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Year 2 - Alimentary > Liver & Biliary system conditions > Flashcards

Liver & Biliary system conditions Flashcards

1
Q

Transmission of viral hepatitis A (2)

A

Food/water: faecal-oral

Body fluids - sexual fluids, blood to blood

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2
Q

Which hepatitis viruses are associated with chronic liver disease (3)

A

B,C,D

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3
Q

Hepatitis A risk factors (4)

A

Age 5-14
Sex between men
Living in endemic region
Contact with infected person

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4
Q

Hepatitis A symptoms (4) /signs (4)

A 
Symptoms:
Nausea/vomiting - ABRUPT ONSET
RUQ pain - ABRUPT ONSET
Malaise - ABRUPT ONET
Jaundice - typically 2 wks after infection/other symptoms
Signs:
Fever - ABRUPT ONSET
Hepatomegaly 
Steatorrhoea
Dark urine

JAUNDICE APPEARS IN HEP A MUCH QUICKER THAN ALL THE OTHER TYPES

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5
Q

Hepatitis A investigations (2)

A

Diagnostic - IgM anti-hepatitis A antibodies

LFTs - elevated serum transaminases, elevated bilirubin

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6
Q

Hepatitis A treatment (2)

A

NO SPECIFIC TREATMENT; ONLY SUPPORTIVE; body will clear virus itself

If not vaccinated for hep A:
-hep A vaccine or normal immunoglobulin

If confirmed hepatitis A:
-Supportive care - rest, analgesia

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7
Q

Who is the hepatitis A immunisation targeted at (5)

A 
Travellers to endemic regions
Patients with chronic liver disease
Haemophiliacs (have impaired clotting ability)
Occupational exposure
Men who have sex with men
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8
Q

How is hepatitis B transmitted

A

Through body fluids - blood to blood or sexual fluid

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9
Q

Hepatitis B infection pathophysiology

A

Virus doesn’t actually kill hepatocytes

Host immune response (particularly cellular) to the viral antigens causes the liver injury

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10
Q

Hepatitis B risk factors (5)

A 
HBV infected mother passing onto baby
IV drug use
Sex between men
Multiple sexual partners
Family history of HBV/chronic liver disease
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11
Q

Antigens of HBV + what do they indicate if detected (4)

A

Hepatitis B surface antigen (HBsAg) - indicates active replication; disappears after acute infection

Hepatitis B early antigen (HBeAg) - indicates active replication of HBV; in early acute stage then disappears

Hepatitis B core antigen (HBcAg) - indicates active replication of HBV, not detected in blood

HBV DNA - indicates active replication of HBV

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12
Q

Hepatitis B symptoms (5)/ signs (5)

*but what’s the important thing to remember

A

*MAJORITY ASYMPTOMATIC until cirrhotic

Symptoms:
Fever/chills 
Fatigue 
Arthralgia
RUQ pain 
Nausea/vomiting 
Signs:
Hepatomegaly 
Jaundice
Dark urine
Ascites 
Spider naevi
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13
Q

Hepatitis B investigations

  • bloods (3)
  • specific serology (antigen, PCR, 4 antibodies)
A
  • LFTs (elevated aminotransferases (ALT/AST), alk phos)
  • FBC
  • U+Es - hyponatraemia, high urea
  • Serum HBsAg (surface antigen) - FIRST TEST; disappears after acute infection
  • HBV DNA
  • Serum anti-HBs (anti hep B surface antigen antibody) - appears wks after surface antigen disappears; suggests resolved acute infection
  • Serum IgM anti-HBc (IgM anti hep B core antigen antibody) - appears during acute infection
  • Serum IgG anti-HBc - develops after IgM
  • Serum anti-HBe (hepatitis B envelope antibody)
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14
Q

4 antibodies produced against HBV + do they indicate acute or chronic infection

A

Anti-HBs (hep B surface antigen antibody) - suggest resolved infection, lifelong immunity

