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3B General Care > Hepatobillary > Flashcards

Hepatobillary Flashcards

1
Q

4 connections of the liver to the peritoneum

A

left triangular
right triangular
coronary ligament
falciform ligament (—> ligamentum teres –> round ligament connects to umbilicus)

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2
Q

Blood supply of the liver

A

portal vein and the hepatic artery

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3
Q

functions of the liver

A
  1. digestion - bile to digest fats
  2. metabolism (everything from the portal vein, particularly fatty acids –> ATP)
  3. detoxification
  4. storage (glycogen, vit KADE, B12, iron and copper)
  5. Produces: prothrombin, albumin and fibrinogen
  6. Immunity - produces Kuppfer cells that line the sinusoids, also produces immunoglobulins
  7. breaks down bilirubin
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4
Q

Kuppfer cells

A

fixed macrophages part of the mononulcear phagocyte system

digests pathogens from the intestinal circulation

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5
Q

What is on a LFT?

A 
total bilirubin
alt 
ast
alt: ast
ALP
GGT
albumin
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6
Q

ALT

Alanine transaminase

A

raised in cell injury e.g. hepatocytosis / hepatitis

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7
Q

High bilirubin in isolation

A

Gilbert’s disease

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8
Q

GGT

gamma glutamyl transpepsidase

A

enzyme produced by the liver
induced by the liver
raised serum GGT in isolation –> indicates drinking
rises the same as ALP in bile duct pathology (but less specific)

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9
Q

ALP

alkaline phosphatase

A

raised in bile duct pathology

also raised in bony disease - mets/ osteomalcia/ osteoporosis/ growing pains

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10
Q

Other tests in liver pathology

A 
Clotting 
Viral serology (HBV, HCV, HIV)
ESR
Urine MSU
Ultrasound (elastography - fibroscan)
Biopsy 
MRI
ERCP (endoscopic retrograde cholangiopancreatography_
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11
Q

Complications of ERCP

A

bleeding
acute pancreatitis
acute cholangitis

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12
Q

Symptoms of liver pathology

A 
Jaundice
Bleeding (coagulopathy)
RUQ pain 
Pain radiating to back on digesting fats
Oedema/ Ascites 
Steatorrhoea
Dark urine 
Increased drug toxicity 
Prone to infections 
Fatigue
Malaise
Itching
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13
Q

Spider naevi

A

common and benign in isolation
more than 3 suggest liver disease
probable presence of oesophageal varices as well
caused by telangiectasis

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14
Q

Signs of liver disease

A 
Clubbing 
Palmar erythema 
Dupytrens contracture
Hepatic flap 
Raised JVP
Xanthalosmas
Scleral jaundice 
Gynaecomastia 
Hepatomegaly
Splenomegaly 
Spider naveii
Acites (shifting dullness)
Peripheral oedema 
Purpuric rash
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15
Q

Sinusoid

A
  • blood from hepatic artery & portal vein (mixed together)
  • lined by hepatocytes and Kupffer cells
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16
Q

Hepatocytes

A

line sinusoids
make bile acids, bile pigments and cholesterol
–> secreted into canaliculi

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17
Q

Bile acid independent components of bile

A

produced by ductal cells that line the bile ducts

  • stimulated by the hormone secretin
  • makes bile alkaline
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18
Q

Journey of bile

A

stored in the gall bladder
- r/l hepatic duct –> common hepatic duct –> gall bladder

–> cycstic duct –> common bile duct (joined by the pancreatic duct)

  • enters the duodenum via ampulla of Vater
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19
Q

Function of bile

A
  • emulsifies fats
  • digests fat soluble minerals and vitamins
  • excretes bilirubin
  • cholesterol homeostasis
  • enterohepatic recirculation
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20
Q

Bilirubin cycle

A

Haem –> uncongugated bilirubin (insoluble, yellow)

  • -> conjugated in hepatocytes to glucuronic acid (soluble, green)
  • -> biliary tree –> small intestine

