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MD2 GIT > Chronic Liver Disease > Flashcards

Chronic Liver Disease Flashcards

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1
Q

List 7 key functions of the liver

A

Synthesis of clotting factors (except factor 8)
Glucose homeostasis (gluconeogenesis, glycogen storage)
Albumin synthesis
Conjugation and clearance of bilirubin
NH3 metabolism (urea cycle)
Drug metabolism and clearance
Immune (dealing with gut-derived bacteria and bacterial products)

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2
Q

Describe the liver enzyme pattern seen in hepatocellular injury or necrosis

A

ALT, AST elevation

Very high ALTs in acute viral hepatitis, acute drug toxicity, ischaemia

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3
Q

Describe the liver enzyme pattern seen in intra- or extra-hepatic cholestasis

A

ALP, GGT elevation
Minor elevation of transaminases
Typical of biliary obstruction, liver infiltration, cholestatic reactions to drugs

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4
Q

Which is more liver-specific: ALT or AST?

A

ALT predominantly from the liver

AST from many sites

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5
Q

What forms of liver disease tend to present with a mixed picture in terms of the liver enzyme pattern?

A

Alcoholic liver disease

Fatty liver disease

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6
Q

List 5 symptoms of CLD

A 
Fatigue
Weight loss (muscle) or gain (ascites)
Bleeding (haematemesis from varices)
Abdominal distension (ascites)
Confusion (encephalopathy)
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7
Q

List 3 clinical signs of CLD

A

Spider naevi
Splenomegaly
Jaundice

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8
Q

What pattern of liver enzymes is typically seen in CLD?

A

Low albumin
Raised bilirubin
AST>ALT (AST not routine)
NB LFTs may be normal

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9
Q

Describe the coagulopathy seen in CLD

A 
Prolonged INR (or high normal 1.2-1.3)
Low platelets (or normal, e.g. under 200)
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10
Q

80 year old woman presents with abnormal LFTs (ALT 54, AST 58, ALP 200)
40 years earlier had severe hepatitis with hepatic failure (encephalopathy and peripheral oedema) after trip to QLD, managed at Fairfield Hospital in ICU
Negative viral and AI serology at the time and made a full recovery
PHx: HTN, mitral valve prolapse
Rx: verapamil, esomeprazole, frusemide
SHx: lives alone (widowed) nearby children
No alcohol (current or past)
No FHx of liver disease
O/E: 3 spider naevi, no other peripheral signs of liver disease, no palpable hepato-splenomegaly, no ascites or oedema, loud pan-systolic murmur consistent with MR
Ix?

A

Ix: FBE, LFTs, coags

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11
Q

What do we look for O/E in CLD?

A

Stigmata of CLD
Signs of underlying aetiology
Signs of decompensation

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12
Q

Stigmata of CLD

A 
Clubbing
Leuconychia
Palmar erythema
Spider naevi
Gynaecomastia
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13
Q

Signs of liver decompensation

A

Jaundice
Ascites/oedema
Bruising

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14
Q

Signs of underlying aetiology for CLD

A

Dupuytren’s contracture (EtOH)

Parotidomegaly (EtOH)

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15
Q

What is clubbing? Mechanism in CLD?

A

Increase in soft tissue of distal fingers/toes

Arterial hypoxaemia due to pulmonary AV shunt?

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16
Q

What is leuconychia? Mechanism in CLD?

A

Opacification of the nail bed

Hypoalbuminaemia or compression of capillary flow by EC fluid

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17
Q

Mechanism of palmar erythema in CLD

A

May be due to excess oestrogens and altered micro-vasculature

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18
Q

4 causes of Dupuytren’s contracture

A

CLD due to alcohol
Manual labour
Anti-epileptics
DM

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19
Q

Mechanism of parotidomegaly in alcoholism

A

Fatty infiltration due to alcohol toxicity +/- malnutrition

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20
Q

Describe the characteristic appearance of a spider naevus

A

Central arteriole with radiating small vessels

Blanches on compression

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21
Q

Where are spider naevi typically seen?

A

SVC distribution

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22
Q

What number of spider naevi is abnormal?

A

> 2 abnormal

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23
Q

What are multiple spider naevi pathognomonic of?