IgM anti-HBc (IgM hep B core antigen antibody) - indicate acute infection

IgG anti-HBc - indicate resolved acute or chronic infection

Anti-HBe (hepatitis B envelope antibody) - indicate inactive infection if HBeAg negative

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15
Q

Hepatitis B treatment (5)

  • acute infection (2)
  • chronic infection (3)
A

Acute infection
-supportive care (rest, analgesia)
+/- oral antivirals - if progresses to very SEVERE or liver failure

Hepatitis B vaccine (only works to prevent or in very recent exposure before person has been infected)

Chronic infection:

  • Oral antivirals (entacovir) OR pegylated interferon
  • Liver transplant - if decompensating cirrhosis
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16
Q

Complications of hepatitis B, C + D infection (3)

A

Chronic hepatitis –> liver cirrhosis –> HCC/ESLD

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17
Q

Transmission of hepatitis C

A

Body fluids - blood, sexual

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18
Q

Which hepatitis viruses are RNA (4) /DNA (1) viruses

A

RNA virus - A,C,D,E

DNA virus - B

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19
Q

What enzyme do RNA viruses need to replicate

A

Reverse transcriptase

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20
Q

Hepatitis C risk factors (5)

A 
IV DRUG USE
BLOOD TRANSFUSIONS
Unsafe medical practices
Heavy alcohol use
HIV
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21
Q

Hepatitis C symptoms (3) /signs (4) + do they appear in acute or chronic HCV

A

Asymptomatic until cirrhotic

Symptoms -
fatigue (acute + chronic hep C),
arthralgia/myalgia (chronic hep C)

Signs - 
fever (acute hep C), 
jaundice (chronic), 
ascites (chronic), 
HE (chronic)
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22
Q

Hep C investigations (3)

  • serology (antibody, antigen)
  • bloods
A

ELISA for serum anti-HCV antibody
PCR for HCV RNA
LFTs - elevated aminotransferases, esp ALT (alanine aminotransferase)

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23
Q

Hep C treatment (2)

A

Oral antiviral combo x2

Liver transplant - if liver failure

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24
Q

Transmission of hepatitis D

A

Transmitted by body fluids - blood or sexual contact

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25
Q

What is special about hepatitis D infection

A

Only infects those that are already infected with HBV as it needs HBV to be able to survive inside body

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26
Q

Surface antigen of HDV (hint: HDV can only exist with HBV infection as well)

A

Same as surface antigen of HBV:

HBsAg

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27
Q

Hepatitis D risk factors (3)

A

Carrying HBV
IV drug use
Sex between men

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28
Q

Hepatitis D symptoms/signs

A

Same as HBV

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29
Q

Hepatitis D investigations (3)

-serology (2 antibodies, 1 antigen)

A

Serum IgM anti-HDV
Serum IgG anti-HDV
HDV RNA - by doing PCR

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30
Q

Hepatitis D treatment

  • prevention
  • medical
A

INCURABLE

Prevented by HBV vaccine
Pegylated interferon alpha (slows spreading but doesn’t cure)

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31
Q

Transmission of hepatitis E

A

Food/water: faecal-orcal transmission

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32
Q

What is the commonest hepatitis infection in grampian

A

Hep E

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33
Q

Hepatitis E risk factors (3)

A

Poor sanitation areas
Undercooked meat/contaminated meat
Pregnant women/infected mother to child

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34
Q

What is fulminant hepatitis + when is it likely to occur

A

Acute liver failure

Occurs more frequently when hepatitis E occurs during pregnancy

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35
Q

Hepatitis E symptoms (5) /signs (4)

A 
Symptoms -
Fever, 
nausea/vomiting, 
anorexia, 
fatigue, 
RUQ pain
Signs-
Jaundice 
--> dark urine
-->steatorrhoea
Hepatomegaly
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36
Q

Hepatitis E investigations (2)

-serology (antibody, antigen)

A

Serum IgM anti-HEV

HEV RNA

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37
Q

Hepatitis E treatment (3)

A

No specific treatment
Very resistant to treatment
Maintain good hygiene

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38
Q

Complications of hepatitis E

A

Acute liver failure (fulminant hepatitis)