–> urobilogen (by bacterial proteases ) excreted in stool (90%) and urine (10% - reabsorbed by portal circulation and is excreted by the kidneys)

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21
Q

Pre-hepatic jaundice

A

increased breakdown of haemoglobin

  • newborn jaundice
  • malaria
  • haemolytic anaemia
  • sickle cell/ beta thalassemia
  • polycythemia rubra vera (PCV)
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22
Q

Pre-hepatic jaundice investigations

A

evidence of haemolysis - on FBC

- slightly elevated LFTs

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23
Q

Hepatic jaundice (unconjugated bilirubin)

A

impaired bilirubin metabolism

- normally genetic (e.g. Gilberts syndrome)

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24
Q

Hepatic jaundice (conjugated bilirubin)

A 
hepatocyte damage usually with some cholestatis 
Causes: 
- Viruses
- Drugs
- NAFLD
- AFLD
- Pregnancy
- Haemochromatosis
- Autoimmune hepatitis

Pale stools and dark urine as excreted as urobilogen

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25
Q

Post hepatic jaundice

A

impaired hepatic excretion
- cholestatis –> pale stools and dark urine

  • primary biliary cirrhosis, primary sclerososing cholangitis, tumours (pancreatic), pancreatitis, ascending cholangitis, strictures
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26
Q

Fulminant liver failure

A

massive necrosis of liver cells –> severe impairment of liver function + hepatic encephalopathy
-acute on chronic

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27
Q

Causes of fulminant liver failure

A 
Hepatocellular carcinoma
Paracetamol overdose, isoniasid, Reyes syndrome
Acute fatty liver of pregnancy 
Alpha-1 antitrypsin deficiency 
Autoimmune hepatitis 
Wilson's disease
Viral hepatits
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28
Q

Hepatic encephalopathy

Causes

A

Protein metabolism –> alanine –> pyruvate and glutamine
glutamine + NH3 –> glutamate –> urea

Ammonia crosses BBB into astrocytes –> glutatmate –> glutamatine

Glutamine has a strong osmotic affect –> cerebral oedema

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29
Q

Hepatic encephalopathy

A

Jaundiced patient
Small liver
Clotting dysfunction

  1. Altered mood/ behaviour, sleep distrubance (reversal of sleep pattern) and dyspraxia. No liver flap.
  2. increasing drowsiness, confusion, slurred speech and liver flap, inappropriate behaviour/ personality change
  3. Incoherent, restless, liver flap, stupor,
  4. Coma
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30
Q

Hepatic encephalopathy investigations

A 
LFT - raised ALT/AST, sky high bilirubin
derranged clotting -INR 
U&E, FBC, glucose, paracetamol level, viral serology 
EEG 
CT head 
Cultures - blood, urine, ascitic fluid
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31
Q

Management of hepatic encephalopathy

Transfer to specialist liver unit

A
  1. INR > 3
  2. Presence of encephalopathy
  3. Hypotension after fluid resus
  4. Metabolic acidosis
  5. Deterioration of prothrombin time
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32
Q

Management of hepatic encephalopathy/ fulminant liver failure

A
  1. Assessing for transfer to specialist
    - -> if paracetamol OD N-acetyl cysteine
  2. Sepsis
  3. Manage coagulopathy
  4. Fluid status
  5. Blood glucose

consider enemas/ lactulose to reduce nitrogenous producing bacteria
TRANSPLANT

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33
Q

Metabolic liver diseases

A
  • haemachromatosis
  • Wilson’s disease
  • alpha-1 antitryspin deficiency
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34
Q

Haemachromatosis (hereditary)

A

one of the most common inherited conditions in europe.

