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Sirpi's Phase 2A Medicine > Hepatology + Pancreatobilliary Disease > Flashcards

Hepatology + Pancreatobilliary Disease Flashcards

1
Q

What are 4 functions of the liver?

A

Detoxification of xenobiotics
Synthesis of plasma proteins and clotting factors
Site of gluconeogenesis
Production of bile

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2
Q

Clinical presentation of acute liver injury

A

Malaise
Nausea
Anorexia
Jaundice (occasionally)

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3
Q

Clinical presentation of chronic liver injury

A

Ascites, Oedema
Haematemesis (varices)
Malaise, anorexia,
Bruising, itching
Palmar erythema, spider naevi, clubbing
Hepatomegaly
Fetor hepaticus - patient breath smells like rotten eggs and garlic

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4
Q

What are examples of liver function tests?

A

Serum bilirubin
Serum albumin
Prothrombin time

Liver enzymes:
Serum alkaline phosphatase (ALP)
Serum aspartate aminotransferase (AST)
Serum alanine aminotransferase (ALT)
Gamma glutamyl transpeptidase (GGT)

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5
Q

What is the relevance of checking aminotransferase (ALT/AST) levels?

A

These enzymes are contained in hepatocytes and leak into the blood with liver cell damage.

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6
Q

What is a consequence of chronic liver disease?

A

Can lead to liver fibrosis and eventually cirrhosis.

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7
Q

What can be calculated using ALT and ALP as a clinical indicator?

A

ALT:AST ratio

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8
Q

What would the ALT:AST ratio be like in viral hepatitis?

A

ALT>AST (>1)

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9
Q

What would the ALT:AST ratio be like in alcoholic liver disease/steatohepatitis?

A

AST>ALT (<1)

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10
Q

What is an indicator of liver cirrhosis in viral hepatitis?

A

ALT:AST ratio <1 (AST higher than ALT)

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11
Q

What would cause raised serum ALP levels?

A

Intrahepatic and extrahepatic cholestatic disease of any cause, due to increased synthesis.

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12
Q

What is jaundice?

A

Yellowing discolouration of the skin and eyes due to hyperbilirubinaemia causing bilirubin deposition.

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13
Q

Aetiology of pre-hepatic jaundice

A

Gilbert’s syndrome (underactivy in UDP glucoronyltransferase enzyme)
Crigler-Najjar syndrome - deficiency in UDP glucoronyltransferase.
Haemolysis

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14
Q

What can cholestatic jaundice be classified into?

A

Hepatic and post-hepatic jaundice.

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15
Q

Aetiology of hepatic/intrahepatic jaundice

A

Viral hepatitis (ABCD, EBV)
Alcoholic hepatitis
Hepatocellular carcinoma
Congestive heart failure

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16
Q

Aetiology of post-hepatic/extrahepatic jaundice

A

Gall stone in bile duct
Cholangitis (bile duct inflammation)
Bile duct carcinoma

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17
Q

Which type of jaundice is caused by high levels of uncongugated bilirubin?

A

Pre-hepatic jaundice

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18
Q

Which type of jaundice is caused by high levels of conjugated bilirubin?

A

Cholestatic (intra + extrahepatic) jaundice.

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19
Q

Clinical presentation of pre-hepatic jaundice

A

Normal urine
Normal stools
No itching
Normal LFTs

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20
Q

Clinical presentation of cholestatic jaundice

A

Dark urine
Pale stools
Itching - gets worse when feeling hot.
Abnormal LFTs
Upper abdomen pain radiating to shoulder.

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21
Q

Investigation of jaundice

A

Abdominal ultrasound to check for biliary obstruction
Check for viral markers
Liver enzymes (ALT, ALP, AST)

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22
Q

Aetiology/risk factors for cholelithiasis (hepatobilliary stones)

A

Female, fat (obesity), fertile (multiparity), forty, fair.

Haemolytic anaemia

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23
Q

Clinical presentation of hepatobilliary stones

A

Epigastric/right hypochondriac colic
Despite colic name, severe, constant crescendo-ing pain.
Can increase after a fatty meal.
Can radiate to shoulder due to diaphragmatic irritation.

