Hepatobiliary Flashcards

1
Q

What are the two types of gallstones?

A

Cholesterol

Bile pigment

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2
Q

What are risk factors for gallstones?

A
Increasing age
Female
FHx
DM
Multiparity
Obesity
Rapid weight loss
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3
Q

How do gallstones present?

A

Biliary colic
N + V
Acute + chronic cholecysitis

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4
Q

Describe biliary colic

A

Colicky abdominal pain which is worse after eating and after fatty foods. Pain may radiate to the right shoulder.

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5
Q

How do you investigate gallstones?

A

Bloods: serum bilirubin, alkaline phosphatase, aminotransferase
Abdo USS

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6
Q

How do you manage gallstones?

A

Cholecystectomy
IV fluids + Abx
Opiate analgesia

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7
Q

What are some complications of gallstones?

A
Liver congestion
Oesophageal reflux
Malabsorption in SI
Acute + chronic pancreatitis
Digestion issues
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8
Q

What is acute cholecystitis?

A

Follows impaction of a store in the cystic duct or neck of gallbladder. Obstruction to gallbladder emptying causes increased gallbladder glandular secretion = progressive distension. Compromised blood supply to gallbladder and inflammatory response to bile retained in gallbladder = infection.

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9
Q

Clinical features of acute cholecystitis?

A

RUQ pain
Fever
Murphy’s sign
Tenderness + guarding

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10
Q

How do you manage acute cholecystitis?

A

USS

Cholescystectomy within 48hrs

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11
Q

Complications of acute cholecystitis?

A

Empyema + perforation = peritonitits

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12
Q

What is chronic cholecystitis?

A
Chronic inflammation of the gallbladder often found in association with gallstones.
- usually asymptomatic
- chronic EUQ pain
- fatty food intolerance
USS: small, shrunken gallbladder
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13
Q

What is choledocholithiasis?

A

Bile duct stones

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14
Q

What is ascending cholangitis?

A

Infection of the biliary tree and most often occurs secondary to common bile duct obstruction by gallstones.

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15
Q

How does ascending cholangitis present?

A

Charcot’s triad:

  • fever
  • jaundice
  • RUQ pain
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16
Q

How do you diagnose ascending cholangitis?

A

Bloods:
- raised neutrophil count, ESR, CRP, serum bilirubin, serum alkaline phosphatase, ALTs and ASTs

Imaging:

  • Abdo US (dilatation of common bile duct)
  • MRI
  • CT scan
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17
Q

How do you treat acute cholangitis?

A

IV Abx: cefotaxime + metronidazole

Urgent biliary draining with ERCP + sphinctectomy

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18
Q

What is ERCP?

A

Endoscopic retrograde cholangio-pancreatography

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19
Q

What are some risk factors for Hep A?

A

Shellfish, travellers, food handlers

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20
Q

Which hepatitis has a high mortality in pregnancy?

A

Hep E

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21
Q

Which hepatitis can lead to HCC?

A

Hep B

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22
Q

What is fulminant hepatitis?

A

Hepatic failure with encephalopathy. Develops in less than 2 weeks in a pt with a previous normal liver.

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23
Q

Most common causes of fulminant hepatitis?

A

Viral hepatitis

Paracetamol overdose

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24
Q

What is autoimmune hepatitis?

A
Immune cells attack hepatocytes.
Associated with:
- HLA
- Hashimoto's thyroiditis
- Grave's disease
Treated: corticosteroids + azathioprine
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25
Q

What is cirrhosis?

A

End-stage of all progressive chronic liver disease, once fully developed it is irreversible.

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26
Q

What is a main risk factor for cirrhosis?

A

Chronic alcohol abuse

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27
Q

What is seen on histology in cirrhosis?

A

Loss of normal hepatic architecture with riding fibrosis + nodular regeneration.

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28
Q

How does cirrhosis present?

A
  • leuconychia
  • clubbing
  • palma erythema
  • spider naevi
  • bruising
  • xanthalasma
  • hepatomegaly
  • loss of body hair
  • ankle swelling + oedema
  • dupuytren’s contracture
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29
Q

How is cirrhosis diagnosed?

A
Child-Pugh classification
Liver biopsy
LFTs
Biochemistry
US, MRI, Endoscopy
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30
Q

What is the child-pugh classification?

A

Ascites, encephalopathy, increased bilirubin, decreased albumin, long PTT.

