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Mechanisms of Disease > Accessory Digestive Organs and Metabolic Disorders > Flashcards

Accessory Digestive Organs and Metabolic Disorders Flashcards

1
Q

What liver syndrome is described as an absence of general functions, where cells do not function properly?

A

Hepatic failure

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2
Q

What liver syndrome is described as architectural disruption and fibrosis within nodules of hepatocytes?

A

Cirrhosis

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3
Q

True or false. Liver cirrhosis has rapid onset of symptoms.

A

False. Nodules of functional tissue are sufficient for maintenance; can be asymptomatic early on

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4
Q

What is the function of Kupffer cells?

A

Resident macrophages of the liver

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5
Q

What is the function of quiescent stellate cells?

A

Vitamin A storage

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6
Q

What are the functions of activated stellate cells (myofibroblasts)? (4)

A
  1. Proliferation
  2. Contraction
  3. Chemotaxis
  4. Fibrogenesis
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7
Q

What causes activation of stellate cells?

A

Release of cytokines from Kupffer cells

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8
Q

What is the difference between jaundice and icterus?

A
  • Jaundice: yellowing of skin
  • Icterus: yellowing of sclera
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9
Q

What is the function of bilirubin?

A
  • End product of heme catabolism to be excreted
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10
Q

How is bilirubin excreted?

A
  • Conjugated to glucuronic acid
  • Excreted in bile
  • Eventually fecal matter
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11
Q

What is cholestasis?

A

Impaired bile formation/flow

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12
Q

Does massive hepatocyte damage (necrosis) occur in acute or chronic hepatitis?

A

Acute

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13
Q

True or false. Acute hepatitis can be symptomatic or asymptomatic

A

True

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14
Q

What systemic viruses can cause acute hepatitis? (2)

A
  • Yellow fever
  • Mononucleosis
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15
Q

What are the frequencies of chronic liver disease among the hepatitis viruses?

A
  1. HepA - Never
  2. HepB - 5-10%
  3. HepC - >80%
  4. HepD - 10% coinfection w/ HepB; 90-100% superinfections
  5. HepE - Only in immunocompromised
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16
Q

True or false. HepA infections are never chronic

A

True

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17
Q

Spontaneous clearance of HepB surface antigen (HBsAg) occurs in ____% of chronic hepatitis cases in western countries.

A

1-2%

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18
Q

What causes HepC infections to become chronic?

A
  • Reactivation of endogenous HCV strain
  • RNA is not fully cleared
  • Emergence of new mutant strain
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19
Q

What are the symptoms of chronic hepatitis? (9)

A
  1. Fatigue
  2. Malaise
  3. Loss of appetite
  4. Mild jaundice
  5. Hepatic tenderness
  6. Hepatomegaly or splenomegaly
  7. Hyperglobulinemia
  8. Hyperbilirubinemia
  9. Increased serum transaminase
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20
Q

In what zone of a hepatic nodule would you expect to see viral damage?

A

Zone 1

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21
Q

How does a necrotic liver present histologically? (2)

A
  1. Congested
  2. Bile accumulation
22
Q

How does an acetaminophen overdose in the liver present histologically? (3)

A

Confluent necrosis in zone 3 surrounding the central vein

23
Q

Why is acetaminophen toxic to the liver?

A

Metabolized to reactive intermediates that can kill cells

24
Q

What is the normal use for chlorpromazine?

A
  • Dopamine antagonist
  • Treats schizophrenia
25
Q

Why is chlorpromazine toxic to the liver?

A
  • Forms insoluble complexes in bile which leads to cholestasis
  • Metabolites inhibit membrane enzymes and impair cytoskeletal functions
26
Q

What proof is Jack Daniel’s? (yes she said this in lecture)

A

80 proof

27
Q

Mild ethanol injury results from moderate alcohol intake, which equates to ________

A

6 beers or 8 oz of 80 proof liquor in 1 session

28
Q

What is steatosis?