Can be accompanied by nausea/vomiting.

Can cause jaundice + associated symptoms if in billiary tree.

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24
Q

What conditions can be caused by gallbladder stones?

A

Cholecystis
Obstructive jaundice (Mirrizi syndrome)

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25
Q

What conditions can be caused by intra and extrahepatic stones?

A

Primary sclerosing cholangitis
Pancreatitis
Obstructive jaundice

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26
Q

Management of hepatobilliary stones

A

Gall bladder stones;
Laparoscopic cholecystectomy
Bile acid dissolution therapy (<1/3 success)

Bile duct stones:
ERCP with stent placement

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27
Q

Aetiology of acute cholecystitis

A

Cholelithiasis

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28
Q

Pathophysiology of cholecystitis

A

Obstruction causes distension of gall bladder due to increased bile storage.
Can result in ischaemia, progressive inflammation, and infection.

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29
Q

Clinical presentation of cholecystitis

A

Biliary colic
Can progress to right upper quadrant pain due to peritoneal involvement.
Fever
Murphy’s sign - pain during inspiration when examiner’s hands are on the gall bladder.

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30
Q

Investigation of acute cholecystitis

A

First line: Abdominal ultrasound

LFTs: Normal-High ALP, ALT, bilirubin

Raised CRP, ESR

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31
Q

Management of acute cholecystis

A

IV fluids
Opiate analgesia
IV antibiotics
Laparoscopic cholecystectomy

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32
Q

What bacteria are associated with cholecystitis?

A

Klebsiella
Escherichia coli
Enterococcus
Pseudomonas species
Bacteroides fragilis,

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33
Q

Clinical presentation of acute/ascending cholangitis

A

Reynold’s pentad:

Biliary colic (RUQ pain)
Fever
Cholestatic jaundice - dark urine, pale stools and skin may itch
Confusion/altered mental state
Hypotension

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34
Q

Investigation of acute/ascending cholangitis

A

Abdominal ultrasound - FL
MRCP - GS

FBC: Elevated neutrophil count

Raised ESR, CRP

LFTs:
Raised serum bilirubin - bile duct obstruction if very high
Raised serum ALP
High ALT + AST, (ALT>AST)

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35
Q

Management of acute/ascending cholangitis

A

ERCP or laporoscopic cholesystectomy
IV antibiotics - cefotaxime, metronizadole

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36
Q

Aetiology of drug induced liver injury

A

Antibiotics
CNS drugs
Analgesics

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37
Q

Examples of antibioitics that can cause drug induced liver injury

A

Rifampicin
Flucloxacillin
Co-amoxiclav (augmentin)

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38
Q

How does paracetamol get metabolised by the liver normally?

A

Normally, mostly P2 metabolism.
Some levelof PI metabolism via oxidation which causes toxic NAPQI production
It is conjugated with glutathione and subsequently excreted.

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39
Q

Hepatic pathphysiology of paracetamol overdose induced liver injury

A

Large amounts of paracetamol causes shunting to P1 metabolism, causing increased NAPQI production.
Glutathione depletion occurs, causing NAPQI buildup.

Can lead to kidney tubular necrosis and hepatic failure if left untreated.

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40
Q

Clinical presentation of paracetamol induced liver injury

A

Anorexia, nausea and vomiting
Acute RUQ pain
Jaundice, confusion.

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41
Q

Investigation of paracetamol induced liver injury

A

Raised ALT, PTT (>70 sec)
Metabolic acidosis (pH <7.3)
Raised creatinine

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42
Q

Management of paracetamol induced liver injury

A

Activated charcoal
IV N-Acetylcysteine - replenishes glutathione stores

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43
Q

What is ascites?

A

Ascites is the accumulation of free fluid within the peritoneal cavity.

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44
Q

Aetiology of ascites

A

Liver cirrhosis
Portal hypertension
Peritonitis, TB
Nephrotic syndrome
Hypoalbuminemia (low oncotic pressure)
Ovarian, uterine, neoplasia

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45
Q

Pathophysiology of ascites

A

Portal hypertension = splanchnic vasodilation causing fluid leakage and activation of RAAS = fluid retention.