Scored 1-3
<7 is good
>10 is bad
Risk of vatical bleeding is high if >8

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31
Q

Complications of cirrhosis?

A

Coagulopathy
Encephalopathy
Hypoalbuminaemia
Portal hypertension

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32
Q

How is cirrhosis treated?

A
Alcohol abstinence
Good nutrition
Avoid NSAIDs
Reduce salt intake
USS every 6months
Liver transplant
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33
Q

How do drugs impair liver function?

A
  • disruption of intracellular calcium homeostasis
  • disruption of bile canalicular transport mechanisms
  • induction of apoptosis
  • inhibition of mitochondrial function
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34
Q

Which drugs impair liver function?

A
  • Abx (augmente, flucloxacillin, TB drugs, erythromycin)
  • CNS drugs (chlorpromazine, carbamazepine)
  • Immunosupressants
  • Analgesia (diclofenac)
  • GI drugs (PPIs)
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35
Q

What drugs don’t cause liver injury?

A
Low dose aspirin
NSAIDs
BB
Ace-i
Thiazides
CCB
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36
Q

What is a fatal dose of paracetamol?

A

12g/adult

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37
Q

What happens in paracetamol overdose?

A

Liver glutathione is depleted so NAPQI can’t be conjugated and deactivated = hepatoxicity and para-induced kidney injury.

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38
Q

Clinical picture of paracetamol overdose?

A
First 24hrs asymptomatic
- RUQ pain
Jaundice
AKI
Metabolic acidosis
Hypoglycamia
Encephalopathy
Rash
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39
Q

How do you treat paracetamol overdose?

A

IV N-acetylcysteine
Activated charcoal
Chlorphenamine

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40
Q

How do you treat aspirin poisoning?

A

IV sodium bicarbonate

Haemodialysis

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41
Q

What is ascites?

A

Accumulation and effusion of free serous fluid within the peritoneal cavity.

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42
Q

What are the causes and RF for ascites?

A

Causes: local inflammation, low protein, low flow
RF: high sodium diet, hepatocellular carcinoma, portal hypertension

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43
Q

How does ascites present?

A
Distended abdomen
Peripheral oedema
Fullness in flanks + shifting dullness
Jaundice
Mild abdo pain + discomfort
Nausea, constipation, cachexia, weight loss
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44
Q

How is ascites diagnosed?

A

Demonstrate shifting dullness

Diagnostic aspiration of fluid with ascitic tap

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45
Q

What are the types of protein measurement?

A

Transduate = protein <30g/L
- PHTN, constrictive pericarditis, heart failure, Budd-Chiari syndrome

Exudate = protein >30g/L
- malignant, peritonitis, pancreatitis, nephrotic syndrome,

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46
Q

How do you treat ascites?

A

Paracentesis (drain fluid)
Shunts (TIPS)
Decrease sodium retention/increase excretion
Diuretic (oral spirolactone)

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47
Q

What is a pre-hepatic cause of portal HTN?

A

Portal vein thrombosis

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48
Q

What are some intra-hepatic causes of portal HTN?

A

cirrhosis, fibrosis, schistosomiasis, sarcoidosis

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49
Q

What are some post-hepatic causes of portal HTN?

A

RH failure, constrictive pericarditis, IVC obstruction

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50
Q

What are common sites for varices?

A
Gastro-oesophageal junction
Rectum
Left renal vein
Retroperitoneum
Diaphragm
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51
Q

How does portal HTN present?

A
Often asymptomatic
Splenomegaly
GI bleeding
Ascites
Hepatic encephalopathy
Vatical haemorrhage
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52
Q

How is portal HTN managed?

A

Measure portal HTN
Treat with TIPS
Propanolol
Salt restriction + diuretics

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53
Q

What is TIPS?

A

Transjugular intrahepatic portosystemic shunt

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54
Q

What is primary biliary cirrhosis?

A

Chronic disorder with progressive destruction of small bile ducts leading to cirrhosis.

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55
Q

How does primary biliary cirrhosis present?

A
PRURITIS
Dry eyes
Joint pain
Vatical bleeding
Lethargy + fatigue
Jaundice
Asymptomatic
56
Q

How do you diagnose primary biliary cirrhosis?

A

Raised anti-mitochondrial antibodies
USS
Liver biopsy

57
Q

How is primary biliary cirrhosis treated?

