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Gastrology > Clinical Liver disease - LFTs, investigations, patterns > Flashcards

Clinical Liver disease - LFTs, investigations, patterns Flashcards

1
Q

Isolated ALP elevation

A

Bone issue

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2
Q

Isolated transaminase

A

Muscle

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3
Q

Isolated bilirubin

A

haemolysis

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4
Q

Liver function is demonstrated by

A

Albumin
Bilirubin
Prothrobin time

not reflected by degree of abnormality of transaminase

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5
Q

Transaminases reflect

A

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
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6
Q

Investigations of abnormal liver blood tests

A

• 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)

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7
Q

Likely cause of asymptomatic abnormal liver blood tests

A

NON-ALCOHOLIC FATTY LIVER DISEASE (nafld)

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8
Q

NAFLD findings

A

negative serological assessment; increased echogencity on ultrasound; minimal elevation of AST/AT tends to stay silent until complications develop

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9
Q

What does NAFLD progress to>

A

NASH (non alcoholic steatohepatitis

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10
Q

Associated conditions of NAFLD?

A

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.

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11
Q

Typical features of NAFLD

A
  • obese
  • FPB: elevated
  • alcohol intake less
  • AT/ALT ration
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12
Q

Typical features of ALD

A
  • 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
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13
Q

Clinical specturem of ALD

A

Malaise > Nausea > Hepatomegaly > Fever > Jaundice > Sepsis > Encephalopathy > Ascites > Renal Failure> Death

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14
Q

Patterns of alcholic liver disease (LFTS)

A
  • Raised AST : ALT ratio: preferential AST elevation as mitochondrial disease and pyridoxine deficiency
  • AST not >500 (ALT usually
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15
Q

The newly jaundiced ALD patient

A

• ‘Clinically relevant’ Alcoholic Hepatitis
• Essential Features: recent excess alcohol, Bilirubin > 80mol/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%

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16
Q

How to score the glasgow hepatitis score (GAHS)

A 
Age 
WCC
UREA
PT ratio
Bilirubin

score out of 1/2/3 for each section

17
Q

Signs of chronic liver disesae and /or portal hypertension

A

Chronic Liver Disease: stigmata: spiders,
fœtor, encephalpathy. ‘synthetic dysfunction’:
prolonged prothrombin time, hypoalbuminaemia.

Portal Hypertension: caput medusa, hypersplenism: Thrombocytopenia (pancytopenia).

18
Q

Assessment of chronic liver disease

A

Child-pugh core
• Grade A = 5-6 – Mild
• Grade B = 7-9 – Moderate
• Grade C = 10-15 – Severe

19
Q

Liver fibrosis staging

A

• Stage 1 = portal fibrosis, stage 2 = portal fibrosis with septa, stage 3 = bridging fibrosis – diffuse and then marked. Stag 4 = cirrhosis – nodular formation.

20
Q

Fibroscan

A
  • 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.
21
Q

Portal hypertension pathophysiology

A
  • 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
22
Q

portal hypertension causes

A 
Hypersplenism 
encephalopathy 
oesophaeal varices 
ascites 
hepato-renal syndrome 
Hyperdynamic circulation
23
Q

Assesment of ascited: diagnostic tap

A

• 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%

24
Q

differential diagnosis relative to SAAG

A

• SAAG11g/l = Liver cirrhosis with portal hypertension. Budd-Chiari syndrome. Congestive heart failure. Constrictive pericarditis. Tricuspid insufficiency.

25
Q

Management of ascites

A
  • 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
26
Q

Hepatorenal syndrome (HRS)

A
  • 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.
27
Q

Precipitating factors

A

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

28
Q

Scoring system used in hepatic encephalopathy

A 
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.
29
Q

What is acute liver failure

A

‘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.

30
Q

Ischaemic hepatitis

A
  • 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).
31
Q

Drug induced hepatitis

A
  • Acute Hepatitis: Phenytoin; Amiodarone. anaesthetic agents, H2 receptor antagonists
  • Acute Cholestasis/ Cholestatic Hepatitis: amoxycillin/ clavulonic acid; macrolides; flucloxacillin; ceftriaxone. Ibuprofen; dextropropoxyphene (co-proxomol). Chlorpromazine

Gastrology (19 decks)

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