Hypoalbuminaemia = low oncotic pressure = fluid leakage.

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46
Q

Clinical presentation of ascites

A

Abdominal swelling, distended abdomen.
Shifting dullness - muffled sound upon abdominal percussion.
Peripheral oedema

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47
Q

Management of ascites

A

Fluid and salt restriction
Diuretics - spironolactone, furosemide
Fluid drainage - paracentesis
Trans-jugular intrahepatic portosystemic shunt (TIPS)

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48
Q

What parameter after ascites paracentesis can be used to asses the cause of ascites?

A

Serum–ascites albumin gradient
(Serum albumin - ascities fluid albumin)

> 1.1 g/dl indicates portal hypertension.

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49
Q

Pathophysiology of alcohol-induced hepatic steatosis.

A

Ethanol metabolisation causes altered redox potential in liver.
Causes increased fatty acid synthesis and decreased fatty acid oxidation.
Can lead to fat-laden swelling of cells (steatosis)

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50
Q

Clinical presentantation of alcohol-induced hepatic steatosis

A

Vomiting, nausea, diarrhoea - due to general GI effects of alcohol
Maybe hepatosplenomegaly.

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51
Q

Investigation of alcohol-induced hepatic steatosis

A

FBC: Macrocytic anaemia indicates heavy drinking.

Liver biochem: Raised ALT and AST

FL: Abdominal ultrasound

GS: Liver biopsy - fatty infiltration

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52
Q

Management of alcohol-induced hepatic steatosis

A

Drinking cessation

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53
Q

Pathophysiology of alcohol-induced hepatitis

A

Excessive alcohol can cause infiltration by neutrophils & cause hepatocyte necrosis

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54
Q

Investigation of alcohol-induced hepatitis

A

Liver biopsy: Mallory bodies, large mitochondria.
FBC: Leucocytosis
Raised serum bilirubin, AST, ALT, ALP, PT

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55
Q

Clinical presentation of alcohol induced hepatitis

A

Jaundice
Ascites
Fever
Hepatomegaly

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56
Q

Management of alcohol induced hepatitis

A

Enteral feeding to maintain nutrition.
Antibiotics, antifungal prophylaxis.

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57
Q

Aetiology of portal hypertension

A

Pre-hepatic: Portal vein thrombosis
Intra-hepatic: Liver cirrhosis, schistosomiasis
Post-hepatic: Budd-Chiari syndrome (hepatic vein thrombosis)

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58
Q

Pathophysiology of portal hypertension

A

Increased intrahepatic resistance due to injury causes portal hypertension.
Results in splanchnic vasodilation and lowered BP.

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59
Q

Complications of portal hypertension

A

Gastroesophageal varices, splenomegaly.

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60
Q

What is a varice?

A

Pathologically enlarged veins.

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61
Q

Aetiolology of oesophageal varices

A

Portal hypertension
Cirrhosis
Schistosomiasis infection
Alcoholism

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62
Q

Pathophysiology of oesophageal varices

A

Drop in systemic BP due to portal hypertension causes RAAS activation and increased CO.
Results in high circulating volume which can cause oesophageal varice formation.
Can start bleeding if portal pressure above 12mmHg.

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63
Q

Clinical presentation of oesophageal varices.

A

Haematemesis
Melaena
Abdominal pain
Hypotension and tachycardia
Splenomegaly

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64
Q

Investigation of oesophageal varices

A

Endoscopy to find source of bleeding.

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65
Q

Management of oesophageal varices.

A

IV terlipressin to increase systemic BP
Endoscopic variceal banding.

Propanolol prophylaxis.

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66
Q

Aetiology of non-alcoholic fatty liver disease

A

Obesity
Hypertension
Type 2 diabetes
Hyperlipidaemia

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67
Q

Pathophysiology of non-alcoholic fatty liver disease

A

Oxidative stress injury and other factors lead to lipid peroxidation in the presence of fatty infiltration and inflammation.

Fibrosis is caused by insulin resistance which can induce connective tissue growth factor.

