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What do the liver and exocrine pancreas mainly produce?
Digestive enzymes
Liver functions
Functions include:
ā¢ storage of glucose as glycogen
ā¢ secretion of proteins into circulation (albumin and fibrinogen)
ā¢ albumin, which pulls fluids back into the blood vessels to prevent edema
ā¢ fibrinogen & blood clotting factors
ā¢ conversion of ammonia to urea (ammonia is toxic in high amounts, especially to brain cells)
ā¢ filtration of blood & removal of bacteria
ā¢ production of bile
ā¢ elimination of bilirubin (broken down RBCs)
Jaundice
Yellow or greenish pigment of the skin caused by hyperbilirubinemia
Caused by:
ā¢ liver disease
ā¢ excessive destruction of RBCs
ā¢ obstruction of bile flow (occlusion of common bile duct)
Manifestations:
ā¢ yellow skin & sclera
ā¢ itchy skin (pruritus)
In liver disease & bile obstruction - will also see:
ā¢ dark-colored urine
ā¢ clay-colored stools
Hepatitis A, B, and C viruses
Acute: Hepatitis A & B
ā¢ flu-like symptoms: fever, malaise, nausea, vomiting, anorexia
ā¢ hepatomegaly (enlarged liver)
ā¢ jaundice
ā¢ dark-colored urine
ā¢ clay-colored stool
ā¢ pruritus (itching)
ā¢ elevated liver enzymes (ALT, AST)
Chronic: Hepatitis C
ā¢ usually asymptomatic
Hepatitis A is usually acquired through fecal matter and oral methods
Hepatitis B is usually acquired through blood transfusions, semen, and vaginal fluid
Hepatitis C is usually acquired through blood
Alcohol-induced liver disease
Alcoholic fatty liver (steatosis)
ā¢ Acetaldehyde (toxic byproduct of alcohol
metabolism)
ā¢ damages hepatocytes
ā¢ Impairs oxidation of fatty acids
ā¢ Result: fat accumulates in & around hepatocytes
ā¢ manifestations: usually asymptomatic
Alcoholic hepatitis
ā¢ inflammation & necrosis of liver cells
ā¢ outcome depends on the severity of the damage
Manifestations:
ā¢ anorexia
ā¢ nausea, vomiting
ā¢ abdominal tenderness
ā¢ low grade fever
ā¢ fatigue and weakness
Alcoholic cirrhosis
ā¢ end-stage alcoholic liver disease (irreversible damage)
Nonalcoholic fatty liver disease
The build up of extra fat in liver cells that is not caused by alcohol consumption
Caused by:
ā¢ obesity
ā¢ genetic inheritance
ā¢ rapid weight loss, resulting in fats in the blood
ā¢ diabetes or medication
Progression:
ā¢ steatosis
ā¢ steatohepatitis
ā¢ fibrosis
ā¢ cirrhosis
Manifestations:
ā¢ early stages: none or fatigue, pain in upper right quadrant of the abdomen
ā¢ later stages: same as cirrhosis
Cirrhosis
End-stage liver damage from a variety of causes leading to scarring (fibrotic tissue) and liver failure
Caused by:
ā¢ viral hepatitis
ā¢ chronic alcohol abuse
ā¢ nonalcoholic fatty liver disease
ā¢ toxic effects of drugs & chemicals
ā¢ bile duct obstruction
Portal hypertension
Abnormally high blood pressure in the portal vein
Most common cause:
ā¢ cirrhosis
Manifestations:
ā¢ hepatic encephalopathy
ā¢ splenomegaly
ā¢ ascites
ā¢ portosystemic shunts causing:
ā¢ esophageal varices
ā¢ caput medusa
ā¢ hemorrhoids
Ascites
Accumulation of fluid in the peritoneal cavity
Most often caused by:
ā¢ liver disease (cirrhosis, portal HTN)
Manifestations:
ā¢ abdominal distention
ā¢ weight gain
ā¢ difficulty breathing
ā¢ loss of appetite
Cholelithiases
Formation of stones in the gallbladder (gallstones)
Caused by:
ā¢ precipitation of substances contained in bile, primarily . . .
ā¢ too much cholesterol
ā¢ too much bilirubin
ā¢ not enough bile acids
Risk factors:
ā¢ female
ā¢ obesity
ā¢ middle age (over 40)
ā¢ pregnancy
ā¢ oral contraceptive use
ā¢ high-fat, high-cholesterol, low-fiber diet
ā¢ rapid weight loss
ā¢ Native American ancestry
ā¢ family history
ā¢ gallbladder, pancreas, or ileal disease
Pancreatitis
Acute or chronic inflammation of the pancreas
Prematurely activated pancreatic enzymes cause injury and an intense inflammatory response which leads to autodigestion of pancreatic tissue
Most common causes:
ā¢ gallstones
ā¢ alcohol abuse