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1b. GASTROINTESTINAL > Liver Disease > Flashcards

Liver Disease Flashcards

1
Q

Name the three zones of liver hepatocytes.

A

Periportal (outer), midacinar, pericentral (inner)

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2
Q

Why is the liver important?

A

Large functional reserve. No replacement

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3
Q

Describe how scar formation (fibrosis) occurs in hepatocytes.

A

Quiescent stellate cells activated by Kupffer cells (releasing PDGF, TNF, ET-1, TGF-B) into myofibroblasts, laying down collagen and destroying hepatocytes

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4
Q

Define acute liver failure.

A

80-90% functionality lost. No prior liver disease

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5
Q

Describe the cellular change seen in acute liver failure.

A

Massive hepatic necrosis

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6
Q

What are the two most common causes of liver failure?

A

Acute - acetaminophen/paracetamol

Chronic - alcohol

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7
Q

Describe the symptoms seen in acute liver failure.

A

Nausea, vomiting, jaundice, icterius

Encephalopathy and coagulopathy

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8
Q

Describe the cellular changes seen in cirrhosis.

A

Diffuse transformation into regenerative nodules, fibrous band formation, vascular shunts.

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9
Q

Which classification system is used for cirrhosis?

A

Child-Pugh (A-C)

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10
Q

Describe the main symptoms seen in chronic liver disease.

A

Anorexia, weight loss, weakness, pruritus, hyperoestrogenaemia

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11
Q

What is usually the cause of death in chronic liver disease?

A

Encephalopathy, variceal bleeds, and infection (if predisposed)

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12
Q

Describe the transmission, symptoms, and antibodies seen in hepatitis A.

A

Faecal-oral route, poor sanitation/hygiene, shellfish
Acute illness - fatigue, anorexia, jaundice
IgM initially, then anti-HAV IgG

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13
Q

Describe the causes and risks seen in hepatitis D.

A

Co-infection/Superinfection with HBV

IV Drug users and multiple blood transfusions

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14
Q

Broadly describe hepatitis E.

A

Zoonotic. Enteric and equatorial. Generally self limiting and acute. Chronic in immunosuppressed.

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15
Q

Describe the causes and overview of symptoms seen in different groups of patients suffering from HBV.

A

Blood, birthing, ‘bonking’
65% - asymptomatic, 25% constitutional, 10% chronic
Usually self-limiting

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16
Q

Describe the antigens seen in hepatitis B infection.

A

HBsAg, HBeAg, IgM, Total anti-HBc, anti-HBVs
First three appear in acute phase
Second two remain through life

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17
Q

What is the purpose of treatment in HBV?

A

Slow disease progression, prevent carcinoma

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18
Q

Describe the disease progression of hepatitis C.

A

75% are chronic (> 6 months). Infection to cirrhosis > 20 years, to HCC > 30 years

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19
Q

Why is there no vaccine for HCV?

A

Quasispecies cause genetic variablity and different genotypes 1-6.

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20
Q

Describe the four different types of progression in alcoholic liver disease.

A

Days - steatosis -> reversible
Weeks - hepatitis -> may be reversible
Months - fibrosis -> irreversible
Years - cirrhosis -> irreversible

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21
Q

Describe the LFTs and chemicals seen in alcoholic liver disease.

A

Acetylaldehyde (from alcohol metabolism) decreases glutathione, sensitising to injury.
P450 increases toxic metabolism
Increased bilirubin, alk phos
AST higher than ALT (unlike other disease)

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22
Q

Describe the two types of autoimmune hepatitis.

Name the two main triggers.

A

Type 1 - any age, commoner. ANA/SMA/anti-SLA/LP, AMA
Type 2 - mainly younger. Anti-LKM-1, ACL-1
Viruses and drugs/toxins

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23
Q

What are the two main treatments for autoimmune hepatitis?

A

Immunosuppression (80% survival), liver transplant

24
Q

Describe the gender spread and histology of PBC and PSC.

A

PBC - female. florid duct lesions, Mallory-Denk bodies, hepatomegaly
PSC - male with UC. Obliterate fibrosis, ‘beading’

25
Q

Which treatments are used for PBC and PSC?

A

PBC - ursodeoxycholic acid/transplant

PSC - cholestyramine, endoscopic dilatation/transplant

26
Q

Name the two types of reaction by drugs to the liver.

