Treatment of Hyperlipidaemia Flashcards

1
Q

What is atherosclerosis?

A

response to injury - as you accumulate risk factors you damage your vascular internal and inevitably you end up with some form of atherosclerosis -

risk factors:

smoking, diabetes etc

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2
Q

what are some modifiable risk factors for cardiovascular disease?

A

•Modifiable

–Smoking

–Dyslipidaemia

  • raised LDL cholesterol
  • low HDL cholesterol
  • raised triglycerides

–Raised blood pressure

–Diabetes mellitus

–Obesity

–Dietary factors

–Lack of exercise

–Excess alcohol consumption

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3
Q

what is the single greatest predictor of cardiovscular disease?

A

family history

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4
Q

what are the good/bad types of lipids?

A

low density lipoprotein = bad

high density lipoprotein?= good

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5
Q

describe the process of atherosclerosis and it’s association with hyperlipidemia

A

As you damage the endothelium – monocytes attack to the endothelium = oxidized LDLs are taken up by monocytes which then migrate into the subendothelium and then plaque developments form

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6
Q

how are lipoproteins classified?

A

by density

Based on density:

  • Chylomicrons (non-atherogenic)
  • Very low-density lipoprotein (VLDL)

•Intermediate-density lipoprotein (IDL)

•Low-density lipoprotein (LDL)

•High-density lipoprotein (HDL).

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7
Q

how do you raise your good cholesterol?

A

you raise your HDL cholesterol - by consistently exercising - it’s one of the reasons that exercise works

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8
Q

Why is HDL good for you?

A

Mechanism may be

due to reverse cholesterol

transport (Probably other mechanisms e.g. antiinflammatory, antioxidative.)

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9
Q

what is the difference between primary prevention and secondary prevention in CVD?

A

primary = stop heart attack from occuring in the first place

secondary = stop heart attack from occuring again with drug therapy

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10
Q

the more risk factors….?

A

the more aggressive the treatment

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11
Q

obesity raises the risk of morbidity from… ?

A
  • Hypertension
  • Dyslipidemia
  • Type II diabetes mellitus
  • Coronary heart disease
  • Stroke
  • Gallbladder disease
  • Osteoarthritis
  • Sleep apnea
  • Cancer
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12
Q

are triglycerides bad for you?

A

yes. rarely you’ll find isolated raised triglycerides - it’s usually involved with other condiitons

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13
Q

a 65 year old diabetic, hypothyroidetic, obese, boozy, and he is on the pill, presents to the clinic with a raised cholesterol… what do you do?

A

if you have a primary reason for high cholesterol - treat it - find the cause and stomp on it

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14
Q

how do statins work?

A
  • The statins are the most effective and best-tolerated agents for treating dyslipidemia.
  • These drugs are competitive inhibitors of HMG-CoA reductase
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15
Q

what do you use to lower triglycerides?

A

with a fibrate

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16
Q

what is the effect of statins?

A

lower LDL

raise HDL

lower Triglycerides

17
Q

why might you use a different statin?

A

people have differences in metabolism - so if you have side effects on one, use a different one

18
Q

what are some proven adverse effects of statins?

A

•Myopathy

  • defined as muscle pain or weakness combined with large increases in blood concentrations of creatinine kinase
  • Diabetes you will cause in some people
  • It is likely that the risk of haemorrhagic stroke is increased
  • the net benefit of the drug far outweighs the side effects
19
Q

what are some myths about statins ?

A

nocebo - if you tell someone about the side effects, they’ll start to feel like they have them- it’s the opposite of the placebo

muscle pain?- muscle pain on a placebo is the same as muscle pain on statins

memory loss?- nope

cataracts? nope

erectile dysfunciton? Nope

Will you find evidece of this in literature? Yes. Do the statins cuase this? No.

20
Q

risk of myopathy with statins increases with what?

A

increases with concentration

21
Q

what factors may increase statin risk?

A

drugs that effect the catabolism of statins - increase risk of myopathy

measure a CK before prescribing a Statin in the following situations.

  • Renal impairment
  • Hypothyroidism
  • Personal or family history of hereditary muscular disorders
  • Previous history of muscular toxicity with a statin or fibrate
  • Alcohol abuse
  • Elderly patient
  • Clinical monitoring is essential in these patients
  • If CK levels are significantly elevated do not use a Statin
22
Q

how do fibrates work?

A

we don’re really know - invovles interaction with the nuclear transcription factor PPAR that regulates several genes invovled in lipid metabolism

23
Q

What are Bile-Acid binding sequestrants?

A

bile-acid binding resins stop absorption of bile - they are very effective drugs - they are not absorbed by the body so they are super safe!

24
Q

the benefits of statin therapy depends on what?

A

depends on the individuals absolute risk

  • Lowering LDL by 2 mmol/L for 5 years in 10,000 patients would typically prevent major vascular events from occurring in about 1000 patients (10% absolute benefit) with pre-existing occlusive vascular disease (secondary prevention).
  • And in 500 patients (5% absolute benefit) who are at increased risk but have not yet had a vascular event (primary prevention)
25
Q

What is the biggest concern with statins? What increases this risk?

A

myopathy = biggest risk

  • increase risk of this with concentration of statins or drugs that effect statin catabolism
26
Q

is it true to say that statins are extremely beneficial for a small subgroup of the population and not effective for a larger group?

A

that’s a fair statement - you cannot measure individual risk. You cannot prove that someone ‘would have’ had a heart attack if not on statins