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Year 3 > Cirrhosis (GI) > Flashcards

Cirrhosis (GI) Flashcards

1
Q

Define cirrhosis.

A

Pathological end stage of any chronic liver disease, characterised by fibrosis and conversion of normal liver architecture to structurally abnormal nodules called regenerative nodules

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2
Q

Who does cirrhosis occur more in?

A

M>F 2:1

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3
Q

What causes the bumpy texture of a cirrhotic liver?

A

Liver cells come together to form regenerative nodules separated by fibrotic scar tissue

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4
Q

Is liver scarring in cirrhosis reversible?

A

No

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5
Q

What can cirrhosis lead to?

A

Portal hypertension, liver failure + hepatocellular carcinoma

  • damaged hepatocytes lining perisinusoidal space activate stellate cell –> TGF-b secretion –> collagen production –> fibrosis
  • fibrotic tissue compresses sinusoids and vessels –> portal hypertension + reduced liver function
  • portal htn –> fluid pushed out of veins and sinusoids –> fluid in peritoneal cavity = ascites + splenomegaly (as fluid backs into spleen)
  • can cause a porto-systemic shunt where high pressures divert blood away from liver and favours systemic circulation
  • reduced detoxification by liver –> toxin accumulation in brain –> hepatic encephalopathy (mainly ammonia)
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6
Q

What are the common causes of cirrhosis? (3)

A
  • alcohol-related liver disease (ALD)
  • non-alcoholic fatty liver disease (NAFLD)
  • chronic viral hepatitis (B and C)
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7
Q

What are the clinical features of cirrhosis? (10)

A
  • abdominal distension
  • jaundice and pruritus
  • haematemesis and melaena (haemorrhage due to varices)
  • encephalopathy
  • hand and nail features (leukonychia, palmar erythema, clubbing, Dupuytren contracture)
  • spider naevi (>4, fill from centre)
  • gynaecomastia (reduced oestrogen metabolism)
  • hepatomegaly and splenomegaly
  • hepatic fetor - sweet putrid breath
  • muscle wasting and anorexia (malnutrition and hypercatabolism)
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8
Q

Why do we get abdominal distension in cirrhosis?

A

Decompensated cirrhosis secondary to reduced hepatic excretion of conjugated bilirubin

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9
Q

What do jaundice and pruritus in cirrhosis suggest?

A

Decompensated cirrhosis secondary to reduced hepatic excretion of conjugated bilirubin

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10
Q

What do haematemesis and melaena suggest in cirrhosis?

A

Decompensated cirrhosis secondary to GI haemorrhage due to varices

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11
Q

Why do we get encephalopathy in cirrhosis and what can this lead to?

A

Due to excess ammonia, can lead to:

  • confusion
  • altered GCS
  • asterixis - inability to maintain sustained posture with subsequent brief, shock-like, involuntary movements
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12
Q

What hand and nail features are seen on examination in cirrhosis? (4)

A
  • leukonychia (hypoalbuminaemia)
  • palmar erythema
  • clubbing
  • Dupuytren contracture (alcohol-related liver disease)
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13
Q

What facial features are seen on examination in cirrhosis? (8)

A
  • telangiectasia
  • spider naevi (>4 and fill from centre)
  • jaundiced sclera
  • rhinophyma
  • parotid gland swelling
  • paper money skin appearance
  • red tongue
  • seborrhoeic dermatitis
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14
Q

What abdominal features are seen on examination in cirrhosis? (6)

A
  • collateral circulation
  • hepatosplenomegaly
  • distension, shifting dullness, fluid thrill (ascites due to portal htn)
  • caput medusae
  • bruising
  • loss of secondary sexual hair + testicular and breast atrophy
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15
Q

What is the A-J of liver failure/cirrhosis?

A
  • Asterixis
  • Bruising
  • Clubbing
  • Dupuytren’s contracture
  • Erythema (palmar)
  • Fetor hepaticus (strong smelly breath)
  • Gynaecomastia
  • Hepatomegaly + Hair loss
  • Itching + Icterus
  • Jaundice + JVP
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16
Q

What are the clinical features of portal hypertension? (4)

A
  • ascites
  • splenomegaly
  • caput medusae - cluster of swollen veins in abdomen
  • causes swelling of veins (varices) in oesophagus and rectum
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17
Q

What two scoring systems can be used to determine cirrhosis severity?

A
  • Child-Pugh classification
  • MELD (Model for End-stage Liver Disease)
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18
Q

What is an easy way to remember the Child-Pugh scoring system for cirrhosis severity?

A

ABCDE; each parameter scored 1,2,3

  • Albumin - lower the worse (>35, 28-35, <28)
  • Bilirubin - higher the worse, and same for rest (<34, 34-51, >51)
  • Clotting - PT (<4, 4-6, >6)
  • Distension - ascites
  • Encephalopathy

Graded A B or C:

  • A: <7
  • B: 7-9
  • C: >9
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19
Q

What is the MELD score for cirrhosis severity?

A

MELD = 3.8xln[serum bilirubin] + 11.2xln[INR] + 9.57xln[serum creatinine] + 6.43

The higher the score, the higher the mortality:

  • 40+: 71.3%
  • 30-39: 52.6%
  • 20-29: 19.6%
  • 10-19: 6.0%
  • <9: 1.9%
20
Q

What are some risk factors for cirrhosis? (7)

A
  • alcohol misuse –> ALD
  • obesity –> NAFLD
  • IVDU –> hep B&C
  • unprotected intercourse –> hep B&C
  • blood transfusion –> hep B&C
  • country of birth –> endemic hep B&C
  • tattoos
21
Q

What are the first-line investigations for cirrhosis? (3)

A
  • LFTs
  • liver biopsy
  • transient elastography - evidence of fibrosis without biopsy
22
Q

What is the most specific and sensitive investigation for cirrhosis?