A

Ursodeoxycholic acid
ADEK vitamins
Bisphosphonates

To treat pruritus:
- colestyramine, naloxone, naltrexone

58
Q

What are the 3 clinical syndromes of alcohol liver disease?

A
  1. fatty change
  2. alcoholic hepatitis
  3. alcoholic cirrhosis
59
Q

How does alcoholic liver disease present?

A
Rapid onset jaundice
RUQ pain
Ascites
Nausea
Anorexia
Hepatic encephalopathy
Fever
Tender hepatomegaly
60
Q

What investigations are done for alcoholic liver disease?

A
FBC - raised WCC, MCV but low platelets
Low sodium
Raised AST + ALT, bilirubin and GGT
Low serum albumin
Raised PPT
USS liver + biliary
61
Q

How do you manage alcoholic liver disease?

A
STOP DRINKING
Fluids, painkillers, vitamins
Adequate nutritional intake
Corticosteroids
Pentoxifylline
62
Q

What is hereditary haemochromatosis?

A

Autosomal recessive gene. Inherited disorder of iron metabolism where there is increased intestinal iron absorption so iron is deposited in joints liver, heart, pancreas etc. It leads to fibrosis and functional organ failure.

63
Q

What causes hereditary haemochromatosis?

A
  • HFE gene mutation on chromosome 6
  • high intake of iron and chelating agents
  • alcoholics may have iron overload
64
Q

How does hereditary haemochromatosis present?

A

TRIAD:

  1. bronze skin pigmentation
  2. hepatomegaly
  3. diabetes mellitus

Hypogonadism
Cirrhosis
Joint pain
Dilated cardiomyopathy

65
Q

How is hereditary haemochromatosis diagnosed?

A
  • raised iron + ferritin
  • HFE gene
  • MRI (iron overload)
  • liver biopsy
  • ECH/ECHO
66
Q

How is hereditary haemochromatosis treated?

A
Venesection 
Chelation therapy - desferrioxamine
Low iron diet
Screening 1st degree relatives
Treat any other complications (e.g. diabetes)
67
Q

What is Wilson’s disease?

A

Rare inherited disorder of biliary copper excretion with too much copper in the liver and CNS.

  • autosomal recessive disorder of gene on Chr 13
  • molecular defect within a copper-transporting ATPase
68
Q

How does Wilson’s disease present?

A

Children have hepatic problems
- hepatitis, cirrhosis, fulminant liver failure

Young adults have CNS problems
- tremor, dysarthria, dysphagia, dyskinesia, dementia

KAYSER-FLEISCHER RING

69
Q

What is a Kayser-fleischer ring?

A

Seen in Wilson’s disease

Copper deposition in corner = greenish-brown pigment at the corneoscleral junction.

70
Q

How is Wilson’s disease diagnose?

A

24hr urinary copper excretions = high
Liver biopsy
Low serum copper, low caerulopasmin
MRI: basal ganglia + cerebellar degeneration

71
Q

How is Wilson’s disease treated?

A
  • Penicillamine (lifelong chelating agent)
  • Avoid foods high in copper
  • Liver transplant if severe
  • Screen siblings
72
Q

SE of penicillamine?

A

Skin rash
Low WCC, Hb + platelets
Haematuria
Renal damage

73
Q

What foods are high in copper?

A

Liver, chocolate, nuts, mushrooms, shellfish

74
Q

What is alpha-1-antitrypsin deficiency?

A

Inherited autosomal recessive conformational disease

- alpha-1-antitrypsin gene is located on Chr 14

75
Q

What is the role of alpha-1-antitrypsin gene?

A

To inhibit proteolytic enzyme: neutrophil elastase

SO deficiency causes protein retention in liver (cirrhosis + HCC) and emphysema in lung.

76
Q

How dos alpha-1-antitrypsin deficiency present?

A

Children: Cirrhosis, hepatitis + cholestatic jaundice
Adults: dyspnoea, emphysema

77
Q

How is alpha-1-antitrypsin deficiency diagnosed?

A

Decreased serum alpha-1-antitrypsin levels

Most symptomatic patients are homozygotes with a PiZZ phenotype

78
Q

How is alpha-1-antitrypsin deficiency treated?

A

No specific treatment
Treat complications
Stop smoking

79
Q

What are clinical features of liver failure?

A
Hepatic encephalopathy
Abnormal bleeding
Ascites
Jaundice
Cerebral oedema
80
Q

What is hepatic encephalopathy?