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39
Q

What is alcoholic liver disease + 3 stages of alcoholic liver disease

A

Direct alcohol toxicity causing fatty change of liver

  • Steatosis –> alcoholic hepatitis –> cirrhosis
  • STILL REVERSIBLE AT THIS STAGE
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40
Q

Cause of alcoholic liver disease

A

CHRONIC ALCOHOL

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41
Q

Alcoholic liver disease pathophysiology

A

Abnormal lipid retention in hepatocytes (steatosis) –> large triglyceride fat vacuoles accumulate –> fatty liver

May be accompanied by progressive inflammation –> steatohepatitis

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42
Q

Alcoholic liver disease risk factors (4)

A

Chronic alcohol
Female
Hepatitis C
Obesity

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43
Q

Alcoholic liver disease symptoms (3) /signs (4)

A

Symptoms:
Abdominal pain - RUQ
Fatigue/malaise
Anorexia

Signs:
Hepatomegaly 
Ascites 
Weight loss OR gain
Dupuytren's contracture - in advanced disease
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44
Q

Alcoholic liver disease investigations

  • LFTs (5)
  • imaging (1)
A

LFTs

  • AST, ALT (AST: ALT = >2:1)
  • gamma GT - high
  • bilirubin - high
  • albumin - low as synthetic liver function decreased

Liver ultrasound

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45
Q

What is the AST:ALT ratio in alcoholic liver disease/ alcoholic hepatitis

A

AST: ALT = >2:1

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46
Q

Alcoholic liver disease treatment (5)
-lifestyle - most important one of all
-medical (3)
+/- medical

A

ALCOHOL ABSTINENCE - 1st line

Treat alcohol withdrawal - benzodiazepine

Nutritional supplements (thiamine)

Immunisations - for flu, hep A/B

+/- Steroids (prednisolone) if:

  • Glasgow alcoholic hepatitis score >9
  • Maddrey’s discrimination function >32
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47
Q

What is the criteria for giving steroids in ALD (2)

A

Glasgow alcoholic hepatitis score >9

Maddrey’s discrimination function >32

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48
Q

Complications of ALD (3)

A

Hepatic encephalopathy
Portal hypertension
GI bleed

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49
Q

What is autoimmune hepatitis

A

Chronic inflammatory disease caused by auto-antibodies attacking hepatocytes

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50
Q

Cause of autoimmune hepatitis

A

Idiopathic

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51
Q

Pathophysiology of autoimmune hepatitis

-combination of what factors

A

Interaction between genetics, environmental trigger, and immune dysregulation

In the genetically predisposed, environmental agent can trigger a pathogenic process leading to liver necrosis and fibrosis

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52
Q

Autoimmune hepatitis risk factors (2)

A

Female

Genetic predisposition

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53
Q

Autoimmune hepatitis symptoms (4) /signs (4)

A 
Symptoms:
Fatigue/malaise
Anorexia
RUQ pain
Pruritus - MILD
Signs:
Jaundice
Fever
Hepatomegaly
Spider naevi
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54
Q

Autoimmune hepatitis investigations

  • LFTs (4)
  • autoantibodies (2)
  • definitive diagnosis
A

LFTs

  • ALT - high
  • AST - high
  • albumin - low
  • bilirubin - high

Anti nuclear antibodies
Smooth muscle antibodies

LIVER BIOPSY

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55
Q

What liver function test is more specific for alcohol related liver injury

A

Gamma GT - raised

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56
Q

Autoimmune hepatitis treatment (1 +/- 1)

A

Steroids - prednisone

+/- other immunosuppressant (azathioprine)

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57
Q

Complications of autoimmune hepatitis

  • of long term corticosteroids
  • of the disease itself
A

Osteoporosis, diabetes, hypertension due to corticosteroids
Acute/chronic liver failure
End stage liver disease and HCC are unlikely

