L16 Liver Flashcards

1
Q

What are the cytosolic hepatocellular enzymes checked for hepatocyte integrity?

A
  1. AST
  2. ALT
  3. LDH
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2
Q

What are the consequences of liver failure?

A

Within the liver itself
1. Coagulopathy –> impaired hepatic synthetic function
2. Hepatic encephalopathy –> altered level of consciousness due to impaired ammonia metabolism
3. Cholestasis –> impaired bile secretion

Affecting other organs:
4. Hepatorenal, hepatopulmonary syndrome

Generalised:
5, Portal hypertension (chronic&raquo_space;> acute)

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3
Q

Pathophysiology of portal hypertension

A
  1. Increased resistance at portal sinusoids
    - Scarring –> disrupted blood flow
    - Vasoconstriction
    - Sinusoidal remodelling
  2. Increased portal venous flow
    - Splanchnic vasodilation
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4
Q

Effects of portal hypertension

A
  1. Increased pressure in the peritonieal cavity –> ascites
  2. Formation of collateral vessels to dissipate the pressure, giving rise to varices
  3. Hepatoencephalopathy
  4. Splenomegaly –> bleeding
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5
Q

Common terminal events in liver failure

A
  1. Hepatic encephalopathy
  2. Bleeding from esophageal varices
  3. Sepsis

Chronic: hepatocellular carcinoma

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6
Q

What are the 2 examples of diseases which prove that not all end-stage chronic liver disease is cirrhotic?

A
  1. Primary billiary cholangitis
  2. Primary sclerotic cholangitis
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7
Q

Does hepatitis A cause chronic hepatitis?

A

NO

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8
Q

What is a risk factor for hepatocellular carcinoma?

A
  1. Chronic liver failure
  2. Hep B viral infection
  3. NAFLD
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9
Q

What are the inflammatory cell infiltrate that are present in both acute and chronic hepatitis?

A

Mononuclear T-cells

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10
Q

Drug and toxin induced liver injury can occur through [3]

A
  1. Direct toxicity
  2. Hepatic conversion of xenobiotic to active toxin
  3. Immune-mediated mechanisms
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11
Q

What are the most common drug / agent that is responsible for the development of ALF and CLF

A
  1. ALF: paracetamol
  2. CLF: alcohol
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12
Q

Pathogenesis of fatty liver disease

A
  1. Increase lipid synthesis due to increased NADH
  2. acetyl induced lipid peroxidation
  3. Increased hypoxia and oxidative stress (ROS)
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13
Q

Pathophysiology of jaundice

A

Pre-hepatic (production)
1. Excessive production (hemolysis)

Hepatic
1. Decreased hepatic uptake
2. Impaired bilirubin conjugation
3. Impaired bile flow

Post-hepatic
1. Duct obstruction

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14
Q

What are the most common causes of acute pancreatitis?

A
  1. Gallstones
  2. Alcohol
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15
Q

3 protective mechanism of the pancreas from its own enzymatic secretions

A
  1. Secretion of zymogens (inactive enzymez)
  2. Activation by tripsyn (in duodenum), minimal intra-pancreatic activation
  3. Acinar and ductal cells secrete trypsin inhibitor –> further prevent the activation of enzymes
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16
Q

What is cirrhosis?

A

Diffuse transformation of the liver into regenerative parenchymal nodules surrounded by fibrous scarring and variable degrees of vascular shunting

17
Q

What are the characteristics of liver cirrhosis?

A
  1. Diffuse hepatic involvement
  2. Long-standing necrosis
  3. Fibrosis
  4. Nodular parenchymal replacement with disruption in lobular arrangement
18
Q

What are the risk factors of liver cirrhosis?

A
  1. Alcoholic liver disease
  2. Viral infection (Hep B and C)
  3. Chronic autoimmune hepatitis
  4. Chronic billiary obstruction
19
Q

What happens at the hepatic parenchyma in liver cirrhosis?

A
  1. Progressive fibrosis
  2. Collagen synthesis in chronic inflammatory state
  3. Release of cytokines
  4. Toxins
  5. Shunts production
20
Q

Gross and microscopic appearance of liver cirrhosis

A

Gross
1. Firm
2. Shrunken
3. Nodular
4. Irregular surface

Microscopic
1. Disruption of lobar arrangement
2. Fibrosis