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68
Q

Investigation of non-alcoholic fatty liver disease

A

Abdominal ultrasound - shows steatosis.
Liver biopsy - Mallory bodies.

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69
Q

Management of non-alcoholic fatty liver disease

A

Lifestyle advice - weight loss, low cholesterol diet, exercise
Pioglitazone

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70
Q

What can cause coma in patients with liver disease?

A

Hepatic encephalopathy
Hyponatraemia
Hypoglycaemia

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71
Q

Aetiology of liver cirrhosis

A

Hepatocellular carcinoma
Hepatitis B,C,D
Non-alcoholic fatty liver disease
Chronic alcoholism - most common cause.

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72
Q

What is liver cirrhosis?

A

End stage, irreversible liver damage characterized by loss of lobular architecture.

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73
Q

Pathophysiology of liver cirrhosis

A

Liver injury causes necrosis and apoptosis, releasing cell contents and
reactive oxygen species (ROS).

Activation of Kupffer cells causes myofibroblast proliferation.

Myofibroblasts cause collagen deposition and fibrosis.

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74
Q

What are the types of liver cirrhosis?

A

Micronodular and macronodular cirrhosis

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75
Q

Characteristics of micronodular liver cirrhosis

A

Regenerating nodules are usually
<3mm in size with uniform involvement of the liver;

76
Q

Characteristics of macronodular liver cirrhosis

A

The nodules are of variable size with non-uniform distribution - can be caused by infection.

77
Q

Aetiology of macronodular liver cirrhosis

A

Viral hepatitis

78
Q

Aeitology of micronodular liver cirrhosis

A

Alcohol or biliary tract disease.

79
Q

What state can the liver be left in upon cirrhosis?

A

Compensated - still some liver function left
Decompensated - end stage liver failure

80
Q

What score can be used to determine the prognosis of liver cirrhosis?

A

Child-Pugh score.

81
Q

Risk factors for primary billiary cholangitis

A

Female, smoking, 40-50 age.
Associated with other autoimmune disorders - hashimoto’s, Sjorgen’s, Keratoconjunctivitis.

82
Q

Pathophysiology of primary billiary cholangitis

A

T-cell mediated autoimmune reaction causing bile duct damage.

Chronic granulomatous inflammation which can result in cholestasis.

83
Q

Clinical presentation of primary billiary cholangitis.

A

Itching
Fatigue
Jaundice
Abdominal pain
Hepatomegaly

84
Q

Investigation of primary biliary cholangitis

A

LFTs: Raised ALP, conj bilirubin, GGT
Low albumin
Serology - antimitochondrial antibodies.
Liver biopsy: Portal tract infilitration with leukocytes

85
Q

Management of primary biliary cholangitis

A

Ursodeoxycholic acid - bile acid analogue
Vitamin ADEK supplements

86
Q

Aetiology/risk factors of primary sclerosing cholangitis

A

Male gender
Association with ulcerative colitis and cholangiocarcinoma.

87
Q

Pathophysiology of primary sclerosing cholangitis

A

Progressive fibrosis, stricturing and scarring of the bile ducts.

88
Q

Investigation of primary sclerosing cholangitis

A

Raised ALP and GGT

MRCP - gold standard, beading” of intra/extrahepatic bile ducts

Serology - pANCA

89
Q

Clinical presentation of primary sclerosing cholangitis

A

Itching, pain, chills jaundice, inflammatory bowel disease

90
Q

Management of primary sclerosing cholangitis

A

Symptomatic management:
- Colestyramine for pruritus (itching)
- Vitamin ADEK supplements
- Liver transplant

91
Q

What does ERCP and MRCP stand for?

A

Endoscopic retrograde cholangiopancreatography

Magnetic resonance cholangiopancreatography

92
Q

How would primary sclerosing cholangitis appear histologically?

A

Periductal oedema, onion skin appearance.

93
Q

What is haemochromatosis?

A

Inherited metal storage disorder causing iron deposition in organs.

94
Q

Aetiology of haemochromatosis

A

Autosomal recessive mutation on HFE gene (chromosome 6)
Male gender

95
Q

Pathophysiology of haemochromatosis

A

The HFE gene protein interacts with transferrin receptor 1 causing intestinal uptake of iron exceeding transferrin binding capacity.

