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Hepatic Disease Flashcards

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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
Gilbert's syndrome ix
investigation: rise in bilirubin following prolonged fasting or IV nicotinic acid
26
Gilbert's syndrome no treatment required
true
27
Haemochromatosis is
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
28
Haemochromatosis Epidemiology
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
29
Haemochromatosis early symptoms include
fatigue, erectile dysfunction and arthralgia (often of the hands)
30
Haemochromatosis gonadal sx
hypogonadism (2nd to cirrhosis and pituitary dysfunction - hypogonadotrophic hypogonadism)
31
Haemochromatosis liver sx
stigmata of chronic liver disease, hepatomegaly, cirrhosis, hepatocellular deposition)
32
Haemochromatosis can cause 'bronze' skin pigmentation | diabetes mellitus
true
33
Haemochromatosis - Reversible complications
Cardiomyopathy | Skin pigmentation
34
Haemochromatosis - Irreversible complications
Liver cirrhosis** Diabetes mellitus Hypogonadotrophic hypogonadism Arthropathy
35
There is continued debate about the best investigation to screen for haemochromatosis. general population: testing family members:
general population: transferrin saturation testing family members: genetic testing for HFE mutation
36
Haemochromatosis Diagnostic tests
molecular genetic testing for the C282Y and H63D mutations | liver biopsy: Perl's stain
37
Typical iron study profile in patient with haemochromatosis
transferrin saturation > 55% in men or > 50% in women raised ferritin (e.g. > 500 ug/l) and iron low TIBC
38
Management haemochromatosis?
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
Haemochromatosis x rays?
Joint x-rays characteristically show chondrocalcinosis
40
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)
True
41
transjugular intrahepatic portosystemic shunting (TIPSS) may precipitate encephalopathy
True
42
Hepatic encephalopathy Features
confusion, altered GCS asterix: 'liver flap' constructional apraxia
43
Hepatic encephalopathy - EEG
triphasic slow waves on EEG
44
Hepatic encephalopathy - raised/low ammonia level
raised ammonia level
45
Grading of hepatic encephalopathy
Grade I: Irritability Grade II: Confusion, inappropriate behaviour Grade III: Incoherent, restless Grade IV: Coma
46
hepatic encephalopathy Precipitating factors
``` 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
Hepatic encephalopathy mx
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
Hepatic encephalopathy lactulose is thought to work by
promoting the excretion of ammonia and increasing the metabolism of ammonia by gut bacteria
49
Hepatic encephalopathy antibiotics such as rifaximin are thought to
modulate the gut flora resulting in decreased ammonia production
50
Hepatocellular carcinoma (HCC) most common cause?
Chronic hepatitis B is the most common cause of HCC worldwide with chronic hepatitis C being the most common cause in Europe.
51
The main risk factor for developing HCC is liver cirrhosis
true
52
HCC tends to present early
false | presents late
53
HCC presentation
features of liver cirrhosis or failure decompensation in a patient with chronic liver disease raised AFP
54
Hepatocellular carcinoma | Screening with ultrasound (+/- alpha-fetoprotein) should be considered for high risk groups such as:
patients liver cirrhosis secondary to hepatitis B & C or haemochromatosis men with liver cirrhosis secondary to alcohol
55
Hepatocellular carcinoma mx
``` early disease: surgical resection liver transplantation radiofrequency ablation transarterial chemoembolisation sorafenib: a multikinase inhibitor ```
56
O/E How would the liver feel in Cirrhosis:
if early disease, later liver decreases in size. Associated with a non-tender, firm liver
57
O/E How would the liver feel in Malignancy
metastatic spread or primary hepatoma. Associated with a hard, irregular. liver edge
58
O/E How would the liver feel in Right heart failure
firm, smooth, tender liver edge. May be pulsatile
59
hepatorenal syndrome pathophysiology
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
hepatorenal syndrome has been categorized into two types | Type 1 HRS
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
hepatorenal syndrome has been categorized into two types | Type 2 HRS
Slowly progressive | Prognosis poor, but patients may live for longer
62
Hepatorenal syndrome: management
vasopressin analogues volume expansion with 20% albumin transjugular intrahepatic portosystemic shunt
63
There are 4 inherited causes of jaundice you need to be aware of:
Gilbert's syndrome Crigler-Najjar syndrome Dubin-Johnson syndrome Rotor's syndrome
64
Inherited causes of jaundice associated with Unconjugated hyperbilirubinaemia
Gilbert's syndrome | Crigler-Najjar syndrome
65
Inherited causes of jaundice associated with Conjugated hyperbilirubinaemia
Dubin-Johnson syndrome | Rotor syndrome
66
Gilbert's syndrome is always malignant
false | usually benign
67
Gilbert's syndrome genetics?
autosomal recessive | mild deficiency of UDP-glucuronyl transferase
68
Crigler-Najjar syndrome, type 1 genetics?
autosomal recessive | absolute deficiency of UDP-glucuronosyl transferase
69
Crigler-Najjar syndrome, type 1 usually survive to adulthood
false | do not survive to adulthood
70
Crigler-Najjar syndrome, type 2 is more/less common than type 1
more common
71
Crigler-Najjar syndrome, type 2 more/less severe than type 1
less severe
72
Crigler-Najjar syndrome, type 2 may improve with?
phenobarbital
73
Dubin-Johnson syndrome genetics?
autosomal recessive. Relatively common in Iranian Jews | mutation in the canalicular multidrug resistance protein 2 (MRP2) results in defective hepatic excretion of bilirubin
74
Dubin-Johnson syndrome and rotor syndrome are benign
true
75
Inherited causes of jaundice results in grossly block liver?
Dubin-Johnson syndrome
76
Inherited causes of jaundice due to defect in the hepatic uptake and storage of bilirubin
Rotor syndrome
77
Wilson's disease is
an autosomal recessive disorder characterised by excessive copper deposition in the tissues
78
Wilson's disease is caused by a defect in which gene?
Wilson's disease is caused by a defect in the ATP7B gene located on chromosome 13.
79
Wilson's disease onset of symptoms is usually
between 10 - 25 years
80
Wilson's disease: Children usually present with: young adults:
Children usually present with liver disease whereas the first sign of disease in young adults is often neurological disease
81
WD | Features result from excessive copper deposition in the tissues, especially (which organs?)
brain, liver and cornea
82
Wilson's disease - liver sx
hepatitis, cirrhosis
83
Wilson's disease - neuro sx
basal ganglia degeneration speech, behavioural and psychiatric problems are often the first manifestations also: asterixis, chorea, dementia, parkinsonism
84
Wilson's disease - eye disease
Kayser-Fleischer rings
85
Wilson's disease can give you blue nails
true
86
Wilson's disease assoc w which syndrome
renal tubular acidosis (esp. Fanconi syndrome
87
Wilson's disease diagnosis?
slit lamp examination for Kayser-Fleischer rings reduced serum caeruloplasmin reduced total serum copper increased 24hr urinary copper excretion
88
Wilson's disease mx
penicillamine (chelates copper) has been the traditional first-line treatment trientine hydrochloride
89
Ischaemic hepatitis causes marked increases in ?levels - exceeding 1000 international unit/L or 50 times the upper limit of normal
aminotransferase

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