Pancreas and Liver Flashcards
What are the two vessels in the dual blood supply to the liver?
Portal vein (blood from intestines - 2/3) Hepatic artery (fresh oxygenated blood - 1/3)
3 components of the portal tract/triad
Hepatic artery
Portal vein
Bile duct
4 Functions of the liver
Excretion (bile)
Metabolic (fats, carbs, protein, drugs)
Storage (carbs, fat, vitamins)
Synthesis (proteins like albumin)
Cirrhosis
Nodular fibrosis
Reduction of function
Clinical signs of chronic liver disease
Jaundice (yellowing of skin, organs due to excess bile)
Varices (expanded blood vessels at risk of bleeding)
Splenomegaly
Kidney and lung symptoms
Ascites (fluid accumulation in the abdominal cavity)
Encephalopathy (mental difficulties)
Hepatitis A virus
ssRNA
Spread via fecal oral route (contaminated food or water)
Latency period 15-45 days
Brief illness
No chronic disease
Vaccine available
Acute hepatitis - inflammation with areas of hepatocyte necrosis and apoptosis
Hepatitis B virus
dsDNA virus
Acquired via parenteral, vertical, or sexual transmission
Latency period 40-180 days
Can cause acute and chronic liver disease
Children: high risk or chronic liver disease, adults are low risk
Vaccine available
Hepatocytes have ground glass cytoplasmic inclusions of HBV
Hepatitis C virus
ssRNA virus
Acquired via sexual and parenteral transmission
Major cause of chronic liver disease (may be asymptomatic for years)
No vaccine, but successful treatment available
Portal based inflammation, including lymphoid aggregate
Hepatitis D virus
ssRNA but incomplete virus
Needs HBV to replicate!
May be infected at the same time (more aggressive chronic disease but better)
Infection after HBV (may cause liver failure)
Hepatitis E virus
ssRNA virus
Fecal oral and zoonotic* routes of infection
Typically causes a mild-severe acute hepatitis like HAV
May cause chronic liver disease in certain populations (immunosuppressed, pregnant)
Steatosis
More than 5% fat in the liver
Steatohepatitis
Fat injures the cell organelle and membranes, with eventual necrosis and collapse of the cytoskeleton
Necrosis and resulting inflammation induce fibrosis
Called ballooning degeneration because the cells get enlarged
Get “chicken wire” fibrosis pattern because every cell is surrounded
Autoimmune hepatitis
Autoimmune disorder
Immune (plasma) cells injure hepatocytes
Young females
Most patients have other autoimmune disorders
Clinical presentations range from asymptomatic to liver failure
Steroids and immunosuppression to treat
Primary Biliary Cholangitis
Autoimmune disease
Typical patient is middle aged female
Immune-mediated destruction of SMALL bile ducts
URSO treatment (mimics bile salts so body produces less)
Florid duct lesions
In primary biliary cholangitis
It is granulomatous inflammation which destroys the small bile ducts
Primary Sclerosing Cholangitis
Unknown etiology, possible autoimmune component
Patients are usually young males*
Associated with ulcerative colitis
Fibro-obliterative destruction of large bile ducts
No treatment available
Periductal “onion-skin” fibrosis surrounding and destroying the bile duct
Alpha-one-anti-trypsin deficiency
Autosomal recessive disorder
Accumulation of this leads to hepatocyte injury
Hereditary Hemochromatosis
Autosomal recessive
HFE gene on chromosome 6
Liver normally produces hepcidin, which binds to transglutaminase in small intestinal cells and regulates iron absorption
In these patients the hepcidin production is altered, so intestine absorbs too much iron
Iron is deposited in hepatocytes and other body sites, causing injury
Wilson’s disease
Autosomal recessive
Low or decreased ceruloplasmin (copper carrier protein)
Leads to an accumulation of Cu in tissues, with associated damage
2 types of liver cancer
Hepatocellular carcinoma (from hepatocytes) Cholangiocarcinoma (from bile ducts - adenoma)
Papilla of Vater
Where the common bile duct and pancreatic duct coalesce and empty into the duodenum
Exocrine pancreas
Secretes digestive enzymes into duodenum
Ex: amylase, lipase, peptidases
Endocrine pancreas
Secretes hormones into circulation so they can act at distant body sites
Ex: insulin and glucagon
Diabetes cause and symptoms
Caused by hyperglycemia
Symptoms: polyuria, polydypsia, polyphagia, organ damage
Type 1 or type 2
Type 1 Diabetes
Sudden onset in childhood
Patients typically not obese
Autoimmune disease with antibodies targeting insulin-producing endocrine pancreatic cells
Insulin producing cells destroyed
Absolute deficit of insulin
Patients require exogenous insulin therapy
Type 2 Diabetes
Typically middle aged, obese, may have other metabolic syndrome components
Insulin receptors on target tissues have insulin resistance
Treat with lifestyle alteration, oral medications, insulin
Acute pancreatitis
Acute inflammation of the pancreas
Exocrine pancreatic cell death
Release of digestive enzymes, damaging remaining pancrea and adjacent fat
Autodigestion
Chronic pancreatitis
Fibrosis and mild inflammation of pancreas
Gradual onset
May be preceded by acute pancreatitis
Alcohol is etiology in 70%
Results in: endocrine and exocrine insufficiency, pain, increased risk of pancreatic cancer
Pancreatic ductal adenocarcinoma
Most common pancreatic cancer Usually middle-aged to elderly patients Most occur in the head of the pancreas Leads to jaundice 80% of patients have cancer outside of their pancreas at the time of diagnosis Poor prognosis
