Cirrhosis
Cirrhosis
Cirrhosis
Juke R Saketi
Internal Medicine Department,
Gastroenterology Hepatology Subdivision,
Medical Faculty Padjadjaran University/
Hasan Sadikin Hospital Bandung
Pathophysiology
• Slow, insidious, progressive, chronic
• Fibrous bands replace normal liver
structure
• Cell degeneration occurs
• Liver attempts to regenerate cells but cells
are abnormal and disorganized
• Causes abnormal blood and lymph flow
• Results in more fibrous tissue formation
Normal Liver
Incidence of Cirrhosis
• Postnecrotic
• Biliary
• Cardiac
Laennec’s Cirrhosis
• Most common type of cirrhosis
• Also called alcoholic or portal
• Alcohol causes inflammation to liver
cells
• Leads to fatty deposits and
hepatomegaly
• Scarring formed and liver cells
destroyed
• Malnutrition and more alcohol accelerate
the damage
Postnecrotic Cirrhosis
• Caused by viral hepatitis or
hepatotoxins
• Scar tissue destroys liver
lobes
• Liver initially enlarges but
then shrinks in size
• 10 – 30% of all cirrhoses
Biliary Cirrhosis
• Caused by chronic biliary
obstruction or stasis of bile,
biliary inflammation, or hepatic
fibrosis
• Excessive bile leads to liver cell
destruction and formation of
nodules in the lobes
• 5 – 10% of all cirrhoses
Cardiac Cirrhosis
• Abdominal x-ray
• Upper GI series
• Angiography
• Abdominal CT
• EGD
• Liver biopsy
• Nuclear scan
Signs and Symptoms
• Neurological
Asterixis Paraesthesias
LOC Sensory
disturbances
Behavorial changes Cognitive
changes
Skin
Spider angiomas Palmar erythma
Jaundice Pruitis
hair production caput medusa
pigmentation Bruising
White Nails
Caput Medusae
Spider Angiomas
Palmar Erythema
More Signs and Symptoms
• GI
Abdominal pain Anorexia
Ascites Diarrhea
Clay colored stools Fetor hepaticus
Gastritis GI bleeding
N/V Varices
Malnutrition
“White Nails”
More Signs and Symptoms
• Cardiovascular
Dysrhythmias Portal
hypertension
Collateral circulation Fatigue
Peripheral edema
• Endocrine
Gynecomastia Amenorrhea
aldosterone, ADH, estrogens,
glucocorticoids
More Signs and Symptoms
• Respiratory
Dyspnea Hypoxia
• Blood
Anemia DIC
Thrombocytopenia
WBCs
Hypokalemia Hypocalcemia
Hypo/Hypernatremia
Hypomagnesia
More Signs and Symptoms
• Immune
Susceptibility to infections
Leukopenia
Renal
Urinary output
Complications
• Portal hypertension
– Ascites
– Varices
• Coagulation defects
• Jaundice
• PSE (portal systemic
encephalopathy)
• Hepatorenal syndrome
Portal Hypertension
• Increased pressure within the portal
vein
• Results in obstruction of blood flow
through the portal vein
– Blood tries to find new ways around
obstructed area = collateral circulation
• Causes venous distention in entire GI
tract
Ascites
• Accumulation of plasma in the peritoneal
cavity
– Caused by increased pressure forcing fluid out of
intravascular space into cavity
– Plasma contains albumin so circulating proteins
decreased
– serum osmotic pressure
– Intravascular fluid depletion stimulates kidney to
conserve sodium and water = hydrostatic
pressure and creates more ascites
Ascites
Varices
• Occur anywhere in the GI tract
especially
– Esophageal
Hemorrhoids
• Bleeding esphageal varices
– Caused by thin walled veins
that are irritated, distended and
eventually rupture
Chemical irritants
Mechanical trauma
Esophagus pressure
Prone to hemorrhage – medical
emergency
Esophageal Varices
Coagulation Defects
• Susceptible to bleeding
• Bruises easily
• Does not clot
– Esophageal varices
bleeding
Jaundice
• Due to hepatocellular destruction or
hepatic obstruction
– Hepatocellular – cannot metabolize
bilirubin so it builds up
– Obstruction – clogs bile ducts so excretion
is not possible
Jaundice
PSE
• Also known as
hepatic coma
• Seen in end stage
hepatic failure
• Can be insidious or
rapid onset
depending on the
severity of liver
disease
• Caused by impaired
ammonia
metabolism
PSE Continued
• Usually protein breaks down into
ammonia in GI tract, then ammonia into
urea --- excreted by the kidneys
• Liver cannot convert ammonia into urea
– Results in serum ammonia levels
– Toxic to the central nervous system
PSE Continued