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Abdominal > Liver > Flashcards

Liver Flashcards

0
Q

Hypoalbuminaemia found in

A

Liver dysfunction
Hyper catabolic states - sepsis, chronic inflammation
Increased loss due to nephrotic syndrome

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1
Q

Determine liver synthetic function by measuring…

A

Prothrombin time - clotting factors are synthesised in liver, increases if impaired function
Serum albumin decreases if impaired function

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2
Q

Prolonged prothrombin time can be due to

A

Liver dysfunction

Vit K deficiency in biliary obstruction (iv v.K improves clotting)

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3
Q

Gilbert’s disease

A

Increased bilirubin, other biochemistry normal

Due to inherited defect in bilirubin metabolism

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4
Q

Isolated rise in serum bilirubin - causes

A

Gilbert’s disease
Haemolysis
Ineffective erythropoiesis (premature RBC death in bone marrow)

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5
Q

Very high bilirubin levels most common in…

A

Biliary tract obstruction

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6
Q

Aminotransferases are…

A

Enzymes in hepatocytes, leak if damage

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7
Q

High levels aminotransferases in

A

Acute hepatitis - 20-50 times normal

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8
Q

Aspartate aminotransferases (AST)

A

Found in liver, heart, skeletal muscle

Raised serum conc on hepatitis, myocardial infarct, skeletal muscle damage

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9
Q

Alanine aminotransferases (ALT’s)

A

More specific to liver damage than ASTs

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10
Q

Alkaline phosphatase is situated in

A

Canalicular and sinusoid all membranes of liver

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11
Q

Alkaline phosphatase is increased in

A

Cholestasis - impaired bile flow from any cause
Pregnancy - as produced in placenta
Produced in bone, so growing children, bony metastases, Paget’s disease

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12
Q

Gamma - GT is a..

A

Liver microsomal enzyme induced by alcohol and enzyme inducing drugs

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13
Q

Gamma-GT raised in

A

Alcohol abuse
Enzyme inducing drugs eg phenytoin
In cholestasis rises in line with serum alkaline phosphatase (similar pattern of excretion)

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14
Q

Predominant elevation of serum aminotransferases indicates…

A

Hepatocellular injury

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15
Q

Predominant elevation of serum bilirubin and alkaline phosphatase indicates…

A

Cholestatic disorder

Eg primary biliary cirrhosis, primary sclerosing cholangitis, extra hepatic bile duct obstruction

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16
Q

Isolated rise in bilirubin most likely due to…

A

Gilbert’s disease

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17
Q

Use of ultrasound in hepatobiliary disease

A

Usually first imaging investigation

Useful tests for lesions in gall bladder, bile duct

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18
Q

Endoscopic US (ultrasound probe at scope tip) used for…

A

Detect and stage pancreatic carcinomas
Assess bile ducts
Confirm malignancy

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19
Q

MRI use…

A

Investigate focal liver disease

Allergies to iodine based contrast, so no contrast CT

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20
Q

MRCP

A

Magnetic Resonance Cholangiopancreatography
High quality images pancreatic and bile ducts
Similar to ERCP - replacing its diagnostic, not therapeutic use

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21
Q

ERCP

A

Endoscope to second part duodenum, image pancreatic and bile ducts with radio graphic contrast via ampulla of vater

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22
Q

Percutaneous transhepatic Cholangiopancreatography (PCT)

A

Inject contrast into biliary system via intrahepatic duct
Performed if biliary dilatation if ERCP failed
If obstruction, bypass stent can be inserted

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23
Q

Acute liver disease presentation

A

May be asymptomatic
Early stages - lethargy, anorexia, malaise
Later - Jaundice

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24
Q

Chronic liver disease complications

A

Ascites
Oesophageal varices - haematemesis, melaena
Hepatic encephalopathy - confusion, drowsiness

