in a week)
Hepatopumonary syndrome
Vasodilations in the lungs, hypoxia due to low pressure
not fixing, transplant
hepatic encephalopathy (altered mental status)
Gut derived neurotoxins accumulate and cross BBB–> CNS changes
Asterixis- do the stop sign
Grade 0-good, Grade 4- coma, Grade 2- confusion
Give LActulose- to lower pH, Rifaximin- cant generate ammonia (nitrogenous waste products enter brain, lactulose, bacteria convert it to lactic acid which causes NH3–> Nh4 the excretable form)
Fulminannt liver failure
Acute liver failure- hepatocyte necrosis, coagulopathy, encephalopathy
Cerebral edema- inability of liver to metabolize ammonia, ammonia and glutamate converted by action of glutamine synthetase into glutamine by brain astrocytes-,astrocyte swelling leads to cerbral edema, cerebral herniation is leading cause fo death- ACCUTE disease
