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Alimentary System > Liver Failure and Jaundice > Flashcards

Liver Failure and Jaundice Flashcards

1
Q

When is jaundice detectable?

A

When serum bilirubin is >50 micro mol/L.

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2
Q

How is bile mainly produced?

A

From Hb breakdown in the spleen.

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3
Q

Explain bilirubin metabolism

A
  1. Unconjugated bilirubin bound to albumin and travels to liver.
  2. Glucuronyl transferase conjugates bile into bilirubin glucuronide, which makes bile water soluble.
  3. Bilirubin glucuronide excreted to duodenum. Bacteria in the gut degrade bilirubin glucuronide into urobilinogen or stercobilinogen (both water soluble).
  4. Some urobilinogen reabsorbed and excreted by kidneys. Some converted to stercobilinogen.
  5. Stercobilinogen (majority) oxidised to stercobilin in GI tract.
  6. 10% stercobilin reabsorbed and returns to liver via portal circulation.
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4
Q

How are bile salts reabsorbed from portal circulation into the liver?

A

Via an active transport mechanism.

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5
Q

What % of bile salts are old and recycled?

A

95%

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6
Q

What are the 3 types of Jaundice?

A
  1. Haemolytic - haemolytic anaemias (e.g. SCD - more RBC breakdown). Increased serum urobilinogen but otherwise normal liver biochemistry.
  2. Congenital - impaired conjugation of bilirubin with glucuronic acid/inappropriate handling of bilirubin. Raised bilirubin, otherwise normal.
  3. Cholestatic - failure of bile secretion by the liver/bile duct obstruction.
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7
Q

Does unconjugated bilirubin pass into urine?

A

No

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8
Q

Gilberts syndrome is a form of congenital jaundice. Explain

A

Autosomal dominant.

UDP-glucuronyl transferase mutation, less conjugation of bilirubin.

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9
Q

Differentiate intrahepatic cholestasis and extra hepatic cholestasis

A

Intrahepatic cholestasis = hepatocellular swelling/abnormalities at a cellular level of bile secretion

Extrahepatic cholestasis = obstruction of bile flow distal to bile canaliculi. Charcterised by pale stool and dark urine.

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10
Q

Which proteins are not synthesised in the liver?

A

Gamma globulins

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11
Q

4 functions of the liver

A
  1. Synthesis/metabolism of protein
  2. Blood sugar maintenance
  3. Lipid metabolism
  4. Metabolism, excretion of bilirubin and bile acids
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12
Q

What are the 2 most common causes of liver disease?

A

Alcohol
Non-alcoholic fatty liver disease

In the developing world, chronic viral hepatitis B and C are the commonest

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13
Q

What are the symptoms of liver disease?

A 
Lethargy
Anorexia
Malaise
Pruritus (itchy skin)
RUQ pain
Later on:
Peripheral swelling
Abdominal bloating
Bruising
Vomiting blood
Confusion/somnolence
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14
Q

What are some signs of liver disease

A
  1. Jaundice
  2. Spider naevi
  3. Loss of body hair
  4. Gynaecomastia
  5. Testicular atrophy
  6. Palmar erythema
  7. Xanthelasma
  8. Finger clubbing
  9. Dupuytrens contracture
  10. Ascites
  11. Hepato(/spleno)megaly
  12. Caput medusa
  13. Oedema
  14. Weight loss
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15
Q

What is cirrhosis?

A

Often final common pathway for liver disease.

Necrosis of liver cells, then fibrosis and nodule formation. Leads to portal hypertension

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16
Q

What are the causes of cirrhosis?

A

Alcohol
Hep B/C

Develops in response to chronic liver injury

17
Q

What are the 2 types of liver cirrhosis?

A

Micronodular - uniform, small nodules. Ongoing alcohol damage/biliary tract disease
Macronodular - often following viral chronic hepatitis.

(can also be mixed)

18
Q

When does acute liver failure occur?

A

Massive loss of hepatocytes.

“Severe hepatic dysfunction occurring within 6 months of onset of liver disease symptoms. Clinical manifestation is hepatic encephalopathy or coagulopathy”

19
Q

What are the 3 classes of acute liver failure?

A
  1. Hyperacute - 1 week of jaundice onset
  2. Acute - 8-28 after jaundice
  3. Subacute - 5-12 weeks after jaundice
20
Q

What are the clinical features of acute liver failure?

A
  1. JAUNDICE
  2. CNS complications
  3. Renal failure - v lethal
  4. Sepsis - v common
  5. CVS complications - HF / hypotension
  6. Metabolic complications - hypoglycaemia and hypoxia
21
Q

What roles does the liver play in coagulation?

A
  1. Synthesis of coagulation factors. Factor V affected first, factor 7 declines first due to short half life.
  2. Inhibition of fibrinolysis
  3. Clearance of activated coagulation factors
  4. Absorption of vitamin K
22
Q

3 signs of coagulation defect?

A

Bleeding
Oozing at venipuncture sites (excessive fibrinolysis)
Bruising

23
Q

Chronic liver failure - when?

A

Deterioration in liver function superimposed on chronic liver disease.

Alimentary System (15 decks)

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