Clinical Liver disease - LFTs, investigations, patterns Flashcards
Isolated ALP elevation
Bone issue
Isolated transaminase
Muscle
Isolated bilirubin
haemolysis
Liver function is demonstrated by
Albumin
Bilirubin
Prothrobin time
not reflected by degree of abnormality of transaminase
Transaminases reflect
Type of damage and degree of damage
8-10,000 u/per/l - toxic or ischaemic cause 300-3000 - acute viral hepatitis 150-350 - alcoholic 30-150 - chronic 25-70- cirrhosis
Investigations of abnormal liver blood tests
• Ultrasound: Biliary disease; hepatic vein thrombosis (Budd-Chiari)
• Chronic viral hepatitis: HBV, HCV
• Autoimmune liver disease: ANA / SMA / LKM (AIH); AMA (PBC);
Immunoglobulins igG in autoimmune > PBC
Immunoglobulins IgM in PBC > AIH
In alcoholics raised in IgA
• Metabolic liver disease: Ferritin (haemochromatosis – (>1000 = end organ damage); Caeruloplasmin(copper binding protein (Wilson’s Disease); 1 anti-trypsin deficiency (chronic liver and ling disease)
Likely cause of asymptomatic abnormal liver blood tests
NON-ALCOHOLIC FATTY LIVER DISEASE (nafld)
NAFLD findings
negative serological assessment; increased echogencity on ultrasound; minimal elevation of AST/AT tends to stay silent until complications develop
What does NAFLD progress to>
NASH (non alcoholic steatohepatitis
Associated conditions of NAFLD?
o Acquired metabolic conditions e.g. obesiy, diabetes, hyperlipidaemia.
o Inborn errors of metabolism e.g. Wilson’s disease
o Surgical procedures: biliopancreatic diversion, small bowel resection.
o Drugs/toxins: Amiodarone, steroids, isoniazid.
Typical features of NAFLD
- obese
- FPB: elevated
- alcohol intake less
- AT/ALT ration
Typical features of ALD
- Variable weight
- FPB: normal
- alcohol intake more
- AT/ALT ration .1/5
- GGT - markedly elevated
- Triglycerides - markedly elevated
- HDL- cholesterol - elevated
- Mean corpuscular volume - elevated
Clinical specturem of ALD
Malaise > Nausea > Hepatomegaly > Fever > Jaundice > Sepsis > Encephalopathy > Ascites > Renal Failure> Death
Patterns of alcholic liver disease (LFTS)
- Raised AST : ALT ratio: preferential AST elevation as mitochondrial disease and pyridoxine deficiency
- AST not >500 (ALT usually
The newly jaundiced ALD patient
• ‘Clinically relevant’ Alcoholic Hepatitis
• Essential Features: recent excess alcohol, Bilirubin > 80mol/l. Exclusion of other liver disease. AST 1.5)
Must be less than 1000
• Characteristic Features: hepatomegaly fever leucocytosis hepatic bruit
• SHORT-TERM MORTALITY AS HIGH AS 60%
How to score the glasgow hepatitis score (GAHS)
Age WCC UREA PT ratio Bilirubin
score out of 1/2/3 for each section
Signs of chronic liver disesae and /or portal hypertension
Chronic Liver Disease: stigmata: spiders,
fœtor, encephalpathy. ‘synthetic dysfunction’:
prolonged prothrombin time, hypoalbuminaemia.
Portal Hypertension: caput medusa, hypersplenism: Thrombocytopenia (pancytopenia).
Assessment of chronic liver disease
Child-pugh core
• Grade A = 5-6 – Mild
• Grade B = 7-9 – Moderate
• Grade C = 10-15 – Severe
Liver fibrosis staging
• Stage 1 = portal fibrosis, stage 2 = portal fibrosis with septa, stage 3 = bridging fibrosis – diffuse and then marked. Stag 4 = cirrhosis – nodular formation.
Fibroscan
- Used to conduct transient elastography on the liver - medical imaging modality based on mechanical tissue excitation and ultrasound measurements. It will map the elasticity of the liver and measure the stiffness.
- Liver Stiffness Measurement (LSM):
- Probe created a shear elastic wave and then the speed of its propagation is measured – Vs.
- Stiffness – E α Vs2
- A cirrhotic liver will be much stiffer than a normal liver and therefore will have a higher liver stiffness measurement.
