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Gastroenterology > Liver Disease > Flashcards

Liver Disease Flashcards

1
Q

What investigations would indicate alcoholic hepatitis?

A
  • raised gamma GT and ALP
  • AST:ALT >2
  • raised bilirubin
  • decreased albumin, urea, potassium, platelets
  • increased PTT
  • EEG showing slow waves - encephalopathy
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2
Q

What is the typical histopathology in alcoholic hepatitis?

A
  • centrilobular ballooning
  • steatosis
  • neutrophilic inflammation
  • cholestasis
  • Mallory-Hyaline inclusions (eosinophilic intracytoplasmic aggregates)
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3
Q

Management of acute alcoholic hepatitis:

A
  • pabrinex
  • diuretics for ascites/paracentesis
  • glucocorticoids (Maddrey’s discriminant function)
  • pentoxyphylline
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4
Q

Diagnosis of cirrhosis:

A
  • transient elastography

- thrombocytopenia most sensitive finding cirrhosis in chronic liver disease

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5
Q

What does the Child Pugh classification for cirrhosis take into account?

A
  • bilirubin
  • albumin
  • PTT
  • encephalopathy
  • ascites
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6
Q

What does the MELD score for cirrhosis take into account?

A
  • serum bilirubin
  • INR
  • serum creatinine
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7
Q

Drugs causing hepatocellular damage:

A
  • paracetamol
  • sodium valproate, phenytoin
  • MAOIs
  • halothane
  • anti-TB: isoniazid, rifampicin, pyrazinamide
  • statins
  • alcohol
  • amiodarone
  • methyldopa
  • nitrofurantoin
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8
Q

Drugs causing cholestatic damage:

A
  • COCP
  • Abx: flucloxacillin, co-amoxiclav, erythromycin
  • anabolic steroids, testosterones
  • phenothiazines: chlorpromazine, prochlorperazine
  • sulphonylureas
  • fibrates
  • rare: nifedipine
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9
Q

Drugs causing liver cirrhosis:

A
  • methotrexate
  • methyldopa
  • amiodarone
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10
Q

Most common organisms for pyrogenic liver abscess in adults and children:

A
  • adults: e. coli

- children: staph aureus

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11
Q

Management of pyrogenic liver abscess:

A

-drainage
-amoxicillin, ciprofloxacin and metronidazole
(ciprofloxacin and clindamycin)

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12
Q

Benign liver lesions:

A
  • haemangioma: most common, ring of fibrous tissue, hyperechoic
  • liver cell adenoma: 90% in female, COCP, sharply demarcated with no capsule, mixed echoity and heterogenous structure, hypodense on CT before contrast
  • mesenchymal hamartomas
  • polycystic liver disease: autosomal dominant
  • cystadenoma: rare, malignant potential, multiloculated, large anechoic fluid-filled area with irregular margins, surgical resection
  • liver abscess
  • amoebic abscess: treat with metronidazole
  • hyatid cysts: echinococcus infection
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13
Q

Gilbert’s syndrome:

A
  • autosomal recessive
  • defective bilirubin conjugation
  • UDP glucuronosyltransferase deficiency
  • unconjugated hyperbilirubinaemia, jaundice
  • investigation: increased bilirubin following prolonged fasting or IV nicotinic acid
  • no treatment
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14
Q

What is haemachromatosis caused by?

A
  • autosomal recessive
  • disorder of iron absorption and metabolism
  • mutations HFE gene on both chromosome 6 copies (C282Y and H63D)
  • hepcidin affected which inhibits ferroprotein
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15
Q

Features of haemachromatosis:

A
  • early: fatigue, erectile disfunction, arthralgia
  • bronze skin (reversible)
  • diabetes
  • liver disease
  • cardiac failure secondary to dilated cardiomyopathy (reversible)
  • hypogonadism
  • arthritis
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16
Q

Investigations for haemachromatosis and management:

A
  • test for C282Y and H63D mutations
  • liver biopsy: Perl’s stain
  • increased transferrin saturation, ferritin and iron
  • low total iron binding capacity
  • joint x-ray shows chondrocalcinosis
  • manage with venesection and desferrioxamine
17
Q

What causes hepatic encephalopathy?

