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Life Maintenance > Clinical Hepatology > Flashcards

Clinical Hepatology Flashcards

1
Q

What are the main functions of the liver?

A

Metabolism/Detoxification
Synthesis and secretion
Storage and blood filtration

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2
Q

How vital is liver function to survival?

A

Very.

Acute or chronic liver failure is associated with a high risk of death

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3
Q

What are the normal parameters included in liver function tests? What do they indicate?

A

Total bilirubin, conjugated vs. unconjugated
Diagnosis of jaundice, liver disease severity

Aminotransferases: AST and ALT:
hepatocellular damage, liver disease progression

Alkaline phosphatase, ALP:
cholestasis, biliary obstruction, hepatic infiltration Dx

Albumin:
Chronic liver disease severity

Prothrombin time:
Severity of hepatic synthetic function

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4
Q

In which conditions are bilirubin levels (LFTs) likely to be abnormal? What are the different type of bilirubin that can be detected?

A

Conjugated (water-soluble):
defects in hepatic bilirubin excretion

Unconjugated (water-insoluble)
Increased Hb breakdown
Defects in hepatic uptake/conjugation
Reduced albumin or other plasma protein conjugates

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5
Q

What symptoms often present in liver disease? Other things to look out for in history?

A

Sx Often general, non-specific
Duration of abnormal LFTs are important

Asymptomatic

Jaundice (pruritus + dark urine + pale faeces, RUQ pain, fevers + rigors)
Confusion
GI bleeding
Abdo distension

weight loss
tiredness
nausea
anorexia
arthralgia
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6
Q

What is pruritus?

A

itching

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7
Q

What are the risk factors for liver disease?

A

EtOH
Drugs (prescribed, oral contraceptive, alternative)
IV drug use
Blood borne virus (BBV) - sexual history, ethnic origin
Recreational drug use - cocaine, MDMA, ecstasy, Khat (akin to speed)

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8
Q

What other diseases are co-morbidities for liver diseases? Which liver diseases do they increase risk for?

A

DM, obesity, hyperlipideamia - NAFLD
Autoimmunity, atopy - autoimmune liver disease
HIV - viral hepatitis, cholangiopathy
Emphysema - ATA1 (antitrypsin) deficiency
Sickle cell disease - sickle hepatopathy
Heart failure - ischaemic/congestive hepatopathy
IBD - primary sclerosing cholangitis (PSC)

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9
Q

During physical examination, what can be indicative of liver disease? What pathologies do these indicate?

A

Abdo exam

Normal

Liver flap/confusion (acute LF)
isolated jaundice (acute viral hepatitis)
jaundice, tenderness, excoriation marks (biliary obstruction)
spider naevi, palmar erythema, gynaecomastia, striae, caput medusa (cutaneous stigmata of chronic liver disease)

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10
Q

How may a patient with cirrhosis present on examination?

A 
liver usually small/shrunken
Portal hypertension - splenomegaly 
If decompensated: 
scleral icterus (jaundice of sclera)
abdo distension
oedema
asterixis (hand tremor on extension of wrist = liver flap)
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11
Q

What is the medical term for a liver flap? How can it be described?

A

Asterixis

hand tremor on extension of wrist

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12
Q

What pathologies might cause hepatomegaly without any other stigmata of chronic liver disease?

A 
malignancy 
fatty liver 
infections (viral, malaria, leptospirosis) 
right sided HF
metabolic storage disease
polycystic disease
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13
Q

What pathologies might cause hepatomegaly with other stigmata of chronic liver disease?

A 
EtOH (alcoholic hepatitis)
Budd Chiari syndrome
haemachromotosis
primary sclerosing cholangitis (PSC)
NAFLD
hepatocellular carcinoma (HCC)
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14
Q

What are causes of acute liver disease?

A 
Drugs 
EtOH 
infection
autoimmune 
vascular
Ischaemia
Inherited/genetic

Usually goes via acute hepatitis before reaching acute liver failure

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15
Q

What are the causes of chronic liver disease?

A 
autoimmune
drugs
inherited/genetic
EtOH
infection 
NAFLD
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16
Q

What are the main parameters in a “liver screen?”

A

Viral serology (Acute vs. chronic hepatitis)
Autoimmune (autoantibodies)
Fatty liver disease (fasting glucose/lipid profile)
Metabolic/genetic (HFE genotype: indicative of haemachromatosis; 24h urinary copper; ATA1 status)
Other (serum ACE, TFTs, CK, LDH, coeliac serology, tumour markers e.g. AFP)

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17
Q

Which autoantibodies are indicative of autoimmune aetiology in liver disease?

A

non-organ specific:
ANA: anti-nuclear
AMA: anti-mitochondrial
SMA: anti-smooth muscle

liver-specific:
LKA: anti-liver kidney antigen
p-ANCA: perinuclear anti-neutrophil cytoplasmic antibodies

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18
Q

What is the AFP test? In which other conditions may it be elevated?