A

Cirrhosis

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24
Q

Mechanism of gynaecomastia in CLD

A

Imbalance of oestrogen:testosterone OR secondary to medication (spironolactone)

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25
Q

Mechanism of jaundice in decompensated CLD

A

Reduced bilirubin processing and excretion (including gall stones, HCC or portal vein thrombosis)

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26
Q

Mechanism of ascites in decompensated CLD

A

Abdominal free fluid due to combination of reduced oncotic pressure (low albumin) and increased portal pressure

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27
Q

Mechanism of coagulopathy in decompensated CLD

A

Reduced clotting factors,thrombocytopaenia

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28
Q 
ALP 170 U/L
GGT 88 U/L
ALT 54 U/L
AST 58 U/L
Bilirubin 17 umol/L
Albumin 36 g/L
INR 1.1
Platelets 125 x 10^9/L
What do these results suggest?
What further tests would help?
A 
Mixed elevation of liver enzymes
AST>ALT suggests possible cirrhosis
Normal synthetic function
Possible portal HTN (low platelets)
Further Ix: hepatitis serology, ANCA, ANA, AMA, ASMA, ALKM, liver U/S, consider liver biopsy
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29
Q

What does a positive ANCA and ANA indicate?

A

??

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30
Q

What is looked for on liver U/S in CLD?

A 
Hepatic echogenicity
Any focal lesions
Liver and spleen size
Portal vein diameter and flow
Presence or absence of ascites
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31
Q

Describe the sonographic appearance of a cirrhotic liver

A

Coarsened hepatic echogenicity

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32
Q

How might liver biopsy be performed?

A

Via intercostal approach

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33
Q

Describe the histopathological progression of CLD

A

F0: normal
F1: peri-portal fibrosis, no septa
F2: peri-portal fibrosis with a few septa
F3: numerous septa, no architectural distortion
F4: architectural distortion and nodule formation

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34
Q

When is staging fibrosis useful?

A

If it would alter Mx

Liver biopsy often useful in this case

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35
Q

What are the risks of liver biopsy and how common are these?

A 
Minor complications (e.g. pain): 14%
Major complications (e.g. haemorrhage/perforation): 0.2-1.0%
Mortality: 0.009%-0.2%
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36
Q

What alternative is there to liver biopsy and when is this indicated?

A

FibroScan

For patients with HCV (remains a research tool for other conditions)

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37
Q

What is FibroScan and how does it work?

A

Transient elastography: probe induces an elastic wave through the liver, velocity of wave is evaluated in a region located located from 2.5cm to 6.5cm below the skin surface

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38
Q

What measurement does FibroScan provide?

A

Liver Stiffness Measurement (LSM): absent or mild fibrosis, significant fibrosis, severe fibrosis, cirrhosis
Median LSM >13 kPa suggests cirrhosis

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39
Q

ARFI

A

Acoustic Radiation Force Imaging

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40
Q

What is ARFI?

A

High power ultrasonic waves are used to displace tissue for the purpose of tissue characterisation and measurements
Acoustic waves displace energy into the tissue; this energy generates a force that causes displacement of the tissue
These motions are used to derive information about the tissue

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41
Q

What is the “rule of 3s” for identifying the cause of CLD?

A

Big 3: HBV, HCV, alcohol
AI 3: AIH, PBC, PSC
Metabolic 3: haemochromatosis, Wilson’s disease, alpha-1 antitrypsin deficiency
Other 3: fatty liver disease (NASH), Budd-Chiari (hepatic vein thrombosis), chronic biliary obstruction (e.g. tumour, CF)

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42
Q

What are 4 main functions of the liver and how are these related to staging of CLD?

A

Make proteins include clotting factors: low levels of albumin/clotting factors results in coagulopathy, bleeding, ascites and oedema
Processes bilirubin: failure to excrete results in jaundice
Metabolises drugs and toxic waste (e.g. ammonia): build up of waste products leads to encephalopathy
First port for blood from intestines: portal HTN results in ascites, splenomegaly and varices (+/- bleeding)

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43
Q

List 3 other problems which may result from CLD

A

Hepatorenal syndrome (renal failure due to CLD)
HCC (aka hepatoma but NOT benign)
Metabolic failure

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44
Q

What kinds of liver disease is HCC associated with?

A

Cirrhosis from any cause

HBV in the absence of cirrhosis

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45
Q

What is the presentation of metabolic failure related to CLD?

A

Hypoglycaemia (late)

Feminisation/masculinisation

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46
Q

What does “decompensation” in the context of CLD refer to?

A

Any of the following: jaundice, ascites/oedema, coagulopathy, variceal bleeding, hepatorenal syndrome

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47
Q

What does “hepatic failure” refer to?