A
  • excess absorption of ammonia and glutamine form bacterial breakdown of proteins in the gut
  • mostly with acute liver failure
  • TIPSS can precipitate
18
Q

Grading of hepatic encephalopathy:

A
  • grade I: irritability
  • grade II: confusion, inappropriate behaviour
  • grade III: incoherent, restless
  • grade IV: coma
19
Q

Precipitating factors of hepatic encephalopathy:

A
  • infection e.g. spontaneous bacterial peritonitis
  • GI bleed
  • post TIPS
  • constipation
  • drugs: sedatives, diuretics
  • hypokalaemia
  • renal failure
  • increased dietary protein
20
Q

How do you manage hepatic encephalopathy:

A
  • lactulose: promotes ammonia excretion and increased metabolism by gut bacteria
  • rifaxamin: modules gut flora to decrease ammonia production
21
Q

Causes of hepatomegaly:

A
  • cirrhosis
  • malignancy
  • RHF
  • viral hepatitis
  • glandular fever
  • Malaria
  • abscess
  • hyatid disease
  • haematological malignancies
  • haemachromatosis
  • primary biliary cirrhosis
  • sarcoidosis, amyloidosis
22
Q

Associations of primary biliary cholangitis:

A
  • Sjogren’s
  • RA
  • systemic sclerosis
  • thyroid
23
Q

Diagnosis of primary biliary cholangitis:

A
  • anti-mitochondiral antibodies
  • smooth muscle antibodies
  • increased serum IgM
24
Q

Treatment of primary biliary cholangitis:

A
  • pruritus: cholestyramine

- ursodeoxycholic acid first line

25
Q

Associations primary sclerosing cholangitis:

A
  • UC
  • Crohn’s less common
  • HIV
26
Q

Investigations for primary sclerosing cholangitis:

A
  • multiple biliary strictures - beaded appearance on ERCP/MRCP
  • p-ANCA may be positive
  • liver biopsy
27
Q

Complications of primary sclerosing cholangitis:

A
  • cholangiocarcinoma

- increased risk of colorectal cancer

28
Q

What is Wilson’s disease?

A
  • autosomal recessive
  • impaired copper excretion and excessive deposition in tissues
  • defect in ATP7B gene on chromosome 13
  • children present with liver disease, adults with neurological
29
Q

Features of Wilson’s disease:

A
  • liver injury
  • neuro: basal ganglia degeneration, asterisks, chorea, dementia, Parkinsonism
  • Kayser Fleischer rings: green iron ring in Descemet membrane
  • RTA: Fanconi
  • haemolysis
  • blue nails
30
Q

How do you diagnose Wilson’s disease?

A
  • slit lamp
  • decreased serum caeruloplasmin, total serum copper
  • increased free copper and 24 hour urinary copper excretion
  • raised LFTs
  • biopsy - copper deposits
31
Q

How do you treat Wilson’s?

A
  • pencillamine chelates copper
  • trientine hydrochloride alternative
  • tetrathiomolybdate
32
Q

What is Budd-Chiari?

A
  • hepatic vein thrombosis
  • caused by: polycythaemia rubs vera, thrombophilia, pregnancy, COCP
  • sudden sever abdo pain, ascites, tender hepatomegaly
  • US with Doppler flow studies
33
Q

Type I hepatorenal syndrome:

A
  • rapidly progressive
  • doubling of serum creatinine or halving clearance over period of less than 2 weeks
  • very poor prognosis
34
Q

Type II hepatorenal syndrome:

A
  • slowly progressive
  • poor prognosis
  • may liver longer
35
Q

Management of HRS:

A
  • vasopressin analogues: terlipressin
  • volume expansion 20% albumin
  • TIPS
36
Q

Spontaneous bacterial peritonitis: (incl diagnosis and management)

A
  • usually in patients with ascites secondary to liver cirrhosis
  • abdo pain, fever
  • paracentesis: neutrophil >250cells/uL, most commonly e.coli
  • manage with IV cefoxime
37
Q

When would you give someone SBP prophylaxis?

A
  • episode of SBP
  • protein fluid <15g/L and Child Pugh 9 or HRS
  • ciprofloxaxin or norfloxacin
38
Q

How does paracetamol overdose affects LFTs:

A
  • increased ALT
  • normal ALP
  • increased ALT/ALP

Gastroenterology (4 decks)

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