Pancreas and Liver Flashcards

(30 cards)

1
Q

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

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

3 components of the portal tract/triad

A

Hepatic artery
Portal vein
Bile duct

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3
Q

4 Functions of the liver

A

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

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4
Q

Cirrhosis

A

Nodular fibrosis

Reduction of function

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5
Q

Clinical signs of chronic liver disease

A

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)

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6
Q

Hepatitis A virus

A

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

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7
Q

Hepatitis B virus

A

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

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8
Q

Hepatitis C virus

A

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

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9
Q

Hepatitis D virus

A

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)

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10
Q

Hepatitis E virus

A

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)

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11
Q

Steatosis

A

More than 5% fat in the liver

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12
Q

Steatohepatitis

A

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

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13
Q

Autoimmune hepatitis

A

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

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14
Q

Primary Biliary Cholangitis

A

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

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15
Q

Florid duct lesions

A

In primary biliary cholangitis

It is granulomatous inflammation which destroys the small bile ducts

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16
Q

Primary Sclerosing Cholangitis

A

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

17
Q

Alpha-one-anti-trypsin deficiency

A

Autosomal recessive disorder

Accumulation of this leads to hepatocyte injury

18
Q

Hereditary Hemochromatosis

A

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

19
Q

Wilson’s disease

A

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

20
Q

2 types of liver cancer

A
Hepatocellular carcinoma (from hepatocytes)
Cholangiocarcinoma (from bile ducts - adenoma)
21
Q

Papilla of Vater

A

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

22
Q

Exocrine pancreas

A

Secretes digestive enzymes into duodenum

Ex: amylase, lipase, peptidases

23
Q

Endocrine pancreas

A

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

24
Q

Diabetes cause and symptoms

A

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

25
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
26
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
27
Acute pancreatitis
Acute inflammation of the pancreas
28
Exocrine pancreatic cell death
Release of digestive enzymes, damaging remaining pancrea and adjacent fat Autodigestion
29
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
30
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 ```