Disrupts hepcidin expression which does not allow for iron release from cells.

Causes uptake by liver and other organs over a long period and cause fibrosis.

96
Q

Clinical presentation of haemochromatosis

A

Men are more symptomatic.

Triad of grey/bronze skin pigmentation (due to melanin deposition), hepatomegaly and diabetes mellitus

Fatigue
Joint pain - arthropathy, especially MCPs.
Hypogonadism
Arrythmias - palpitations

97
Q

Why are men more symptomatic in haemochromatosis?

A

Women lose iron through menstruation and have lower dietary iron intake.

98
Q

Investigation of haemochromatosis

A

Serum iron - elevated (>30)
Serum ferritin - elevated
Genetic testing for HFE gene
Liver biopsy

99
Q

Management of haemochromatosis

A

Venesection
Low iron diet
Avoid fruits

100
Q

Aetiology of Wilson’s disease

A

ATP7B gene mutation (autosomal recessive)

101
Q

How is copper normally metabolized?

A

Goes from GI tract to liver bound to albumin.
Binds to apoceruloplasmin in the liver, forming ceruloplasmin and secreted into the blood.
Remaining copper excreted into the bile and faeces.

102
Q

Pathophysiology of Wilson’s disease

A

Failure of copper excretion from bile due to defective ceruloplasmin transport causes copper deposition into tissues.

103
Q

Clinical presentation of Wilson’s disease

A

Acute/chronic hepatitis symptoms e.g jaundice

Tremor, dysarthria, involuntary movements and eventually dementia

Kayser–Fleischer ring, - green brown pigment at corneoscleral junction.

104
Q

Investigation of Wilson’s disease

A

Total serum copper - reduced since deposition in tissue.

Ceruloplasmin - decreased

Free copper - increased since less ceruloplasmin for it to be bound to

24 hr Urinary copper - elevated

Liver biopsy

105
Q

Management of Wilson’s disease

A

Lifelong penicillamine - copper chelating agent

Trientine & zinc acetate for maintenance in asymptomatic.

Low copper diet (e.g no choc, peanuts)

106
Q

What is the function of alpha-1-antitrypsin?

A

Prevents tissue damage by inhibits the proteolytic enzyme neutrophil elastase.

107
Q

Aetiology for alpha-1-antitrypsin deficiency?

A

SERPINA1 protein mutation - autosomal recessive.

108
Q

Pathophysiology of alpha-1-antitrypsin deficiency

A

Causes panacinar emphesyma in the lungs through alveolar duct collapse.

Liver tissue damage leads to cirrhosis and hepatocellular carcinoma.

109
Q

Clinical presentation of alpha-1-antitrypsin deficiency

A

Children: Liver disease, like cirrhosis, jaundice, hepatitis, etc.

Adutls: COPD, emphysema etc with no smoking history.

110
Q

Investigation of alpha-1antitrypsin deficiency

A

Low serum α1-antritrypsin

Liver biopsy: PAS positive globules containing misfolded a1 antitrypsin

CXR - Barrel chest
CT chest shows emphysema
Spirometry shows obstruction (FEV:FVC <0.7)

111
Q

Management of alpha-1 antitrypsin deficiency

A

Smoking cessation
Management of complications.

112
Q

Pathophysiology of Budd-Chiari syndrme

A

Obstruction to the venous outflow of the liver owing to occlusion of the hepatic vein.

113
Q

Aetiology of Budd-Chiari syndrome

A

Hepatocellular carcinoma, polycythaemia, thrombus formation, renal tumours.

114
Q

Clinical presentation of acute Budd-Chiari syndrome

A

Abdominal pain
Nausea
Vomiting
Tender hepatomegaly
Ascites

115
Q

Clinical presentation of chronic Budd-Chiari syndrome

A

Hepatosplenomegaly
Mild jaundice
Ascites
Negative hepatojugular reflux
Portal hypertension.