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25
Q

Pruritus (itching) found in

A

Cholestatic jaundice - any cause

Especially - primary biliary cirrhosis

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26
Q

Signs in compensated chronic liver disease

A 
Xanthelasma
Spider naevi
Gyanaecomastia
Small/large liver
Splenomegaly
Testicular atrophy
Hands - clubbing, dupuytrens contracture
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27
Q

Decompensated liver disease signs

A 
Neurological - disorientation, drowsy, coma
Hepatic flap
Ascites
Dilated veins on abdomen (caput medusa)
Oedema
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28
Q

General liver signs

A

Jaundice
Fever
Loss of body hair

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29
Q

Bilirubin is derived predominantly from…

A 
Haemoglobin breakdown in spleen
Carried in blood bound to albumin
Conjugated in liver
Excreted in bile to small intestine
Terminal ileum - converted to urobilinogen and excreted, or re absorbed, excreted by kidneys
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30
Q

3 clinical categories of jaundice

A 
Haemolytic jaundice
Congenital hylerbilirubinaemia (impaired conjugation)
Cholestatic jaundice (failure of bile excretion - abnormal LFTs)
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31
Q

Haemolytic jaundice

A

Increased breakdown RBCs, increased bilirubin
Mild
Causes = haemolytic anaemias

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32
Q

Congenital hylerbilirubinaemia

A

Most common Gilbert’s syndrome, 5% population
Asymptomatic, often incidental finding
Reduced conjugation
Other LFTs normal

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33
Q

Two types Cholestatic jaundice

A

Intrahepatic cholestasis - hepatocellular swelling / abnormalities at a cellular level of bile excretion
Extrahepatic cholestasis - obstruction of bile flow distal to bile canaliculi
Both - conjugated bilirubin so pale stools, dark urine

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34
Q

Causes intrahepatic cholestatic jaundice

A

Viral / alcoholic hepatitis
Drugs
Cirrhosis
Pregnancy

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35
Q

Causes extrahepatic jaundice

A 
Common duct stones
Carcinoma - bile duct, head of pancreas, ampulla of vater
Biliary stricture
Sclerosing cholangitis
Pancreatitis
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36
Q

Investigating jaundice - three things plus some

A

Serum liver biochemistry - confirm jaundice
US examination
Serum viral markers
Also - prothrombin time, serum autoantibodies

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37
Q

Serum biochemistry in jaundice

A

Confirms jaundice, larger rise AST - hepatitis, larger rise alkaline phosphatase - extra hepatic obstruction

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38
Q

Hepatitis serum viral markers

A

Hepatitis A and B - serum viral markers present in acute viral hepatitis
Hepatitis C - antibodies develop late, RNA detectable by 2 weeks

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39
Q

US examination shows dilated bile ducts in…

A

Extra hepatic cholestasis

May identify level of cause eg gall stones, tumours

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40
Q

Acute hepatitis causes

A

Mostly viral

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41
Q

Acute hepatitis progression

A

Usually self limiting

Occasional progression to massive cell necrosis

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42
Q

Acute hepatitis - clinical features

A

May be jaundiced
Enlarged, tender liver
Lab evidence of raised aminotransferases

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43
Q

Acute hepatitis assess disease severity by…

A

Prothrombin time

Serum bilirubin

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44
Q

Chronic hepatitis is…

A

Sustained inflammation of liver >6 months

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45
Q

Most common cause chronic liver disease world wide is…

A

Viral hepatitis

Causing chronic liver disease, cirrhosis, hepatocellular carcinoma

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46
Q

Hepatitis A epidemiology

A 
Most common
Particularly children and young adults
Faeco-oral transmission route
Ingestion contaminated food - shellfish
Most infectious just before onset jaundice
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47
Q

Clinical features hepatitis A

A

Average incubation period 28 days
Nonspecific nausea, anorexia, distaste for cigarette
Then some jaundiced, dark urine, pale stools, prodrome improves
Moderate hepatomegally, spleen palpable 10%
Self limiting 3-6 weeks
Rare - coma and death

