L 23. Hyperlipidaemia 2 Flashcards

1
Q

Patients with a … CV risk will have the …. from lifestyle modifications and what are they?

A

Patients with a high CV risk have the GREATEST benefits from lifestyle modifications.
Healthy diet, Regular exercise, weight management, Smoking cessation.

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2
Q

Reduction in body weight: what will improve ?

A

improves lipid profile

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3
Q

Overweight patients have an increased risk of developing?

A

Atherosclerosis

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4
Q

What type of fats need to be reduced for CV patients?

A

Transfats and saturated fats, needs to be reduced

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5
Q

Exercise per day and per week?

A

30 mins/day

2.5 hours/week

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6
Q

For high CV risk patients the DIET and exercise alone will be adequate?

A

Diet and exercise alone will not be adequate to achieve the necessary improvements in lipid profile

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7
Q

What is the primary prevention for hyperlipidaemia impact?

A

Only has sole elevated cholesterol. And the Patients with no evidence of CHD or other atherosclerotic disease.

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8
Q

Who does secondary prevention for hyperlipidemia impact?

A

Patients who have conditions alongside elevated cholesterol (e.g angina, MI patients, coronary artery bypass patients etc)

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9
Q

What is the first-line drug for lipid-lowering therapy?

A

STATINS!!!!

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10
Q

What are the 5 main classes of drug for CV patients which can lower the lipid?

A
  1. Statins
  2. Fibrates
  3. Bile acid binding agents
  4. Cholesterol absorption inhibitors
  5. Nicotinic acid derivatives
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11
Q

What is the drug class of statins?

A

HMG-CoA reductase inhibitors.

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12
Q

What is the mechanism of statin work?

A

Statins work by inhibiting the conversion of HMG-CoA to mevalonic acid and later to cholesterol, therefore they are effective in lowering LDL().

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13
Q

What proportion of concentration will we achieve within 2 weeks of statins administration?

A

25 to 62%

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14
Q

We will receive full effect within how many weeks of statin administration?

A

4 weeks

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15
Q

Doubling the statin dose achieves an extra… reduction in LDL

A

6% (only a small added reduction)

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16
Q

Inhibiting the cholesterol pathway, what will also inhibit?

A

Production of byproducts in the cholesterol pathway

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17
Q

Which statin is first line for most patients?

A

Atorvastatin.

18
Q

What are the other Statin Options? What do we do if a patient is not tolerated after atorvastatin in?

A

Atorvastatin, rosuvastatin, pravastatin, simvastatin

Will use simvastatin and rosuvastatin

19
Q

When does cholesterol synthesis peak?
Therefore when are statins recommended to be taken?
Which statin doesn’t need to adhere to this?

A

Statins recommended to be taken at night. But no evidence best taken at night.
Atorvastatin has a longer half life so dosing time doesn’t matter (just consistency and adherence does)

20
Q

What are some examples of statin interactions? What happens?

A

CYP3A4 inhibitors increase statin concentration

e.g azoles, macrolides, antidepressants, grapefruit juice.

21
Q

What is the ADRs of statins?

A

Elevated liver enzymes, myopathy, rhabdomyolysis

Myopathy vs rhabdomyolysis

22
Q

What is rhabdomyolysis? What patient may feel?

A

Rhabdo= started
Myo= Muscle
Lysis= Breakdown
Patients may feel muscle necrosis

23
Q

Myopathy: muscle pain with creatinine kinase 10x normal

A

Rhabdomyolysis: muscle necrosis and release of intracellular muscle constituents in the bloodstream (myopathy + brown urine + myoglobinuria)

24
Q

Statins in pregnancy and breastfeeding?

A

NOT to be used in pregnancy or breastfeeding.

25
Q

How fibrates are used for CV patients?

A

Fibrates are used along with statins. They do not use it alone.

26
Q

How do fibrates work?

A

Increase some apoproteins and decrease others to reduce triglyceride rich lipoproteins, causing a decrease in LDL.

27
Q

Common side effects from fibrates

A

Well tolerated
GI disturbances: Dyspepsia, abdo pain, diarrhoea, flatulence, rash, muscle pain, fatigue.
Myopathy + rhabdomyolysis can occur with statin use.

28
Q

Fibrates in pregnancy and breastfeeding?

A

NOT in preg and breastfeeding

29
Q

What do you need to check before starting fibrates?

A

Creatinine kinase (CK) levels

30
Q

Bile acid binding agent what are they? Give an examples

A

Cholestryamine and colestipol

31
Q

How do bile acid-binding agents work? What effect does this have?

A

Binds to bile acids produced from cholesterol, then this complex (resin-bile acid) is excreted in faeces.
Causes hepatic cholesterol to be converted into bile to replace lost bile = decreased stored cholesterol

32
Q

What are the Bile acid-binding agent’s side effects? How do you minimize this?

A

GI (constipation, bloating, flatulence).

Minimize by increasing fluid intake.

33
Q

Are bile acid binding agents all good in pregnancy and breastfeeding?

A

NOT, avoid in pregnancy and breastfeeding

34
Q

Cholesterol absorption inhibitor example

A

Ezetimibe

35
Q

How do cholesterol absorption inhibitors work?

A

They interact with a cholesterol transporter in the intestinal brush border to stop cholesterol reabsorption in GI.

36
Q

Cholesterol absorption inhibitors should be prescribed…

A

With a statin, fibrate, or nicotinic acid derivative

37
Q

Are cholesterol absorption inhibitors safe in preg/bfeeding?

A

Not safe, avoid in pregnancy and breastfeeding

38
Q

Nicotinic acids and derivatives are ….

A

No longer recommended as monotherapy or in conjunction with other lipid-lowering drugs.

39
Q

What is the Monitoring for statins?

A

Non-fasting lipid levels every 12 months.

CK if symptoms of muscle pain (if too high will decrease/discontinue statin use)

40
Q

Steps for high cholesterol treatment?

A

Lifestyle modifications + statins