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4th year passmedicine by topic > Hepatic Disease > Flashcards

Hepatic Disease Flashcards

1
Q

The causes of ascites can be grouped into

A

serum-ascites albumin gradient (SAAG) <11 g/L

or a gradient >11g/L

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2
Q

SAAG > 11g/L indicates

A

portal hypertension

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3
Q

SAAG > 11g/L most common cause

A

Liver disorders
(cirrhosis/alcoholic liver disease
acute liver failure
liver metastases)

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4
Q

SAAG > 11g/L non liver causes?

A

right heart failure
constrictive pericarditis

Budd-Chiari syndrome
portal vein thrombosis
veno-occlusive disease
myxoedema

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5
Q

SAAG <11g/L causes?

A

Hypoalbuminaemia
Malignancy
Infections

other - pancreatitisis, bowel obstruction, biliary ascites, postoperative lymphatic leak, serositis in connective tissue diseases

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6
Q

Ascites mx

A

reducing dietary sodium - fluid restriction is sometimes recommended if the sodium is < 125 mmol/L

aldosterone antagonists: e.g. spironolactone

drainage if tense ascites (therapeutic abdominal paracentesis)

prophylactic antibiotics to reduce the risk of spontaneous bacterial peritonitis

transjugular intrahepatic portosystemic shunt (TIPS) may be considered in some patients

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7
Q

Budd-Chiari syndrom is

A

hepatic vein thrombosis, is usually seen in the context of underlying haematological disease or another procoagulant condition.

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8
Q

Budd-Chiari syndrome caues?

A

polycythaemia rubra vera
thrombophilia
pregnancy
combined oral contraceptive pill: accounts for around 20% of cases

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9
Q

Budd-Chiari syndrome thrombophilias?

A

activated protein C resistance, antithrombin III deficiency, protein C & S deficiencies

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10
Q

Budd-Chiari syndrome triad

A

abdominal pain: sudden onset, severe
ascites → abdominal distension
tender hepatomegaly

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11
Q

Budd-Chiari syndrome ix

A

ultrasound with Doppler flow studies is very sensitive and should be the initial radiological investigation

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12
Q

Carcinoid syndrome

usually occurs

A

metastases are present in the liver and release serotonin into the systemic circulation

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13
Q

Carcinoid syndrome sx

A

flushing (often earliest symptom)
diarrhoea
bronchospasm
hypotension

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14
Q

Carcinoid syndrome valve disease?

A

right heart valvular stenosis

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15
Q

Carcinoid syndrome endocrine disorders?

A

other molecules such as ACTH and GHRH may also be secreted resulting in, for example, Cushing’s syndrome

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16
Q

Carcinoid tumours ix

A

urinary 5-HIAA

plasma chromogranin A y

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17
Q

Carcinoid tumours mx

A

somatostatin analogues e.g. octreotide

diarrhoea: cyproheptadine may help

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18
Q

Drug-induced liver disease is generally divided into

A

hepatocellular, cholestatic or mixed

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19
Q

The following drugs tend to cause a hepatocellular picture:

A 
paracetamol
sodium valproate, phenytoin
MAOIs
halothane
anti-tuberculosis: isoniazid, rifampicin, pyrazinamide
statins
alcohol
amiodarone
methyldopa
nitrofurantoin
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20
Q

The following drugs tend to cause cholestasis (+/- hepatitis):

A

combined oral contraceptive pill
antibiotics: flucloxacillin, co-amoxiclav, erythromycin*
anabolic steroids, testosterones
phenothiazines: chlorpromazine, prochlorperazine
sulphonylureas
fibrates
rare reported causes: nifedipine

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21
Q

Drug-induced liver disease - Liver cirrhosis

A

methotrexate
methyldopa
amiodarone

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22
Q

Gilbert’s syndrome is

A

autosomal recessive* condition of defective bilirubin conjugation due to a deficiency of UDP glucuronosyltransferase.

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23
Q

Gilbert’s syndrome bloods

A

unconjugated hyperbilirubinaemia (i.e. not in urine)

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24
Q

Gilbert’s syndrome sx

A

jaundice may only be seen during an intercurrent illness, exercise or fasting

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25
Q

Gilbert’s syndrome ix

A

investigation: rise in bilirubin following prolonged fasting or IV nicotinic acid

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26
Q

Gilbert’s syndrome no treatment required

A

true

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27
Q

Haemochromatosis is

A

autosomal recessive disorder of iron absorption and metabolism resulting in iron accumulation. It is caused by inheritance of mutations in the HFE gene on both copies of chromosome 6