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48
Q

Drug causes chronic hepatitis

A

Methyl dopa
Nitrofurantoin
Isoniazid
Ketoconazole

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49
Q

Investigation findings Hep A

A

Raised ALT, then raised bilirubin
Bloods - leucopenia, lymphocytosis, high ESR
Severe cases - prothrombin time prolonged

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50
Q

Antibodies in HAV

A

Acute HAV - IgM anti-HAV

Past infection - IgG anti-HAV

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51
Q

HAV prophylaxis

A

Active immunisation with inactivated strain given to travellers, people with chronic liver disease, occupational risk, haemophilia patients treated with clotting factors

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52
Q

HAV passive immunisation

A

With immunoglobulin

Given to close contacts of confirmed HAV cases

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53
Q

HBV epidemiology

A

Vertical transmission most common

Also blood, blood products, sexual intercourse

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54
Q

Acute HBV infection immune response

A

Penetrates hepatocyte, strong cellular immune response
Clearance of infection in 99% infected adults
Anti HBs antibodies develop
Immunity to subsequent infection

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55
Q

Fulminant liver failure

A

Occasional effect of HAV / HBV infection
Hepatic failure with encephalopathy in less than 2 weeks
Due to massive cell necrosis
Presents - hepatic encephalopathy, jaundice, coagulopathy
Complications - hypotension, renal failure, cerebral oedema, hypoglycaemia

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56
Q

HBsAg

A

Appears in blood from about 6 weeks to 3 months after an acute infection, then disappears
If chronic hepatitis, persists and indicates chronic infection / carrier state

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57
Q

HBeAg

A

Rises early, declines rapidly in acute disease
Chronic - persists, correlates with increases severity / infective ty
Anti HBe correlates with decreased HBeAg

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58
Q

Anti HBc

A

First antibody to appear, high titres suggest acute ongoing infection

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59
Q

HBV DNA

A

Suggests continued viral replication

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60
Q

Chronic HBV progression

A

Persistence of HBsAg for >6 months after acute infection = chronic
Progression depends on virulence, age, immunocompetence

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61
Q

Acquisition of HBV at / near birth

A

Immune tolerant phase 20-30 years, high levels replication
Normal ALT, positive HBeAg
Then immune clearance phase active hepatitis, high ALT
Ends with clearance of HBeAg, development anti-HBe

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62
Q

HBV treatment given to…

A

Patients most likely to develop progressive liver disease - high HBV DNA,

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63
Q

HBV / HIV co-infection

A

10-20%

Test all chronic HBV for HIV

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64
Q

Hepatitis C epidemiology

A

UK - iv drug use

Worldwide - blood products, poorly sterilised instruments

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65
Q

Clinical features HCV

A

Acute often mild, jaundice rare, most progress to chronic liver disease
Present with elevated aminotransferases or signs/symptoms CLD

66
Q

Px with cirrhosis secondary to HCV are at increased risk of…

A

Hepatocellular carcinoma

67
Q

Diagnosis of HCV

A

HCV antibody in serum
8 weeks to appear after acute infection
Positive HCV RNA suggests active disease

68
Q

HCV treatment

A

Aims for viral clearance
Depends on genotype (2&3 more responsive so even treat mild)
1&4 less responsive so treat moderate/ severe
IFN-Alfa and ribavirin

69
Q

Autoimmune hepatitis what, who

A

Progressive liver disease
Often associated with autoimmune eg pernicious anaemia, thyroiditis
Most common in young-middle aged women

70
Q

Autoimmune hepatitis aetiology

A

Unknown
Disease characterised by hypergammaglobulinaemia
High IgG, circulating autoantibodies

71
Q

Clinical features autoimmune hepatitis

A

Insidious onset, anorexia, malaise, nausea, fatigue

25% present acute hepatitis - rapid progressive liver disease

72
Q

Treatment autoimmune hepatitis

A

Prednisolone 2-3 weeks

Maintenance dose may be required, and azathiopene as steroid sparing agent

73
Q

Autoimmune hepatitis prognosis

A

Steroid and azathiopene induce remission in over 80% cases

Liver transplant may be necessary

74
Q

Non-alcoholic fatty liver disease

A

Liver biopsy finds changes indistinguishable from alcohol excess
But no heavy drinking

75
Q

Non alcoholic fatty liver disease is associated with..

