Chapter 38 - Disorders of Hepatobiliary and Exocrine Pancreas Functions

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11 Terms

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What do the liver and exocrine pancreas mainly produce?

Digestive enzymes

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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)

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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

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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

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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)

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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

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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

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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

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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

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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

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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