116
Q

Investigation of Budd-Chiari syndrome

A

Early: Hypoalbuminuric ascites fluid
Late: Hyperalbuminuric ascites fluid

Histology - centrilobular compression and necrosis
Ultrasound/CT/MRI - hepatic vein occlusion

117
Q

Management of acute Budd-Chiari syndrome

A

Transjugular intrahepatic portosystemic shunt (TIPS)
Anticoagulant prophylaxis

118
Q

Management of chronic Budd-Chiari syndrome

A

Liver transplant
Anticoagulant prophylaxis.

119
Q

Pathophysiology of hepatic encephalopathy

A

In cirrhosis, portal blood bypasses the liver via collaterals.
Lack of detoxification can cause toxic metabolites like ammonia to build up in the brain.

120
Q

Clinical presentation of hepatic encephalopathy

A

Confusion
Liver flap (asterixes - flapping tremor with wrist extended)
Drowsiness
Coma

121
Q

Investigation of hepatic encephalopathy

A

EEG
Arterial blood ammonia
Check visual evoked responses

122
Q

Management of hepatic encephalopathy

A

Lactulose - reduces colon pH to inhibit NH3 absorption.
Rifaximin - antibiotic that reduces NH3 producing gut bacteria.

123
Q

What is acute liver failure?

A

Acute liver failure (ALF) is defined as acute liver injury with encephalopathy and deranged coagulation (INR >1.5) in a patient with a previously normal liver.

124
Q

Aetiology of acute liver failure

A

Hepatitis ABDE, Cytomegalovirus
Autoimmune hepatitis
Paracetamol overdose, alcoholism
Hepatocellular carcinoma

125
Q

Clinical presentation of acute liver failure

A

Jaundice
Confusion, drowsiness - HE
Spasticity and hyper-reflexia
Cerebral oedema
Fetor hepaticus - patient breath smells like rotten eggs and garlic
Bruising

126
Q

Investigation of acute liver failure

A

Hyperbilirubinaemia
ALT, AST - elevated
Low levels of coagulation factors
High ammonia, low glucose

EEG - encephalopathy
Abdominal ultrasound - liver size, hepatic vein patency.

127
Q

Management of acute liver failure

A

Treat causative problem.

Coagulopathy - IV Vit K
Raised ICP - IV Mannitol
Encephalopathy - Lactulose
Antibiotic prophylaxis

128
Q

Aetiology of chronic liver disease

A

Alcohol
Non alcoholic steatohepatitis (NASH)
Viral hepatitis (B, C)

Immune:
autoimmune hepatitis
primary biliary cholangitis
sclerosing cholangitis

Metabolic:
haemochromatosis
Wilsons
a1 antitrypsin deficiency

Vascular :
Budd-Chiari

129
Q

Viral aetiology of hepatitis

A

Hepatitis ABCDE viruses
EBV, CMV, VZV

130
Q

Organismal aetiology of hepatitis

A

Protozoa -Toxoplasmis gondii

Bacteria - Syphilis, M.tuberculosis

131
Q

Non-infective causes of hepatitis

A

Alcohol
Autoimmune hepatitis
NAFLD

132
Q

What hepatitis viruses usually cause acute hepatitis?

A

A & E

133
Q

Clinical presentation of acute hepatitis

A

Jaundice
Fever (pyrexia)
RUQ abdominal pain
Tender hepatomegaly
Ascites

134
Q

Clinical presentation of chronic hepatitis

A

Palmar erythema
Spider naevi
Dupuytren’s contracture (one or more fingers bending into palm of hand)

135
Q

Investigation of acute hepatitis

A

Raised transaminases (ALT/ALP)
With/without raised bilirubin

136
Q

What can be seen on serology for an acute hepatitis infection?

A

Anti-Hepatitis X Virus core IgM (e.g Anti-HBc IgM)

Hepatitis X Virus Surface Antigen (e.g HBsAg) - indicates ongoing infection

Hepatitis X e Antigen (e.g HBeAg) - indicates active viral replication and high transmissibility.

137
Q

What can be seen on serology for a chronic hepatitis infection?

A

Anti-Hepatitis X Virus core IgG
(e.g Anti-HBc IgG, or HBcAb IgG)

Hepatitis X Virus Surface Antigen (e.g HBsAg) - indicates ongoing infection

If high transmissibility - Hepatitis X e Antigen
(e.g HBeAg)

138
Q

What can be seen on serology for a patient who is vaccinated against hepatitis?

