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Gastroenterology > Cirrhosis > Flashcards

Cirrhosis Flashcards

1
Q

What is cirrhosis?

A

Liver damage characterised by diffuse distortion of basic architecture and replacement with scar tissue and formation of regenerative nodules.

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2
Q

What are the common causes of cirrhosis?

A
  • Fatty liver (alcohol, metabolic syndrome)

- Chronic viral hepatitis: Hep B +/- D, Hep C

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3
Q

What are the less common causes of cirrhosis?

A

1) Primary biliary cirrhosis
2) AI hepatitis
3) Haemochromatosis
4) Chronic Hepatic venous congestion: cardiac cirrhosis, Budd Chiari syndrome.
6) Wilson’s disease
7) Drugs (e.g. methotrexate)
8) a1 anti-trypsin deficiency
10) Glycogen storage disease

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4
Q

What initiates liver fibrosis?

A

Stellate cells, activated by cytokines and ROS

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5
Q

What occurs in liver fibrosis?

A

In the space of Disse, normal matrix is replaced by collagens (predominately 1 and 3), and fibronectin.
Subendothelial fibrosis -> loss of endothelial fenestration -> impaired function.

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6
Q

What are the characteristic features of liver cirrhosis?

A

Regenerating nodules separated by fibrous septa with loss of the normal lobular architecture within the nodules.

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7
Q

What is micronodular cirrhosis?

A

Regenerating nodules

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8
Q

What is macronodular cirrhosis?

A

Regenerating nodules >3mm

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9
Q

What are the first tests to order in suspected cirrhosis?

A 
LFTs (deranged)
GGT (elevated)
Serum Albumin (reduced)
Serum Sodium (reduced)
APTT (prolonged)
Platelet count (reduced)
Hep B/C Abs
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10
Q

What are the best indicators of liver function?

A

Serum albumin and prothrombin time.

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11
Q

What causes hyponatremia of patients with cirrhosis?

A

Low sodium indicates severe liver disease due to a defect in free water clearance or to excess diuretic therapy.

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12
Q

What imaging utilised to assess/diagnose cirrhosis? Outline expected features.

A

US: liver surface nodularity, changes to liver size, ascites, splenomegaly, increased diameter of portal vein.
CT: hepatosplenomegaly, ascites, collateral circulation (varices), liver surface texture.

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13
Q

What imaging can be used to detect HCC?

A

Arterial phase contrast CTA

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14
Q

How is cirrhosis classified?

A
  • Compensated: findings consistent with cirrhosis present but hepatic synthetic function preserved with no evidence of complications of portal HTN.
  • Decompensated: complications of liver dysfunction with decreased synthesis and portal HTN.
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15
Q

What are the RFx for cirrhosis?

A

Alcohol abuse, IVDU, unprotected sex, obesity, blood transfusion.

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16
Q

What are the key diagnostic features of cirrhosis on Hx and Ex?

A
  • Presence of RFx
  • Abdo distension
  • Jaundice and pruritus
  • Coffee ground vomitus and maelena
  • Hand and nail features (leukonychia, palmar erythema, spider angiomata)
  • Facial features (jaundice, telangiectasia)
17
Q

How is cirrhosis severity scored?

A

Child Pugh and MELD

18
Q

What is the Child Pugh scoring system?

A

CP A, B or C based on:
Ascites, hepatic encephalopathy, serum bilirubin, albumin, APTT and INR.
A = well compensated –> B = decompensated

19
Q

How is cirrhosis managed?

A
  • Treatment of underlying chronic liver disease and prevention of superimposed hepatic insult
  • Monitor for complications
  • Sodium restriction and diuretic therapy for ascites
  • 2nd = liver transplant
20
Q

What are the common causes of death in cirrhotic patients?

A
  • Renal failure (hepatorenal syndrome)
  • Sepsis
  • GI bleed
  • HCC
21
Q

What are the stages of cirrhosis?

A
  • S1: compensated and asymptomatic. Can last 10-20y w/ norm life expectancy
  • S2: onset first decompensation (typically development of ascites, variceal bleeding, encephalopathy).
22
Q

Complications of cirrhosis?

A

VARICES

  • Varices
  • Anaemia
  • Renal failure
  • Infection
  • Coagulopathy
  • Encephalopathy
  • Sepsis
23
Q

What are the haematology complications of cirrhosis?

A
  • Pancytopenia (from hypersplenism): first platelets > WBC >Hb.
  • Decreased clotting factor synthesis = prolonged INR, bruising and bleeding.
24
Q

What proportion of patients with cirrhosis develop varices / vatical haemorrhage?

A
  • 50% cirrhotics will develop varies

- ~30% develop haemorrhage (mortality then = 30%+)

25
Q

What is the strongest predictor of variceal development in cirrhosis?

A

hepatic venous pressure gradient >10mmHg.

26
Q

Management of oesophageal varies?

A

Resuscitation, ABx, vasoactive drugs + endoscopic band ligation or sclerotherapy, TIPS.

27
Q

What are the classifications of renal failure in cirrhosis?

A
  • Pre renal (usually over diuresis)
  • Acute tubular necrosis
  • Hepatorenal syndrome
28
Q

What are the types of hepatorenal syndrome?

A
  • Type I: sudden and acute renal failure (rapid doubling of Cr over 2/52)
  • Type II: gradual increase in Cr with worsening liver function (Cr doubling over years)
29
Q

When is hepatorenal syndrome likely to develop?

A
  • overdiuresis or dehydration (e.g. V/Diarrhoea)
  • GI bleed
  • Sepsis
30
Q

Treatment for type I hepatorenal syndrome?

A

-Octreotide + midodrine + albumin
Increases renal blood flow by increasing systemic vascular resistance.
Definitive Rx = liver transplant.

31
Q

What is the presumed aetiology of hepatopulmonary syndrome?

A

?VQ mismatch, intrapulmonary shunting and limitation of O2 diffusion. Relates to failure of damaged liver to clear circulating pulmonary vasodilators vs production of vasodilating substance by liver.

32
Q

What is the clinical triad of hepatopulmonary syndrome?

A
  • Liver disease
  • Increase A-a gradient on RA
  • Evidence of intrapulmonary vascular abnormalities
33
Q

What is platypnea?

A

Increase in dyspnoea when upright, improved with recumbency.

34
Q

What is orthodeoxia?

A

Desaturation in upright position, improved with recumbency.

35
Q

What are the clinical features of hepatopulmonary syndrome?

A
  • Dyspnoea, platypnea, orthodeoxia.
  • Hyperdynamic circulation with CO>7L/min at rest.
  • Decreased pulmonary and systemic resistance (intrapulmonary shunting)
36
Q

How is hepatopulmonary syndrome diagnosed?

A

Contrast enhanced echo:
inject air bubbles into peripheral vein; air bubbles appear in left ventricle after 3rd heartbeat (normal = no air bubbles; VSD = air bubbles

37
Q

Rx hepatopulmonary syndrome?

A

Only proven treatment is transplant.

Gastroenterology (54 decks)

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