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Z YEAR 1 BRS Gastroentology > Liver Failure > Flashcards

Liver Failure Flashcards

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1
Q

What are normal Bilirubin levels?

A 
•Normal plasma [bilirubin (BR)] – 17 μmol/L
•If [BR] ↑s > 30 μmol/L 
 → yellow sclera & mucous membranes
•If [BR] ↑s > 34 μmol/L 
 → skin turns yellow
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2
Q

What is cholestasis?

A
  • Cholestasis - slow/cessation of bile flow
  • Cholestasis - normally results in jaundice
  • Jaundice does not necessarily mean there is cholestasis
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3
Q

What are prehepatic causes of jaundice?

A
  1. Haemolysis
    - Haemolytic anaemia
    - Toxins
  2. Massive transfusion (transfused erythrocytes short-lived)
  3. Large haematoma resorption
  4. Ineffective erythropoiesis
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4
Q

What are specific defects in intrahepatic causes of jaundice?

A 
1. ↓ed BR uptake 
•Gilberts syndrome
2.. ↓ed conjugation BR 
•Crigler-Najar syndrome
3. ↓ed secretion BR into biliary canaliculi
•Dubin-Johnson syndrome
•Rotor syndrome
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5
Q

What are other causes of intrahepatic jaundice?

A

1.Intrahepatic cholestasis (↓ed outflow):
•Sepsis, TPN & drugs
2. Liver failure (acute & chronic)

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6
Q

What happens in liver failure?

A

When rate of hepatocyte death > regeneration

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7
Q

Describe the pathophysiology in liver failure?

A
  • Combination of apoptosis &/or necrosis
  • Apoptosis (e.g. Acetaminophen=Paracetamol):
  • Necrosis (ischaemia):
  • Clinical result = catastrophic illness
  • Can rapidly lead to coma/death due to multi-organ failure
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8
Q

What is fulminant hepatic failure in acute liver failure?

A
  • Fulminant hepatic failure = rapid development (< 8wks) of severe acute liver injury
  • impaired synthetic function (INR/PT, albumin)
  • encephalopathy
  • previously normal liver or well-compensated liver disease
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9
Q

What is sub-fulminant hepatic in acute liver failure?

A

< 6 months

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10
Q

What happens in chronic liver failure?

A
  • Over years

* Cirrhosis

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11
Q

What are the common causes of acute liver failure in west?

A
  • Toxins (West)
  • Paracetamol
  • Amanita phalloides
  • Bacillus cereus
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12
Q

What are the common causes of acute liver failure in the east?

A
  • Inflammation (East)
  • Exacerbations of chronic Hep B (Hong Kong)
  • Hepatitis E (India)
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13
Q

What are the pregnancy causes of acute liver failure?

A

•AFLP, HELLP syndrome, hepatic infarction, HEV, Budd-Chiari

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14
Q

What are some causes of acute liver failure with Idiosyncratic drug reactions?

A
  • Single Agent: Isoniazid, NSAID’s, valproate

* Drug combinations: Amoxicillin/clavulanic acid, trimethoprim/sulphamethoxazole, rifampicin/isoniazid

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15
Q

What vascular diseases can causes acute liver disease?

A

•Ischaemic hepatitis, post-OLTx hepatic artery thrombosis, post-arrest, VOD

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16
Q

What are the metabolic causes of acute liver disease?

A
  • Wilson’s disease

* Reye’s syndrome

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17
Q

What are the inflammatory causes of chronic liver failure?

A

•chronic persistent viral hepatitis

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18
Q

What else can cause chronic liver failure?

A
  • Alcohol abuse
  • Non alcoholic steatohepatitis (NASH)
  • Autoimmune Hepatitis, PBC, PSC
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19
Q

What drug side effects can lead to chronic liver failure?

A

folic acid antagonists phenylbutazone

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20
Q

What are cardiovascular causes of chronic liver failure?

A

•↓venous return - right heart failure

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21
Q

What are some inherited diseases that can lead to chronic liver failure?

A

•Glycogen storage diseases, Wilson’s disease, Galactosaemia, Haemochromatosis, α1-antitrypsin deficiency

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22
Q

What can chronic liver failure lead to?

A

cirrhosis

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23
Q

What are the metabolic and catabolic functions of hepatocyte?

Study These Flashcards
A

synthesis & utilization of carbohydrates, lipids and proteins

24
Q

What are the secretory and excretory functions of hepatocyte?

