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Pathophysiology > W.9: Liver diseases > Flashcards

W.9: Liver diseases Flashcards

1
Q

What is the weight of the human liver?

A

1-1,5kg

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2
Q

How much of the cardiac output does the liver get?

A

25%

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3
Q

Which substance gets excreted through the liver?

A

Copper

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4
Q

What happens to bilirubin in the liver?

A

It gets conjugated with glucoronic acid

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5
Q

A condition that is NOT known to be caused by liver disease?

A

High blood pressure

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6
Q

How many percent of the blood supply to the liver goes through the hepatic a.?

A

20% (systemic, oxygenated)

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7
Q

How many percent of the blood supply to the liver goes through the portal vein?

A

80% (rich in nutrients, deoxygenated)

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8
Q

Exocrine function of the liver

A
  • Bile production
  • Excretion of cholesterol, bilirubin, copper
  • Emulsification of fat
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9
Q

Characteristic for zone 1 of the liver (outer)

A
  • Good oxygenation
  • Metabolism: gluconeogenesis, urea cycle
  • Sensitive to: direct toxins
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10
Q

Characteristic for zone 3 of the liver (inner)

A
  • Poor oxygenation
  • Metabolism: Glycolysis, lipogenesis
  • Sensitive to: Secondary toxins (toxins that the liver produces itself), circulatory problems, biliary obstruction
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11
Q

What are the macrophages of the liver called?

A

Kupffer cells (80% of all tissue macrophages)

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12
Q

Filtration of the blood of the splanchnic bed

A
  • Filtration of microbes, immunogenic materials
  • Biotransformation
  • Temporary storage of materials (not lipids)
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13
Q

Filtration of systemic blood

A

Excretion, synthesis, metabolism

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14
Q

Phases of biotransformation

A
  1. Activation: Apolar substance absorbed and gets activated to a reactive substance by cytochrome P450
  2. Increase of polarity: Reactive, active substance is transformed to a polar substance (eg. via conjugation with glucuronic acid, glutathione or methylation)
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15
Q

What can happen with biotranformation eg. in the case of alcohol abuse?

A

The two phases can be unsynchronized, phase 1 can become faster than phase 2 and leads to increased toxicity (reactive substances that will damage the liver)

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16
Q

Metabolic consequences of liver diseases: Carbohydrates

A
  • Postprandial hyperglycemia

- Hypoglycemia after prolonged fasting in alcoholics

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17
Q

Metabolic consequences of liver diseases: Proteins

A
  • Decrease in albumin and coagulation factors (albumin only produced in the liver)
  • Hepatic coma
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18
Q

Metabolic consequences of liver diseases: Lipids

A

Fatty liver

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19
Q

Clinical signs of liver diseases

A
  • Nausea, temp., fatigue
  • Palpable, tender liver, splenomegaly
  • Jaundice, palmar erythema, spider naevi, excorations, less body hair
  • Bleeding tendency
  • Confusion, coma
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20
Q

What are the symptoms of portal hypertension?

A
  • Ascites
  • Caput Medusae
  • Esophageal varices
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21
Q

Causes of aquired parenchymal liver diseases

A
  • Toxic effects: Alcohol, mushroom, drugs
  • Infections (hepatotropic and other viruses)
  • Autoimmune disorders
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22
Q

Causes of congenital parenchymal liver diseases

A
  • Inherited hyperbilirubinemias

- Other genetic syndromes (eg. hemochromatosis, Wilson’s disease)

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23
Q

When do we use the CAGE test?

A

To find out if someone is an alcoholic

24
Q

CAGE test - What does the letters stand for?

