Cirrhosis Flashcards

1
Q

What is cirrhosis?

A

Diffuse pathologic process, characterised by fibrosis and conversion of normal liver architecture to structurally abnormal nodules known as regenerative nodules.

It can arise from a variety of causes and is the final stage of any chronic liver disease.In general, it is considered to be irreversible in its advanced stages, although there can be significant recovery if the underlying cause is treated.

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2
Q

What are the most common causes cirrhosis?

A
  • Alcohol-related liver disease
  • Nonalcoholic fatty liver disease (NAFLD and associated steatohepatitis)
  • Chronic viral hepatitis
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3
Q

Give examples of metabolism, cholestatic, autoimmune, billiary and drug causes of cirrhosis

A

Metabolic disorders: hemochromatosis, Wilson disease, alpha-1 antitrypsin deficiency, glycogen storage diseases and abetalipoproteinemia

Cholestatic and autoimmune liver diseases: primary biliary cholangitis, primary sclerosing cholangitis, autoimmune hepatitis, autoimmune cholangiopathy, and immunoglobulin G4 (IgG4)-related disease

Biliary obstruction: mechanical obstruction, biliary atresia and cystic fibrosis

Drug: amiodarone and methotrexate

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4
Q

Briefly differentiate between compensated and decompensated cirrhosis

A

Compensated- when the liver can still function effectively and there are no, or few, noticeable clinical symptoms

Decompensated- when the liver is damaged to the point that it cannot function adequately and overt clinical complications (such as jaundice, ascites, variceal haemorrhage, and hepatic encephalopathy) are present

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5
Q

What risk factors are associated with cirrhosis?

A
  • Alcohol misuse
  • IV drug use
  • Unprotected intercourse
  • Obesity
  • Country of birth
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6
Q

What are the signs of cirrhosis?

A
  • Abdominal distension
  • Jaundice and pruritis
  • Hand and nail features (e.g. leukonychia, palmar erythema and spider nevi)
  • Facial features (e.g. telangiectasia, spider nevi and jaundiced sclera)
  • Abdominal features (e.g. collateral circulation, hepatosplenomegaly and distension)
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7
Q

What are the symptoms of cirrhosis?

A
  • Haematemesis (blood in vomit)
  • Melena (black stool)
  • Constitutional symtoms e.g fatigue, weakness, and weight loss
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8
Q

What investigations should be ordered for cirrhosis?

A
  • LFTs
  • Gamma-glutamyl transferase (GGT)
  • Serum albumin
  • Serum sodium
  • Prothrombin time
  • Platelet count
  • Antibodies to hepatitis C virus
  • Hepatits B surface antigen
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9
Q

Why investigate LFTs? And what may this show?

A
  • Aminotransferase levels increase with hepatocellular damage; normal AST and ALT levels do not preclude the diagnosis of cirrhosis
  • Deranged
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10
Q

What ratio of AST:ALT predicts cirrhosis?

A

≥1

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11
Q

Why investigate gamma-glutamyl transferse (GGT)? And what may this show?

A
  • Increase in this liver microsomal enzyme represents enzyme activation that can be induced by alcohol and certain drugs
  • Elevated
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12
Q

Why investigate serum albumin? And what may this show?

A
  • A decrease in the serum albumin is a marker of hepatic synthetic dysfunction
  • Reduced
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13
Q

Why investigate serum sodium? And what may this show?

A
  • Hyponatremia is a common finding in cirrhotic patients with associated ascites and worsens as the liver disease progresses
  • Reduced
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14
Q

Why investigate prothombin time? And what may this show?

A
  • Prolongation of the prothrombin time is a marker of hepatic synthetic dysfunction
  • Prolonged
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15
Q

Why investigate platelet count? And what may this show?

A
  • The presence of thrombocytopenia (platelet count <150,000 mm³) is the most sensitive and specific laboratory finding for the diagnosis of cirrhosis in the setting of chronic liver disease and results from portal hypertension with hypersplenism and platelet sequestration
  • Reduced
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16
Q

Why investigate antibodies to hepatitis C virus? And what may this show?

A
  • Presence of immunoglobulin G (IgG) antibodies to hepatitis C virus (confirmed with hepatitis C virus-RNA) is indicative of chronic hepatitis C infection
  • Present
17
Q

Why investigate hepatits B surface antigen? And what may this show?

A
  • A detectable hepatitis B surface antigen is indicative of hepatitis B infection, regardless of viral DNA level. E-antigen/e-antibody and viral DNA should be measured to assess disease phase
  • Present
18
Q

Briefly describe the treatment of cirrhosis

A
  • Treatment of underlying chronic liver disease and prevention of superimposed hepatic insult
  • Monitoring for complications
  • Sodium restriction and diuretic therapy for ascites
19
Q

When would a patient with cirrhosis be considered for liver transplantation?

A

Patients who develop complications of cirrhosis such as hepatocellular carcinoma or signs of decompensation (ascites, jaundice, variceal hemorrhage, portal systemic encephalopathy, or hepatorenal syndrome) should be referred for liver transplant evaluation without delay.

20
Q

How can superimposed hepatic insult be avoided in cirrhosis patients?

A

Superimposed hepatic insult may be prevented through the avoidance of alcohol and other hepatotoxic drugs (e.g., nonsteroidal anti-inflammatory drugs [NSAIDs] and high doses of acetaminophen [>2 g/day]), immunization against hepatitis A and B for susceptible patients, management of metabolic risk factors, maintenance of adequate nutrition, and regular exercise.

21
Q

Briefly describe sodium restriction and diuretic therapy in cirrhotic patients with ascites

A

Ascites is the most common complication of cirrhosis.

Treatment involves a no added salt diet and the use of diuretics. First-line diuretic should be spironolactone to maintain normal serum potassium.

22
Q

What are the complications of cirrhosis?

A
  • Ascites
  • Gastroesophageal varices
  • Hepatocellular carcinoma
  • Bleeding and thrombosis
23
Q

What differentials should be considered in cirrhosis?

A
  1. Constrictive pericarditis
  2. Budd-Chiari syndrome
  3. Portal vein thrombosis
24
Q

How does cirrhosis and constrictive pericarditis differ?

A
  • Differentiating signs and symptoms:
    • Elevated jugular venous pressure, tachycardia, and atrial fibrillation
    • Heart sounds: quiet, third heart sound (ventricular knock) present
  • Differentiating investigations:
    • ECG: tachycardia, atrial fibrillation, low-voltage QRS complexes, T-wave abnormalities
    • Doppler ultrasound: ventricular filling abnormalities
25
Q

How does cirrhosis and Budd-Chiari syndrome differ?

A
  • Differentiating signs and symptoms:abdominal pain, diarrhea, and progressively worsening ascites.
  • Differentiating investigations:
    • Doppler ultrasound and abdominal CT: absence of hepatic vein filling
    • Abdominal CT: rapid contrast clearing of caudate lobe
26
Q

How does cirrhosis and portal vein thrombosis differ?

A
  • Differentiating signs and symptoms: signs and symptoms of the underlying cause such as acute pancreatitis, ascending cholangitis or abdominal sepsis
  • Differentiating investigations:
    • Magnetic resonance (indirect) or direct angiography: normal hepatic venous pressure gradient (measure of portal pressure)
    • Doppler ultrasound and abdominal CT: portal vein filling defect, absence of flow in the portal vein
27
Q

Describe what is shown in the picture

A