Week 206 - Myocardial Infarction Flashcards

1
Q

What type of inheritance pattern does Familial Hyperlipidaemia have?

A

Autosomal Dominant

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2
Q

List 3 clinical signs of hyperlipidaemia.

A

1) Xanthelasma
2) Tendon xanthomata
3) Corneal arcus

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3
Q

What is considered the ideal total cholesterol blood level?

A

<5mmol/L

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4
Q

What is considered to be a very high cholesterol level?

A

> 7.8mmol/L

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5
Q

Which chromosome holds the gene responsible for Familial Hypercholesterolaemia?

A

Chromosome 19

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6
Q

What is the main aim of non-drug treatment for hypercholesterolaemia?

A

Maintaining a lean body weight

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7
Q

What lifestyle changes should be encouraged to manage hyperlipidaemia?

A

Reduce – fat intake, alcohol consumption
Smoking cessation
Avoid thiazides, oestrogens and non-selective B-blockers
Increase exercise

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8
Q

What is the most potent pharmacological treatment for hypercholesterolaemia?

A

Statins

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9
Q

In which groups of patients should you be particularly careful when prescribing statins?

A

 Children
 Women of reproductive age
cholesterol is source of steroid hormones so reducing cholesterol could also reduce steroid hormone production

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10
Q

When should statins be taken and why?

A

In the evening > cholesterol synthesis is most active at night

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11
Q

What is the reasonably common alternative pharmacological treatment for hypercholesterolaemia/hyperlipidaemia?

A

Fibrates

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12
Q

What do fibrates (fibric acid derivatives) do?

A

Reduce blood triglyceride levels by:
-Decreasing VLDL production in liver (therefore reducing triglyceride carrier potential)
-Modestly increase HDL levels
Have NO effect of LDL levels

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13
Q

What is the function of a lipoprotein?

A

To carry/transport lipids in the blood

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14
Q

Describe the process of atherosclerotic plaque formation.

A

Damage/insult on the endothelial lining which releases factors such as ADP and *** causing platelets and macrophages to adhese and aggregate. Lipids, calcium and cellular debris accumulate too and smooth muscle cells begin to form a fibrous cap over the plaque > plaque is now unable to disperse.

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15
Q

What do macrophages become within an atherosclerotic plaque?

A

Foam cells

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16
Q

How does Aspirin work as an antithrombotic drug?

A

It irreversibly inhibits platelet cyclo-oxygenase-1 (COX-1) through acetylation. COX-1 catalyses thromboxane and prostaglandin production > reduces thromboxane A2 and prostaglandin

17
Q

What is prostacyclin (PG12)?

A

A vasodilator and platelet inhibitor produced by platelets and vascular endothelium.

18
Q

What clinical sign is virtually diagnostic of heterozygous familial hypercholesterolaemia?

A

Tendon Xanthomata > occurs in ~70% of all affected individuals

19
Q

What two major clinical signs occur around the eyes of many individuals with familial hypercholesterolaemia?

A

Xanthelasma and corneal arcus (premature)

20
Q

What are yellow, fatty plaque lesions associated with hyperlipidaemia that occur on the body in areas besides the eyes?

A

Xanthomas (xanthelasma is the most common form of xanthoma)

21
Q

Why is chromosome 19 associated with Familial hypercholesterolaemia?

A

Because the LDL receptor is coded for on chromosome 19 and it is dysfunction of any of the 5 steps involved in LDL receptor function that can result in the condition

22
Q

How is familial hypercholesterolaemia best managed?

A

With a statin. High dose atorvastatin has been proven to reverese intimal thickening that occurs in FH

23
Q

How do statins work in the treatment of hypercholesterolaemia?

A

They inhibit HMG CoA in the liver – the rate limiting step in cholesterol synthesis. Increase the removal of LDL and IDL( by inc. their receptors), decrease the production of LDL and VLDL. Slightly increase HDL

24
Q

Why are fibrates contraindicated in gallstone disease?

A

They themselves can cause gallstone formation by increasing cholesterol excretion via bile

25
Q

Why should fibrates be used with caution in renal impairment?

A

May increase creatinine levels

26
Q

List the main contraindications of fibrates.

A

Severe hepatic impairment, hypoalbuminaemia, primary biliary cirrhosis, gallstone disease, nephrotic syndrome, pregnancy and breast-feeding