Liver Cirrhosis - Etzion Flashcards
Which cells are responsible for liver fibrosis?
Hepatic stellate cells (deposit scar matrix)
Sinusoidal endothelial cells (SEC-bind together and increase pressure)
Lymphocytes (Th1,Th2,B cells,NK & dendritic cells)
Kupffer cells and bone marrow derived macrophages
Produce ECM, regulate sinusoidal hemodynamics, increase blood flow resistance in the liver and cause portal HTN.
Ascites and portal hypertension (how the splanchnic circulation leads to accumulation of fluid
Splanchnic and vasodilatation causes lymph formation from elevation of hydrostatic pressure
Perpetuation from arterial underfilling
Hyperdynamic state in splanchnic arterial system
In systemic arterial system there is a low effective blood volume
Major consequences of PHTN
Ascites and SBP
-Respiratory distress from pressure on diaphragm, pleural effusion (R sided), pancystitis
Variceal bleeding
1/3 cirrhotics develop varices, 5-15%/yr
Red wale and cherry red spots are more prone to bleeding
Defines decompensation: 70% die within a year
Hepatic encephalopathy
Hepatorenal syndrome
Hepatopulmonary syndrome
Diagnosis of ascites
Physical examination
Bulging flanks, fluid wave, shifting dullness
U.S- when fluid amount is small
Diagnostic paracenthesis
Total protein & albumin
CBC & differential
cultures
SAAG = albumin concentration in serum-ascitic fluid
high gradient >1.1g/dL
Lab findings:
Moderately elevated transaminases and ALP, GGT (if alcoholic), Bilirubin (normal if compensated, elevated as progressive)
Elevated IgG (autoimmune) and IgM (primary biliary cirrhosis)
Decreased albumin
Increased PT
Hyponatremia (poor prognosis)
Anemia
Thombocytopenia (won’t cause spontaneous bleeding but may complicate treatment)
MELD score used for liver transplantation
Treatment of ascites
Dietary Na restriction ( <2g/d)-hard to measure
Duiretics :
spironolactone (distal tubule)
fusid
Check for compliance and compensating (measure Na in urine)
Raise duiretic dosage
Large volume paracentesis (LVP) + albumin
Consider TIPS or transplant
Spontaneous Bacterial Peritonitis
Cause, diagnosis, treatment
Spontaneous infection of the ascitic fluid w/o an intrabdominal source
30% of ascitic pts; up to 25% in hospital mortality
Translocation of flora from permeable gut to mesenteric LD with seeding of ascitic fluid
E.coli, enterococus, S. aureus, S. viridans
If more than 2 organisms identified, suspect secondary bacterial peritonitis (from gut)
Suspect any patient with ascitis and:
Abdominal pain
Fever
Altered mental status
Elevated WBC
Ascitic fluid cell count> 250 neutrophils mm3 (treat empirically with second generation cephalosporins)
Culture ascitic fluid
Treat patients with variceal bleeding or previous infection prophylactically (high incidence)
Hepatic Enceophalopathy:
Causes, diagnosis, treatment
Alteration in mental status and cognitive function occurring in the presence of liver failure
Portosystemic shunting leads to CNS exposure to gut derived neurotoxins
Ammonia level usually elevated but correlation is poor with severity of liver disease
ALF- brain edema and swelling of gray matter leading to severe encephalopathy in weeks to months. Cerebral herniation most feared complication.
Treatment aimed at reduction of brain edema (manitol, hyperosmal saline-draw water out of interstitium)
R/O overt or occult GI bleeding
Is there is ascites- tapp for infection (especially if pt is confused)
Measure electorytes and correct disturbances
Look for asterixis (flapping hand)
Lactulose colonic acidification (diarrhea)
Nonabsorbable AB-neomycin, metronidazole
Rifaximin- less side effects
Zinc preperation
Transplant list
Risk factors of Cirrhotic Liver Disease
Previous Hx of hepatitis/Family Hx of CLD
Transfusions/operation
travel
Illicit drug use
Alcohol consumption
Diabetes
Presence of autoimmune diseases
Medication history and herbal preperations
Physical features in cirrhotic liver disease
Spider angiomata
Palmar Erythema
Nail changes
Dupuytren’s Contracture (bendy hands)
Gynecomastia
Hypogonadism
Splenomegaly
Caput medusae