  • -> increased absorption of iron, reduced function of transferrin
  • accumulates in the liver (as this is where Fe is stored), heart, skin, endocrine tissue –> fibrosis –> cirrhosis
  • treat with chelation and regular venesection
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35
Q

Haemachromatosis symptoms

A

Early –> tiredness, arthralgia

Initial skin bronzing –> slate grey skin

Triad of 
Bronzed skin (increased melanin), massive hepatomegaly, DM, (hypogonadism, cardiomyopathy/ arrythmias, increased risk of HCC)
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36
Q

Haemochromatosis investigations

A

Fe and Ferritin
Normal LFTs
Genetic testing
Fibroscan

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37
Q

Haemochromatosis treatment

A

Venesection 1 unit every 1-3 weeks

Monitor HbA1C

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38
Q

Wilson’s disease

Heptatolenticular degenertaion

A

rare, recessively inherited disorder

  • decreased secretion of copper into biliary system
  • reduced incorporation of copper into procaeruloplasmin (precursor of caeruloplasmin)
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39
Q

Symptoms of wilsons disease

A

copper accumulates in

  • liver –>cirrhosis and fulminant liver failure
  • basal ganglia of the brain –> parkinsonism & dementia
  • cornea –> Kayser-Fleischer rings
  • renal tubules
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40
Q

Diagnosis of Wilsons

A

low total serum copper & caeruloplasmin
increased 24 hr urinary copper excretion
increased copper in a liver biopsy specimen

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41
Q

Treatment of wilson’s disease

A

Chelation: penicillamine or trientene

Reduce copper absorption: zinc

Liver transplant with end-stage liver disease

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42
Q

Alpha-1 anti-tripsin deficiency

A

reduced hepatic production of a1-AT (normally inhibits proteolytic enzyme –> neutrophil elastase
- genetic variants medium (M), slow (S) or very slow (z)

Chronic liver disease due to accumulation of abnormal protein in the liver & early onset emphysema

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43
Q

Diagnosis of Alpha-1 anti-tripsin deficiency

A

low serum a1-AT, genotype assessment

histology: a1-AT containing globules in hepatocytes

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44
Q

Treatment of Alpha-1 anti-tripsin deficiency

A

as for chronic lung and liver disease

smoking cessation, IV augmentation of a1-AT

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45
Q

Fatty liver disease

alcoholl

A

steatosis –>

hepatocytes contain macrovesicular droplets of triglycerides

  • typically asymptomatic
  • may be hepatomegaly
  • lab tests normal (may have elevated MCV and gamma GT)
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46
Q

Alcoholic hepatitis

biopsy

A

ballooned hepatocytes that contain amorphous eosinophillic material –> Mallory bodies
- fibrosis and foamy degeneration of hepatocytes

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47
Q

Clincial features of AFLD

A 
rapid onset jaundice 
nausea
anorexia
RUQ pain 
encephalopathy
fever 
ascities
tender hepatomegaly
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48
Q

Investigations of AFLD

A

FBC- leucocytosis, elevated MCV, thrombocytopenia
Serum Electrolytes- hyponatraemia, elevated serum creatinine indicates hepatorenal syndrome
- LFTs- elevated AST &AKT - disproportionate rise in AST, raised, bilirubin, low serum albumin and prolonged PT
-MC&S
-USS - liver & biliary tree
- Liver biopsy

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49
Q

Management of alcoholic hepatitis

A

supportive treatment
adequate nutrional intake
corticosteroids (40mg/day for 4 weeks) reduce inflammatory process (CI in renal failure, infection or bleeding)

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50
Q

Alcoholic cirrhosis

A
  • final stage of liver disease from alcohol abuse
  • destruction of liver archetcture & fibrosis
    regenerating nodules produce micronodular cirrhosis
    Pts may be asymptomatic
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51
Q

Primary sclerosing cholangitis

A

chronic chloestatic liver disease
progressive obliterating fibrosis of intra & extrahepatic ducts –> cirrhosis

  • Cholangiocarcinoma in 15% pts
  • may be caused by cryptosporidium infection in pts with AIDS
  • raised ALP
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52
Q

