Chronic liver disorders Flashcards

(50 cards)

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
What is intractable ascites
Ascites not responding to aggressive diuretic use
26
What are the options for Intractable ascites
Repeated paracentesis | Radiological placement of intraheaptic portal venous hunts to reduce splanchnic pressure
27
What is spontaneous bacterial peritonitis
The spontaneous onset of bacterial infection of ascitic fluid in the setting of liver disease
28
What are the majority of the causative organisms in spontaneous bacterial peritonitis
Gram negative
29
What are the investigation required to diagnose SBP
paracentesis and identification of ascitic neutrophils | Gram stain and culture of ascitic fluid
30
What is the management of SBP?
Empiric therapy is with IV cephalosponins but may be guided by past culture and IV albumin
31
What do varices result from
Collateral flow from the portal system through the coronary vein of the stomach in the azygous vein
32
Where do varices lie
Submucosally
33
What are varices graded by
According to their size and the presence of overlying mucosal lesion
34
What is the management for varices
Primary prophylaxis - following diagnosis of varices but proper to the development of a bleeding complication Secondary prophylaxis - instituted after an episode of bleeding
35
What is the current favoured initial treatment for primary prophylaxis
Beta blockers
36
What is the modality of first choice
Band ligation
37
What are some second line modalities
Sclerotherapy | splanchnic vasoconstrictors
38
When does hepatic encephalopathy result
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
When does hepatic encephalopathy result
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
What is the management of hepatic encephalopathy
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
What is hepatorenal syndrome
Renal dysfunction in chronic liver disease
42
Who does hepatorenal syndrome occur in
Patients with chronic or acute liver disease
43
What are the 2 classes of hepatorenal syndrome
Early and late (type 1 and type 2)
44
How is the diagnoiss of HRS made
Through exclusion
45
What is the management of HRS
Correcting reversible factors: Hypovolaemia Infection Presence of nephrotoxins
46
What is the only definitive treatment for HRS
Liver transplantation
47
What is hepatopulmonary syndrome
Pulmonary dysfunction in association with chronic liver disease
48
What is the common complaint from patients with hepatopulmonary syndrome
Shortness of breath
49
What 3 things does the diagnosis of HPS rely on
The demonstration of: liver disease or portal hypertension Elevated age-adjusted alveolar-arterial oxygen gradient AaPO2 Evidence of intrapulmonary vasodilatation
50
What is involved in the management for HPS
Liver transplantation | Oxygen supplementation