A

NH3 builds up in circulation (due to liver failure) which goes to brain and causes brain damage as it is neurotoxic. It stops the Kreb’s cycle so causes irreparable cell damage and neural cell death.
Symptoms:
- confusion, coma, liver flap, drowsiness, cerebral oedema, irritability, constructional apraxia, asterixis

81
Q

What are the main causes of liver failure?

A
Virus: Hep ABE, CMV, EBV, HSV
HCC
Drugs
Acute fatty liver of pregnancy
Wilsons 
A1ATD
82
Q

What investigations are done for liver failure?

A

Bloods

  • hyperbilirubinaemia
  • raised ALT + AST
  • low coagulation factor, high PTT
  • low glucose, high NH3

Imaging
- EEG, US, CXR, Doppler US

Microbiology

83
Q

How is liver failure treated?

A
Treat cause
IV mannitol for raised ICP
IV Vit K
IV glucose
PPI
Liver transplant
84
Q

What is primary sclerosis cholangitis?

A

A biliary disease characterised by inflammation and fibrosis of intra and extra-hepatic bile ducts. Leads to strictures +/- gallstones.

85
Q

What is primary sclerosis cholangitis assoc with?

A

Ulcerative colitis
Crohn’s
HIV

86
Q

How does primary sclerosis cholangitis present?

A

Prutitis + jaundice
RUQ pain
Fatigue
Rigors

87
Q

How is primary sclerosis cholangitis investigated?

A

ERCP
ANCA
MRCP
Liver biopsy

88
Q

Complications of primary sclerosis cholangitis?

A

Cholangiocarcnioma

Increased risk of colorectal cancer

89
Q

How is primary sclerosis cholangitis managed?

A

Cholestyramine (for pruritis)

Monitor for HCC

90
Q

What is seen on EEG in hepatic encephalopathy?

A

Triphasic slow waves

91
Q

What is the grading used for hepatic encephalopathy?

A

I - irritable
II - confused, inappropriate behaviour
III - incoherent, restless
IV - coma

92
Q

How is hepatic encephalopathy managed?

A

Lactulose
Rifaximin
Neomycin

93
Q

What is spontaneous bacterial peritonitis?

A

A form of peritonitis usually sen in patients with ascites secondary to liver cirrhosis?

94
Q

What are the clinical features of spontaneous bacterial peritonitis?

A
Vague Sx
Fever
Change in mental state
Abdo tenderness
GI bleeding
N + V
Chills
95
Q

How is spontaneous bacterial peritonitis diagnosed?

A

Paracentesis of ascitic fluid

- neutrophil count >250 cells/ul

96
Q

How is spontaneous bacterial peritonitis treated?

A

IV cefotaxime
Abx prophylaxis after 1 ep
Consider liver transplant

97
Q

What is non-alcoholic fatty liver disease?

A

A spectrum of disease:

Steatosis > Non-alcoholic steatohepatitis > progressive disease (fibrosis, cirrhosis)

98
Q

What are RF for NAFLD?

A
Obesity
Hyperlipidaemia
T2DM
Jejunoileal bypass
Sudden weight loss/starvation
99
Q

Investigations for NAFLD?

Mx for NAFLD?

A

Enhanced liver fibrosis blood test (ELF)
Fibroscan

Weight loss

100
Q

What is Budd-Chiari syndrome?

A

Hepatic vein thrombosis
Occlusion of the hepatic vein obstructs venous outflow from the liver = stasis and congestion within the liver which leads to hypoxic damage and necrosis of hepatocytes.

101
Q

What can cause Budd-Chiari syndrome?

A
Polycythaemia rubra vera
Thrombophilia
OCP
Pregnancy
Myeloproliferative disorders
Irradiation
102
Q

Clinical features of Budd-Chiari syndrome?

A
  • RUQ pain (sudden onset + severe)
  • ascites
  • tender hepatomegaly
  • jaundice
103
Q

Investigations for Budd-Chiari syndrome?

A

Doppler USS

  • abnormal flow in hepatic veins
  • thickening, tortuosity + dilatation of hepatic vein walls

Abnormal LFTs

104
Q

Management for Budd-Chiari syndrome?

A

TIPS to restore hepatic venous drainage

Anticoagulation + thrombolysis

105
Q

What is cholangiocarcinoma?

A

Cancer of biliary tree (in or out of liver)

  • slow growing
  • mostly distal extra hepatic or perihilar
  • 90% ductal adenocarcinoma, 10% SCC
106
Q

RF for cholangiocarcinoma?

