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Gastrointestinal (LECTURE NOTES) > Chronic liver disorders > Flashcards

Chronic liver disorders Flashcards

1
Q

What does chronic liver disease result from

A

Hepatocellular injury and necrosis often with a degree of underlying fibrosis of the liver

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2
Q

When does jaundice result

A

When the liver’s capacity to convert and excrete bilirubin as bile is exceeded

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3
Q

What can jaundice result from

A

Over production of bilirubin

reduction in the eliminatory capactiy of the liver

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4
Q

What is bilirubin

A

The breakdown product of haem

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5
Q

Where is bilirubin found

A

Bound to albumin in the plasma but at the hepatocyte membrane, it dissociates and enters the hepatocyte

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6
Q

What is prehepatic jaundice

A

increased degradation of haem leading to haem concentrations that cannot be cleared by the normal conjufative mechamisms resultin in predominately unconjugated hyperbilirubinaemia

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7
Q

What is hepatic jaundice

A

Liver damage and or inflammation affecting the conjugative and excretory ability of the liver so that the normal bilirubin load cannot be excreted. This results in a predominately unconjugated or mixed conjugated and unconjugated hyperbilirubinaemia

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8
Q

What is postheaptic jaundice

A

Obstruction of the biliary outflow tract at any level, leading to an inability to excrete conjugated bilirubin in bile resulting in a conjugated hyperbilirubinaemia

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9
Q

Is unconjugated bilirubin in water soluble or insoluble

A

Insoluble (cannot be excreted in urine)

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10
Q

What is conjugated bilirubin converted to in the terminal ileum

A

Urobilinogen

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11
Q

Bilirubin that is not reabsorbed is further converted to what and what does this do

A

Urobilin then stercobilin

It gives faeces its normal colour

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12
Q

What gives clues about the cause of jaundice

A

Observation of the stool and testing for the different byproducts of haem excretion in the blood and urine

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13
Q

What results in pale stool and dark urine

A

Obstruction of the biliary system

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14
Q

What is portal hypertension defined as

A

The gradient reaching 12mmHg or greater

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15
Q

What does increased pressure in the portal system result in

A 
Collateral vessel formation
Ascites 
increased risk of hepatorenal syndrome 
hepatic encephalopathy 
Splenomegaly
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16
Q

What is the management for portal hypertension

A

First line is with a non-selective B blocker: propanolol to reduce the pressure within the portal system

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17
Q

What is ascites

A

The presence of fluid in the peritoneum

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18
Q

What are the two main pathogenic mechanisms for asictes

A

Transudation and exudation

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19
Q

What are transudates:

A

Hydrostatic: result of portal hypertension and resultant increases in the pressure in splanchnic vessels
Oncotic: the result of lowered serum albumin as the synthetic function of the liver decreases
Fluid retention: renal hypoperfusion resulting from portal hypertension causes release of renin and hence a secondary hyperaldosteronism; this results in salt and water retention and contributes to ascites

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20
Q

What are exudates

A

They result from an inflammatroy or neoplastic process at the peritoneal surface causing increased production of peritoneal secretions

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21
Q

What is the function of the Serum-to-ascites albumin gradient

A

To determine whether ascites is related to transudation or exudation

22
Q

How is SAAG calculated

A

Serum albumin conc. - Ascites albumin conc.

23
Q

What is the general management of ascites

A

treat the underlying liver condition

Improvement of nutritional status in order to maximise serum albumin

24
Q

What are the specific management for asicties

A

Reduction of hydrostatic pressure in the splanchnic vasculature with diuretics - spironolactone!
Abdominal paracentesis - removing the fluid through a drain

25
Q

What is intractable ascites

A

Ascites not responding to aggressive diuretic use

26
Q

What are the options for Intractable ascites

A

Repeated paracentesis

Radiological placement of intraheaptic portal venous hunts to reduce splanchnic pressure

27
Q

What is spontaneous bacterial peritonitis

A

The spontaneous onset of bacterial infection of ascitic fluid in the setting of liver disease

28
Q

What are the majority of the causative organisms in spontaneous bacterial peritonitis

A

Gram negative

29
Q

What are the investigation required to diagnose SBP

A

paracentesis and identification of ascitic neutrophils

Gram stain and culture of ascitic fluid

30
Q

What is the management of SBP?

A

Empiric therapy is with IV cephalosponins but may be guided by past culture and IV albumin

31
Q

What do varices result from

A

Collateral flow from the portal system through the coronary vein of the stomach in the azygous vein

32
Q

Where do varices lie

A

Submucosally

33
Q

What are varices graded by

A

According to their size and the presence of overlying mucosal lesion

34
Q

What is the management for varices

A

Primary prophylaxis - following diagnosis of varices but proper to the development of a bleeding complication
Secondary prophylaxis - instituted after an episode of bleeding

35
Q

What is the current favoured initial treatment for primary prophylaxis

A

Beta blockers

36
Q

What is the modality of first choice

A

Band ligation

37
Q

What are some second line modalities

A

Sclerotherapy

splanchnic vasoconstrictors

38
Q

When does hepatic encephalopathy result

A

When toxic metabolites cannot be excreted by the diseased liver; they bypass the liver due to portosystemic shunts and produce direct effects on the brain

39
Q

When does hepatic encephalopathy result

A

When toxic metabolites cannot be excreted by the diseased liver; they bypass the liver due to portosystemic shunts and produce direct effects on the brain

40
Q

What is the management of hepatic encephalopathy

A

Correction or reduction in factors that precipitate the onset of encephalopathy
Non-digestable disaccharides (lactulose)
Reduction of protein in the diet may be reasonable in the short term

41
Q

What is hepatorenal syndrome

A

Renal dysfunction in chronic liver disease

42
Q

Who does hepatorenal syndrome occur in

A

Patients with chronic or acute liver disease

43
Q

What are the 2 classes of hepatorenal syndrome

A

Early and late (type 1 and type 2)

44
Q

How is the diagnoiss of HRS made

A

Through exclusion

45
Q

What is the management of HRS

A

Correcting reversible factors:
Hypovolaemia
Infection
Presence of nephrotoxins

46
Q

What is the only definitive treatment for HRS

A

Liver transplantation

47
Q

What is hepatopulmonary syndrome

A

Pulmonary dysfunction in association with chronic liver disease

48
Q

What is the common complaint from patients with hepatopulmonary syndrome

A

Shortness of breath

49
Q

What 3 things does the diagnosis of HPS rely on

A

The demonstration of:
liver disease or portal hypertension
Elevated age-adjusted alveolar-arterial oxygen gradient AaPO2
Evidence of intrapulmonary vasodilatation

50
Q

What is involved in the management for HPS

A

Liver transplantation

Oxygen supplementation

Gastrointestinal (LECTURE NOTES) (29 decks)

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