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

Accessory Digestive Organs and Metabolic Disorders Flashcards

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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)

Study These Flashcards
A
  1. Congested
  2. Bile accumulation
22
Q

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

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A

Confluent necrosis in zone 3 surrounding the central vein

23
Q

Why is acetaminophen toxic to the liver?

Study These Flashcards
A

Metabolized to reactive intermediates that can kill cells

24
Q

What is the normal use for chlorpromazine?

Study These Flashcards
A
  • Dopamine antagonist
  • Treats schizophrenia
25
Why is chlorpromazine toxic to the liver?
* Forms insoluble complexes in bile which leads to cholestasis * Metabolites inhibit membrane enzymes and impair cytoskeletal functions
26
What proof is Jack Daniel's? (yes she said this in lecture)
80 proof
27
Mild ethanol injury results from moderate alcohol intake, which equates to \_\_\_\_\_\_\_\_
6 beers or 8 oz of 80 proof liquor in 1 session
28
What is steatosis?
* Fatty deposits in the liver * Caused by mild ethanol injury
29
What are the effects of ethanol on hepatocytes? (4)
1. Affects membrane function (chemical) 2. Induces/inhibits enzymes that detoxify foreign compounds 3. Enhances oxygen toxicity 4. Oxidized to acetaldehyde
30
What are the effects of acetaldehyde on hepatocytes? (2)
1. Inhibits protein export and metabolism 2. Alters redox potential
31
What are the symptoms of preeclampsia/eclampsia? (4)
1. Maternal hypertension 2. proteinuria 3. Peripheral edema 4. Hypercoagulability
32
What is HELLP syndrome?
* H = hemolysis * EL = elevated liver enzymes * LP = low platelets
33
What causes preeclampsia/eclampsia?
* Hemorrhage into space of Disse * Fibrin deposits in periportal sinusoid * Leads to necrosis of hepatocytes
34
\_\_\_\_ is the systemic retension of bilirubin and other solutes such as excess cholesterol, xenobiotics, and other waste products.
Cholestasis
35
What is the cause of cholestasis?
* Impaired bile flow: * accumulation of bile in hepatocytes * Obstruction of bile channels * Defects in hepatocyte bile secretion
36
What are the symptoms of cholestasis?n (4)
1. Jaundice 2. Pruritis (itching) 3. Skin xanthomas (cholesterol accumulation) 4. Malabsorption in the intestines
37
What is canalicular cholestasis?
* Most common form of cholestasis as a result of sepsis * Bile plugs within centrilobular bile canaliculi * Activated Kupffer cells * Mild portal inflammation
38
What is ductular cholestasis?
* 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
By what 3 mechanisms can sepsis cause cholestasis?
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
What is cholecystitis?
* Inflammation of the gall bladder * Almost always associated with gall stones
41
How does acute cholecystitis present clinically? (4)
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
Insulinomas, somatostatinomas, and glucagonomas are caused by an overgrowth of what pancreatic cell types?
* Glucagonoma - alpha cells * Insulinoma - beta cells * Somatostatinoma - delta cells
43
What is steatorrhea?
Impaired pancreatic excretion
44
What is cholethiasis?
Impaired bile secretion
45
What are the symptoms of a glucagonoma?
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
What infectious disease is known to cause acute pnacreatitis?
Mumps
47
What enzymes are activated in acute pancreatitis and can lead to autodigestion? (3)
1. Trypsin (or other proteases) - normally in duodenum 2. Elastase - microvascular leakage 3. Lipase - fat necrosis
48
Aside from inappropriate activation of certain enzymes, what else can lead to autodigestion in acute pancreatitis? (2)
1. Thromboses 2. Hemorrhage
49
What is the most common cause of chronic pancreatitis? Why?
* Long-term alcohol abuse * Increased excretion → duct obstruction * Directly toxic to acinar cells
50
Describe the pathology of chronic pancreatitis. (3)
1. Parenchymal fibrosis 2. Reduced **exocrine** acini 3. Duct dilation/concretions
51
What are the symptoms of pancreatitis? (6)
1. Upper abdominal pain 2. Nausea/vomiting 3. Fever 4. Tachycardia 5. Sweating 6. Icterus/jaundice
52
What is the treatment for pancreatitis?
* IV fluids * No food * Medicine for pain

Mechanisms of Disease (13 decks)

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