L 23. Hyperlipidaemia 2 Flashcards

(40 cards)

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
How fibrates are used for CV patients?
Fibrates are used along with statins. They do not use it alone.
26
How do fibrates work?
Increase some apoproteins and decrease others to reduce triglyceride rich lipoproteins, causing a decrease in LDL.
27
Common side effects from fibrates
Well tolerated GI disturbances: Dyspepsia, abdo pain, diarrhoea, flatulence, rash, muscle pain, fatigue. Myopathy + rhabdomyolysis can occur with statin use.
28
Fibrates in pregnancy and breastfeeding?
NOT in preg and breastfeeding
29
What do you need to check before starting fibrates?
Creatinine kinase (CK) levels
30
Bile acid binding agent what are they? Give an examples
Cholestryamine and colestipol
31
How do bile acid-binding agents work? What effect does this have?
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
What are the Bile acid-binding agent’s side effects? How do you minimize this?
GI (constipation, bloating, flatulence). | Minimize by increasing fluid intake.
33
Are bile acid binding agents all good in pregnancy and breastfeeding?
NOT, avoid in pregnancy and breastfeeding
34
Cholesterol absorption inhibitor example
Ezetimibe
35
How do cholesterol absorption inhibitors work?
They interact with a cholesterol transporter in the intestinal brush border to stop cholesterol reabsorption in GI.
36
Cholesterol absorption inhibitors should be prescribed...
With a statin, fibrate, or nicotinic acid derivative
37
Are cholesterol absorption inhibitors safe in preg/bfeeding?
Not safe, avoid in pregnancy and breastfeeding
38
Nicotinic acids and derivatives are ....
No longer recommended as monotherapy or in conjunction with other lipid-lowering drugs.
39
What is the Monitoring for statins?
Non-fasting lipid levels every 12 months. | CK if symptoms of muscle pain (if too high will decrease/discontinue statin use)
40
Steps for high cholesterol treatment?
Lifestyle modifications + statins