Chronic Liver Disease Flashcards

1
Q

What is CLD?

A

Disease process of the liver involving progressive destruction & regeneration of liver parenchyma, leading to fibrosis & cirrhosis

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2
Q

How long?

A

> 6 months

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3
Q

Causes

A

Inflammation (chronic hepatitis, cirrhosis & hepatocellular carcinoma)

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4
Q

What is fibrosis?

A

excess fibrous connective tissue, replacement of normal tissue by scar tissue

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5
Q

What is cirrhosis?

A

chronic disease of the liver marked by degeneration of cells, inflammation, and fibrous thickening of tissue. It is typically a result of alcoholism or hepatitis

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6
Q

What is compensated cirrhosis?

A

Liver can still function properly, few clinical signs

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7
Q

What is decompensated cirrhosis?

A

Abnormal liver function, overt clinical complications

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8
Q

what is the prognosis?

A

Compensated: >12 yeats
Decompensated: 2 years

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9
Q

What % of cardiac output constitutes the liver?

A

25%

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10
Q

What is the blood supply to the liver?

A

75% portal vein

25% hepatic artery

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11
Q

What is the porta hepatis?

A

Where the R & L bile duct combine to form the common hepatic duct (from the liver)

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12
Q

What combines to form the common bile duct?

A

Common hepatic duct & cystic duct

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13
Q
Functions of the liver:
Bilirubin
Albumin
Lipid
Bile
A

Conjugation & elimination of bilirubin

Albumin synthesis

Lipid metabolism

Formation of bile`

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14
Q

What does bile do?

A

Aids digestion of lipids

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15
Q
Functions of the liver:
Clotting factors
Glucose
Hormone & drug 
Nitrogen
A

Synthesis of clotting factors

Gluconeogenesis

Hormone & drug inactivation

Degradation (nitrogen excretion)

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16
Q

Sign of CLD in men

A

Gynaecomastia

17
Q

Hand signs

A

Xnthoma, clubbing, dupuytrens contracture, asterixis, erythema

18
Q

Skin signs

A

Spider naevi, purpura

19
Q

What are signs of hepatic encephalopathy?

A

Confusion, agitation, irritability, sleep disturbance, lethargy, disorientation, slurred speech, coma

20
Q

What causes hepatic encephalopathy?

A

Increased nitrogenous waste products in the brain (ammonia & glutamine)

21
Q

What is hepatic encephalopathy usually predisposed by?

A

Dehydration, infection, constipation, GI bleed

22
Q

What drugs may trigger encephalopathy?

A

Benzos, opiates, diuretics

23
Q

What causes ascites?

A

• Fluid accumulation in the peritoneal cavity from splanchnic vasodilation, sodium & water retention

24
Q

Why do people with CLD get oesophageal varices?

A

Portal HTN causes varices a a result of dilatation of the veins in the oesophagus & stomach

25
Why are people with CLD at increased risk of infection?
Immune dysfunction E.g. spontaneous bacterial peritonitis
26
What is hepatorenal syndrome?
Decrease in renal blood flow leading to reduced GFR
27
What bloods would you do?
LFT, serum albumin, PT Viral markes Haem: macrocytic anaemia, folate deficiency
28
What biochemical tests?
``` Alpha 1 antitrypsin (cirrhosis) Alpha fetoprotein (usually produced in foetus, but can be raised in liver cancer) ```
29
investigation in jaundice
USS - assessing hepatic & portal vein patency
30
When would you consider CT?
After USS
31
What must you check before liver biopsy?
Coagulation status
32
What must you do with all patients with decompensated liver disease?
Refer to a hepatologist
33
Management of upper GI bleed
``` IV volume support/ transfusion Balloon tamopnade (temporary measure) ```
34
Management of ascites
Diuretics/ paracentesis
35
Management of encephalopathy why?
Non-absorbable disaccharides (lactulose) Reduce pH of colon & promote amonia excretion Antibiotics to reduce enteric bacterial prod of ammonia
36
Reviewing cirrhosis in primary care (3)
Review medications Ensure underlying disease is being managed Ensure specialist follow-up & screesning for complications