Symptoms of PSC (primary sclerosing cholangitis

A

pruritus, jaundice or cholangitis

60% ANCA positive

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53
Q

Diagnosis of PSCE(primary sclerosing cholangitis)

A

MRCP (magnetic resonance cholangiopancreatography)

Liver biopsy

54
Q

Treatment of PSC (primary sclerosing cholangitis)

A

ERCP

High dose ursodeoxycholic acid may slow disease progression

55
Q

Budd Chiari syndrome

A

occlusion of hepatic vein obstructs venous outflow from the liver

  • -> stasis & congestion within the liver
  • -> hypoxic damage and necrosis of hepatocytes
56
Q

Budd Chiari syndrome

aetiology

A

hypercoaguable state associated with:

  • myeloproliferative disorders
  • malignancy
  • oral contraceptives
  • inherited thrombophilias
57
Q

Budd Chiari syndrome

Clinical features

A

depends on extent & rapidity of hepatic vein occlusion
- venous collateral circulation may have developed

  • RUQ pain, hepatomegaly, jaundice & ascites
  • acute may present with fulminant hepatic failure
  • chronic –> cirrhosis –> portal hypertension & varices
58
Q

Investigations of Budd Chiari syndrome

A

Doppler US

  • abnormal flow in major hepatic vein or IVC
  • thickening, tortuosity & dilatation of the walls of the hepatic veins
  • Hepatosplenomgaly, ascites & caudate hypertrophy
59
Q

Treatment of Budd Chiari syndrome

A
  • Restore hepatic venous drainage (thrombolysis, angioplasty, stent or TIPS)
  • treatment of complications of ascites/portal HTN
  • detection & treatment of underlying hypercoaguable disorder
60
Q

Gall stone formation (cholesterol)

A

excess of cholesterol in bile

  • either relative deficiency of bile salts and phospholipids
  • relative excess of cholesterol (supersaturated or lithogenic bile)
61
Q

Gall stone formation (pigment stones)

A

bilirubin polymers and calcium bilirubinate

  • pts with chronic haemolysis e.g. hereditary spherocytosis and sickle cell disease & cirrhosis
  • may also form after cholecystectomy with duct strictures
62
Q

Clinical presentation of Gall Stones

A

Biliary pain

  • recurrent episodes of severe constant pain RUQ
  • subsides after several hours
  • may radiate to right shoulder/ right sub-scapular
  • often associated with vomiting
63
Q

Risk factors for cholesterol gallstones

A 
Increasing age
female
Family history 
Multiparity 
Obestity ± metabolic syndrome 
Rapid weight loss
Diet
Ileal disease/resection 
DM
Acromegaly 
Liver cirrhosis
64
Q

Gall stone investigations

A
  • History and USS
  • Raised serum alkaline phosphate & bilirubin
  • absence of inflammatory features (fever, WCC, local peritonism differentiates from acute cholecystitis)
65
Q

Management of Gall Stones

A
  • analgesia
  • elective cholecystectomy
  • Abnormal LFTs/ dilated common bile duct = pre-operative MRCP
66
Q

What is acute cholecystitis?

A

impaction of a stone in the cystic duct or neck of gall bladder

67
Q

Clinical features of acute cholecystitis

A
  • similar to biliary colic
  • progression to severe pain localised in RUQ
  • fever and tenderness with muscle guarding
  • Pain worse on inspiration (Murphy’s sign)
68
Q

Complication sof acute cholycystitis

A

empyema

perforation with peritonitis

69
Q

Acute Cholecystitis Investigations

A

WCC- leucocytosis
Serum liver Biochem- may be mildly abnormal
Abdominal US - gall stones and distended gall bladder

70
Q

Management of cholecystitis

A

conservative- NBM, IV fluids, analgesia & IV abx (cefotaxime)
Cholecystectomy within 48hrs