A
  • Fatty deposits in the liver
  • Caused by mild ethanol injury
29
Q

What are the effects of ethanol on hepatocytes? (4)

A
  1. Affects membrane function (chemical)
  2. Induces/inhibits enzymes that detoxify foreign compounds
  3. Enhances oxygen toxicity
  4. Oxidized to acetaldehyde
30
Q

What are the effects of acetaldehyde on hepatocytes? (2)

A
  1. Inhibits protein export and metabolism
  2. Alters redox potential
31
Q

What are the symptoms of preeclampsia/eclampsia? (4)

A
  1. Maternal hypertension
  2. proteinuria
  3. Peripheral edema
  4. Hypercoagulability
32
Q

What is HELLP syndrome?

A
  • H = hemolysis
  • EL = elevated liver enzymes
  • LP = low platelets
33
Q

What causes preeclampsia/eclampsia?

A
  • Hemorrhage into space of Disse
  • Fibrin deposits in periportal sinusoid
  • Leads to necrosis of hepatocytes
34
Q

____ is the systemic retension of bilirubin and other solutes such as excess cholesterol, xenobiotics, and other waste products.

A

Cholestasis

35
Q

What is the cause of cholestasis?

A
  • Impaired bile flow:
    • accumulation of bile in hepatocytes
    • Obstruction of bile channels
    • Defects in hepatocyte bile secretion
36
Q

What are the symptoms of cholestasis?n (4)

A
  1. Jaundice
  2. Pruritis (itching)
  3. Skin xanthomas (cholesterol accumulation)
  4. Malabsorption in the intestines
37
Q

What is canalicular cholestasis?

A
  • Most common form of cholestasis as a result of sepsis
  • Bile plugs within centrilobular bile canaliculi
  • Activated Kupffer cells
  • Mild portal inflammation
38
Q

What is ductular cholestasis?

A
  • Type of cholestasis that results from sepsis
  • Dilated canals of Hering and bile ductules with bile plugs
  • Edema and presence of neutrophils in stroma
  • Hepatocyte death is possible
39
Q

By what 3 mechanisms can sepsis cause cholestasis?

A
  1. DIrect effects due to infection within the liver (abcess or cholangitis)
  2. Ishcemia due to hypotension (esp. if liver is cirrhotic)
  3. Circulating microbial products (esp. with Gram(-) bacteria)
40
Q

What is cholecystitis?

A
  • Inflammation of the gall bladder
  • Almost always associated with gall stones
41
Q

How does acute cholecystitis present clinically? (4)

A
  1. Enlarged, tense gall bladder
  2. Wall is thickened and fluid-filled (edematous)
  3. Hemorrhages beneath serosa
  4. May be covered with fibrinous exudate (sign of more severe disease)
42
Q

Insulinomas, somatostatinomas, and glucagonomas are caused by an overgrowth of what pancreatic cell types?

A
  • Glucagonoma - alpha cells
  • Insulinoma - beta cells
  • Somatostatinoma - delta cells
43
Q

What is steatorrhea?

A

Impaired pancreatic excretion

44
Q

What is cholethiasis?

A

Impaired bile secretion

45
Q

What are the symptoms of a glucagonoma?

A
  1. Hyperglycemia (due to excessive glucose mobilization)
  2. Characteristic rash due to malnutrition
  3. Excess amino acid uptake for use as fuel to produce more glucose
46
Q

What infectious disease is known to cause acute pnacreatitis?

A

Mumps

47
Q

What enzymes are activated in acute pancreatitis and can lead to autodigestion? (3)

A
  1. Trypsin (or other proteases) - normally in duodenum
  2. Elastase - microvascular leakage
  3. Lipase - fat necrosis
48
Q

Aside from inappropriate activation of certain enzymes, what else can lead to autodigestion in acute pancreatitis? (2)

A
  1. Thromboses
  2. Hemorrhage
49
Q

What is the most common cause of chronic pancreatitis? Why?

A
  • Long-term alcohol abuse
    • Increased excretion → duct obstruction
    • Directly toxic to acinar cells
50
Q

Describe the pathology of chronic pancreatitis. (3)

A
  1. Parenchymal fibrosis
  2. Reduced exocrine acini
  3. Duct dilation/concretions
51
Q

What are the symptoms of pancreatitis? (6)

A
  1. Upper abdominal pain
  2. Nausea/vomiting
  3. Fever
  4. Tachycardia
  5. Sweating
  6. Icterus/jaundice
52
Q

What is the treatment for pancreatitis?

A
  • IV fluids
  • No food
  • Medicine for pain

Mechanisms of Disease (13 decks)

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