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58
Q

What is non-alcoholic fatty liver disease + the 3 stages of NAFLD

A

Fatty change of the liver not due to alcohol

Steatosis –> non-alcoholic steatohepatitis (NASH) –> fibrosis + cirrhosis

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59
Q

Hypothesised cause of NAFLD, although not 100% clear

A

Insulin resistance

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60
Q

Pathophysiology of NAFLD (5)

A

Insulin resistance –> fatty accumulation in liver (steatosis) –> inflammation (NASH) –> healing of inflammation by fibrosis –> cirrhosis

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61
Q

NAFLD risk factors (4)

A

Obesity
Diabetes
Hypercholesterolaemia
Hypertension

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62
Q

NAFLD/hepatic steatosis (3)/ signs (2)

A

Symptoms:
Fatigue
Malaise
RUQ pain

Signs:
Hepatosplenomegaly
Truncal/central obesity

ASYMPTOMATIC until advanced

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63
Q

NAFLD investigations

  • gold standard
  • LFTs (4) + is ALT or AST higher
  • other bloods
  • imaging
  • scoring system for NAFLD
A

LIVER BIOPSY - gold standard

LFTs

  • ALT > AST = NAFL
  • bilirubin - high
  • gamma GT - high
  • AlkP - high

FBC, U+Es, Lipid panel - high total cholesterol

Ultrasound

NAFLD score (age, diabetes, AST:ALT, platelet, albumin)

64
Q

NAFLD treatment

  • lifestyle (2)
  • medical (2)
  • surgical if
A 
Weight loss 
Diet change
Insulin sensitiser - metformin (if have diabetes)
Statins (if have high cholesterol)
Liver transplant (if ESLD)
65
Q

What is jaundice and what is it caused by

A

Increased circulating bilirubin due to altered metabolism of bilirubin in any of the 3 pathways of bilirubin metabolism (pre-hepatic, hepatic or post-hepatic)

66
Q

Pathophysiology of pre-hepatic jaundice

A

Increased release of haemoglobin from RBCs due to increased haemolysis –> increased circulating bilirubin

67
Q

Pathophysiology of hepatic jaundice + name the 2 causes of hepatic jaundice

A

Defective uptake of bilirubin –> defective conjugation of bilirubin –> defective excretion of bilirubin

DUE TO:
Cholestasis (bile accumulation in liver –> reduced bile flow to duodenum)
or
intra-hepatic bile duct obstruction (PSC, PBC, tumours)

68
Q

Pathophysiology of post-hepatic jaundice + name the 3 causes of post-hepatic jaundice

A

Defective transport of bilirubin by the biliary ducts due to:

Gallstones (cholelithiasis), gallbladder disease,
extra-hepatic duct obstruction

69
Q

Jaundice risk factors (4)

A

Chronic alcohol
IV drug use
Travel history to endemic regions
Sexual activity with hep C/D people

70
Q

Jaundice symptoms (3)/ signs (3)

A 
Yellow eyes and skin
Symptoms- 
fatigue, anorexia, pruritus
Signs- 
Steatorrhoea, dark urine, weight loss
71
Q

Jaundice investigations (2)

A

Serum bilirubin

Ultrasound

72
Q

Jaundice treatment (2)

A

No treatment for jaundice in adults

Treat cause to get rid of jaundice, e.g. treat hepatitis, gallstone blockage

73
Q

What is cirrhosis

A

End stage liver disease caused by progressive fibrosis, response of liver to chronic injury

74
Q

Causes of cirrhosis (7)

A

Chronic injury from:

Chronic alcohol/ alcoholic liver disease
Chronic hepatitis B + C
Metabolic disorders - NAFLD, OBESITY, excess copper (haemochromatosis, Wilson’s disease)
Autoimmune - autoimmune hepatitis, PBC, PSC
Drugs - methotrexate

75
Q

Pathophysiology of cirrhosis

A

Healing of chronic inflammation by fibrosis –> liver tissue replaced by scar tissue –> loss of normal liver structure –> impaired function –> liver failure

Stellate cells activated, collagen produced

76
Q

Cirrhosis symptoms (2) /signs (11)