A

Presence of porto-systemic encephalopathy (PSE)

48
Q

What Ix should be performed before a TOE in a patient with CLD

A

Gastroscopy to screen for oesophageal varices

49
Q

Describe the Child-Pugh system for classification of CLD

A

Encephalopathy: none = 1, I-II/suppressed = 2, III-IV = 3
Ascites: none = 1, mild = 2, severe = 3
INR: under 1.7 = 1, 1.7-2.2 = 2, >2.2 = 3
Albumin: >35 = 1, 28-35 = 2, under 28 = 3
Bilirubin: under 34 = 1, 35-50 = 2, 50 = 3

Class A: 5-6 points
Class B: 7-9 points
Class C: 10-15 points

50
Q

What is the 1 and 2 year survival rate for classes A, B and C in the Child-Pugh scoring system?

A

A: 1 year survival 100%, 2 year 85%
B: 1 year survival 81%, 2 year 57%
C: 1 year survival 45%, 2 year 35%

51
Q

What is MELD and when is it used?

A

Model for End-stage Liver Disease
9.6 logE (creatinine (umol/L)/8) + 3.8 logE (bilirubin (umol/L)/17.1) + 11.2 logE (INR) + 6.4
Gives score between 6 and 40; lower scores under 20
Used for transplant listing

52
Q

What are some of the advantages and limitations of MELD?

A

Continuous, objective variables

BUT can’t calculate at bedside and subject to lab variability

53
Q

CLD patient undergoes mitral valve repair and later develops exertional dyspnoea
O/E: dullness to percussion and reduced breath sounds on R
CXR: fluid on R side of chest, echo shows good cardiac function
Dx?
Mx?

A

Dx: CLD with hepatic hydrothorax (ascites which tracks into pleural space)
Mx: increased diuretics with spironolactone and frusemide, occasional drainage via U/S and replacement of fluid with IV concentrated albumin

54
Q

Why do we try and avoid using normal saline in patients with decompensated liver disease?

A

Ascites

55
Q

List 9 complications of CLD

A 
Jaundice
Bleeding varices
Ascites (and SBP)
Encephalopathy
Hepatorenal syndrome
HCC
Nutrition
OP
Infection (CLD patients should be vaccinated)
56
Q

How should CLD be managed?

A

Treating the cause

Managing and preventing complications

57
Q

How should alcoholism be treated?

A

Encourage abstinence
?inpatient detox/withdrawal
Support/counselling
Pharmacological interventions (anti-craving medications)

58
Q

How is HBV treated?

A 
Oral nucleos(t)ide analogues
Peg-IFN
59
Q

How is HCV treated? When do you not treat?

A

Peg-IFN + ribavirin +/- new agents

Not if decompensated CLD

60
Q

How should haemochromatosis as an underlying cause of CLD be treated?

A

Venesection

61
Q

How is AIH treated?

A

Prednisolone +/- azathioprine/mercaptopurine

62
Q

How is PBC treated?

A

Urso-deoxycholic acid

63
Q

How is PSC treated?

A

ERCP +/- stent or balloon dilatation occasionally

64
Q

What possible causes of jaundice should be considered in a CLD patient?

A

Portal vein thrombosis
Biliary obstruction (tumour, gallstone)
Infection (esp SBP)

65
Q

What forms of fluid retention may be seen in CLD patients?

A

Ascites
Oedema
Pleural effusions

66
Q

What is the mechanism of fluid retention in CLD?

A

Renal Na+ and H2O retention via activation of RAAS

67
Q

How is fluid retention in CLD managed?

A

Salt and fluid restriction
Large volume paracentesis (ascitic tap)
Diuretics (spironolactone/amiloride, frusemide)

68
Q

What are the possible locations of varices in CLD?

A

Oesophageal
Gastric
Rarely duodenal

69
Q

Describe 2 methods of primary prophylaxis for bleeding varices in CLD

A

Variceal band ligation (banding)

Non-selective B-blockers (propanolol)

70
Q

List 5 secondary treatments for bleeding varices in CLD

A 
Octreotide or terlipressin
Abx (reduces bacterial translocation)
Endoscopic banding (or sclerotherapy)
Senstaken-Blakemore (SB) tube
TIPSS
71
Q

TIPSS

A

Transjugular intrahepatic portosystemic stent/shunt

72
Q

What is an SB tube?