A

Obesity, T2DM, hypertension, hyperlipidaemia

Considered the liver component of ‘metabolic syndrome’

76
Q

NAFLD pathogenesis

A

Not entirely known
Thought that insulin resistance is key, then ‘second hit’ oxidative injury, progresses to inflammatory component - steatohepatitis (NASH)

77
Q

Clinical features non-alcoholic fatty liver disease

A

Most asymptomatic
Mild elevation aminotransferases picked up
Hepatomegaly common

78
Q

Management non alcoholic fatty liver disease

A

No proven effective therapy
Treat risk factors
Transplant may be needed for end stage disease

79
Q

Cirrhosis

A

Results from necrosis of liver cells
Then fibrosis, nodule formation
Therefore impairment of liver cell function, gross distortion anatomy, portal hypertension

80
Q

Aetiology cirrhosis

A

Alcohol, viral hepatitis

81
Q

Histologically two types cirrhosis

A

Micronodular - small, uniform, ongoing alcohol/ biliary tract disease
Macronodular - variable size, normal acini in larger nodules, chronic viral hepatitis
Some is mixed.

82
Q

Clinical features hepatitis

A

Secondary to portal hypertension / liver cell failure

83
Q

Decompensated cirrhosis has…

A

Encephalopathy, ascites, varicella haemorrhage

84
Q

Compensated cirrhosis has NO

A

Ascites, encephalopathy, varicella haemorrhage

85
Q

Liver biochemistry in cirrhosis

A

May be normal

Often some increase serum alkaline phosphatase and aminotransferases

86
Q

FBC in cirrhosis

A

Thrombocytopenia at most diagnoses

Leukopenia, anaemia develop later

87
Q

Measure liver function in cirrhosis with

A

Prothrombin time and serum albumin

88
Q

Serum electrolytes in cirrhosis

A

Low sodium - severe liver disease secondary to impaired free water clearance / excess diuretic therapy
Elevated serum creatinine associated with worse prognosis

89
Q

Serum alpha-fetoprotein (AFT) in cirrhosis

A

Usually undetectable post partum
May be raised in chronic liver disease
High level suggests hepatocellular carcinoma

90
Q

Aetiology of cirrhosis

A

Response to any chronic liver injury

Liver biopsy to confirm severity, type

91
Q

Further investigations in cirrhosis

A

Seek and treat oesophageal varices - endoscopy

US for HCC and assess patency portal and hepatic veins

92
Q

Cirrhosis management

A 
Manage complications
Underlying problems - halt progress
Screen for HCC
End stage consider transplant
Flu vaccine
93
Q

Portal vein formed from union of

A 
Superior mesenteric (gut)
Splenic vein (spleen)
94
Q

Portal vein carries blood to

A

Liver

Accounts for 75% hepatic vascular inflow

95
Q

Blood vessel passage in liver

A

enter liver via hilum (porta hepatis)
Passes into hepatic sinusoids via portal tracts
Leaves liver through hepatic veins to join IVC

96
Q

Normal portal pressure

A

5-8mmHg

97
Q

Three types blockage hepatic blood flow

A

Prehepatic - due to blockage portal vein before liver
Intrahepatic - from distortion of liver architecture
Post hepatic - venous blockage outside liver - rare

98
Q

Most common cause portal hypertension

A

Cirrhosis

99
Q

1cause prehepatic portal hypertension

A

Portal vein thrombosis

100
Q

3 causes intrahepatic portal hypertension

A

Cirrhosis
Alcoholic hepatitis
Schistosomiasis

101
Q

Two causes post hepatic portal hypertension

A

Right heart failure

Constrictive pericarditis

102
Q

Common signs portal hypertension

A

Splenomegaly
GI bleeding
Ascites
Hepatic encephalopathy

103
Q

Management bleeding oesophageal varices

A

Endoscopic therapy - eg band ligation
Pharmacological - emergency control bleeding
Balloon tamponade if endoscopy fails - inflate gastric balloon, pull back to block blood G-O junction !aspiration pneumonia, oesophageal rupture!