A

tests for abundance of alpha-foetoprotein
can be indicative of liver disease and/or malignancy
Is often elevated in the 2nd trimester of pregnancy

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19
Q

What do massive AST/ALT elevations indicate? (>1000)

A

Acute liver injury

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20
Q

What is the AST/ALT level usually at for alcohol-related injury?

A

usually <300

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21
Q

What are the 4 most common causes to consider when AST/ALT is >1000?

A

Drugs/toxins
e.g. paracetamol, ecstasy, anti-tuberculous, anti-convulsants, NSAIDs, herbs

Viruses
e.g. A, B, (±D), E, CMV, EBV, HSV

Ischaemia
e.g. hypotension/shock, cocaine

Autoimmune hepatitis

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22
Q

What are the medical consequences of cocaine use?

A 
cardiac arrhythmias
coronary artery spasm
MI
CVA
haemorrhage
seizures
hallucinations
intestinal ischaemia 
acute liver injury 
rhabdo
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23
Q

How does cocaine cause hepatic injury?

A

Toxicity occurs hours-days after acute OD
usually involves other organs too
causes acute hepatic necrosis
Abnormal prothrombin time can indicate DIC
Antibodies are absent
centrolobular (zone 3) necrosis and fatty change

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24
Q

What is Disseminated Intravascular Coagulation (DIC)?

A

condition where spontaneous blood clots form throughout body
This causes clotting factors and platelets to be used up, and so bleeding may ensue
May present clinically with haematuria, malaena, and organ failure
Findings: low platelets, high INR, high D-dimer

25
Q

What are rare causes of AST/ALT elevations >1000?

A

malignancy within liver (primary or metastases)

Budd-Chiari

26
Q

How is acute liver failure defined?

A

fulminant = sudden/severe onset
onset of hepatic encephalopathy <8 weeks of first Sx
AND in absence of pre-existing liver disease

27
Q

How are acute liver failure syndromes defined?

A 
= Grady scale (Lancet, 1993)
3 categories:
hyper acute 
acute
Subacute

Looks at time interval between jaundice and encephalopathy, risk of cerebral oedema and survival ratios

28
Q

What is defined by HYPERACUTE liver failure syndrome (acc: Grady, 1993)?

A

<7 days: between jaundice and encephalopathy

very high: risk of cerebral oedema

36% survival chances

29
Q

What is defined by ACUTE liver failure syndrome (acc: Grady, 1993)?

A

8-28 days: between jaundice and encephalopathy

high: risk of cerebral oedema

7% survival chances

30
Q

What is defined by SUBACUTE liver failure syndrome (acc: Grady, 1993)?

A

5-12 weeks: between jaundice and encephalopathy

low: risk of cerebral oedema

14% survival chances

31
Q

What is the main consideration when looking at indicators of poor prognosis in acute LF?

A

paracetamol-induced
VS.
non-paracetamol induced

32
Q

What are the main indicators of poor prognosis in PARACETAMOL-INDUCED acute LF?

A 
pH < 7.3 following fluid resuscitation (irrespective of grade of encephalopathy)
OR
PT >100s (INR >6.5) 
Creatinine > 300mmol/L 
Grade III-IV encephalopathy 
(lactate > 3mmol/L)
33
Q

What are the main indicators of poor prognosis in NON-PARACETAMOL-INDUCED acute LF?

A

pH < 7.3 following fluid resuscitation
PT > 100s (irrespective of grade of encephalopathy)

OR

Any 3 of the following:
age < 10 or >40 years
Aetiology: non-A-non-B (NANB) or drug induced 
Jaundice to enceph. <7 days
PT> 50s (INS>3.5) 
Bilirubin > 300 umol/L)
34
Q

What is the scale used to grade (hepatic) encephalopathy?

A

Grade 1: slight disorientation
Grade2: more drowsy/disorientation, responds appropriately to verbal stimulation
Grade 3: extreme agitation
Grade 4: coma

35
Q

What is the mortality figures for chronic liver disease?

A

5th cause of death in UK
20-50% increases in EtOH predicted in next decade
15-25% of population have increased BMI
increased incidence of chronic viral disease
dual pathology: progression of liver disease increases

36
Q

What are the main macroscopic changes associated with liver cirrhosis?

A

Nodules (micro/macro)
Fibrous septa between nodules
Creating tough liver structure

37
Q

What are the main parameters used to stage cirrhosis severity?
(D’Amico et al, 2010)

A

Staging goes from full compensation (stages 1-2) to increasing decompensation (stages 3-5)
Increased severity correlates with increased hepatic venous pressure gradient (portal hypertension)

38
Q

What are the stages of cirrhosis severity? Which clinical features define each stage?

A

Stage 1: no varices (fully compensated cirrhosis), 7% chance of 5 year mortality

Stage 2: varies (compensated), 8% of 5 year mortality

Stage 3: bleeding (varices),decompensated, 19% of 5 year mortality

Stage 4: ascites, decompensated, 45% risk of 5 year mortality

Stage 5: ascites and bleeding, decompensated, 56% risk of 5 year mortality

39
Q

What is considered the normal hepatic venous pressure gradient?

A

10mm Hg

40
Q

What is the Child-Pugh score?

