Cirrhosis Flashcards

1
Q

what is it?

A

chronic liver damage with replacement of normal liver architecture with diffuse fibrosis

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2
Q

Cirrhosis is considered DECOMPENSATED when?

A

if becomes complicated by any of GAJE;

GI bleed

Ascites

Jaundice

Encephalopathy

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3
Q

Aetiology/Risk factors?

A

Chronic alcohol misuse (most common in the UK)

Chronic viral hepatitis (hep B/C - most common worldwide)

Autoimmune hepatitis

Drugs (e.g. methotrexate, hepatotoxic drugs)

Inherited;
a1-antitrypsin deficiency 
Haemochromatosis  
Wilson's disease  
Galactosaemia  
Cystic Fibrosis  

Vascular ;
Budd-Chiari Syndrome
Hepatic Venous Congestion

Chronic Biliary Diseases;
Biliary atresia

Unknown: 5-10%

Non-Alcoholic Steatohepatitis (NASH) ;
Associated with obesity, diabetes, total parenteral nutrition, hyperlipidaemia

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4
Q

Presenting symptoms?

A

Early non-specific symptoms:

Anorexia 
Nausea  
Fatigue  
Weakness 
Weight loss  

Symptoms due to decreased liver synthetic function:
Easy bruising
Abnormal swelling
Ankle oedema

Symptoms due to reduced detoxification function: 
Jaundice  
Personality change  
Altered sleep pattern  
Amenorrhoea 
Galactorrhoea 

Symptoms due to portal hypertension:
Abdominal swelling
Haematemesis
PR bleeding or melaena

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5
Q

signs of any chronic liver disease?

A
ABCD;
Asterixis 
Ascites 
Bruises  
Clubbing  
Dupuytren's contracture 

Palmar erythema
Jaundice
Gynaecomastia
Leukonychia

Parotid enlargement
Spider naevi
Scratch mark (from cholestatic pruritis)

Enlarged liver (may be shrunken in the later stages)
Testicular atrophy
Caput medusae
Splenomegaly

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6
Q

Ivx?

A

FBC: low platelets + Hb = because of hypersplenism as a result of portal hypertension

LFTs - may be normal but often get:
High AST, ALT, ALP, GGT and bilirubin
Low albumin
Low Na

Clotting: prolonged PT

Serum AFP (alpha-fetoprotein = tumour marker for liver cancer):
Raised in chronic liver disease
High levels may suggest hepatocellular carcinoma

invx to determine cause; viral serology etc

Ascitic tap; IMPORTANT: ascitic tap with neutrophils > 250/mm3 = spontaneous bacterial peritonitis (SBP)

abdo US, CT, MRI

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7
Q

What is the Child-Pugh grading system?

A

Child-Pugh Grading - score for estimating the prognosis in chronic liver disease/cirrhosis. It is based on 5 factors:

Albumin  
Bilirubin 
PT 
Ascites  
Encephalopathy 

Cirrhosis can be divided into Classes using the Child-Push grading system:
Class A: 5-6
Class B: 7-9
Class C: 10-15

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8
Q

Management of cirrhosis?

A

1st - Treat underlying cause;

  • whether hep A or haemochromatosis etc
  • sodium restriction + diuretics for ascites
  • avoid, alcohol, opiates, nsaids drugs affecting liver

2nd line; liver transplant

encephalopathy

  • Use lactulose and phosphate enemas
  • lactulose reduces the absorption of ammonia from the gut
  • helps prevent encephalopathy caused by ammonia reaching the brain
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9
Q

ascites ivx and mx management?

A

Initially:
Diagnostic paracentesis; take sample for cultures and biochemistry (albumin, amylase, bnp, ADA)

Calculate the Serum ascitic albumin gradient - SAAG

Give prophylactic antibiotics if GI bleeding present.

————————- Treatment:
Mainstay 1+2:
1. Diuretics (spironolactone with/without furosemide)

  1. Dietary sodium restriction

Monitor weight

Fluid restrict if plasma sodium < 120 mmol/L.

Give abx if SBP

Monitoring:
There is a risk of hyponatraemia so stop diuretics if this happens

Avoid alcohol and NSAIDs

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10
Q

causes of ascites?

A

Other causes of portal hypertension that may be associated with ascites include congestive heart failure, constrictive pericarditis, alcoholic liver disease, fulminant hepatitis, subacute hepatitis, massive liver metastasis, and Budd-Chiari syndrome.

Conditions causing hypo-albuminaemia such as nephrotic syndrome and protein-losing enteropathy may result in ascites. Peritoneal diseases including infectious peritonitis and malignancies can also cause ascites.

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11
Q

How does SAAG help to narrow differentials of ascites?

A
SAAG ≥11 /L (or 1.1mg/dL)
Portal hypertension:
Cirrhosis
Cardiac failure
Portal vein thrombosis*
Hypothyroidism*
SAAG <11 /L
Peritoneal carcinomatosis
Peritoneal tuberculosis
Pancreatitis*
Bowel perforation*
Nephrotic syndrome*
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12
Q

How is refractory ascites treated?

A

As the liver disease progresses the ascites may no longer respond to medication. This is known as untreatable or refractory ascites.

They will have:

  1. Therapeutic paracentesis (with human albumin replacement)
    • so drainage every few weeks in the hospital

Last line:

  1. TIPSS - transjugular intrahepatic portosystemic shunt
    - placing a small tube (stent) in the liver
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13
Q

purpose for SAAG?

calculation?

A

SAAG = (serum albumin) − (albumin level of ascitic fluid).

Tells us whether the ascites is due to high oncotic pressure or hydrostatic pressure?

high saag means higher albumin in serum so hydrostatic pressure imbalance hence fluid being pushed out of circulation.

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14
Q

what are major factors in pathogenesis of ascites in cirrhosis?

A

Sodium retention is a major factor in pathogenesis

And water retention

due to activation of the RAS and sympathetic NS causing release of ADH

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