104
Q

Ascites is

A

Presence of fluid in peritoneal cavity

105
Q

Commonest cause ascites is

A

Cirrhosis

106
Q

Pleural effusion in ascites

A

Usually right sided

107
Q

Causes ascites - transudate

A

Portal hypertension
Hepatic outflow obstruction
Cardiac failure

108
Q

Causes ascites - exudate

A

Peritoneal carcinomatosis
Peritoneal TB
Pancreatitis
Nephrotic syndrome

109
Q

Cirrhotic ascites and high neutrophil count (>250)

A

Bacterial peritonitis

110
Q

Management ascites - cirrhotic

A

Dietary sodium restriction, plus spironolactone
Frusemide added if poor response
Maybe paracentesis, plus albumin infusion

111
Q

Aim of ascites treatment

A

Lose 0.5kg weight/day

Too rapid diuresis - intravascular depletion, encephalopathy

112
Q

Rising creatinine / hyponatraemia in management ascites…

A

Inadequate renal perfusion

So temporary cessation diuretic therapy

113
Q

Spontaneous bacterial peritonitis in cirrhotic ascites patients

A

Occurs in 8%
Mortality rate 10-15%
Mostly E-Coli
Perform diagnostic aspiration and empiric antibiotics

114
Q

Portosystemic (hepatic) encephalopathy

A

Occurs in advanced chronic/acute hepatocellular disease
Also following TIPS shunts
Failure of toxin breakdown

115
Q

Clinical features hepatic encephalopathy

A

Drowsy, comatose
Increased tone, hyperreflexia
Chronically - irritable, slurred speech, reversed sleep

116
Q

Signs hepatic encephalopathy

A

Fetor hepaticus - sweet smelling breath
Asterixis
Constructional apraxia

117
Q

Hepatic encephalopathy investigations

A

EEG

Arterial blood ammonia

118
Q

Factors precipitating hepatic encephalopathy

A

High dietary protein
GI haemorrhage
Constipation
Infection…

119
Q

Management hepatic encephalopathy

A

Laxatives - lactulose, limits ammonia absorption
Antibiotics decrease bowel flora therefore ammonia production
Initially restrict protein

120
Q

Hepatorenal syndrome

A

Development AKI if advanced liver disease
Due to peripheral vasodilatiation, hypovolaemia
Decreased renal perfusion
Diagnosis - oliguria, rising serum creatinine, low urine sodium

121
Q

Hepatopulmonary syndrome

A

Inteapulmonary vascular dilatation in chronic liver disease, hypoxaemia, can be breathless on standing
Diagnose by echo, improve with liver transplant

122
Q

Liver transplantation

A 
Liver failure, any cause
Psychological assessment
Education
Few over 65 years
6 month abstinence if alcohol related
123
Q

Primary biliary cirrhosis

A

Type of chronic liver disease
Destruction of bile ducts, cholestasis, cirrhosis
Predominantly women middle age
Abnormal immuneregulation inherited anti-mitochondrial antibodies often present

124
Q

Primary biliary cirrhosis features

A 
Pruritus, sometimes jaundice
Advanced - hepatosplenomegaly, xanthelasma
Raised serum alkaline phosphatase
Autoantibodies
Steatorrhoea
125
Q