A
  • Have you felt the need to Cut down on your drinking?
  • Have you ever felt Annoyed by criticism of your drinking?
  • Have you had Guilty feelings about drinking?
  • Do you ever take a morning Eye opener (a drink first thing in the morning to steady your nerves or get rid of a hangover)?
25
Q

Systemic biochemical consequences of alcohol intake

A

Lactate acidosis (-> plasma uric acid increase)

26
Q

Cytosolic biochemical consequences of alcohol intake

A

Inhibition of gluconeogenesis (-> fasting hypoglycemia)

27
Q

Mitochondrial biochemical consequences of alcohol intake

A
  • Inhibition of the citrate cycle

- Inhibition of beta-ox. of fatty acids (-> statosis)

28
Q

Threshold dose for liver injury in case of alcohol

A

Men: 60-80g/day over years
Women: 20-40g/day

29
Q

Why is the alcohol threshold for liver disease lower in woman than in men?

A

Because the alcohol dehydrogenase activity of the stomach is less in women than in men

30
Q

Most common cause of severe acute liver injury?

A

Paracetamol poisoning

31
Q

There exists a vaccine against which hepatitis types?

A

HAV, HBV, HDV, HEV

32
Q

A vaccine does not exist for which type of hepatitis?

A

HCV

33
Q

Route of infection: HAV

A

Fecal-oral

34
Q

Route of infection: HBV

A

Percutaneous, perinatal, sexual

35
Q

Route of infection: HCV

A

Percutaneous

36
Q

Route of infection: HDV

A

Percutaneous, perinatal, sexual

37
Q

Route of infection: HEV

A

Water

38
Q

Can hepatitis caused by HAV and HEV become chronic?

A

No, never

39
Q

How many of the cases of hepatitis caused by HCV becomes chronic? (%)

A

50-70%

40
Q

Can hepatitis caused by HCV be cured?

A

Yes, effective drugs exist and can cure most cases, but the therapy is really expensive

41
Q

What causes chronic hepatitis?

A

Virus, drugs or autoimmune diseases

42
Q

Hepatic cirrhosis leads to

A

Progressive, irreversible destruction of liver parenchyma

43
Q

What causes liver cirrhosis?

A

Alcohol (Laennec cirrhosis), NASH, chronic infection, biliary obstruction, congestion, inherited metabolic desease

44
Q

What does NAFLD stand for and how common is it?

A

Non-alcoholic fatty liver, 30% of the population

45
Q

NAFLD can progress to …? In how many percent of the cases?

A

NASH (non alcoholic steatohepatis) in around 10% in 10 years

46
Q

NASH can progress to…? In how many percent of the cases?

A

Cirrhosis in around 10% of the cases in 10 years

47
Q

Cirrhosis can progress to

A

HCC (hepatic carcinoma)

48
Q

Prevention of NASH

A

Slow, mild weight reduction and increasing physical activity

49
Q

Consequences of liver cirrhosis

A

Destruction of cells, fewer microvilli, fibrosis, capillarization

50
Q

Clinical consequences of cirrhosis: Portal hypertension

A
  • Esophageal varices, bleeding
  • Splenomegaly, hypersplenia
  • Spontanous bacterial peritonitis
  • Ascites
  • Hepatic encephalopathy
51
Q

Clinical consequences of cirrhosis: Loss of parenchyma

A
  • Ascites
  • Hepatic encephalopathy
  • Bleeding tendency
  • Hypalbuminemia
52
Q

Clinical consequences of cirrhosis: Other

A
  • Hepatorenal syndrome

- Hepatocellular carcinoma

53
Q

Why is bleeding from esophageal varices dangerous?

A

Because the pressure is high, it is difficult to access, the patient may have a bleeding tendency, the protein getting into the stomach may trigger the development of hepatic coma

54
Q

What is caput medusae?

A

Dilation of the periumbilical veins

55
Q

What are the two main factors playing a role in the development of ascites?

A

Decreased albumin synthesis and increased portal pressure

56
Q

Major factor in the development of hepatic encephalopathy

A

Insufficiency of the urea cycle in the liver

57
Q

Hepatorenal syndrome

A
  • Renal failure developing as a result of hepatic insufficiency with unknown cause
  • Kidneys sense severe hypovolemia, no parenchymal damage in the kidneys so they can be successfully transplanted

Pathophysiology (14 decks)

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