71
Q

Acute cholangitis

A

infection of biliary tree

72
Q

Causes of acute cholangitis

A 
secondary to obstruction by gall stones 
biliary strictures after surgery 
chronic pancreatitis
PSC
HIV cholangiopathy
Biliary stents
73
Q

Clinical features of acute cholangitis

A

Charcot’s triad: Fever (with rigors), Jaundice, RUQ pain

74
Q

Investigations for Acute Cholangitis

A 
WCC- leucocytosis 
\+ Blood cultures (E. Coli)
LFTs - cholestatic pic (raised serum bilirubin & ALP)
USS - dilated CBD
MRCP
ERCP
75
Q

Management of Acute Cholangitis

A

Resuscitation and volume replacement
Pain relief
IV Abx ((cefotaxime/ ciprofloxacin) + metronidazole)
Relief of Obstruction - ERCP ± sphincterotomy

76
Q

Pathogenesis of Acute pancreatitis

A
  • elevation in intracellular calcium
  • leads to activation of intracellular proteases & release of pancreatic enzymes
  • Acinar cell injury & necrosis –> promotes migration of inflammatory cells from microcirculation into the interstitium
  • -> local inflammatory response, systemic inflammatory response, single/ multiple organ failure
77
Q

Clinical features of acute pancreatitis

A

epigastric or upper abdominal pain radiating through to the back + Nausea & Vomiting
- Epigastric/ general abdo tenderness, guarding and rigidity
- Coma & Multi-organ failure
Eccymosis around the umbilicus (Cullen’s sign) or flanks (Grey Turner’s sign) indicate severe necrotising pancreatitis

78
Q

Causes of Acute Pancreatitis

A

I: Idiopathic

G: Gall stones
E: Ethanol (alcohol)
T: Trauma

S: steroids
M: Mumps/ Malignancy
A: Autoimmune
S: scorpion sting/ spider bite
H: Hyperlipidaemia/ hypercalcaemia
E: ERCP
D: Drugs
79
Q

Causes of Chronic Pancreatitis

A 
Alcohol
Tropical diseases
Autoimmune
Idiopathic 
Hereditary - trypsinogen and protein defects, cystic fibrosis
80
Q

ACute Pancreatitis blood tests

A

LFTS- raised serum amylases/ lipase

FBC/ CRP/ U&Es/ ABG/ plasma calcium

81
Q

Acute Pancreatitis radiology

A

Erect CXR - exclude peptic ulcer
Abdominal USS
Spiral CT/ MRI

82
Q

Management of Acute pancreatitis (mild disease)

lasts 5-7 days

A 
Medical therapy 
-pain control (avoid opioids)
NBM
IV fluids (may need up to 5L / day)
?NG tube
monitor for complications
83
Q

Management of Acute pancreatitis (predicted severe disease)

A 
Medical therapy 
Consider HDU/ ITU
Prophylactic Abx
NG/NJ feeding 
ERCP
84
Q

Complications of acute pancreatitis

A

Acute- hyperglycaemia, hypocalcaemia, renal failure, shock

85
Q

Pathogenesis of chronic pancreatitis

A

inappropriate activation of enzymes leads to precipitation of protein plugs within the duct lumen
–> nidus for calcification

–> Cytokine activation –> pancreatic inflammation, irreversible morphological changes ± permanent impairment of function

86
Q

Clinical features of chronic pancreatitis

A

-Epigastric abdominal pain (intermittent or constant)
radiating to the back
- Severe weight loss (due to anorexia)
- DM & steatorrhoea (due to endocrine (insulin) and exocrine (lipase) insufficiency)
- Jaundice due to CBD obstruction

87
Q

Investigations for chronic pancreatitis

A

Abdo X-ray / US / CT- pancreatic calcification
MRCP / endoscopic US
Functional assessment - feacal elastase (reduced)

88
Q

Treatment of chronic pancreatitis

A
  • stop drinking alcohol
  • opiates for pain relief
  • surgical resection with drainage of pancreatic duct into small bowel
  • ERCP for small stones or strictures
  • pancreatic enzyme supplication
89
Q