A

Antibody to Hepatitis B Virus Surface Antigen
(e.g Anti-HBs)

139
Q

What can be seen on serology for a patient who has hepatitis immunity through a past infection?

A

Antibody to Hepatitis B Virus Surface Antigen
(e.g Anti-HBs)

Anti Hepatitis X Virus Core IgG (e.g HBcAb IgG)

140
Q

Mode of transmission of hepatitis A and E

A

Faecal-oral route

141
Q

Aetiology/risk factors for hepatitis A & E

A

Contaminated food + water
Immunocompromised patients

142
Q

Prevention of hepatitis A

A

Active immunisation

143
Q

Management of hepatitis E

A

If chronic infection (viral RNA > 6 months), treat with rivabarin.

144
Q

Which hepatitis viruses have vaccinations?

A

Hepatitis B & C

145
Q

Aetiology/risk factors of hepatitis B, C, D

A

IV drug users
Tatoos
Infected mothers
Unprotected sex

146
Q

Mode of transmission of hepatitis B, C, D

A

Blood borne + body fluids
Unprotected sex
Mother to child

147
Q

Management of chronic hepatitis B

A

If chronic or severely ill, DNA polymerase inhibitors tenofovir, entecavir + pegylated interferon alpha.

148
Q

Complications of chronic hepatitis C

A

Liver cirrhosis and failure
Hepatocellular carcinoma

149
Q

Prevention of hepatitis B, C, D

A

Antenatal viral screening
Childhood and healthcare worker immunisation - B
Screening of blood products
Barrier contraceptives

150
Q

Pathophysiology of hepatitis D

A

Defective RNA requiring HBsAg for viral replication.

Can be co-infection or superinfection post hepatitis B

151
Q

Investigation of hepatitis D

A

Serology:

Co-infection: Anti HBV IgM and Anti HDV IgM

Superinfection: Anti HBV IgG and Anti HDV IgM

152
Q

Management of hepatitis D

A

Pegylated interferon-a

153
Q

Management of hepatitis C

A

Direct acting antiviral therapy

Ex. Elbasvir/Grazoprevir + ribavarin

154
Q

Pathophysiology of T1 autoimmune hepatitis

A

Associated with HLA-DR4 and DR3.

Can have anti-nuclear antibodies (ANA)
Anti smooth muscle antibodies (ASMA)
Anti soluble liver antigen/liver pancreas antibody (ASLA/LP)

Affects middle aged women mainly.

155
Q

Pathophysiology of T2 autoimmune hepatitis

A

Associated with HLA DQB1, DRB1

Can have anti-liver kidney microsome antobodies (LKM1), anti-liver cytosol 1 antibody (LC1).

Affects children and young adults mainly.

156
Q

Investigation of autoimmune hepatitis

A

Raised immunoglobulins

Serology: Relevant antibodies

Liver biopsy: Piecemeal necrosis (interface hepatitis).

157
Q

Investigation of hepatobilliary stones

A

First line: Abdominal ultrasound.

Can also do MRCP - esp if in billiary tree.

High ALT if infection

158
Q

Aetiology of cholangiocarcinoma

A

Primary sclerosing cholangitis
Fluke worm infection

159
Q

Clinical presentation of cholangiocarcinoma

A

Abdominal pain +/- ascites
Malaise
Jaundice
Dark urine
Pale stools

160
Q

Investigation of cholangiocarcinoma

A

First line: Abdominal ultrasound
Gold standard: MRCP
LFT - raised bilirubin and ALP

161
Q

Management of cholangiocarcinoma

A

Surgical resection
ERCP with stenting

162
Q

Aetiology of hepatocellular carcinoma

A

Liver cirrhosis, viral hepatitis (esp B and C), alcoholic liver disease, NAFLD

163
Q

Clinical presentation of hepatocellular carcinoma

A

Weight loss
Hepatomegaly
Jaundice
Ascites
Hepatic encephalopathy
Pruritus

164
Q

Investigation of hepatocellular carcinoma

A

First line - abdominal ultrasound
Gold standard - abdominal CT
Serum α-fetoprotein - tumour marker in HCC, will be raised.

