Pancreas and Liver

Question 1

What are the two vessels in the dual blood supply to the liver?

Answer 1

Portal vein (blood from intestines - 2/3)
Hepatic artery (fresh oxygenated blood - 1/3)

Question 2

3 components of the portal tract/triad

Answer 2

Hepatic artery
Portal vein
Bile duct

Question 3

4 Functions of the liver

Answer 3

Excretion (bile)
Metabolic (fats, carbs, protein, drugs)
Storage (carbs, fat, vitamins)
Synthesis (proteins like albumin)

Question 4

Cirrhosis

Answer 4

Nodular fibrosis

Reduction of function

Question 5

Clinical signs of chronic liver disease

Answer 5

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)

Question 6

Hepatitis A virus

Answer 6

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

Question 7

Hepatitis B virus

Answer 7

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

Question 8

Hepatitis C virus

Answer 8

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

Question 9

Hepatitis D virus

Answer 9

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)

Question 10

Hepatitis E virus

Answer 10

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)

Question 11

Steatosis

Answer 11

More than 5% fat in the liver

Question 12

Steatohepatitis

Answer 12

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

Question 13

Autoimmune hepatitis

Answer 13

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

Question 14

Primary Biliary Cholangitis

Answer 14

Autoimmune disease
Typical patient is middle aged female
Immune-mediated destruction of SMALL bile ducts
URSO treatment (mimics bile salts so body produces less)

Question 15

Florid duct lesions

Answer 15

In primary biliary cholangitis

It is granulomatous inflammation which destroys the small bile ducts

Question 16

Primary Sclerosing Cholangitis

Answer 16

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

Question 17

Alpha-one-anti-trypsin deficiency

Answer 17

Autosomal recessive disorder

Accumulation of this leads to hepatocyte injury

Question 18

Hereditary Hemochromatosis

Answer 18

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

Question 19

Wilson’s disease

Answer 19

Autosomal recessive
Low or decreased ceruloplasmin (copper carrier protein)
Leads to an accumulation of Cu in tissues, with associated damage

Question 20

2 types of liver cancer

Answer 20

Hepatocellular carcinoma (from hepatocytes)
Cholangiocarcinoma (from bile ducts - adenoma)

Question 21

Papilla of Vater

Answer 21

Where the common bile duct and pancreatic duct coalesce and empty into the duodenum

Question 22

Exocrine pancreas

Answer 22

Secretes digestive enzymes into duodenum

Ex: amylase, lipase, peptidases

Question 23

Endocrine pancreas

Answer 23

Secretes hormones into circulation so they can act at distant body sites
Ex: insulin and glucagon

Question 24

Diabetes cause and symptoms

Answer 24

Caused by hyperglycemia
Symptoms: polyuria, polydypsia, polyphagia, organ damage
Type 1 or type 2

Question 25

Type 1 Diabetes

Answer 25

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

Question 26

Type 2 Diabetes

Answer 26

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

Question 27

Acute pancreatitis

Answer 27

Acute inflammation of the pancreas

Question 28

Exocrine pancreatic cell death

Answer 28

Release of digestive enzymes, damaging remaining pancrea and adjacent fat
Autodigestion

Question 29

Chronic pancreatitis

Answer 29

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

Question 30

Pancreatic ductal adenocarcinoma

Answer 30

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