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
2
Q
What is the typical histopathology in alcoholic hepatitis?
A
- centrilobular ballooning
- steatosis
- neutrophilic inflammation
- cholestasis
- Mallory-Hyaline inclusions (eosinophilic intracytoplasmic aggregates)
3
Q
Management of acute alcoholic hepatitis:
A
- pabrinex
- diuretics for ascites/paracentesis
- glucocorticoids (Maddrey’s discriminant function)
- pentoxyphylline
4
Q
Diagnosis of cirrhosis:
A
- transient elastography
- thrombocytopenia most sensitive finding cirrhosis in chronic liver disease
5
Q
What does the Child Pugh classification for cirrhosis take into account?
A
- bilirubin
- albumin
- PTT
- encephalopathy
- ascites
6
Q
What does the MELD score for cirrhosis take into account?
A
- serum bilirubin
- INR
- serum creatinine
7
Q
Drugs causing hepatocellular damage:
A
- paracetamol
- sodium valproate, phenytoin
- MAOIs
- halothane
- anti-TB: isoniazid, rifampicin, pyrazinamide
- statins
- alcohol
- amiodarone
- methyldopa
- nitrofurantoin
8
Q
Drugs causing cholestatic damage:
A
- COCP
- Abx: flucloxacillin, co-amoxiclav, erythromycin
- anabolic steroids, testosterones
- phenothiazines: chlorpromazine, prochlorperazine
- sulphonylureas
- fibrates
- rare: nifedipine
9
Q
Drugs causing liver cirrhosis:
A
- methotrexate
- methyldopa
- amiodarone
10
Q
Most common organisms for pyrogenic liver abscess in adults and children:
A
- adults: e. coli
- children: staph aureus
11
Q
Management of pyrogenic liver abscess:
A
-drainage
-amoxicillin, ciprofloxacin and metronidazole
(ciprofloxacin and clindamycin)
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
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
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
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
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
25
Associations primary sclerosing cholangitis:
- UC
- Crohn's less common
- HIV
26
Investigations for primary sclerosing cholangitis:
- multiple biliary strictures - beaded appearance on ERCP/MRCP
- p-ANCA may be positive
- liver biopsy
27
Complications of primary sclerosing cholangitis:
- cholangiocarcinoma
| - increased risk of colorectal cancer
28
What is Wilson's disease?
- 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
Features of Wilson's disease:
- 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
How do you diagnose Wilson's disease?
- slit lamp
- decreased serum caeruloplasmin, total serum copper
- increased free copper and 24 hour urinary copper excretion
- raised LFTs
- biopsy - copper deposits
31
How do you treat Wilson's?
- pencillamine chelates copper
- trientine hydrochloride alternative
- tetrathiomolybdate
32
What is Budd-Chiari?
- hepatic vein thrombosis
- caused by: polycythaemia rubs vera, thrombophilia, pregnancy, COCP
- sudden sever abdo pain, ascites, tender hepatomegaly
- US with Doppler flow studies
33
Type I hepatorenal syndrome:
- rapidly progressive
- doubling of serum creatinine or halving clearance over period of less than 2 weeks
- very poor prognosis
34
Type II hepatorenal syndrome:
- slowly progressive
- poor prognosis
- may liver longer
35
Management of HRS:
- vasopressin analogues: terlipressin
- volume expansion 20% albumin
- TIPS
36
Spontaneous bacterial peritonitis: (incl diagnosis and management)
- 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
When would you give someone SBP prophylaxis?
- episode of SBP
- protein fluid <15g/L and Child Pugh 9 or HRS
- ciprofloxaxin or norfloxacin
