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Pathology 3000 > Liver and Pancreas - Final Exam > Flashcards

Liver and Pancreas - Final Exam Flashcards

1
Q

Function of liver (4)

A
  1. Excretion (bile)
  2. Metabolic (fats, carbohydrates, proteins, drugs)
  3. Storage (carbohydrates, fats, vitamins)
  4. Synthesis (albumin)
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2
Q

Chronic liver disease

A

Many diseases
Liver has only few stereotypic ways to respond to injury
Most liver diseases result in cirrhosis (nodular fibrosis)

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3
Q

Clinical signs of chronic liver disease (6)

A
  1. Jaundice
  2. Varices
  3. Splenomegaly (black up in portal vein and splenic vein)
  4. Kidney and lung symptoms
  5. Ascites
  6. Encephalopathy
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4
Q

Ascites

A

Fluid accumulation in abdominal cavity - expanded stomach

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5
Q

Encephalopathy

A

Mental difficulties

Increase ammonia in blood

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6
Q

Hepatotropic viruses

A

Cause chronic liver disease
Viruses that specifically target hepatocytes
Hepatitis A, B, C, D, E
May present as acute or chronic

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7
Q

Hep A virus composition

A

Single stranded RNA

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8
Q

Hep A spread

A

Faecal-oral route by contaminated food or water

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9
Q

Hep A clinical features

A

15-45 days after exposure
Brief illness - days unless immunocompromised
No chronic disease
Vaccine available
Acute hepatitis: inflammation with areas of hepatocyte necrosis

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10
Q

Hep B virus composition

A

dsDNA

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11
Q

Hep B spread

A

Parenteral, vertical (from mom), or sexual transmission

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12
Q

Hep B clinical features

A

40-180 days
Can cause acute and chronic liver disease (chronic more likely if at birth(
Vaccine available

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13
Q

Hep B histology

A

Hepatocytes contain ground-glass cytoplasm inclusions of HBV
Pink, glassy inclusion (usually granular)
Expanded endoplasmic reticulum
Retraction artifacts around inclusion

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14
Q

Hep C virus composition

A

ssRNA

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15
Q

Hep C spread

A

Via sexual and parenteral transmission (blood products, shared needles, tattoos, neddlestick)

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16
Q

Hep C clinical features

A

Major cause of chronic liver disease
May be asymptomatic for many years
Cancer associated
No vaccine, but successful treatment (>95%, but expensive)
HCV infection with portal-based inflammation and lymphoid aggregate

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17
Q

Hep D virus composition

A

ssRNA - incomplete

Needs HBV to replicate

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18
Q

Coinfection of HDV and HBV

A

Infected at the same time

Often more aggressive than HBV alone

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19
Q

Superinfection of HDV and HBV

A

Infected with HDV after HBV

May cause fulminant liver failure

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20
Q

Hep E virus composition

A

ssRNA

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21
Q

Hep E spread

A

Faecal-oral and zoonotic roots of infection

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22
Q

Hep E clinical features

A

Mild-severe acute hepatitis

May cause chronic liver disease in certain population (immunosuppressed)

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23
Q

Fatty liver disease

A

Chronic liver disease
Alcoholic or non-alcoholic
Normal liver is 5% fat
Steatohepatitis

24
Q

Steatosis

A

Fat accumulation in liver

>5% fat

25
Q

Steatohepatitis

A

Fat injures cell organelles and membrane
Eventual necrosis and collapse of cytoskeleton
Necrosis resulting in inflammation and inducing fibrosis
Deluming degeneration

26
Q

Non-alcoholic fatty liver disease risk factors (4)

A
  1. Obesity
  2. Diabetes
  3. Metabolic syndromes
  4. Certain drugs
27
Q

Autoimmune hepatitis

A

Autoimmune disorder
Immune cells (plasma cells) injure hepatocytes
Commonly in young females
Most patients have other autoimmune disorders
Areas of necrosis and plasma cell inflammation

28
Q

Clinical features of autoimmune hepatitis

A

Asymptomatic to fulminant liver failure

Steroids and immunosuppression to treat

29
Q

Primary biliary cholangitis

A

Sclerosis
Autoimmune disease
Middle-aged females
Immune mediated destruction of small bile ducts
URSO treatment
Granulomatous inflammation - florid duct lesions

30
Q

URSO treatment

A

To treat primary biliary cholangitis
Bile acid mimic
Tricks body to produce less bile acid