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28
Q

Haemochromatosis Epidemiology

A

1 in 10 people of European descent carry a mutation in the genes affecting iron metabolism, mainly HFE
prevalence in people of European descent = 1 in 200, making it more common than cystic fibrosis

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29
Q

Haemochromatosis early symptoms include

A

fatigue, erectile dysfunction and arthralgia (often of the hands)

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30
Q

Haemochromatosis gonadal sx

A

hypogonadism (2nd to cirrhosis and pituitary dysfunction - hypogonadotrophic hypogonadism)

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31
Q

Haemochromatosis liver sx

A

stigmata of chronic liver disease, hepatomegaly, cirrhosis, hepatocellular deposition)

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32
Q

Haemochromatosis can cause ‘bronze’ skin pigmentation

diabetes mellitus

A

true

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33
Q

Haemochromatosis - Reversible complications

A

Cardiomyopathy

Skin pigmentation

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34
Q

Haemochromatosis - Irreversible complications

A

Liver cirrhosis**
Diabetes mellitus
Hypogonadotrophic hypogonadism
Arthropathy

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35
Q

There is continued debate about the best investigation to screen for haemochromatosis.
general population:
testing family members:

A

general population: transferrin saturation

testing family members: genetic testing for HFE mutation

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36
Q

Haemochromatosis Diagnostic tests

A

molecular genetic testing for the C282Y and H63D mutations

liver biopsy: Perl’s stain

37
Q

Typical iron study profile in patient with haemochromatosis

A

transferrin saturation > 55% in men or > 50% in women
raised ferritin (e.g. > 500 ug/l) and iron
low TIBC

38
Q

Management haemochromatosis?

A

Venesection is the first-line treatment
monitoring adequacy of venesection: transferrin saturation should be kept below 50% and the serum ferritin concentration below 50 ug/l
desferrioxamine may be used second-line

39
Q

Haemochromatosis x rays?

A

Joint x-rays characteristically show chondrocalcinosis

40
Q

many patients with liver cirrhosis may develop subtle symptoms such as mild cognitive impairment before the features become more recognisable (‘minimal’ or ‘covert’ hepatic encephalopathy)

A

True

41
Q

transjugular intrahepatic portosystemic shunting (TIPSS) may precipitate encephalopathy

A

True

42
Q

Hepatic encephalopathy Features

A

confusion, altered GCS
asterix: ‘liver flap’
constructional apraxia

43
Q

Hepatic encephalopathy - EEG

A

triphasic slow waves on EEG

44
Q

Hepatic encephalopathy - raised/low ammonia level

A

raised ammonia level

45
Q

Grading of hepatic encephalopathy

A

Grade I: Irritability
Grade II: Confusion, inappropriate behaviour
Grade III: Incoherent, restless
Grade IV: Coma

46
Q

hepatic encephalopathy Precipitating factors

A 
infection e.g. spontaneous bacterial peritonitis
GI bleed
post transjugular intrahepatic portosystemic shunt
constipation
drugs: sedatives, diuretics
hypokalaemia
renal failure
increased dietary protein (uncommon)
47
Q

Hepatic encephalopathy mx

A

treat any underlying precipitating cause

lactulose first-line, with the addition of rifaximin

other options include embolisation of portosystemic shunts and liver transplantation in selected patients

48
Q

Hepatic encephalopathy lactulose is thought to work by

A

promoting the excretion of ammonia and increasing the metabolism of ammonia by gut bacteria

49
Q

Hepatic encephalopathy antibiotics such as rifaximin are thought to

A

modulate the gut flora resulting in decreased ammonia production

50
Q

Hepatocellular carcinoma (HCC) most common cause?

A

Chronic hepatitis B is the most common cause of HCC worldwide with chronic hepatitis C being the most common cause in Europe.

51
Q

The main risk factor for developing HCC is liver cirrhosis

A

true

52
Q

HCC tends to present early

A

false

presents late

53
Q

HCC presentation

A

features of liver cirrhosis or failure
decompensation in a patient with chronic liver disease
raised AFP

54
Q

Hepatocellular carcinoma

Screening with ultrasound (+/- alpha-fetoprotein) should be considered for high risk groups such as:

A

patients liver cirrhosis secondary to hepatitis B & C or haemochromatosis
men with liver cirrhosis secondary to alcohol

55
Q

Hepatocellular carcinoma mx

A 
early disease: surgical resection
liver transplantation
radiofrequency ablation
transarterial chemoembolisation
sorafenib: a multikinase inhibitor
56
Q

O/E How would the liver feel in Cirrhosis:

A

if early disease, later liver decreases in size. Associated with a non-tender, firm liver

57
Q

O/E How would the liver feel in Malignancy

A

metastatic spread or primary hepatoma. Associated with a hard, irregular. liver edge

58
Q

O/E How would the liver feel in Right heart failure

A

firm, smooth, tender liver edge. May be pulsatile

59
Q

hepatorenal syndrome pathophysiology

A

vasoactive mediators cause splanchnic vasodilation which in turn reduces the systemic vascular resistance

‘underfilling’ of the kidneys. This is sensed by the juxtaglomerular apparatus which then activates the renin-angiotensin-aldosterone system, causing renal vasoconstriction which is not enough to counterbalance the effects of the splanchnic vasodilation.