A

Liver biopsy

23
Q

What are the adverse effects of a liver biopsy to diagnose cirrhosis?

A

Bleeding and pain

24
Q

What other techniques are now used more than liver biopsy in diagnosing cirrhosis? (2)

A
  • transient elastography - named ‘Fibroscan’ and passes 50MHz wave into liver to measure stiffness and fibrosis
  • acoustic radiation force impulse imaging
25
Q

What test is recommended for patients with non-alcoholic fatty liver disease?

A

Using enhanced liver fibrosis score to screen for patients who need further testing

26
Q

What other scans are done for investigating cirrhosis? (2)

A
  • upper GI endoscopy - check for varices in patients with new cirrhosis diagnosis
  • liver US (and AFP) every 6 months - to check for hepatocellular cancer
27
Q

What do LFTs show in liver cirrhosis?

A
  • deranged - AST and ALT increase with hepatocellular damage
  • normally ALT > AST - except for alcohol-related liver disease
  • ALD –> AST:ALT = 2:1
28
Q

What does serum albumin show in cirrhosis?

A

Reduced - marker of hepatic synthetic dysfunction

29
Q

What does prothrombin time show in cirrhosis?

A

Prolonged - marker of hepatic synthetic dysfunction

30
Q

What does serum sodium show in cirrhosis?

A

Reduced - common finding in cirrhotic patients with ascites as they are hypovolaemic and hyponatraemic

31
Q

What are platelets like in cirrhosis?

A

Reduced as portal HTN –> hypersplenism + platelet sequestration

32
Q

What is the most sensitive and specific lab finding for diagnosis of liver cirrhosis in those with chronic liver disease?

A

Thrombocytopenia (platelet count <150,000mm3)

33
Q

How do we diagnose SBP (cirrhosis)?

A

Paracentesis - neutrophil count >250cells/ul

34
Q

What are some differential diagnoses for cirrhosis? (10)

A
  • Budd-Chiari syndrome (abdominal pain, diarrhoea, progressively worsening ascites)
  • portal vein thrombosis (Sx of underlying cause e.g. chronic pancreatitis, ascending cholangitis, abdominal sepsis)
  • splenic vein thrombosis (Sx of pancreatitis)
  • nodular regenerative hyperplasia
  • idiopathic portal hypertension
  • constrictive pericarditis (raised JVP, tachycardia, AF, S3)
  • IVC obstruction (Sx of renal cell carcinoma)
  • schistosomiasis
  • sarcoidosis
  • vitamin A intoxication, arsenic and vinyl chloride toxicity
35
Q

What is the principle of cirrhosis management?

A

Treatment of underlying chronic liver disease/cause and prevention of superimposed hepatic insult

36
Q

What do we recommend if liver disease is alcoholic?

A

Abstinence from alcohol and good nutrition

37
Q

What are some hepatotoxic drugs to avoid in liver disease/cirrhosis? (4)

A
  • NSAIDs
  • paracetamol
  • methotrexate
  • amiodarone
38
Q

How do we manage liver cirrhosis with encephalopathy?

A
  • lactulose - reduces ammonia absorption from gut
  • secondary prophylaxis - rifaximin
39
Q

How do we manage ascites in cirrhosis? (3)

A
  • sodium restriction
  • diuretic - spironolactone
  • paracentesis to drain
40
Q

How do we manage spontaneous bacterial peritonitis (cirrhosis)?

A

Prophylactic Abx (ciprofloxacin or norfloxacin)

41
Q

What surgeries can we do if complications of cirrhosis or signs of decompensation? (2)

A
  • liver transplant
  • transjugular intrahepatic portosystemic shunt (TIPS) - to reduce portal hypertension - if not suitable for liver transplant
42
Q

What does transjugular intrahepatic portosystemic shunt (TIPS) reduce the risk of?

A

Oesophageal varices secondary to portal hypertension

43
Q

How do we manage oesophageal varices secondary to portal hypertension?

A
  • IV terlipressin (vasoactive agent - vasopressin analogue)
  • IV Abx
  • vitamin K
  • blood transfusion if Hb<7g/dL
  • prophylaxis: propranolol, endoscopic variceal band ligation with PPI
  • Sengstaken-Blakemore tube if uncontrolled haemorrhage
  • TIPS if others fail
44
Q

How do we monitor complications in cirrhosis? (3)

A
  • abdominal US - ascites
  • upper GI endoscopy - gastro-oesophageal varices
  • USS, CT, MRI - hepatocellular carcinoma detection
45
Q

What are some complications of cirrhosis?

A
  • ascites
  • gastro-oesophageal varices which may rupture (enlarged veins –> caput medusae)
  • hepatocellular carcinoma
  • bleeding and thrombosis (from varices/deranged clotting/HCC)
  • spontaneous bacterial peritonitis (neutrophils>250cells/mm3, Abx prophylaxis if risk)
  • hepatic encephalopathy (give lactulose)
  • hepatorenal syndrome
  • hypogonadism and feminisation
46
Q

Describe the overall prognosis of cirrhosis.

A

Overall median survival is 10 years but prognosis depends on stage of disease

Year 3 (203 decks)

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