Biochemical Functions Of The Liver Flashcards

1
Q

What hapoens in the liver?

A
  1. Liver glycogen- in fasted and fed states. Glucose homeostasis.
  2. Can process fatty acids to ketone bodies, fuel that is critical for surviving during starvation.
  3. Almost ALL plasma proteins produced in liver.
  4. Xenobiotic metabolism
  5. Hormones and waste products processed like bilirubin.b4 elimination
  6. Bile made
  7. Liver only site of urea cycle- ammonia toxicity.
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2
Q

What happens in the carbohydrate metabolism?

A

Store glucose as glycogen in fed state anspd break it down and make glucose from non carbs in fasted states.

Glucogenolysis and gluconeogenesis

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3
Q

What happens in Drug metabolism?

Metabolism of Xenobiotics

A
  1. Inactivation of compund
  2. Increased water solubility of the compound. - facilitating excretion by kidneys or in bile.

Drug metabolism occurs in 2 stages:
Phase 1. : P-450 mixed function oxidases- these enzymes xatalyse oxidations. Require NADPH.

Phase 2: polar molecules being added in products of phase 1 to produce water soluble products.

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4
Q

What can induce cytochrome P-450?

A

Drugs- narrow therapeutic index- warfarin, digioxin, cyclosporin.

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5
Q

Hormone Inactivation

A
  1. Metabolism and inactivation of adrenaline and noraderenalime by monoamine oxidase
  2. De- iodination of thyroxine and triiodothyroine
  3. Insulin reduction to separate chanes A and B
  4. Metabolism and inactivation of steroid hormones : cortisol, testosterone, progesterone and oestradiol. By double bond reduction to form very water soluble products.
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6
Q

What happens in jaundice?

A

Bilirubin accumulates: 1. Xs formation
2. Inadequate removal in bile

Icterus- jaundice:
1. Massive breakdown of erythrocytes (haemolysis) leading to overproduction of bilirubin from Hb catabolism (unconjucated)

  1. Intrahepatic defect for disposal.
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7
Q

Does neonatal jaundice has to be treated?

A

Yes but normal as ligandin system still immature in first few days.
H/w if left, high levels of unconjugayed bilirubin can cause kernicterus- possibly a motor disorder if enters CNs.

Tx: phototherapy- where bilirubin in skin convreted to a water soluble derivative

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8
Q

LFTs what do they include?

A

Liver has a great reserve activity. 80% damage and still can be no change in LFts. Significant liver damage not aasc w/ glucose, even tho we know most of it metabolised there.

  1. Serum albumin
  2. PT: prtothrombin time of plasma-> indicates synthetic activity of liver
  3. ALP : as a measure of Cholestasis
  4. Aminotransferases: AST/ALT : inflammation and necrosis test
  5. Serum bilirubin

⬆️ PT : sensitive for synthetic activity- dependend on Factor 7 - short half life. involved in extrinsic coagulation- Vit K dependent so we know vit K status as well.

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9
Q

Whre is ALP coming from?

A
Serum ALP: derived from liver, 
Bone
Intestine
Placenta
Kidney

⬆️ assc w/ obstructive and cholestatic liver disease.
When the liver is damaged, as in viral hepatitis- ALT more liver specific (involved in gluconeogenic pathway from alanine to glucose. )

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10
Q

When liver damage is due to hepatitis, the ratio of ALT to AST is greater than 1?

A

True, unless the damage is due to severe alcoholism, the Alt/ast ratio is greater than 1. ALT somwhat soecific to livwr due to its gluconeogenic pathway.

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11
Q

Is ALP assc with cholesistatic jaundice?

A

Yes, as ALP can oroginate from the bile ducts. So elevated in obstruction.

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12
Q

Is the liver the site of synthesis of 25- hydroxycholecalciferol?

A

No, cholecalciferol made in skin and 25- hydroxylation in the liver gives the precursor of the hormone calcitriol which is made in the kidney.

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13
Q

What are purines catabolised to?

A

Uric acid

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14
Q

What are some tests for liver damage?

A

GGT, ALP, AST/ALT

Serum bilirubin

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15
Q

What tests measure actual liver function?

A

Serum albumin and prothrombin time.

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16
Q
55year old pt
Serum Bilirubin:14
ALP: 134iu/L
AST:70
ALT: 90 iu/L
What does this indicate?
A

Suggest intrahepatic disease. Ask about alcohol.
Says occasional…
What to do next: Reoeat LFTs, viral markers, serum autoantibodies, serum ferritin.
Would an USs be helpful?
No- pattern of biliary or pancreatic disease. Take hx, not helpful again.
Notice a few spider navi.
HCV antibodies: chronic hepatitis–> HCV RNA, liver biopsy.. Ask for drugs… Treated with pegylated interferon + ribavirin.

17
Q

What do the viral markers mean?

A
  1. HbsAg: Acute or Chronic infection
  2. HbeAg: Acute Hep B . Persistance implies: continuous infective stage, development of chronicity, increased severity of disease.
  3. HBV DNA-implies viral replication (found in serum and liver, alsompresent in HbsAg -ve patients due to mutant viruses.)
  4. Anti-HBs: immunity to HBV: previous exposure or vaccination
  5. Anti-HBe: seroconversion
  6. Anti-HBc- Acute Hepatitis B (high titre)
  7. IgM: chronic hepatitis (low titre)
  8. IgG: past exposure to hepatitis (HbsAg -ve)