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Clinical Hepatology Flashcards

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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)?

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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
What are rare causes of AST/ALT elevations >1000?
malignancy within liver (primary or metastases) | Budd-Chiari
26
How is acute liver failure defined?
fulminant = sudden/severe onset onset of hepatic encephalopathy <8 weeks of first Sx AND in absence of pre-existing liver disease
27
How are acute liver failure syndromes defined?
``` = 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
What is defined by HYPERACUTE liver failure syndrome (acc: Grady, 1993)?
<7 days: between jaundice and encephalopathy very high: risk of cerebral oedema 36% survival chances
29
What is defined by ACUTE liver failure syndrome (acc: Grady, 1993)?
8-28 days: between jaundice and encephalopathy high: risk of cerebral oedema 7% survival chances
30
What is defined by SUBACUTE liver failure syndrome (acc: Grady, 1993)?
5-12 weeks: between jaundice and encephalopathy low: risk of cerebral oedema 14% survival chances
31
What is the main consideration when looking at indicators of poor prognosis in acute LF?
paracetamol-induced VS. non-paracetamol induced
32
What are the main indicators of poor prognosis in PARACETAMOL-INDUCED acute LF?
``` 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
What are the main indicators of poor prognosis in NON-PARACETAMOL-INDUCED acute LF?
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
What is the scale used to grade (hepatic) encephalopathy?
Grade 1: slight disorientation Grade2: more drowsy/disorientation, responds appropriately to verbal stimulation Grade 3: extreme agitation Grade 4: coma
35
What is the mortality figures for chronic liver disease?
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
What are the main macroscopic changes associated with liver cirrhosis?
Nodules (micro/macro) Fibrous septa between nodules Creating tough liver structure
37
What are the main parameters used to stage cirrhosis severity? (D'Amico et al, 2010)
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
What are the stages of cirrhosis severity? Which clinical features define each stage?
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
What is considered the normal hepatic venous pressure gradient?
10mm Hg
40
What is the Child-Pugh score?
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
What are the 5 clinical measures used in the Child-Pugh score?
``` 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
What is the relevant scoring for each parameter in Child-Pugh score?
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
How is the Child-Pugh score interpreted?
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
What are the mechanisms by which hepatotoxicity results in acute LF and systemic damage?
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
What is the sengstaken-blakemore tube and what is it used for?
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
What are the precipitants for hepatic encephalopathy?
Protein in gut - food - blood - faeces (constipation) Drugs/toxins - psychoactive - diuretics - EtOH Infection - sepsis - peritonitis
47
What are the management guidelines for encephalopathy?
Treat sepsis + dehydration Give Lactulose: - reduces colonic pH - increases transit Give Antibiotics e.g. rifaximin Dietary protein restriction is rarely necessary
48
What is ascites?
``` 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
How common is ascites as a complication to cirrhosis?
60% of patients with cirrhosis will develop ascites over the next 10 years
50
What is the mortality for ascites?
Cumulative mortality 40% for 1-year, 50% for 2-year Refractory ascites 70% at 1-year Spontaneous Bacterial Peritonitis (SBP) 30-50% mortality
51
What is refractory ascites?
ascites that recurs shortly after therapeutic paracentesis Despite sodium restriction and diuretics No approved medical therapy specifically for refractory ascites
52
What is spontaneous bacterial peritonitis?
``` 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
What is the best method of managing large volume ascites (Grade III)?
Large volume paracentesis (LVP) > diuretics - more effective - reduced risk of hyponatraemia and renal dysfunction - safer
54
What is used to treat/avoid circulatory dysfunction with large volume ascites and LVP?
albumin infusion | best method of expanding plasma volume
55
What medications can cause drug induced cholestasis?
- macrolides e.g. erythromycin (antibiotic) | macrolides work by inhibiting bacterial protein synthesis by blocking translocation
56
At what bilirubin level does jaundice begin to appear?
bilirubin at > 35 umol/L
57
What is Gilbert's syndrome?
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
What is the main cause of secondary hypertension in young adults?
renal disease
59
What are the main endocrine causes of secondary hypertension?
endocrine causes are generally less common - acromegaly - pheochromocytoma - hyperaldosteronism

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