Chronic Liver Disease Flashcards

1
Q

Define Cirrhosis (in pathological terms)

A

An irreversible consequence of chronic hepatic injury w/ 3 key characteristics

  • Destruction of liver cells
  • Chronic inflammation –> fibrosis
  • Hepatocyte regeneration –> nodules
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2
Q

What is the underlying pathology of fibrosis?

A

Due to growth factors released from inflammatory cells/Kupffer cells/hepatocytes
Inflammatory cells due to disease/response to liver cell necrosis

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3
Q

What is the underlying pathology of nodule formation?

A

Due to hepatocyte regeneration
Stellate cell activation –> myofibroblasts formed, secrete collagen –> nodules form
Nodules lack vascular/bile drainage connections

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4
Q

What are the common causes of cirrhosis?

A

Alcoholic liver disease
Cryptogenic liver disease
Non-alcoholic fatty liver disease
Chronic viral hepatitis

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5
Q

What are the less common causes of cirrhosis?

A
AI hepatitis
1o biliary cirrhosis
1o sclerosing cholangitis
Budd-Chiari syndrome
Cystic fibrosis
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6
Q

What are the very rare causes of cirrhosis?

A

Haemochromatosis
Wilson’s
a1-antitrypsin deficiency

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7
Q

What is primary biliary cirrhosis?

A

AI destruction of intrahepatic bile cannaliculi

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8
Q

What are the risk factors for primary biliary cirrhosis?

A

40-60yr old females (90%)

IBD

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9
Q

How does primary biliary cirrhosis present?

A

Jaundice
Pruritis
Skin xanthomas

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10
Q

How is primary biliary cirrhosis diagnosed?

A

Raised anti-mitochondrial antibodies (AMA)

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11
Q

What are the management options for primary biliary cirrhosis?

A

Replacement of fat soluble vitamins

-progressive condition, 6yr average survival

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12
Q

What is primary sclerosing cholangitis?

A

Autoimmune inflammation & fibrosis around the bile ducts in the liver
-2o cirrhosis due to chronic biliary obstruction

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13
Q

What conditions are associated w/ primary sclerosing cholangitis?

A

IBD (70%)

Cholangiocarcinoma (develops in 10-15%)

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14
Q

What are the management options for primary sclerosing cholangitis?

A

No effective treatment except transplantation

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15
Q

What are the classic sx of chronic liver disease?

A
Fatigue
Wt loss/anorexia
Jaundice
Leg swelling
Bleeding/bruising
Itching
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16
Q

What are the classic signs of chronic liver disease?

A

Nails - leuconychia, clubbing
Hands - palmar erythema, duyputren’s contracture, liver flap
Skin - pigmentation, spider naevi, striae
Feminization - gynaecomastia, testicular atrophy, loss of body hair
Portal HTN - caput medusae, hepatosplenomegaly, ascites
Hepatocellular failure - bruising, prolonged clotting

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17
Q

What are the signs of decompensated liver disease?

A

Encephalopathy
Ascites
Jaundice

18
Q

What factors may precipitate chronic liver disease decompensating?

A

Alcohol binge
Variceal bleed
Hepatotoxic drugs
Portal/hepatic vein thrombosis

19
Q

What is the Child-Pugh score?

A

Gives 1/2 yr mortality scores in chronic liver disease using

  • total bilirubin
  • serum albumin
  • PT/INR
  • ascites
  • hepatic encephalopathy
20
Q

What are the complications of chronic liver disease?

A

Hepatocellular failure
Portal HTN
Malignant change
Renal failure (hepatorenal syndrome)

21
Q

How can the severity of chronic liver disease be investigated?

A
Liver function
   -albumin
   -INR
Liver damage
   -LFTs
Complications
   -U&Es
   -ABG
22
Q

How can the type of chronic liver disease be investigated?

A
Liver screen
Imaging
   -USS & duplex
   -endoscopy
   -CT/MRI
23
Q

What investigations make up a liver screen?

A
Viral serology
Serum autoantibodies/immunoglobulins
AFP
Fe studies (hereditary haemochromatosis)
Serum copper/caeruloplasmin (Wilson's)
a1-antitrypsin level
24
Q

What further investigations may be necessary in chronic liver disease?

A
Ascitic tap (MCS)
Liver biopsy
25
Q

What is Wilson’s disease?

A
Inborn error of copper metabolism
Deposition of copper in
   -liver
   -basal ganglia
   -cornea (Kayser-Fleischer rings)
26
Q

What are the appropriate investigations in suspected Wilson’s disease?

A
Serum caeruloplasmin (reduced)
Urinary copper (increased)
Liver biopsy (increased copper)
27
Q

What are the management options for Wilson’s disease?

A

Chelating agents (trientene, D-penicillamine)

28
Q

What is Haemachromatosis?

A

Inherited condition of excess iron deposition leading to fibrosis & organ failure

29
Q

What is the classic triad of sx in Haemachromatosis?

A

Bronze skin discolouration
Hepatomegaly
DM
(also hypogonadism - impotence, testicular atrophy)

30
Q

What are the appropriate investigations in suspected Haemachromatosis?

A

Serum Fe/Ferritin (increased)
Total iron binding capacity (decreased)
Genetic testing
Liver biopsy

31
Q

What are the management options for Haemachromatosis?

A

Vensection

-1 unit/wk

32
Q

What are the common complications of cirrhosis?

A

Portal HTN (varices)
Ascites
Encephalopathy

33
Q

How does portal HTN related to cirrhosis present?

A

Often asymptomatic/just hepatosplenomegaly
90% develop gastro-oesophageal varices over 10 yrs
-1/3 bleed

34
Q

How does ascites related to cirrhosis present?

A

Mild abdo pain common

-if severe suspect spontaneous bacterial peritonitis

35
Q

What are the management options for ascites?

A

Initial bed rest & fluid restriction/low Na diet
Spironolactone
Furosemide (if poor response)
Therapeutic paracentesis/albumin infusion (large volume)

36
Q

What are the signs of spontaneous bacterial peritonitis?

A

Fever
Pain
Deterioration in prev well pt

37
Q

How should spontaneous bacterial peritonitis be managed?

A

IV ceftriaxone

Long term norfloxacin (recurrence high)

38
Q

What causes encephalopathy?

A

Accumulation of nitrogenous waste in circulation

Leads to cerebral oedema

39
Q

What are the grades of encephalopathy?

A

Grade 1 - altered mood/behaviour, sleep disturbances
Grade 2 - increasing drowsiness/confusion
Grade 3 - stupor, incoherence, restlessness
Grade 4 - coma

40
Q

What are the management options of encephalopathy?

A

ICU admission
20o head tilt
Oral lactulose w/ regular enemas
IV manitol/hyperventilation if cerebral oedema