Primary billiard cirrhosis investigations

A

Raised alkaline phosphatase, IgM
Often anti mitochondrial antibodies, antinuclear factor
Liver biopsy - loss of bile ducts, later cirrhosis (staging)

126
Q

Primary biliary cirrhosis prognosis

A

Asymptomatic - near normal

Jaundiced - poor, death in 5 years without transplant

127
Q

Secondary biliary cirrhosis

A

Cirrhosis due to prolonged large duct biliary obstruction

Eg bile duct strictures, CBD stones, sclerosing cholangitis

128
Q

Hereditary haemochromatosis

A

Autosomal recessive, 1in400 prevalence (Caucasian)
Approx 10% population carriers
Excess iron deposition - fibrosis - organ failure

129
Q

Aetiology haemochromatosis

A

Increased iron absorption from small intestine
HFE gene mutation
Few cases due to defects in metabolism

130
Q

Clinical features haemochromatosis

A

Often incidental finding increased iron / ferritin or screening
Less overt disease in women do to iron loss
Symptoms due to iron deposition

131
Q

Symptoms of iron deposition in organs

A 
Liver - hepatomegally, lethargy
Pancreas - diabetes
Myocardium - cardiomegally, heart failure, conduction disturbances
Pituitary - loss of libido, impotence
Joints - arthralgia
Skin - hyperpigmentation
132
Q

Investigations hereditary haemochromatosis

A

Serum liver biochemistry often normal
Serum iron increased, iron binding capacity reduced
Serum ferritin elevated
Genotyping - mutation HFE gene
Non invasive assessment fibrosis/cirrhosis

133
Q

Management haemochromatosis

A

Venesection - 500ml blood removed twice weekly till normal
Then three or four venue sections / year maintenance
If cirrhosis, surveillance for HCC required
Screen relatives HFE mutations

134
Q

Prognosis haemochromatosis

A

Major complication development HCC if cirrhosis

Life expectation fairly normal

135
Q

Wilson’s disease (hepatolenticular degeneration)

A

Rare, recessive inheritance, mutations ATP7B gene
Decreased secretion of copper into biliary system
Copper accumulates in liver - fulminant hepatic failure, cirrhosis
Basal ganglia - Parkinsonism, dementia
Cornea - Keyser-Fleischer rings
Renal tubules

136
Q

Diagnosis Wilson’s disease

A

Demonstrate low serum copper and caeruloplasmin
Increased urinary copper excretion
Increased copper in liver specimen

137
Q

Alpha-1 anti trypsin deficiency

A

Rare cause of cirrhosis
Abnormal protein accumulates in liver
Treat for chronic lung and liver disease - stop smoking!

138
Q

Alcohol and liver…

A

Most common cause liver disease western world
Alcohol is hepatotoxic
Only 15% excessive drinkers develop cirrhosis
3 major findings - fatty change, alcoholic hepatitis, alcoholic cirrhosis

139
Q

Three major clinical illnesses associated with excessive alcohol intake

A

Fatty change
Alcoholic hepatitis
Alcoholic cirrhosis

140
Q

Fatty liver change

A

Most common biopsy finding in alcoholics
Can be caused by just a few weeks - macro vascular lipid in hepatocytes
Symptoms often absent, may be hepatomegally
Often normal lab tests
Increased MCV may suggest heavy drinking
Gamma GT usually elevated
REVERSIBLE

141
Q

Alcoholic hepatitis

A

Years of heavy drinking
May coexist with cirrhosis
Swollen hepatocytes contain Mallory bodies, surrounded by neutrophils.
May be fibrosis, degeneration of hepatocytes

142
Q

Alcoholic hepatitis clinical features

A

Rapid onset jaundice
Also nausea, annorexia, RUQ pain
Fever, ascites, encephalopathy, tender hepatomegally

143
Q

Full blood results in alcoholic hepatitis

A

Leukocytosis
Raised MCV
Often thrombocytopenia

144
Q

Liver biochemistry in alcoholic hepatitis

A

Elevated AST, ALT, disproportionate rise AST, but <500
Bilirubin may be markedly elevated
Serum albumin low
Prothrombin time prolonged