A

Symptoms:
Fatigue/weak
Pruritus

Signs:
Jaundice - late stage
Hepatosplenomegaly
Bruising
Ascites
Abdo distension
Peripheral oedema
Hepatic fetor
Spider naevi
Palmar erythema
Leukonychia (white nails)
Clubbing
77
Q

Cirrhosis investigations

  • LFTs
  • other bloods (3)
  • imaging (2)
  • most specific and sensitive test (but don’t always need this if other investigations are suffice)
A

LFTs - AST > ALT, GGT, AlkP, bilirubin, albumin, PT time

U+Es - low sodium
Platelet count - LOW
Serology (for hep B/C)

Abdo USS
Abdo CT

Liver biopsy

78
Q

Cirrhosis treatment

  • medical (2)
  • lifestyle (2)
  • surgical if
A

Treat underlying chronic liver disease (hep C/D, ALD, autoimmune etc)
Diuretics (furosemide + spironolactone) - for ascites
Stop alcohol
Restrict sodium in diet

Liver transplant - if very decompensated

79
Q

Complications of cirrhosis (5)

A 
Portal hypertension
Ascites
Variceal bleeding
HCC
Hepatic encephalopathy
80
Q

Main preceding cause of hepatocellular carcinoma

A

Liver cirrhosis

81
Q

HCC risk factors (6)

A 
Cirrhosis
Chronic hepatitis B + C
Chronic alcohol
Obesity
Diabetes
Family history of HCC
82
Q

HCC symptoms (3)/ signs (7)

A

Symptoms:
RUQ pain
Anorexia
Early satiety - due to ascites compressing stomach

Signs:
Weight loss
Palpable abdo mass
Signs of decompensated cirrhosis
-Abdo distension/ASCITES
-Jaundice
-Variceal bleeding
-Splenomegaly
-HE --> fetor hepaticus, asterixis (flapping tremor)
83
Q

HCC investigations (6)

  • bloods (3)
  • cancer marker
  • imaging (2)
A

FBC
LFTs - elevated aminotransferases, AlkP, bilirubin; low albumin
U+Es

Alpha foetal protein

USS
Contrast CT/MRI

84
Q

HCC treatment (8) - curative (4) /palliative (4)

A 
Curative:
Partial/full hepatectomy
Liver transplant
Radiofrequency ablation
Radiotherapy 
Palliative:
Chemotherapy
Radiotherapy
Tyroskine kinase inhibitor - sorafenib
Hormone therapy - tamoxifen
85
Q

Where does HCC metastasise to (3)

A

Lung, lymph, bone

86
Q

What is a cholangiocarcinoma

A

Malignant tumour of bile duct epithelium (BILE DUCT CANCER)

87
Q

What type of tumour are most cholangiocarcinomas

A

Adenocarcinoma

88
Q

Cholangiocarcinoma risk factors (5)

A 
Age >50
Cholangitis/ PSC
Choledocho-lithiasis (CBD stone)
Ulcerative colitis
Chronic liver disease - alcoholic liver disease, hep C/D
89
Q

Cholangiocarcinoma symptoms (2)/ signs (1)

A

PAINLESS JAUNDICE
Abdominal pain

Weight loss

90
Q

Cholangiocarcinoma investigations

  • LFTs
  • tumour markers (2)
  • imaging (4)
A

LFTs - elevated bilirubin, AlkP, AST, ALT etc

Tumour markers - CA 19-9, CEA

Abdo USS - INITIAL
Abdo CT/MRI
ERCP + biopsy
MRCP - if can’t do above

91
Q

Cholangiocarcinoma treatment

  • if resectable (2)
  • if unresectable (2)
A

Partial liver resection (if intrahepatic tumour)
OR
tumour excision (if extrahepatic tumour)
+/- pre-op biliary stenting

If unresectable:
Liver transplant
+ neoadjuvant chemotherapy +/- radiotherapy

92
Q

Complications of cholangiocarcinoma (2)

