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BNF > Hyperlipidaemia > Flashcards

Hyperlipidaemia Flashcards

1
Q

What are the first choice for treating hypercholesterolaemia or moderate hypertriglyceridaemia?

A

Statins

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2
Q

What should be done in the case of severe hypercholesterolaemia or hypertriglyceridaemia?

A

After trying max dose statin, may need to add another lipid regulating drug e.g. ezetimibe (specialist supervision)

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3
Q

What med is most effective for lowering LDL-cholesterol conc?

A

Statins

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4
Q

What med is most effective for lowering triglyceride conc?

A

Fenofibrate- added to statin if TGs high even after LDL reduced

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5
Q

What is the risk with familial hypercholesterolaemia?

A

Puts patients at high risk of premature coronary heart disease

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6
Q

What should be offered to patients with FH?

A

Lifelong lipid modifying therapy and advice on lifestyle changes

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7
Q

What is 1st line treatment for FH?

A

> High intensity statin (dose where reduction of LDL greater than 40% is achieved)
Dose to be titrated to achieve reduction of LDL greater than 50% from baseline

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8
Q

What is an alternative to a statin if it is not tolerated?

A

> In primary heterozygous FH can give ezetimibe as monotherapy
Combo of statin and ezetimibe can be given if max tolerated statin dose fails to reduce LDL

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9
Q

What should be considered if statin and ezetimibe not appropriate?

A

A fibrate or bile acid sequestrant (cholestyramine or colestipol hydrochloride) [specialist advice]

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10
Q

What is the risk of combining fibrate and statin?

A

Increased risk of rhabdomyolysis

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11
Q

Which fibrate should not be given with statins at all and why?

A

Gemfibrozil–> together it increases risk of rhabdomyolysis considerably

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12
Q

What is one of the last treatment steps in FH if all else fails?

A

Alirocumab and evolocumab

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13
Q

What are some examples of high intensity statins?

A

> Atorvastatin: 20mg, 40mg, 80mg
Rosuvastatin: 10mg, 20mg, 40mg
Simvastatin: 80mg

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14
Q

What is the MHRA advice regarding Simvastatin 80mg?

A

There is an increased risk of myopathy–> only considered in severe hypercholest and high risk of CVD (benefits outweigh risk)

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15
Q

What is the definition of hyperlipidaemia?

A

High blood levels of cholesterol, triglycerides or both

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16
Q

How does HL manifest?

A 
> Cardiovascular disease
--> it causes atherosclerosis which causes: 
> CHD
> Strokes and TIAs
> Peripheral arterial disease
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17
Q

When is primary prevention indicated?

A
  • T1DM
  • T2DM (only if CVD risk >10%)
  • QRisk >10%
  • CKD or albuminuria
  • FH
  • 85+
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18
Q

When is secondary prevention indicatied?

A

In established CVD:

Angina, MI, Stroke, TIA and peripheral arterial disease

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19
Q

What is the risk calculator recommended by NICE?

A

QRISK3: assesses CVD risk in 84 and under

if over 10% then offer primary prevention

20
Q

Which patients is QRISK inaccurate in?

A 
> T1DM
> Established CVD
> Over 85 years
> CKD (eGFR <60)
> FH
21
Q

What level would cholesterol be for hyperlipidaemia diagnosis?

A

6mmol/L total cholesterol

22
Q

What are the total cholesterol targets for a healthy adult and high risk adult?

A

<5mmol/L HEALTHY

<4mmol/L HIGH RISK

23
Q

What are the LDL targets for a healthy adult and high risk adult?

A

<3mmol/L healthy

<2mmol/L high risk

24
Q

What are the HDL and triglycerides target?

A

> 1mmol/L HDL (higher the better)

<1.7mmol/L TG

25
Q

What drugs can cause hyperlipidaemia?

A

> Antipsychotics
Immunosuppressants
Corticosteroids
Antiretrovirals (HIV drugs)

26
Q

What conditions can cause hyperlipidaemia?

A 
> Hypothyroidism
> Liver or kidney disease
> Diabetes
> Family history
> Lifestyle (smoking, excess alcohol, obesity, fatty diet)
27
Q

How do statins work?

A

They lower LDL synthesis by the liver via inhibition of HMG-CoA reductase)

28
Q

What are the atorvastatin doses for primary and secondary prevention?

A 
Primary= 20mg OD
Secondary= 80mg OD
29
Q

What needs to be considered before starting a statin?

A

Any secondary causes of dyslipidemia:

  • Hypothyroidism
  • Uncontrolled diabetes
  • Nephrotic syndrome
  • Liver disease
30
Q

What are some common side effects of statins?

A

> Myopathy, myositis, rhabdomyolysis (Tell patient to report tender, weak and painful muscles)
Interstitial lung disease (report SOB, cough, weight loss)
Diabetes (can raise HbA1c)

31
Q

What patients have a higher risk of muscle toxicity?

A

> Personal or fam history of muscle disorder
High alcohol intake
Renal impairment
Hypothyroidism (treat before giving statin)

32
Q

In what instances are there increased risk of myopathy?

A

> Concomitant ezetimibe or fibrates (esp gemfibrozil)

> Concomitant fusidic acid (restart statin 7 days after ast dose)

33
Q

What monitoring is required with statins?

A

> Baseline lipid profile
Renal function
Thyroid function
HbA1c if high risk of developing diabetes

34
Q

When should you consider discontinuing therapy?

A

> Severe muscle symptoms
Creatine kinase–> is 5X normal
Liver function–> if 3X normal

35
Q

What happens if statin levels increase?

A

Increased myopathy risk

36
Q

What meds can increase statin levels?

A
  • Amiodarone
  • Grapefruit
  • CCB
  • Imidazole/triazole antifungals
37
Q

What interactions can occur with statins and what should be done?

A
  • Macrolides (e.g.clarith): stop statin until abx course done
  • Ezetimibe/fibrate: AVOID
  • Fusidic acid: restart statin 7 days after (oral) dose
38
Q

What are some simvastatin dose adjustments needed for interactions?

A
  • Max 10mg w/fibrate

- Max 20mg w/Amiodarone, amlodipine, diltiazem and verapamil

39
Q

What are some atorvastatin dose adjustments needed for interactions?

A

Max 10mg w/ ciclosporin

40
Q

What are some rosuvastatin dose adjustments needed for interactions?

A

Initially 5mg, max 20mg w/clopidogrel

41
Q

Can statins be taken in pregancy?

A

No- they are teratogenic

42
Q

When should statins be stopped in pregnancy?

A

3 months before conceiving and restart after breastfeeding

43
Q

What is ezetimibe mechanism of action?

A

Reduces blood cholesterol by inhibiting abs of cholesterol from small intestine

44
Q

What is the mechanism of action for fibrates?

A

Lowers TG levels by reducing liver’s production of VLDL (what carries TG around blood) and also speeds up TG removal from blood

45
Q

What is the mechanism of action of bile acid sequestrants?

A

Binds and sequesters bile acids. Liver then makes more bile acid which uses cholesterol to do so- reducing LDL in blood

46
Q

What is important to factor with bile acid sequestrants?

A

Imparis abs of fat sol vitamins (ADEK) and other drugs.

Take other drugs 1 hour before (4h for coleveselam) or 4h after.

BNF (8 decks)

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