A
  • infestation with parasitic worms
  • biliary cysts
  • IBD
  • HBV, HCV, DM
  • primary sclerosis cholangitis
107
Q

Clinical features of cholangiocarcinoma?

A

Fever
Abdo pain +/- ascites
Malaise

108
Q

How is cholangiocarcinoma diagnoes?

A

High bilirubin + high alkaline phosphate
Contrast MRI
ERCP

109
Q

Treatment for cholangiocarcinoma?

A

Complete surgical resection
Stent
Transplant is CI

110
Q

What is hepatocellular carcinoma?

A

Cancer of the hepatocytes

111
Q

RF for HCC?

A
  • male
  • HBV/HCV carriers
  • cirrhosis (alcohol, NAFLD, haemochromatosis)
112
Q

Where can HCC metastasise to?

A

Lymph nodes
Bones
Lungs

113
Q

Clinical features of HCC?

A

Weight loss, fever, anorexia, fatigue
Jaundice, ascites
Ache in R hypochondrium
Enlarged, irregular, tender liver

114
Q

How is HCC diagnosed?

A

Raised serum AFP (alpha-fetoprotein)
USS
Enhanced CT
Liver biopsy

115
Q

How is HCC treated?

A

Surgery resection of isolated lesion
Transplant

HBV vaccination for prophylaxis

116
Q

Describe pancreatic cancer?

A

Mostly adenocarcinomas of ductal origin

Mainly at head of pancreas

117
Q

RF for pancreatic cancer?

A
Increasing age
Smoking
Diabetes
Chronic pancreatitis
HNPCC
Multiple endocrine neoplasia
BRCA2 gene
118
Q

Clinical features of pancreatic cancer?

A
PAINLESS JAUNDICE
Anorexia, weight loss epigastric pain
Steatorrhoea
Diabetes
Atypical back pain
Migratory thrombophlebitis (Trousseau sign of malignancy)
119
Q

Typical features of cancer of head of pancreas?

A

Painless jaundice due to obstruction of CBD

Weight loss

120
Q

Typical features of cancer of body/tail of pancreas?

A

Abdo pain, weight loss + anorexia

121
Q

Investigations for pancreatic cancer?

A

Courvoisseier’s law
Central abdo mass
USS
HRCT

122
Q

What is courvoisserier’s law?

A

Painless jaundice with palpable gallbladder = NOT gallstones

123
Q

What is seen on HRCT for pancreatic cancer?

A

Dilated bile ducts
Mass/lesion
Staging

124
Q

How is pancreatic cancer treated?

A

Whipple’s resection (pancreaticoduodenectomy)
Adjuvant chemo
ERCP if palliative

v poor prognosis (12months)

125
Q

What are the different neuroendocrine tumours of the pancreases?

A

Gastrinoma
Somatostatinoma
VIPoma
Glucagonoma

126
Q

What are the different liver abscesses?

A

Pyogenic
Amoebic
Hyatid

127
Q

Causative agents of pyogenic abscesses?

A
Staph aurea (children)
E coli (adults)
128
Q

What can cause pyogenic abscesses?

A
Biliary sepsis
Infection of tumour or cyst
Direct extension (E.g. from empyema of gallbladder)
Trauma
Haematogenous
129
Q

How are pyogenic abscesses managed?

A

Amoxicillin + ciprofloxacin + metronidazole

USS guided drainage if large

130
Q

What is the causative agent of an amoebic abscess?

A

Entamoeba histoytica

131
Q

What can cause an amoebic abscess?

A

Hx of living/visiting endemic area

Large, single asbecc

132
Q

How is an amoebic abscess diagnosed?

A

Aspiration: anchovy sauce (chocolate-brown material)

Serology

133
Q

How is amoebic abscess treated?

A

Metronidazole

Aspirate if large

134
Q

What is the causative agent of a hyatid cyst?

A

Echinococcus granulosis

tapeworm

135
Q

How is a hyatid cyst diagnosed?

A

serology ELISA

136
Q

How is hyatid cyst managed?

A

Albendazole
Percutaneous Aspiration
Injection of a solicidal agent
Reaspiration

137
Q

Clinical features of a liver abscess?

A
Fever 
Weight loss
Lethargy
RUQ pain +/- pleuritic or R shoulder pain
Tender hepatomegaly
Obstructive jaundice