A

Biliary obstruction

Cholangitis

93
Q

What is cholelithiasis

A

Gallstones present in gallbladder

94
Q

How are gallstones formed

A

Bile is supersaturated with cholesterol

Excess cholesterol precipitates out of solution as solid microcrystals –> crystals aggregate + grow –> gallstones

95
Q

3 types of gallstones

A

Cholesterol (most common)
Pigmented (bilirubin)
Mixed

96
Q

Gallstones risk factors (5)

A 
Obesity
Diabetes
Female
Family history of gallstones
Pregnancy
97
Q

Cholelithiasis symptoms (2) /signs (1) + percentage asymptomatic

A

80% asymptomatic

RUQ/epigastric pain (biliary colic) - SUDDEN INTENSE >30mins
Postprandial pain

RUQ tenderness

98
Q

Cholelithiasis investigations

  • imaging (2)
  • bloods (2)
A

Abdo USS
ERCP/MRCP

LFTs - normal but if progresses to choledocholithiasis then AlkP, bilirubin elevated
Serum lipase/amylase - to see if the pain is pancreatitis
FBC - usually normal

99
Q

Cholelithiasis treatment (4)

  • asymptomatic
  • symptomatic
A

If asymptomatic = no treatment

If non-operable:

  • dissolution (with ursodeoxycholic acid tablets)
  • ERCP + lithotripsy (shock waves to break up gallstones)

If operable:
Laparascopic cholecystectomy

100
Q

Cholelithiasis complications (6)

A

ERCP induced pancreatitis
Cholecystitis
Choledocho-lithiasis
Gallstone ileus (gallstones causing small intestine obstruction)
Mirizzi syndrome –> obstructive jaundice

101
Q

Pathophysiology of acute cholecystitis

A

usually when gallstone blocks cystic duct –> bile trapped in gallbladder –> increased pressure in GB –> inflammation in GB –> PAIN

90% resolves itself as stone dislodges itself

102
Q

Cause of cholecystitis

A

Symptomatic gallstones

103
Q

Pathophysiology of chronic cholecystitis

A

Recurrent acute inflammation due to GALLSTONES REPEATEDLY BLOCKING CYSTIC DUCT –> chronic inflammation and FIBROSIS of gallbladder wall

Contractile function lost so GB can’t release bile

104
Q

Risk factors of cholecystitis (think risk factors of gallstones)

A

Gallstones
Diabetes
Obesity
Female

105
Q

Symptoms (3) /signs (3) of cholecystitis

+ where does the pain spread to

A

RUQ pain - can spread to right shoulder
Postprandial pain
Nausea

Fever
MURPHY’S SIGN
-RUQ tenderness during deep inspiration; tenderness suddenly becomes worse and causes BREATHING TO STOP
Palpable mass - distended GB

106
Q

Investigations of cholecystitis

  • initial imaging
  • bloods (3)
  • further imaging if initial imaging unclear
A

RUQ USS

FBC - high WBC
CRP - high
LFTs - elevated AlkP, bilirubin, gamma GT

HIDA scan if USS unclear - shows cystic duct obstruction

107
Q

Treatment of acute cholecystitis (4)

  • medical (3)
  • surgical
A

IV fluids
Antibiotics
Analgesia - NSAIDs

Cholecystectomy

108
Q

What is choledocho-lithiasis + pathophysiology

A

Common bile duct stones

Gallstones can move out from gallbladder into bile duct and block the bile duct –> BILE DUCT STONES

or stones can form in CBD itself

109
Q

Risk factor of choledocho-lithiasis (CBD stones)

110
Q

Causes of extra-hepatic bile duct obstruction (i.e. bile ducts outwith the liver, e.g. CBD) (4)

A

Migrated gallstones
Bile duct tumours - e.g. cholangiocarcinoma
Benign stricture
External compression (e.g. head of pancreas tumour compressing CBD)