165
Q

Management of hepatocellular carcinoma

A

Surgical resection of tumour
Liver transplant

166
Q

What other regions can a hepatocellular carcinoma metastisize to?

A

Lymph nodes, bones, lungs.

167
Q

Aetiology of pancreatitis

A

I - Idiopathic
- G - Gallstones (majority - 60%)
- E - Ethanol (i.e. alcohol - 30%)
- T - Trauma
- S - Steroids
- M - Mumps
- A - Autoimmune
- S - Scorpion venom
- H - Hyperlipidaemia
- E - ERCP (endoscopic retrograde cholangiopancreatography)
- D - Drugs e.g. azathioprine, furosemide (diuretics), corticosteroids, NSAIDs, ACE inhibitors
- Also pregnancy and neoplasia

168
Q

Pathophysiology of pancreatitis

A

Buildup of pancreatic enzymes can cause tissue autodigestion and haemhorrage.

169
Q

Clinical presentation of pancreatitis

A

Acute epigastric pain radiating to the back.
Retroperitoneal haemhorrage - Cullen and Turner’s sign
Nausea/vomiting
Hypotension due to fluid oedema within gut
Pyrexia

170
Q

What are Cullen’s and Grey Turner’s signs?

A

Cullens - periumbilical ecchymosis (skin discoloration)
Grey Turner’s - left flank discoloration

171
Q

Investigation of pancreatitis

A

Serum amylase - elevated + diagnostic if combined with symptoms and 3x raised.

GS: Raised serum lipase - specific for pancreatitis

Urinalysis - raised urine amylase

CRP - elevated

Abdominal CT - best imaging if biochem not indicative.

172
Q

What scoring system is used to assess the severity of pancreatitis?

A

Apache and Glasgow scoring system.

173
Q

Complications of acute pancreatiits

A

Necrotizing pancreatitis
Pseudocyst formation
Progression into chronic pancreatitis

174
Q

Management of pancreatitis

A

Nil by mouth to reduce pancreatic enzyme secretion.
Analgesia - tramadol
Antibiotic prophylaxis - cefuroxime, metronidazole.

175
Q

Aetiology/risk factors of pancreatic cancer

A

Smoking
Alcohol
Excessive aspirin usage
Old age
Obesity
T2DM

176
Q

Pathophysiology of pancreatic cancer

A

Mostly affects exocrine pancreas.
Mainly occurs in the head of the pancreas, but can be in body or tail.

177
Q

Clinical presentation of pancreatic cancer

A

Abdominal pain radiating to the back - cancer of body/tail.
Painless jaundice + DUPS - cancer of head
Weight loss
Courvoisier’s sign - palpable pancreas/GB with painless jaundice

Steatorreah = obstruction of pancreatic duct

178
Q

Investigation of pancreatic cancer

A

First line - abdominal ultrasound
Gold standard - Abdominal CT with contrast and pancreatic mass protocol.

179
Q

Management of pancreatic cancer

A

Surgical removal of tumour - whipple procedure (pancreatoduodenectomy) for head tumors.
Pancreatectomy for body/tail tumours.

Chemotherapy

180
Q

Differences in acute and chronic pancreatitis

A

Chronic causes irreversible pancreatic damage e.g fibrosis.

Longer duration of disease.

181
Q

What vitamin supplementation is used in chronic pancreatitis?

A

ADEK vitamins because they are fat soluble.

Pancreatitis causes malabsorption of fat due to decreased lipase production.

182
Q

What type of jaundice is raised ALP an indication of?

A

Post-hepatic jaundice

183
Q

What type of jaundice is raised AST/ALT an indiciation of?

A

Intrahepatic jaundice

184
Q

Mangement of alcohol withdrawal

A

Acamprosate/naltrexone - NMDA receptor antagonists.

185
Q

2 causes of asterixis

A

Chronic liver disease
CO2 retention

186
Q
A

Sirpi's Phase 2A Medicine (13 decks)

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