A

Medical device inserted through the nose or mouth and used occasionally in the management of upper GI haemorrhage due to oesophageal varices

73
Q

Octreotide

A

GH, glucagon and insulin inhibitor (somatostatin analogue)

74
Q

Terlipressin

A

Vasopressin analogue

75
Q

What is encephalopathy and how does it present?

A

Reversible impaired brain function

Spectrum of symptoms from mild slowing to coma, or stroke-like syndromes

76
Q

Describe the mechanism of encephalopathy in CLD

A

Ammonia build-up
Oxidative stress
Impaired neurotransmission (e.g. GABA-benzodiazepine neurotransmitters)

77
Q

PSE

A

Portosystemic encephalopathy

78
Q

List 5 causes of encephalopathy

A 
Drugs
Increased ammonia
Dehydration
Portal vein thrombosis or primary HCC
TIPSS
79
Q

What drugs can cause encephalopathy?

A

Benzodiazepines
Alcohol
Narcotics

80
Q

What are some causes of increased ammonia which may lead to encephalopathy?

A

GI bleeding, constipation
Infection
Electrolyte imbalance, alkalosis, hypoxia

81
Q

What is hepatorenal syndrome? What different types exist?

A

Worsening renal function in the setting of CLD

Type I = acute (

82
Q

Mechanism of hepatorenal syndrome

A

More blood flowing in portal system

Less blood flowing to kidneys

83
Q

What changes are seen on UEC in hepatorenal syndrome?

A

Creatinine rises and urinary volume and urinary Na+ fall

84
Q

How does cirrhosis cause OP?

A

Combination of cholestasis, vit D deficiency, physical inactivity, alcohol excess and hypogonadism

85
Q

What treatment options exist if medical therapy fails?

A

Consider liver transplant; we have no truly effective hepatic support systems
Transplant will cure many disorders but in HCV reinfection occurs 100% of the time

86
Q

How long can a liver graft survive?

A

> 20 years

87
Q

List 4 reasons for deferral from liver transplant waiting list

A

Too early (liver function too good, MELD too low e.g. MELD

88
Q

Name 3 factors which limit rates of liver transplantation

A

Donor organ supply
Size
Blood group

89
Q

How are recipients on the liver transplant waiting list ranked?

A

By MELD score

90
Q

Which CLD patients should be referred for transplantation?

A

Anyone with decompensated CLD (ascites, variceal bleeding, encephalopathy, hepatorenal syndrome, HCC)

91
Q

Mr PH, 54 year old man, born in Hong Kong to Chinese parents and lived in Hong Kong, Korea and Singapore
Routine screening for blood donation at age 16 revealed chronic hepatitis B infection
LFTs normal, seen by GP and told no further Ix required
FHx: mother has HTN and renal failure (HBV status unknown), father died of lung cancer aged 63, brother diagnosed with HCC (HBV positive), other siblings HBV positive
Pt requested scan from GP which revealed 9 cm x 7.8 cm HCC in segments 5/6
Referred to liver clinic
Ix: ALT 58/Bilirubin 19/ALP 98/GGT 307, HBV viral load log 6, platelets 220/INR 1.0/albumin 40, HBsAg positive, HBeAg positive, AFP 6
Mx?

A

Started on entecavir
?R hemi hepatectomy (residual L lobe must be at least 0.6% body weight)
?transplantation

92
Q

Describe the Mazzaferro (Milan) criteria for liver transplantation

A

Single lesion 5 cm or less

Up to 3 separate lesions,

93
Q

Describe the UCSF criteria for liver transplantation

A

Single HCC 6.5 cm or less

Up to 3 lesions, largest of which is

94
Q

When and how is downstaging performed?

A

For patients currently outside transplant criteria
Loco-regional therapy provides “bridging” to prevent tumour progression: TACE, radio-embolisation with beads (SIR-Spheres/SIRTEX), RFA

95
Q

TACE

A

Transarterial chemoembolisation

96
Q

RFA

A

Radiofrequency ablation

97
Q

What % of patients can be successfully downstaged?

A

~30-60%

98
Q

What is the difference in survival rates between patients who require downstaging to meet transplant criteria vs patients who do not need downstaging?

A

5-year survival rates are comparable

99
Q

SIR-Spheres/SIRTEX

A

Selective Internal Radiation Therapy (SIRT)

100
Q

What are some possible complications of liver transplantation and how can these be managed?