Epidemiology of pancreatic Ca

A

5th most common causes of cancer death in the western world
men more than women
incidence increases with age (most >60)
Adenocarcinomas of ductal origin

90
Q

Aetiologyy of pancreatic Ca

A

Hereditary
environmental - smoking & obesity
Chronic pancreatitis is pre-malignant

91
Q

Clinical features of pancreatic Ca

head of pancreas/ ampulla of vater

A

painless jaundice (obstruction of CBD) with classic scratch marks and palpable gall ladder (Coursoisier’s law)

weight loss

Central Abdominal mass

92
Q

Clinical features of pancreatic Ca

Body or tail

A 
abdominal pain
weight loss 
anorexia 
DM 
increased risk of thrombophlebitis
93
Q

Incestigation sof pancreatic Ca

A

Diagnosis made by USS/ contrast CT
MRI & endoscopic US for staging
ERCP for palliation

94
Q

Management of pancreatic ca

A

surgical resection
Chemo-radiotherapy
endoscopic stenting for palliation

95
Q

Prognosis of pancreatic ca

A 
vey poor (30-40% 3 yr survival)
locally advanced disease 8-12 months 
metastatic disease 3-6 months
96
Q

Cancer of the bile ducts

epidemiology

A

disease of the elderly with poor prognosis

common in primary sclerosing cholangitis, congenital bile duct abnormalities & infection with liver flukes

97
Q

Cancer of the bile ducts presentation

A

jaundice secondary to bile duct obstruction of metastatic disease
imaging shows bile duct stricture, hilar mass or multiple mets

98
Q

Gilbert’s syndrome

A

common congenital hyperbilirubinaemia
asymptomatic - often found as incidental finding
mutation of UDP-glucuronyl transferase = reduced enzyme activity and reduced conjugation of bilirubin with glucuronic acid

99
Q

Diagnosis of Gilbert’s syndrome

A

uncongugated hyperbilirubinaemia
normal lFTS
normal FBC/ smear and reticulocyte count
Abscence of signs of liver disease

100
Q

Autoimmune hepatitis

aetiology

A

Immunological abnormalities

  • hypergammaglobulinaemia with high IgG
  • presence of circulating autoantibodies
  • interface hepatitis with portal plasma cell infiltration on liver histology
101
Q

Autoimmune hepatitis

clinical features

A 
Anorexia 
Malaise
Nausea
Fatigue
25% acute
75% chronic with signs of liver disease
102
Q

Autoimmune hepatitis

Investigations

A

Circulating antibodies
(anti-nuclear, smooth muscle, soluble liver antigen, liver/kidney microsomal antibodies)
Hypergammaglobulinaemia
Elevated serum bilirubin and aminotransferases

103
Q

NAFLD

Associations

A

Obesity
T2DM
HTN
Hyperlipidaemia

104
Q

Clinical features of NAFLD

A
  • asymptomatic
  • elevated aminotransferases on LFTs
  • hepatomegaly on examination
105
Q

Investigations of NAFLD

A

USS - hyperechoic texture due to diffuse fatty infiltration

106
Q

Management of NAFLD

A

Management of risk factors

107
Q

What is Cirrhosis?

A

Necrosis of liver cells followed by fibrosis and nodule formation
impairment of liver cell function & gross distortion of the liver architecture–> portal hypertension

108
Q

Pathology of cirrhosis

- micronodular

A

uniform small nodules of up to 3mm in diameter

- caused by ongoing alcohol damage or biliary tract disease

109
Q

Pathology of cirrhosis

- macronodular

A

variable nodule size and normal acini with large nodules

- seen after chronic viral hepatitis

110
Q

Clinical features of cirrhosis

A

Secondary to portal hypertension & liver cell failure

Decompensated cirrhosis - encephalopathy, ascites, variceal haemorrhage

111
Q

Investigations of cirrhosis

A

LFTs, FBC, Serum electrolytes, liver biochem, serum alpha-fetoprotein

112
Q

aetiology of cirrhosis

A

response to chronic liver injury

113
Q

Further investigations of cirrhosis

A

Endoscopy - oesophageal varices
USS - Hepatocellular carcinoma
DEXA for osteoporosis