111
Q

Symptoms (2) /signs (3) of CBD obstruction/ choledocholithiasis

A

Abdo pain
Nausea/vomiting

PAINFUL jaundice
Dark urine
Steatorrhoea

112
Q

Investigations of CBD obstruction

  • bloods (1)
  • imaging (3)
A

LFTs - elevated AlkP, bilirubin

USS
MRCP/ ERCP
+/- CT

113
Q

Treatment of CBD obstruction (2)

A

Therapeutic ERCP + lithotripsy (shock waves)

or Laparascopic CBD exploration

114
Q

Complication of CBD obstruction

A

Ascending cholangitis (bile proximal to obstruction infected) - due to bacteria ascending

115
Q

Name 3 autoimmune liver diseases

A

Autoimmune hepatitis
Primary biliary cholangitis
Primary sclerosing cholangitis

116
Q

Name 3 diseases that cause intra-hepatic bile duct obstruction

A

Primary biliary cholangitis
Primary sclerosing cholangitis
Liver tumours

117
Q

What is primary biliary cholangitis

A

AUTOIMMUNE LIVER DISEASE

Chronic disease of the small intrahepatic bile ducts that is characterised by progressive bile duct damage –> intra-hepatic bile duct obstruction

118
Q

Pathophysiology of primary biliary cholangitis

-what autoantibodies involved

A

Anti-mitochondrial autoantibodies attack liver

GRANULOMATOUS inflammation of bile ducts –> loss of intra-hepatic bile ducts –> bile acids build up in liver (CHOLESTASIS) –> fibrosis –> cirrhosis

119
Q

Symptoms (3) /signs (1) of PBC

A

Fatigue
Pruritus
Dry eyes + mouth

Hepatomegaly

120
Q

Investigations of PBC (3)

A

LFTs - all raised, low albumin
Anti-mitochondrial antibody immunofluorescence
Abdo USS - to exclude obstructive lesion

121
Q

Name the liver function tests (7)

A 
Alkaline phosphatase
Gamma GT
Bilirubin
Alanine aminotransferase
Aspartate aminotransferase
Albumin
Prothrombin time
Platelet count
122
Q

When is alkaline phosphatase (ALP) raised + what is it

A

In intra or extra hepatic obstruction, e.g. PBC, PSC, CBD obstruction
It’s an enzyme produced and present in bile ducts

123
Q

Treatment of PBC (3)

-medical

A

Ursodeoxycholic acid (UDCA) - bile acid analogue to dissolve
Prednisolone - if significant inflammation
Antipruritics

124
Q

What is primary sclerosing cholangitis (PSC)

A

Autoimmune liver disease

Chronic progressive cholestatic liver disease –> destruction of the intrahepatic AND/OR extrahepatic bile ducts

Predominantly affects young and middle-aged men, often with underlying IBD

125
Q

Pathophysiology of primary sclerosis cholangitis (PSC)

A

Autoantibodies (no specific autoantibody for PSC) attacking liver –> chronic inflammation + fibrosis of intra/extrahepatic bile ducts –> stricturing of ducts –> cholestasis

Ultimately intra-hepatic ducts are completely destroyed

126
Q

What GI disease is PSC associated with

A

IBD, predominantly MALES

127
Q

Risk factors of PSC (3)

A

Male - unlike most autoimmune diseases
Existing IBD
Genetics

128
Q

Symptoms (3) /signs (3) of PSC

A

Abdo pain - RUQ or epigastric
Fatigue
Pruritus

Jaundice
Weight loss
Fever - episodic

129
Q

Elevation of which 2 LFTs suggest bile duct injury/obstruction

A

ALP

Gamma GT

130
Q

Investigations of PSC (4)

  • bloods (2)
  • imaging (2)
A

LFTs - elevated AlkP, gamma GT
Serum autoantibodies - no specific one for PSC

Abdo USS
MRCP or ERCP

131
Q

Treatment of PSC (5)

  • asymptomatic
  • symptomatic
A

NO EFFECTIVE MEDICAL THERAPY

If asymptomatic – just observe + lifestyle change

  • Antipruritics
  • Immunosuppressants, e.g. prednisolone (if have autoimmune hepatitis as well)
  • ERCP + stent - if symptomatic biliary stricture
  • Liver transplant if end stage liver
132
Q

