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P2 LIVER+ > Liver Injury > Flashcards

Liver Injury Flashcards

1
Q

What is alcoholic liver disease?

A

Build-up of fat in the liver leading to inflammation and eventually cirrhosis

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2
Q

How would you diagnose alcoholic liver disease? (3)

A

Raised AST: ALT > 2:1
Raised GGT
Biopsy: Mallory body + neutrophil infiltrate

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3
Q

How would you treat alcoholic liver disease? (3)

A

Quit alcohol
Treat malnutrition from alcohol: thiamine (vit B1)
Corticosteroids (suppress immune system)

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4
Q

What is non-alcoholic fatty liver disease (NAFLD)?

A

Fat deposits in the liver (not due to alcohol/ viral causes) leading to hepatocyte destruction.

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5
Q

How would you diagnose NAFLD? (2)

A

Raised ALT

Biopsy: Mallory-denk bodies

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6
Q

How would you treat NAFLD?

A

Lifestyle - lose weight, healthy diet, manage diabetes

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7
Q

An autoimmune hepatitis patient would typically present as? (3)

A

Female
Other autoimmune condition
Liver problems

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8
Q

How would you diagnose type 1 (most common) autoimmune hepatitis? (2)

A 
Antinuclear antibodies (ANAs)
Anti-smooth muscle antibodies (ASMA)
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9
Q

How would you diagnose type 2 autoimmune hepatitis? (2)

A

ALKM-1

ALC-1

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10
Q

How would you treat autoimmune hepatitis? (2)

A

Immunosuppressants: prednisolone, azathioprine

Liver transplant

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11
Q

What is alpha-1-antitrypsin (A1AT) deficiency?

A

Autosomal recessive disorder where alpha-1-antitrypsin doesn’t inhibit elastase so too much elastin is broken down

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12
Q

What does alpha-1-antitrypsin deficiency lead to? (2)

A

Emphysema

Cirrhosis

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13
Q

What is the clinical presentation of a pt w/ alpha-1-antitrypsin deficiency? (4)

A

Young person
Cirrhosis
Dyspnoea (difficulty breathing)
No history of smoking

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14
Q

How would you diagnose alpha-1-antitrypsin deficiency? (3)

A

Chest X-ray/ CT: hyperinflated lung/ damaged tissue
Bloods: A1AT levels
Liver biopsy: PAS stain +ve

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15
Q

How would you treat alpha-1-antitrypsin deficiency? (4)

A

IV infusion of normal A1AT protein
Inhalers
Supplemental oxygen
Standard treatments for cirrhosis (lactulose)

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16
Q

What id primary biliary cholangitis (PBC)?

A

Autoimmune destruction intrahepatic biliary ducts leading to cholestasis

17
Q

PBC is common in which pt? (2)

A

Females

Other autoimmune condition

18
Q

What are the clinical presentations of PBC? (6)

A

Pruritus (itch)
Jaundice
Xanthelasma (cholesterol deposits under skin)
Hyperpigmentation
Xerophthalmia (dry eyes = vit A def)
Corneal arcus (cholesterol deposits around cornea)

19
Q

How would you diagnose PBC? (2)

A 
Antimitochondrial antibodies (AMA)
Raised serum cholesterol
20
Q

How would you treat PBC? (4)

A

Ursodeoxycholic acid (UDCA)
Colestryamine for pruritus
KADE supplementation
Bisphosphonates for osteoporosis

21
Q

What is primary sclerosing cholangitis (PSC)? (2)

A

Inflammation, fibrosis and strictures of intra and extrahepatic parts of the biliary tree

Aka onion-skin fibrosis

22
Q

Why is PSC important?

A

Pre-malignant disease, can cause colorectal cancer

23
Q

What are the clinical presentations of PSC? (5)

A 
Pruritus (itch)
Jaundice
Dark urine
Clay coloured stool
Hepatosplenomegaly
24
Q

How would you diagnose PSC? (2)

A

Raised p-ANCAs (antinuclear cytoplasmic antibodies)

MRCP: biliary tracts are beaded or have strictures (‘pruned-tree’)

25
Q

How would you treat PSC? (3)

A

Colestryamine for pruritus
Ursodeoxycholic acid may improve LFT
Liver transplant

26
Q

What is hemochromatosis?

A

Excess iron everywhere

27
Q

What causes hemochromatosis? (2)

A

Autosomal recessive HFE gene disorder (causing excess iron absorption in SI)
Frequent blood transfusions

28
Q

What are the clinical presentations of hemochromatosis? (3 + 1)

A
  • Cirrhosis
  • Diabetes mellitus
  • Skin hyperpigmentation (always tanned look)

Bronze diabetes
Arthralgia from pseudogout

29
Q

How would you diagnose hemochromatosis? (2)

A
  • Blood: increased serum iron, ferritin, decreased transferrin
  • Decreased total iron-binding capacity
30
Q

How would you treat hemochromatosis? (3)

A
  • Bloodletting
  • Deferoxamine (iron chelator)
  • Reduce iron in diet
31
Q

What is Wilson disease?

A

Excess copper build-up in the liver and CNS

32
Q

What causes Wilson disease?

A

Autosomal recessive disorder (ATPB7 in chromosome 13)

33
Q

What are the clinical presentations of Wilson disease? (4)

A
  • Cirrhosis
  • Neurological Sx
  • Psychiatric Sx
  • Kayser-Fleischer ring (visible copper deposits in cornea)
34
Q

How would you diagnose Wilson disease? (3)

A
  • Bloods: raised serum copper; low serum ceruloplasmin
  • Urine: copper
  • Hepatosplenomegaly
35
Q

How would you treat Wilson disease? (2)

A
  • Penicillamine (copper chelator)

- Reduce copper diet (shellfish)

P2 LIVER+ (6 decks)

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