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Z YEAR 1 BRS Gastroentology > Liver Failure > Flashcards

Liver Failure Flashcards

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?

A

synthesis & utilization of carbohydrates, lipids and proteins

24
Q

What are the secretory and excretory functions of hepatocyte?

A

synthesis &secretion of proteins, bile and waste products

25
Q

What are the detoxification and immunological functions of hepatocyte?

A

breakdown of ingested pathogens & processing of drugs

26
Q

What happens in cirrhosis?

A
  • 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
Q

What is normal liver function?

A
  1. Production of clotting factors
  2. Protein synthesis
  3. Detoxification
  4. Glycogen storage
  5. Immunological functionalists and globulin production
  6. Maintenance of homeostasis
28
Q

What are the consequences of hepatocytes failure?

A
  1. Coagulopathy and bleeding
  2. Ascites
  3. Encephalopathy and cerebral oedema
  4. Hypoglycaemia
  5. increased susceptibility to infection
  6. Circulatory collapse, renal failure
29
Q

What is the problem with low albumin?

A

Plasma vol ↓
→ 20 hyperaldosteronism
→ hypokalaemia (↓K+)
→ alkalosis

30
Q

What is the problem with low plasma (clotting factors)?

A

Hepatocytes synthesis all coagulation proteins except von Willebrand factor & factor VIIIC

31
Q

What does choleostasis lead to?

A

•→ 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
Q

What is the mechanism of cholestasis?

A
  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
Q

What are the consequences of cholestasis?

A
  1. Increased bilirubin lead to jaundice
  2. Pruritus (itching)
  3. Cholesterol deposition
  4. Malabsorption
  5. Cholangitis
34
Q

What is portal hypertension and what does it lead to?

A

-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
Q

What are preheptic causes of portal hypertension?

A

PV thrombosis

36
Q

What are postheptic causes of portal hypertension?

A
  • right heart failure

- constrictive pericarditis

37
Q

What are intraheptic causes of portal hypertension?

A
  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
Q

What are portal hypertension causes?

A
  • Increased portal vein pressure causes
    1. Malabsorption
    2. Splenomegaly (anaemia & thrombocytopaenia)
    3. Effect on vasodilators
    4. Encephalopathy
    5. Varices
39
Q

How are vasodilators affected in portal hypertension?

A
  • Vasodilators (glucagon, VIP, substance P, prostacyclins, NO, etc.)
  • → ↓BP → ↑CO → hyperperfusion of abdo. organs & varices
40
Q

Why does portal hypertension cause encephalopathy?

A

Toxins from intestine (NH3, biogenic amines, FFAs, etc.) normally extracted from portal blood by hepatocytes → CNS

41
Q

Why does portal hypertension affect varices?

A

Thin walled collateral vessels + thrombocytopenia & ↓ clotting factors → bleeding +++

42
Q

What is hepatic encephalopathy?

A

apathy, memory gaps, tremor & liver coma

43
Q

How does Hyperammonaemia cause encephalopathy?

A
  • Hyperammonaemia ↑s
  • GI bleeding ↑s colonic proteins
  • liver can’t convert (NH3 NH4+) to urea
44
Q

How does Hypokalaemia cause encephalopathy?

A
  • → intracellular acidosis → activates ammonium formation in proximal tubules → systemic alkalosis.
  • respiratory component with hyperventilatn 20 encephalopathy.
45
Q

How do toxins and false transmitters cause encephalopathy?

A
  • 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
Q

What is the child Pugh score?

A

-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
Q

What is the supportive treatment for encephalopathy?

A
  • reduce protein intake
  • phosphate enemas/lactulose
  • no sedation
48
Q

What is the supportive treatment for hypoglycaemia?

A

infusion 10-50% dextrose

49
Q

What is the supportive treatment for hypocalaemia?

A

10 ml 10% calcium gluconate

50
Q

What is the supportive treatment for renal failure?

A

haemofiltration

51
Q

What is the supportive treatment for respiratory failure?

A

ventilation

52
Q

What is the supportive treatment for hypotension?

A
  • albumin

* vasoconstrictors

53
Q

What is the supportive treatment for infection?

A
  • frequent cultures

* A/Bs

54
Q

What is the supportive treatment for bleeding?

A
  • Vit K
  • FFP
  • platelets
55
Q

What are the causes of death?

A 
-Bacterial and fungal infections
•Circulatory instability
•Cerebral Oedema
•Renal failure
•Respiratory failure
•Acid-base and electrolyte disturbance
•Coagulopathy
56
Q

What are some liver support devices?

A

•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
Q

Describe liver transplant?

A
  • 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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