31
Q

Primary sclerosing cholangitis

A

Unknown etiology, possible autoimmune component
Patients usually young adult males
Associated with ulcerative colitis
Fibro-obliterative destruction of large bile ducts
No treatment, only transplant
Periductal onion-skin fibrosis surrounding destroying bile duct

32
Q

Alpha-1-anti-trypsin deficiency

A

Autosomal recessive disorder

SERPINA gene on chromosome 14

33
Q

SERPINA gene

A

Protease inhibitor

34
Q

Alpha-1-anti-trypsin deficiency in liver

A

Accumulation of A1AT protein leads to hepatocyte injury - droplets in cells
Stained with PAD-S, pink/fuscia, found varying sizes

35
Q

Alpha-1-anti-trypsin deficiency in lungs

A

Absence of A1AT enzyme allows elastase to proceed uninhibited
Destruction of lung parenchyma - emphysema

36
Q

Hereditary haemochromatosis

A 
Autosomal recessive
HFE gene (chromosome 6)
Hepcidin production is altered and intestine absorbs too much ison
Deposited into hepatocytes and other both sites causing injury
37
Q

Hepcidin

A

Binds to transglutaminase in small intestinal cells and regulates iron absorption

38
Q

Wilson’s disease

A 
Autosomal recessive
ATP7B gene (chromosome 13)
Low or decrease in ceruloplasmin
Leads to accumulation of copper in tissues
Irreversible psychosis
39
Q

Ceruloplasmin

A

Copper carrier protein

40
Q

Cirrhosis

A

Caused by viral infection or alcohol
Viral: necrosis, inflammation, fibrosis
Alcohol: scarring, regeneration (liver cells in fibrous nodules)

41
Q

Cirrhosis leads to (3)

A
  1. Increased risk of death (liver failure, bleed from varices, coma)
  2. Possible liver transplantation
  3. Increased risk of cancer
42
Q

Liver cancer (2)

A
  1. Hepatocellular carcinoma

2. Cholagiocarinoma

43
Q

Hepatocellular carcinoma

A

Cancer arising from hepatocytes

44
Q

Cholagiocarcinoma

A

Cancer arising from bile ducts

45
Q

Pancreas function (2)

A
  1. Exocrine pancreas

2. Endocrine pancreas

46
Q

Exocrine pancreas

A

Secretes digestive enzymes into duodenum
Amylase: starch
Lipase: lipids
Peptidases: protein

47
Q

Endocrine pancreas

A

Secretes hormones into circulation

Insulin and glucagon

48
Q

Acini

A

Pancreas cells that secrete thing going into ducts

49
Q

Beta cells

A

Produce insulin

50
Q

Diabetes

A

Systemic disorder characterized by hyperglycemia

Type 1 or type 2

51
Q

Symptoms of diabetes (4)

A
  1. Polyuria (excess urination)
  2. Polydypsia (thirst)
  3. Polyphagia (hunger)
  4. Organ damage
52
Q

Type 1 diabetes

A

Sudden onset in childhood
Patients typically not obese
Autoimmune disease with autoantibodies targeting insulin-producing endocrine pancreatic cells
Patients require exogenous insulin therapy

53
Q

Type 2 diabetes

A

Typically middle-aged
Gradual onset
Obese and other metabolic syndrome components
Insulin-producing cells of endocrine pancreas preserved
Insulin receptors on target tissues have insulin resistance
Lifestyle alterations, oral medications and insulin

54
Q

Acute pancreatitis

A 
Alcohol + bile stones + unknown = 95%
Exocrine pancreatic cell death
Release of digestive enzymes, damaging remaining pancreas and adjacent fat (autodigestion)
Gallstones
Alcohol (slows down secretion)
55
Q

Chronic pancreatitis

A

Fibrosis and mild inflammation of pancreas
Gradual onset
May be preceded by acute pancreatitis
Alcohol is 70% etiology

56
Q

Clinical features of chronic pancreatitis (4)

A
  1. Endocrine insufficiency
  2. Exocrine insufficiency (malabsorption, diarrhea)
  3. Pain (fibrosis entraps nerves)
  4. Increased risk of pancreatic cancer
57
Q

Pancreatic ductal adenocarcinoma

A 
Most common pancreatic cancer
Usually middle aged to elderly
Mostly at head of pancreas
Lead to jaundice (common symptom)
80% have cancer outside their pancreas at time of diagnosis

Pathology 3000 (14 decks)

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