cirrhosis

Question 1

cirrhosis common etiology

Answer 1

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)

Question 2

cirrhosis exam and lab

Answer 2

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)

Question 3

Hepatic fibrosis

Answer 3

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

Question 4

child pugh scoring

Answer 4

albumin, bili, INR, acites, encephalopathy

A (5-6) healthy, up to 15 in C

5 yr survival = 70-75%, B and C for transplant

Question 5

Model for END Stage liver disease (MELD)

Answer 5

looks at INR, bilirubin, creatinine, dialysis
predicts 90 day survival

MELD scores of 15+ get on the list
QMd

Question 6

Portal HTN

Answer 6

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

Question 7

Complications of cirrhosis

Answer 7

Variceal bleeding, Ascites (hyponatremia, spontaneous bacterial peritonitis (SBP), hepatorenal syndrome)
Hepatopulmonary syndrome
Hepatic encephalopathy

Esophageal varices- rupture and bleed

Question 8

esophageal varices treatment

Answer 8

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

Question 9

treatment of ACTIVE variceal hemorrhage, pharmacologic and surgical

Answer 9

Octreotide aka synthetic somatostatin- compresses the portal vein from spewing out more blood.

Variceal band ligation

Question 10

Ascites

Answer 10

bulging of flanks, drained

Portal HTN, low albumin, fluid leakage in the abddomen

Question 11

pathophysiology of ascities

Answer 11

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

Question 12

What happens when you dilate the hepatic/splanchnic artery and decrease the effective circulating volume

Answer 12

Decreased effective circulating volume–> increased vasopressin –> water retention–>

Decreased ef circ volume–> increased RAAS–> sodium Retention–>

–> water retention>sodium retention= hyponatremia via dilution

Question 13

Management of ascites

Answer 13

low NA restricted diet

Diuretics- spironolactone inhibits aldosterone, furosemide (lasix)

Question 14

signs and symptoms in patients with spontaneous bacterial peritonitis (SBP) due to ascites

Answer 14

All patients with cirrhosis are immunocomprimised, and the asictes fluid can become infected (SBP) –> abdominal pain and fever

Question 15

Hepatorenal syndrome, a complication of ascites

Answer 15

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

Question 16

3 types of renal failure in cirrhosis

Answer 16

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)

Question 17

Hepatopumonary syndrome

Answer 17

Vasodilations in the lungs, hypoxia due to low pressure

not fixing, transplant

Question 18

hepatic encephalopathy (altered mental status)

Answer 18

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)

Question 19

Fulminannt liver failure

Answer 19

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