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A

synthesis &secretion of proteins, bile and waste products

25
What are the detoxification and immunological functions of hepatocyte?
breakdown of ingested pathogens & processing of drugs
26
What happens in cirrhosis?
- Necrosis of hepatocyte and release enzymes that cause cytokines - activate Kuppfner cells that realise growth factors stimulates Ito fat cell get myofibrilbast and lots of ECM deposition and fibroblasts activated and lead to fibrosis - Called cholestasis as well, portal hypertension and metabolic failure
27
What is normal liver function?
1. Production of clotting factors 2. Protein synthesis 3. Detoxification 4. Glycogen storage 5. Immunological functionalists and globulin production 6. Maintenance of homeostasis
28
What are the consequences of hepatocytes failure?
1. Coagulopathy and bleeding 2. Ascites 3. Encephalopathy and cerebral oedema 4. Hypoglycaemia 5. increased susceptibility to infection 6. Circulatory collapse, renal failure
29
What is the problem with low albumin?
Plasma vol ↓        → 20 hyperaldosteronism        → hypokalaemia (↓K+)        → alkalosis
30
What is the problem with low plasma (clotting factors)?
Hepatocytes synthesis all coagulation proteins except von Willebrand factor & factor VIIIC
31
What does choleostasis lead to?
•→ liver damage •aggravates any bleeding tendency •↓ bile salts            → ↓ micelles & absorptn of vit  K            → ↓ γ-carboxylation of vit K                 -dependent clotting factors                 prothrombin (II), VII, IX, & X
32
What is the mechanism of cholestasis?
1. Canalicular dilation 2. Decrease cell membrane fluidity 3. Deformed brush border 4. Biliary transporters 5. Increase tight junction permeability 6. Decreased mitochondrial ATP synthesis
33
What are the consequences of cholestasis?
1. Increased bilirubin lead to jaundice 2. Pruritus (itching) 3. Cholesterol deposition 4. Malabsorption 5. Cholangitis
34
What is portal hypertension and what does it lead to?
-Blood doesn't go in portal vein instead side little routes (small blood vessels) •↓ lymphatic flow → makes ascites worse •thrombocytopenia resulting from splenomegaly •oesophageal varices (back pressure) (lots where blood goes) •↓ active clotting factors, thrombocytopenia, & varices → severe bleeding (v low platelets) •exudative enteropathy •↑ ascites → loss of albumin from plasma •favours bacteria in large bowel being “fed” with proteins •↑ liberation of ammonium (toxic to brain)
35
What are preheptic causes of portal hypertension?
PV thrombosis
36
What are postheptic causes of portal hypertension?
- right heart failure | - constrictive pericarditis
37
What are intraheptic causes of portal hypertension?
1. Presinusoidal -chronic hepatitis, PBC, granulomas (schistosomiasis, TB, etc.) 2. Sinusoidal - acute hepatitis, alcohol, fatty liver, toxins, amyloidosis, etc. 3. Postsinusoidal - venous occlusive disease of venules & small veins; Budd– Chiari syndrome (obstruction of large HVs).
38
What are portal hypertension causes?
- Increased portal vein pressure causes 1. Malabsorption 2. Splenomegaly (anaemia &  thrombocytopaenia) 3. Effect on vasodilators 4. Encephalopathy 5. Varices
39
How are vasodilators affected in portal hypertension?
* Vasodilators (glucagon, VIP, substance P, prostacyclins, NO, etc.) * → ↓BP → ↑CO → hyperperfusion of abdo. organs & varices
40
Why does portal hypertension cause encephalopathy?
Toxins from intestine (NH3, biogenic amines, FFAs, etc.) normally extracted from portal blood by hepatocytes → CNS
41
Why does portal hypertension affect varices?
Thin walled collateral vessels + thrombocytopenia & ↓ clotting factors → bleeding +++
42
What is hepatic encephalopathy?
apathy, memory gaps, tremor & liver coma
43
How does Hyperammonaemia cause encephalopathy?
* Hyperammonaemia ↑s * GI bleeding ↑s colonic proteins * liver can’t convert (NH3 NH4+) to urea
44
How does Hypokalaemia cause encephalopathy?
* → intracellular acidosis → activates ammonium formation in proximal tubules → systemic alkalosis. * respiratory component with hyperventilatn 20 encephalopathy.
45
How do toxins and false transmitters cause encephalopathy?
* Toxins (amines, phenols & FFAs) bypass liver → not extracted → encephalopathy. * “false transmitters” (e.g., serotonin) from aromatic amino acids in brain → ↑ed in liver failure * transmitters → encephalopathy.
46
What is the child Pugh score?
-assess disease celerity for end stage liver disease and a prognosticator for peri-op death 1. Bilrubin 2. Serum albumin 3. INR 4. Ascites 5. Hepatic encephalopathy Class A: 5-6 points (15-20 years) Class B: 7-9 (transplant candidates) Class C: 10-15 (1-3 months)
47
What is the supportive treatment for encephalopathy?
* reduce protein intake * phosphate enemas/lactulose * no sedation
48
What is the supportive treatment for hypoglycaemia?
infusion 10-50% dextrose
49
What is the supportive treatment for hypocalaemia?
10 ml 10% calcium gluconate
50
What is the supportive treatment for renal failure?
haemofiltration
51
What is the supportive treatment for respiratory failure?
ventilation
52
What is the supportive treatment for hypotension?
* albumin | * vasoconstrictors 
53
What is the supportive treatment for infection?
* frequent cultures | * A/Bs
54
What is the supportive treatment for bleeding?
* Vit K * FFP * platelets
55
What are the causes of death?
``` -Bacterial and fungal infections •Circulatory instability •Cerebral Oedema •Renal failure •Respiratory failure •Acid-base and electrolyte disturbance •Coagulopathy ```
56
What are some liver support devices?
•Artificial (MARS, Bio-Logic DT) - Albumin exchange system -based on selective removal of albumin-bound toxins from blood •Bioartificial (Hepatocytes in culture) •Hepatocyte transplantation
57
Describe liver transplant?
* 5% of all transplants in UK * 5 year survival rate with OLTx btwn 60-80% * No recurrence of disease BUT patient will require life-long immunosuppression

Z YEAR 1 BRS Gastroentology (11 decks)

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