60
Q

hepatorenal syndrome has been categorized into two types

Type 1 HRS

A

Rapidly progressive

Doubling of serum creatinine to > 221 µmol/L or a halving of the creatinine clearance to less than 20 ml/min over a period of less than 2 weeks

Very poor prognosis

61
Q

hepatorenal syndrome has been categorized into two types

Type 2 HRS

A

Slowly progressive

Prognosis poor, but patients may live for longer

62
Q

Hepatorenal syndrome: management

A

vasopressin analogues

volume expansion with 20% albumin

transjugular intrahepatic portosystemic shunt

63
Q

There are 4 inherited causes of jaundice you need to be aware of:

A

Gilbert’s syndrome
Crigler-Najjar syndrome
Dubin-Johnson syndrome
Rotor’s syndrome

64
Q

Inherited causes of jaundice associated with Unconjugated hyperbilirubinaemia

A

Gilbert’s syndrome

Crigler-Najjar syndrome

65
Q

Inherited causes of jaundice associated with Conjugated hyperbilirubinaemia

A

Dubin-Johnson syndrome

Rotor syndrome

66
Q

Gilbert’s syndrome is always malignant

A

false

usually benign

67
Q

Gilbert’s syndrome genetics?

A

autosomal recessive

mild deficiency of UDP-glucuronyl transferase

68
Q

Crigler-Najjar syndrome, type 1 genetics?

A

autosomal recessive

absolute deficiency of UDP-glucuronosyl transferase

69
Q

Crigler-Najjar syndrome, type 1 usually survive to adulthood

A

false

do not survive to adulthood

70
Q

Crigler-Najjar syndrome, type 2 is more/less common than type 1

A

more common

71
Q

Crigler-Najjar syndrome, type 2 more/less severe than type 1

A

less severe

72
Q

Crigler-Najjar syndrome, type 2 may improve with?

A

phenobarbital

73
Q

Dubin-Johnson syndrome genetics?

A

autosomal recessive. Relatively common in Iranian Jews

mutation in the canalicular multidrug resistance protein 2 (MRP2) results in defective hepatic excretion of bilirubin

74
Q

Dubin-Johnson syndrome and rotor syndrome are benign

A

true

75
Q

Inherited causes of jaundice results in grossly block liver?

A

Dubin-Johnson syndrome

76
Q

Inherited causes of jaundice due to defect in the hepatic uptake and storage of bilirubin

A

Rotor syndrome

77
Q

Wilson’s disease is

A

an autosomal recessive disorder characterised by excessive copper deposition in the tissues

78
Q

Wilson’s disease is caused by a defect in which gene?

A

Wilson’s disease is caused by a defect in the ATP7B gene located on chromosome 13.

79
Q

Wilson’s disease onset of symptoms is usually

A

between 10 - 25 years

80
Q

Wilson’s disease:

Children usually present with:

young adults:

A

Children usually present with liver disease whereas the first sign of disease in young adults is often neurological disease

81
Q

WD

Features result from excessive copper deposition in the tissues, especially (which organs?)

A

brain, liver and cornea

82
Q

Wilson’s disease - liver sx

A

hepatitis, cirrhosis

83
Q

Wilson’s disease - neuro sx

A

basal ganglia degeneration

speech, behavioural and psychiatric problems are often the first manifestations

also: asterixis, chorea, dementia, parkinsonism

84
Q

Wilson’s disease - eye disease

A

Kayser-Fleischer rings

85
Q

Wilson’s disease can give you blue nails

A

true

86
Q

Wilson’s disease assoc w which syndrome

A

renal tubular acidosis (esp. Fanconi syndrome

87
Q

Wilson’s disease diagnosis?

A

slit lamp examination for Kayser-Fleischer rings

reduced serum caeruloplasmin

reduced total serum copper

increased 24hr urinary copper excretion

88
Q

Wilson’s disease mx

A

penicillamine (chelates copper) has been the traditional first-line treatment

trientine hydrochloride

89
Q

Ischaemic hepatitis causes marked increases in ?levels - exceeding 1000 international unit/L or 50 times the upper limit of normal

A

aminotransferase

4th year passmedicine by topic (96 decks)

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