Chronic Liver Disease Flashcards
- Vascular Disease (pericentral): Hepatic venous outflow obstruction; Ischemic necrosis
- Steatophepatitis (pericentral)
- Chronic Hepatitis (periportal)
- Chronic Cholestatic Syndromes (bile duct injury)
Classifications of Chronic Liver Disease
- a histological diagnosis of severe fibrous scarring encircling regenerative nodules of hepatocytes
- Micronodules (3cm): assoc w/ chronic hepatitis
- Results in loss of collagen type III architectural framework between hepatocytes
- associated with clinical liver dysfunction (decreased detoxification and decreased protein synthesis) and portal hypertension
Cirrhosis
- hepatitis C now predominates in U.S. (approximately 26%)
- Alcohol (21%)
- Alcohol + HCV (15%)
- Cryptogenic (18%)
- hepatitis B (15%)
- other causes (5%)
Most common etiologies of cirrhosis
- reside in space of disse between hepatocytes and sinusoidal epithelium
- normally quiescent
- activated during liver injury –> flatten and behave as fibroblasts; release collagen
Stellate Cells
- Jaundice: inadequate metabolism and excretion of bilirubin; a late sign of chronic liver disease
- Palmar Erythema
- Telangiectasia / Spider Angiomata
- Testicular atrophy & gynecomastia: due to failure of the liver to clear circulating estrogenic precursors
- Dupuytren’s contractures: contractures of the palmar fascia; of unknown cause
Stigmata of Chronic Liver Disease
- Portosystemic shunts / Varices
- Ascities
- Congestive splenometgaly/hypersplenism
Consequences of Portal hypertension (due to cirrhosis)
- dilated veins resulting from obstruction to portal blood flow
- especially gastric, esophageal, periumbilical (“caput medusa”) and peri-rectal veins (hemorrhoids)
- high risk of hemorrhage after erosion & coagulopathy
- stasis in the portal circulation is predisposing to thrombosis
- endoscopy (EGD) for diagnosis and treatment
Varices
Normal: HVWP - IVC < 4 mmHg
Cirrhosis: HVWP = IVC > 4mmHg; > 12 mmHg is clinically signficant
Hepatic Venous Wedge Pressure
- Beta blocker (propranolol)
- EGD to band larger varicose
Prophylaxis for Variceal bleeding
- Engorgement and congestion of the spleen related to portal hypertension.
- Complications can include significant sequestration/consumption of RBCs and platelets (thrombocytopenia)
Slpenomegaly
Coagulopathy due to impaired synthesis of:
- coagulation factors (2, 5, 7, 9, 10): increased PT
- epoxide reductase (diminished vit K activtaion)
Hypoalbuminemia with edema: decreases oncotic pressure of the blood
Consequences of decreased protein synthesis
- fluid accumulation in peritoneal space
Pathogenesis:
- New hypothesis: systemic arterial vasodilation: increases in nitroc oxide with increased blood volume in splanchnic circulation
- “overflow hypothesis”: primary renal sodium & water retention; expanded intravascular volume is displaced to the peritoneal space by effects of cirrhosis and portal hypertension
- “compensatory hypothesis” ascites accumulates as a result of cirrhosis and portal hypertension, causing decreased intravascular volume; induces renal retention of sodium and water
Ascites
- Diuretics: Spironolactone or furosemide
- limit salt intake (
Ascites Management
- Renal failure in setting of ascites and cirrhosis
- Marked sodium retention is unresponsive to volume expansion and diuresis
- Kidneys show no tissue pathology
- poor prognosis
- tx: possible TIPS shunt or liver transplant
Hepatorenal Syndrome
- New onset ascites must be tapped
- clear transudate in common causes of uncomplicated cirrhosis
- Serum-ascites albumin gradient: SAAG >1.1 is consistent with portal hypertension; if
Diagnostic Paracentesis
- Infection in the ascites
- translocation of bacteria from gut or seeding from circulation is not cleared due to low opsonins and complement, most commonly due to E. coli, Klebsiella, or Strep. pn.
- Systemic presentation: low-grade fever, abdominal tenderness, encephalopathy, ascites, renal failure
- Labs - high WBC, acidosis; WBC > 500 mm3, polys > 250 mm3
- if clinical evidence, treat empirically with I.V. cefotaxime (broad spectrum)
Spontaneous Bacterial Peritonitis
- a neuro-psychiatric syndrome with signs of mental confusion and neurological instability; early hyper-reflexia and asterixis (flapping tremor) progressing to coma
- due to decreased hepatic clearance
- EEG: triphasic slow waves
- Fetor: odor of mercaptans
- Constructional apraxia: slow to remake the shape with sticks
Dx: measure NH3 ammonia
Tx: reduce the amount of protein in the gut; avoid constipation (prescribe lactulose)
Hepatic Encephalopathy