Complications of PSC (3)

A

Cholangiocarcinoma
Liver failure/cirrhosis
Hepatic encephalopathy

133
Q

What is hepatic encephalopathy + most commonly due to what

A

Decline in brain function that occurs in patients with advanced, acute or chronic liver disease

Commonly due to cirrhosis/liver failure

134
Q

Pathophysiology of hepatic encephalopathy

A

Liver malfunction/failure –> liver can’t adequately remove toxins from blood (lack of ammonia conversion to urea) –> build up of ammonia in blood –> brain dysfunction when ammonia crosses the BBB

135
Q

Causes/risk factors of HE (6)

A 
Cirrhosis
Hypovolaemia
GI bleed
Hypokalaemia
Hypoxia
Acute liver failure
136
Q

Signs of HE (5)

A

Confusion,
Flapping tremor (asterixis)
foetor hepaticus (bad breath)
mood/sleep disturbances

Signs of chronic liver disease/cirrhosis - hepatomegaly etc

137
Q

Investigations of HE

  • bloods (3)
  • imaging (2)
A

LFTs - abnormal
Blood/urine culture - maybe bacteraemia, SBP, UTI
Urine toxin screen

Abdo USS
CT head

138
Q

Treatment of HE (3)

A

Lactulose - laxative
Enema - to clear out bowel
Antibiotics (Rifaximin or neomycin) - only if lactulose not working

139
Q

3 causes of acute liver injury

A

Hepatitis - caused by viruses, alcohol or drugs
Bile duct obstruction
Alcoholic liver disease

140
Q

Which hepatitis viruses usually resolve (2)

141
Q

What is cholestasis

A

Accumulation of bile within hepatocytes or bile canaliculi –> reduced bile flow to duodenum

142
Q

Causes of intra-hepatic bile duct obstruction (3)

A

Primary biliary cholangitis
Primary sclerosing cholangitis
Tumours of liver

143
Q

What is spontaneous bacterial peritonitis (SBP) (2)

A

Acute bacterial infection of ascitic fluid

Can be a feature of advanced end stage liver disease or kidney disease

144
Q

Diagnostic investigation of spontaneous bacterial peritonitis

A

Ascitic tap - to get fluid protein/glucose/WBC level (IF HIGH WHITE CELL THEN DIAGNOSTIC OF BACTERIAL PERITONITIS)

145
Q

Treatment of spontaneous bacterial peritonitis (3)

A

IV Antibiotics
Ascitic Fluid Drainage
IV Albumin Infusion – improves perfusion of kidneys if cause was associated with kidney failure

146
Q

3 stages of alcohol related liver disease

A

Alcoholic fatty liver disease
Alcoholic hepatitis (nothing to do with infectious hepatitis)
Cirrhosis

147
Q

What is liver steatosis

A

Fatty change of the liver, primarily by obesity

148
Q

Is AST or ALT higher in NAFLD

149
Q

Elevated alkaline phosphatase suggests obstruction of what ducts

A

Cystic or bile duct

150
Q

Malignant tumours causing jaundice other than cholangiocarcinoma (3)

A

Gallbladder cancer
Ampullary cancer
Cancer of head of pancreas

151
Q

Name some benign biliary tract diseases (3)

A

Biliary atresia - congenital
Choledochal cysts - congenital
Benign biliary stricture

152
Q

What drugs induce cholestasis

A

Antibiotics, NSAIDs,

153
Q

What tumour is PSC likely to cause

A

Cholangiocarcinoma

154
Q

Tumour marker of HCC

A

Alpha foetal protein

155
Q

What drugs induce liver cirrhosis (2)

A

Amiodarone

Methotrexate

156
Q

What is Charcot’s triad + what condition does it indicate

A

Jaundice, fever and right upper quadrant pain indicating ascending cholangitis

Year 2 - Alimentary (21 decks)

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