(3.2) Cholesterol and Lipid Metabolism Flashcards

1
Q

What is the pathology of Famalial Hypeerlipidaemia? Suggest a treatment for it.

A
  • Mutation of LDL receptor -> increased LDL (moving cholesterol from liver to tissue) in circulation
  • Statin: increases LDL receptors and inhibits HMG-CoA reductase -> reduces Cholesterol synthesis
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2
Q

What is the normal range of Cholesterol and when fasting?

A
  • Normal:
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3
Q

Suggest some ADRs of Statin use.

A
  • Myopathy & Myositis
  • Headache
  • GI complaints
  • Type 2 Diabetes
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4
Q

Suggest two types of Statin and how should each be prescribed (e.g. time of a day)?

A
  • Simvastatin: given before bed (a short half life, to coincide cholesterol peak production in the morning)
  • Rosuvastatin & Atorvastatin: during day (a longer half life, given to those who don’t take before bed)
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5
Q

How do Fibrates work?

A

PPAR-alpha antagonists -> + FA uptake & oxidation & action of lipoprotein lipase -> —TAG & -LDL

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6
Q

Suggest some possible ADRs of fibrates.

A
  • GI complaints
  • Myositis
  • Cholelithiasis
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7
Q

Why shouldn’t Statin and Fibrates be prescribed together?

A

Both cause myopathy -> Rhabdomyolysis

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8
Q

How does Ezetimibe work?

A

Cholesterol lipase inhibitor -> inhibits INTESTINAL cholesterol absorption -> –LDL

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9
Q

Suggest some possible ADRs of Ezetimibe.

A
  • Headache
  • GI complaints
  • Headache
  • Rhabdomyolysis
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10
Q

Suggest the actions of Nicotinic Acid.

A
  • —TAG
  • -LDL
  • +++HDL
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11
Q

Suggest some possible ADRs of Nicotinic Acid.

A
  • Headache
  • Flushing
  • Hepatoxicity
  • Reduced insulin sensitivity -> hyperglycaemia
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12
Q

How does Bile Acid Sequesterants work?

A
  • Bind bile acid -> reduce their reabsorption
  • Bile acid synthesis requires cholesterol, reduced reabsorption leading to increased synthesis -> increase utilisation of cholesterol -> lowers cholesterol level
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