Portal hypertension pathophysiology
- cirrhosis
-elevation of portioal pressure
-causes shunting of the portal blood into portal systemic collaterals and then into the systemic blood
-Portal circulation contains substances that shouldnt enter the systemic system
-It is a vicious cycle – shunting of the portal blood leads to vasodilation – the body perceives that the blood pressure is low and therefore activated systems to increase it and increase volume.
• Vasodilation leads to compensatory activation of the RAAS and release of catecholamine’s
• This leads to sodium retention and renal vasoconstriction causing ascites and hepato-renal syndrome where the kidneys shut off – they are not damaged, just refuse to work
portal hypertension causes
Hypersplenism encephalopathy oesophaeal varices ascites hepato-renal syndrome Hyperdynamic circulation
Assesment of ascited: diagnostic tap
• If a liver disease patient has ascites then you must aspirate it and send the fluid to the lab. Looking for infection, malignancy etc.
• Cell count:
o >500 WBC/ cm3 and >250 neutrophils/cm3 suggest spontaneous bacterial peritonitis
o Inflammatory conditions can also increase WBC count
o Lymphocytosis suggests TB or peritoneal carcinomatosis
• Albumin
o Serum ascites albumin gradient (SAAG) = serum albumin MINUS ascitic albumin g/l
o SAAG >11g/l = portal hypertension
• SBP diagnosed in 20% cirrhotics admitted to hospital, and 2-3% attending for outpatient paracentesis. Early mortality >80% at 30d. Now, best reported is 10%
differential diagnosis relative to SAAG
• SAAG11g/l = Liver cirrhosis with portal hypertension. Budd-Chiari syndrome. Congestive heart failure. Constrictive pericarditis. Tricuspid insufficiency.
Management of ascites
- Low salt diet
- Diuretics
- Spironolactone: Targets the activated RAAS – aldosterone receptor blocker. Start 100mg/day. Max effect 3days. Max dose 400mg/day (divided doses). Side-effects e.g. gynaecomastia, hyperkalaemia, hyponatraemia, impotence.
- Frusemide (Furosemide): Max 160mg/day (divided doses) Side-effects e.g. hyponatraemia.
- Paracentesis – draining fluid 10-15L. If repeated paacenteses is required – consider shunt.
- Transjugular intrahepatic portosystemic shunt (TIPSS) – at this point also consider:
- Liver transplant
- Aim for weight loss of 1kg/day: Monitor renal function and electrolytes
Hepatorenal syndrome (HRS)
- Type 1: rapid decline in function often triggered by SBP (spontaneous bacterial peritonitis). Approaching 100% mortality in 10 weeks.
- Type 2: moderate stable decline. Median survival 3-6 months.
Precipitating factors
Such factors may include: gastrointestinal tract haemorrhage, infections, renal and electrolyte disturbances, use of psychoactive medication, excessive dietary protein and an acute deterioration of liver function in a patient.
• These precipitating factors negatively affect the patient by:
o Further reducing hepatic or cerebral function,
o Increasing ammonia levels or
o Stimulating an inflammatory response.
• Hepatic encephalopathy is a disease caused by the failure of the cirrhotic liver to remove toxins from the blood, which ultimately negatively affects the brains function.
• Therefore identification and removal of precipitating factors should be instituted immediately once hepatic encephalopathy is diagnosed.
• Don’t make it worse: avoid regular sedation; caution with opiates; avoid hyponatraemia
Scoring system used in hepatic encephalopathy
Conn Score (West Haven classification) for Grading Mental State in Hepatic Encephalopathy1 • Conn score is used to grade the mental state in patients with cirrhosis on a scale of 0 to IV, based on the level of impairment of autonomy, changes in consciousness, intellectual function, behaviour, and the dependence on therapy.
What is acute liver failure
‘Acute’ Liver Failure is a potentially reversible consequence of severe liver injury characterised by the development of hepatic encephalopathy in the absence of pre-existing liver disease.
Ischaemic hepatitis
- Not an inevitable consequence of severe shock.
- The liver is relatively resistant to ischaemia.
- Hypotension is typically transient (15-20 minutes).
- Majority of patients have right-sided heart failure: a combination of systemic hypotension and background hepatic congestion.
- In-hospital mortality: 52% (HENRION et al, 2003).
Drug induced hepatitis
- Acute Hepatitis: Phenytoin; Amiodarone. anaesthetic agents, H2 receptor antagonists
- Acute Cholestasis/ Cholestatic Hepatitis: amoxycillin/ clavulonic acid; macrolides; flucloxacillin; ceftriaxone. Ibuprofen; dextropropoxyphene (co-proxomol). Chlorpromazine