A

Used to assess chronic liver disease severity, mainly of cirrhosis
Used to determine prognosis, strength of treatment needed and need for liver transplantation
min score: 5 (mild disease)
max score 15 (severe disease)

41
Q

What are the 5 clinical measures used in the Child-Pugh score?

A 
total bilirubin (mg/dL)
serum albumin (g/dL)
prothrombin time, prolongation (s) or INR (only one to be used)
ascites 
hepatic encephalopathy (Grady stages)
42
Q

What is the relevant scoring for each parameter in Child-Pugh score?

A

total bilirubin:
<2 (1 point)
2-3 (2 points)
>3 (3 points)

serum albumin
>3.5 (1 point)
2.8-3.5 (2 points)
<2.8 (3 points)

PT
<4 (1 point)
4-6 (2 points)
>6 (3 points)

INR
<1.7 (1 point)
1.7-2.3 (2 points)
>2.3 (3 points)

ascites
none (1 point)
mild/suppressed by medications (2 points)
moderate-severe/refractory (3 points)

hepatic encephalopathy
none (1 point)
Grade I-II (2 points)
Grade III-IV (3 points)

43
Q

How is the Child-Pugh score interpreted?

A

3 classes

Class A: 5-6 points total
100% 1-year survival
85% 2-year survival

Class B: 7-9 points total
80% 1-year survival
60% 2-year survival

Class C: 10-15 points total
45% 1-year survival
35% 2-year survival

44
Q

What are the mechanisms by which hepatotoxicity results in acute LF and systemic damage?

A

fibrosis -> more shear stress, endothelial stretching, and VEFG signalling

INCREASED stress -> INCREASED endothelial NOS + NO -> INCREASED vasodilation

splanchnic and peripheral vasodilation causes hyperdynamic vascular state
INCREASED intra-vascular pressure and venous return

-> PORTAL HYPERTENSION

45
Q

What is the sengstaken-blakemore tube and what is it used for?

A

Inserted through the nose or mouth
Management of an upper GI haemorrhage e.g. oesophageal varices post-cirrhosis
Used extensively in 1950s but rarely used now thanks to advent of modern endoscopy
Tube - flexible plastic with internal channels and 2 inflatable balloons
Traction applied to maintain pressure mediated by inflated balloon and to minimise blood flow to oesophageal varices
Derivatives include Minnesota device which has an extra opening to SB tube

46
Q

What are the precipitants for hepatic encephalopathy?

A

Protein in gut

  • food
  • blood
  • faeces (constipation)

Drugs/toxins

  • psychoactive
  • diuretics
  • EtOH

Infection

  • sepsis
  • peritonitis
47
Q

What are the management guidelines for encephalopathy?

A

Treat sepsis + dehydration

Give Lactulose:

  • reduces colonic pH
  • increases transit

Give Antibiotics
e.g. rifaximin

Dietary protein restriction is rarely necessary

48
Q

What is ascites?

A 
Splanchnic vasodilation 
causes oedema as lymph fluid leaks out of blood vessels
Abdo distension 
Reduced effective blood volume 
RAAS activation
renal sodium retention 
ECF expansion
49
Q

How common is ascites as a complication to cirrhosis?

A

60% of patients with cirrhosis will develop ascites over the next 10 years

50
Q

What is the mortality for ascites?

A

Cumulative mortality
40% for 1-year, 50% for 2-year

Refractory ascites
70% at 1-year

Spontaneous Bacterial Peritonitis (SBP)
30-50% mortality

51
Q

What is refractory ascites?

A

ascites that recurs shortly after therapeutic paracentesis
Despite sodium restriction and diuretics
No approved medical therapy specifically for refractory ascites

52
Q

What is spontaneous bacterial peritonitis?

A 
Infection of ascites fluid
Without apparent source
Sx: fever, malaise, abdo distension, LF
Ix: examination of ascites fluid post-paracentesis
Tx: antibiotics e.g. Cefotaxime
53
Q

What is the best method of managing large volume ascites (Grade III)?

A

Large volume paracentesis (LVP) > diuretics

  • more effective
  • reduced risk of hyponatraemia and renal dysfunction
  • safer
54
Q

What is used to treat/avoid circulatory dysfunction with large volume ascites and LVP?

A

albumin infusion

best method of expanding plasma volume

55
Q

What medications can cause drug induced cholestasis?

A
  • macrolides e.g. erythromycin (antibiotic)

macrolides work by inhibiting bacterial protein synthesis by blocking translocation

56
Q

At what bilirubin level does jaundice begin to appear?

A

bilirubin at > 35 umol/L

57
Q

What is Gilbert’s syndrome?

A

mild liver disorder in which bilirubin is not processed correctly by the liver
Caused by mutation in UGT1A1
Rx not usually needed and often this is asymptomatic

58
Q

What is the main cause of secondary hypertension in young adults?

A

renal disease

59
Q

What are the main endocrine causes of secondary hypertension?

A

endocrine causes are generally less common

  • acromegaly
  • pheochromocytoma
  • hyperaldosteronism

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