145
Q

Management severe alcoholic hepatitis

A

Nutritional input, support
Corticosteroids for inflammation
Steroids contraindicated in renal failure, infection, bleeding

146
Q

Alcoholic cirrhosis

A

Final stage liver disease form alcohol abuse
Fibrosis, destruction liver architecture
May be symptomatic, or cirrhotic presentation

147
Q

Primary sclerosing cholangitis

A

Chronic liver disease, progressive fibrosis of intra and extra hepatic ducts, -> cirrhosis
Unknown cause, link ulcerative colitis
Often diagnosed while asymptomatic but with IBD
Raised alkaline phosphatase
Symptomatic - pruritus, jaundice, cholangitis

148
Q

Budd-Chiari syndrome

A

Occlusion hepatic vein- stasis and liver congestion - hypoxia, necrotic damage hepatocytes
Often due to hypercoagulable state - myeloproliferative disorders, thrombocytopenia, OCP, malignancy, inherited thrombophillias

149
Q

Clinical features Budd-Chiari syndrome

A

RUQ pain, hepatomegally, jaundice, ascites
Acute - may -> fulminant hepatic failure
Chronic - cirrhosis, portal hypotension etc
Differentials ! Right heart failure, IVC obstruction, constrictive pericarditis!

150
Q

Budd-Chiari investigations

A

Doppler US - abnormal flow, IVC thickening
Plus non specific signs hepatomegally etc
Biopsy not often necessary

151
Q

Treatment Budd-Chiari syndrome

A

Three aims:
Restore venous drainage, if acute - thrombolysis, stent, angioplasty
Treat portal hypertension ascites complications
Detect underlying hypercoagulable disorder, treat

152
Q

Causes liver abscesses

A

Biliary sepsis, portal pyaema from intra-abdominal sepsis
Trauma, bacteraemia, peri euphoric access
Most common is E Coli
Also strep milleri and anaerobes - bacteriodes

153
Q

Amoebic liver abscess

A

Spread of entamoeba histolytica from bowel to liver via portal vein
Serological tests eg compliment / ELISA
Often recent travel endemic country
Single access right lobe liver

154
Q

Clinical features liver abcess

A

Fever, lethargy, weight loss, abdominal pain
Liver - enlarged, tender,
Right side chest - consolidation/effusion

155
Q

Investigations in liver abcess

A

Non specific infection signs inc low albumin
Raised alkaline phosphatase
US lesions, CT - non enhancing cavities with surrounding rim inflammation

156
Q

Pyogenic liver abcess management

A

Aspirate under radiological control
Pigtail catheter for further drainage
Initial empirical antibiotics, then check

157
Q

Liver tumours

A

Most are metastatic - GI tract, breast, bronchus

Can be confused with cysts

158
Q

Hepatocellular carcinoma

A

5th most common tumour worldwide
Most due to hepB, hepC, pathogens
In patients with CLD / cirrhosis

159
Q

Clinical features HCC

A

Weight loss, abdo pain, anorexia, fevers ascites - rapid development suggests HCC
Focal lesion in cirrhotic liver very likely HCC

160
Q

Hepatocellular carcinoma investigations

A

Serum AFP can be raised (alpha fetoprotein)
US / CT show large filling defects
Biopsy / MRI if diagnostic doubt

161
Q

Management hepatocellular carcinoma

A

Sometimes resection or transplant possible
Percutaneous ablative therapies - high frequency US or ethanol injection can produce tumour necrosis
Transarterial chemoembolisation in large tumours
Iv chemo not much use

162
Q

Prognosis hepatocellular carcinoma

A

Median survival 6-20 months

163
Q

Most common benign liver tumours

A

Haemangiomas - incidental finding

Hepatic adenomas - resect if symptomatic

Abdominal (4 decks)

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