A

Predictable (i.e. paracetamol)

Unpredictable (based on host response)

27
Q

Name the main features of nonalcoholic fatty liver disease.

A

Steatosis with ethanol < 20g.
Metabolic syndrome: diabetes mellitus/insulin issues with hypertension, dyslipidaemia, central obesity, microalbuminuria.

28
Q

How should NAFLD be treated?

A

Reverse underlying cardiovascular issues, exercise and diet

29
Q

Describe haemochromatosis.

A

Iron buildup. Decreases liver size. Hepatomegaly, abdo pain, glucose issues, cardiac dysfunction, arthritis
Treated by regular venesection (phlebotomy)

30
Q

Describe Wilsons disease.

A

Impaired copper secretion.
Diagnosed by ceruloplasmin.
Causes atrophy/cavitation of the brain, Kaiser-Fleischer rings
Copper cholation or zinc based treatment

31
Q

Describe alpha1-antitrypsin deficiency.

A

Usually inhibits proteases. Causes emphysema and liver disease. Smoking cessation and liver transplant

32
Q

Name the two types of nodular hyperplasia.

A

Focal -> single demarcated nodule

Regenerative -> whole liver, looks like cirrhosis

33
Q

What is the main risk of benign adenomas? Name the three main types and the risk associated with them.

A

HNF1-a inactivated: almost no risk
B-caterin: very high
Inflammatory: medium
Almost all associated with oral contraceptive

34
Q

Describe hepatoblastomas.

A

Children under 3. Common in FAP. Resection and chemotherapy

35
Q

Describe the pathogenesis of hepatocellular carcinoma and the main risks.

A

Patients > 60 and after cirrhosis.
HBV, HCV, aflatoxin, alcohol
B-caterin activation/p53 inactivation

36
Q

Name the main causes of death associated with HCC.

A

Cachexia, coma, variceal or tumour rupture

37
Q

Name the main tumour of the biliary duct.

A

Cholangiocarcinoma

38
Q

Are primary or secondary tumours more common?

A

Secondary

39
Q

Describe the three main vessel components of the liver.

A

Hepatic artery (oxygen), portal vein (nutrients), portal vein drains to IVC

40
Q

Name the main investigations for acute liver disease.

A

HISTORY AND EXAM!!

LFTs, prothrombin time, US, virology, biopsy

41
Q

What are the main treatments for acute liver failure?

A

Rest, fluids (no alcohol) and nutrition.

Symptomatic relief from ursodeoxycholic acid with cholestyramine.

42
Q

What are the main treatments for Hep B?

A

Peginterferons -> antiviral treatment (if not tolerated, tenofovir, entecavir)

43
Q

Which factor most increases carcinoma risk from HBV?

A

Initial starting load

44
Q

What treatment is used for PBC?

A

Ursodeoxy, obeticholic acid

45
Q

What treatment is used for autoimmune hepatitis?

A

Corticosteroid (prednisone) and azathioprine

46
Q

What is Budd-Chiari syndrome? What are the causes? What is the treatment?

A

Thrombosis, by webs or protein C/S deficiency

Treated by recanulation or TIPS

47
Q

How is ascites treated?

A

Spironolactone, paracentesis or TIPS

48
Q

How is encephalopathy treated?

A

Lactulose/rifaxalin, transplant

49
Q

What is the prophylaxis of varices?

A

B-blockers, ligation

50
Q

Describe the pathogenesis of hepatorenal syndrome.

A

Accumulation of toxic metabolites, causing the renin-aldosterone cascade. K is lost, Na/H2O retained

51
Q

What are the treatment options for pain relief in liver disease? Which ones should be used?

A

Paracetamol, NSAIDs, opioids

Lowest dose paracetamol (<3g/day) with very low dose opioids if needed

52
Q

Which four main drugs may cause liver disease?

A

Co-amoxiclav, aminoglycosides, quinolones, metronidazole

53
Q

What are the alcohol guidelines in the UK for men and women?

A

14 or less units a week, ideally spread over 3 days

Not in pregnancy

54
Q

What serum markers are seen in alcoholic liver disease?

A

Hypoalbuminaemia, raised prothrombin time, AST>ALT

55
Q

Describe the FRAMES model of alcohol advice.

A

Feedback, Responsibility, Advice, Menu (of options), Empathy, Self-efficacy

1b. GASTROINTESTINAL (10 decks)

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