A

Humoral rejection: plasmapheresis
Infection: e.g. CMV, treated with IV ganciclovir
Anastomotic stricture: ERCP

101
Q

Describe the epidemiology of HCC in Australia

A

9th most common cause of cancer death in Australia
Fastest increasing cause of cancer deaths
18% survival 5 years after diagnosis
Majority associated with chronic viral hepatitis

102
Q

Describe the epidemiology of HCC in Australia

A

9th most common cause of cancer death in Australia
Fastest increasing cause of cancer deaths
18% survival 5 years after diagnosis
Majority associated with chronic viral hepatitis

103
Q

Give some reasons why HCC may be increasing

A

Underdiagnosed: 45% of Australians with HBV are unaware of their status, screening and monitoring not routine, stigma, language barriers, confusion about “carrier status”, Medicare auditing
Undertreated: only ~1/5 of those who could benefit receive antiviral therapy (

104
Q

What are the top countries of birth for chronic HBV in Australia?

A

China
Vietnam
Philippines
Italy

105
Q

What are the top countries of birth for chronic HBV in Australia?

A

China
Vietnam
Philippines
Italy

106
Q

Who should be screened for HBV?

A 
Individuals from countries of high or intermediate prevalence: Aboriginals, Asia, Africa, South Pacific Islands, Middle East (except Cyprus and Israel), European, Mediterranean (Malta and Spain), South and Central America, Eastern Europe (except Hungary), Caribbean
Household contacts
Sexual contacts
IVDU
Multiple sexual partners
MSM
Prisoners
Those with HCV or HIV
Dialysis patients
All pregnant women
All who receive immunosuppressive therapy
107
Q

What qualifies as a high vs intermediate prevalence area?

A

High: HBsAg 8%
Intermediate: HBsAg 2-7%

108
Q

How is HBV screened for and what actions are indicated for a positive result?

A

HBsAg, HBsAb, HBcAb
If HBsAg positive, refer to specialty clinic
If HBcAb positive, risk of reactivation with immunosuppression
Recommend serology testing of household, close and intimate contacts
Vaccinate non-immune individuals

109
Q

Describe the natural Hx of HBV and the changing clinical indications throughout

A

Immune tolerance: high HBV DNA, normal LFTs, HBeAg, monitor every 6-12 months
Immune clearance: high HBV DNA, abnormal LFTs, HBeAg positive, at risk of progression to cirrhosis and HCC therefore should be referred for consideration of treatment
Immune control: low HBV DNA, normal LFTs, HBeAg negative, anti-HBe positive, monitor every 6-12 months
Immune escape: high HBV DNA, abnormal LFTs, HBeAg negative, anti-HBe positive, at risk of progression to cirrhosis and HCC therefore should be referred for consideration of treatment

110
Q

What is the effect of timely screening and Mx on the natural Hx of HBV?

A

Treatments are effective and well tolerated
Rates of cirrhosis decrease by 52%
Rates of HCC decrease by 47%
25% mortality transforms to 97% surviva

111
Q

What is the effect of timely screening and Mx on the natural Hx of HBV?

A

Treatments are effective and well tolerated
Rates of cirrhosis decrease by 52%
Rates of HCC decrease by 47%
25% mortality transforms to 97% surviva

112
Q

7 issues facing GPs in the Mx of HBV

A 
Lack of community awareness
Stigma, language and cultural diversity
Time and inadequate financial support
Unclear referral pathways
Limited feedback from specialists
Lack of prescribing opportunities
Fear of Medicare auditing
113
Q

What are the key domains in the HBV strategy?

A

Increase community awareness, education and decrease stigma in a culturally appropriate way
Increase access to testing and vaccination
Increase clinical Mx and treatment rates
Support research to guide action

114
Q

What is cultural competency and how can it effect medical Mx?

A

Based on shared social experience, cultural characteristics and ancestry
Effects on patient/provider knowledge, attitudes and access
“Cultural competency” aims to improve accessibility and effectiveness of healthcare from cultural and linguistically diverse populations

115
Q

What is cultural competency and how can it effect medical Mx?

A

Based on shared social experience, cultural characteristics and ancestry
Effects on patient/provider knowledge, attitudes and access
“Cultural competency” aims to improve accessibility and effectiveness of healthcare from cultural and linguistically diverse populations

116
Q

What is medical negligence?

A

Medical negligence may involve a patient who receives care below a reasonable standard that results in an injury (or disease) or causes an existing injury to become worse

MD2 GIT (14 decks)

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