114
Q

Management of cirrhosis

A

irreversible & frequently progresses to HCC

Management of complications as they arise

115
Q

Pre-hepatic causes of portal hypertension

A

portal vein thrombosis

116
Q

INtra-hepatic causes of portal hypertension

A 
Cirrhosis 
Alcoholic hepatitis 
Idiopathic non-cirrhotic portal hypertension
Schistosomiasis 
Veno-occlusive disease
117
Q

Post-hepatic causes of portal hypertension

A

Budd-Chiari syndrome
Right heart failure
Constrictive pericarditis
IVC obstruction

118
Q

What is the portal vein?

A

Union of the supermesenteric and splenic veins
75% of hepatic blood flow
enters the liver through the hilum (porta hepatis)
blood passes into hepatic sinusoids via portal tracts

119
Q

Clincial features of portal hypertension

A
  • GI bleeding from oesophageal or gastric varices
  • Ascites
  • Hepatic encephalopathy
120
Q

Aetiology of Ascites

A

peripheral arterial vasodilation reduces effective blood volume

–> activation of sympathetic nervous system and renin-angiotensin system
–> renal salt and water retention
Formation of oedema encouraged by hypoalbuminaemia
localises in abdominal cavity as a result of portal HTN

121
Q

Clinical features of ascites

A

Fullness in flanks
Shifting dullness
Tense ascites is uncomfortable - produces respiratory distress
Pleural effusion and peripheral oedema may also be present

122
Q

Investigation of ascites

A 
Aspiration 
Serum albumin
FBC
gram stain and culture/ cytology 
Amylase to exclude pancreatic ascites
123
Q

Transudate causes of ascites

low protein content
low specific gravity

A 
portal HTN
Hepatic outflow obstruction 
Budd-Chiari
Hepatic veno-occlusive disease 
cardiac failure 
tricuspid regurgitation
constrictive pericarditis
Meig's syndrome
124
Q

Exudate causes of ascites

A 
Peritoneal carcinomatosis
Peritoneal TB
Pancreatitis 
Nephrotic syndrome 
Lymphatic obstruction (chylous ascites)
125
Q

Management of Ascites

A

Diuretics (furosemide)
Paracentesis
Transjugular intrahepatic portsystemic shunt (TIPS)

126
Q

Complications of Ascites

A
  • Spontaneous bacterial peritonitis (e.coli- IV cefotaxime)
127
Q

Primary biliary cirrhosis

A

Chronic disorder with progressive destruction of intrahepatic bile ducts causing cholestatis –> cirrhosis

128
Q

Epidemiology of primary biliary cirrhosis

A

women 40-50

129
Q

Aetiology of Primary biliary cirrhoiss

A

inherited abnormality of immunoregulation - leads to T-lymphocyte mediated attack of bile duct epithelial cells
Possible environmental trigger
AMA antibodies

130
Q

Clinical features of primary biliary cirrhosis

A 
Pruritis ± jaundice
hepatosplenomegaly
xanthelasma
raised serum ALP & autoantibodies
Steatorrhoea
131
Q

Primary biliary cirrhosis investigations

A

Raised serum ALP
Serum AMA (antimitochondrial antibodies)
Raised Serum IgM
Liver biopsy –> loss of bile ducts, lymphocyte infiltration at portal tracts, granuloma formation –> fibrosis –> cirrhosis

132
Q

Management of primary biliary cirrhosis

A

lifelong ursodeoxycholic acid
colestyramine for pruritus
Supplementation of fat soluble vitamins
Liver transplant in severe disease

3B General Care (8 decks)

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