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Clinical Pharmacy 2 > Dyslipidemia > Flashcards

Dyslipidemia Flashcards

1
Q

Hyperlipidemia is an independent risk factor for what?

A
  • CHD (angina, MI)
  • cerebrovascular disease (ischemic stroke, TIA)
  • peripheral artery disease (PAD)
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2
Q

What are some of the modifiable risk factors for CVD?

A
  • reduce saturated fats
  • lack of exercise
  • diabetes
  • hypertension
  • smoking
  • BMI >27
  • waist circumference <94 cm in men and <80 cm in women
  • poor nutrition
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3
Q

What is CVD?

A
  • coronary death, MI, coronary insufficiency, angina, ischemic or hemorrhagic stroke, TIA, PAD, heart failure
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4
Q

Who do we generally need to screen for cholesterol?

A
  • men over 40 years of age
  • women over 40 years of age (or postmenopausal)
  • consider earlier screening in South Asian or First Nations individuals
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5
Q

Who would you screen for cholesterol in regardless of age?

A
  • clinical evidence of atherosclerosis
  • abdominal aortic aneurysm
  • diabetes
  • arterial hypertension
  • current cigarette smoking
  • stigmata of dyslipidemia
  • family history of premature CVD
  • family history of dyslipidemia
  • chronic kidney disease
  • obesity (BMI >30 kg/m2)
  • inflammatory bowel disease
  • HIV infection
  • erectile dysfunction
  • chronic obstructive pulmonary disease
  • hypertensive diseases of pregnancy
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6
Q

Describe LDL cholesterol?

A
  • often called bad cholesterol because the high levels in the blood promote the buildup of plaque in the artery walls
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7
Q

Describe HDL cholesterol?

A
  • good cholesterol because it helps carry LDL cholesterol away from the artery walls
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8
Q

What are triglycerides?

A
  • a type of fat that is found in the blood
  • high triglycerides are associated with excess weight, excessive alcohol consumption and diabetes
  • triglyceride levels are usually measured at the same tome as your blood cholesterol
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9
Q

What is considered a healthy TChol value?

A

< 5.2 mmol/L

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10
Q

What is considered a healthy LDL value?

A

< 3.4 mmol/L

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11
Q

What is considered a healthy HDL value?

A

> 1.0 (men)

> 1.3 (women)

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12
Q

What is considered a healthy triglyceride level?

A

< 1.7 mmol/L

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13
Q

Is it important to fast before a cholesterol test?

A
  • non-fasting lipid profiles have minimal effect on LDL and HDL levels, modest effect on TGs, predict CV risk similar to fasting, increase adherence to testing, decrease lab demands and decrease hypoglycaemia
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14
Q

What drugs can cause drug induced dyslipidemia?

A
  • progestins
  • thiazide diuretics
  • anabolic steroids
  • glucocorticoids
  • beta blockers
  • isotretinoin
  • protease inhibitors
  • cyclosporine
  • mirtazapine
  • sirolimus
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15
Q

What are the conditions that cause dyslipidemia?

A
  • type 2 DM
  • chronic renal failure
  • hypothyroidism
  • nephrotic syndrome
  • cholestatic liver dx
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16
Q

What are the lifestyle factors that can lead to dyslipidemia?

A
  • saturated fats increase lipids
  • refined CHO and simple sugars increase TGs
  • smoking decreases HDL
  • aerobic exercise increases HDL
  • moderate EtOH increases HDL
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17
Q

What are the 3 things that can positively affect the lipid profile and decrease the risk of CV events?

A
  • physical activity (150 minutes of moderate to vigorous activity a week)
  • diet (mediterannean diet- decreases the CV risk to a similar magnitude as statins)
  • stop smoking
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18
Q

When is therapy supposed to be initiated for dyslipidemia according to the framingham study?

A
  • should be initiated if the FRS is >20%
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19
Q

What is now considered the gold standard for assessing dyslipidemia in canada?

A
  • discuss the risks and benefits of moderate or high intensity statins with primary prevention patients based on an individuals risk of CVD
  • for patietns with a 10 year CVD risk of <10%, retest lipids in 5 years with risk estimation
  • for patients with a 10 year risk of 10-19% discuss and offer statins (preferably moderate intensity)
  • for patients with a 10 year CVD risk of >20%, discuss and strongly encourage statins (high intensity)
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20
Q

What are the outcomes of torcetrapib?

A
  • it increases the risk of CVD

- it increases the mortality by 50%

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21
Q

What are the outcomes of using fibrates in CVD and mortality?

A
  • decreases the CVD risk by 10%, has no effect on mortality
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22
Q

What are the outcomes of using ezetimibe in CVD and mortality?

A
  • decreases the CVD risk by 6% and has no effect on mortality
23
Q

What are the outcomes of using statins in CVD and mortality?

A
  • decreases the CVD risk by 25-30% and decreases the mortality risk by 14%
24
Q

What is the relative risk reduction of statins? (IMPORTANT)

A

25-30%

25
Q

What is the efficacy of statins compared to each other?

A
  • consider the efficacy of them to all be the same
26
Q

What is the harm of statins compared to each other?

A
  • consider the harm risk to all be the same
27
Q

What is the drug interactions of statins compared to each other?

A
  • simvastatin and lovastatin > atorvastatin >pravastatin and rosuvastatin
28
Q

What is the general dose that should be started out?

A
  • RCTs used the equivalent of ~10mg of atorvastatin and no need to adjust doses
29
Q

What is considered to be the primary target for LDL levels?

A
  • < 2 mmol/L or >50% decrease in LDL-C
30
Q

What are the 3 main problems that arise when treating to a target LDL of under 2 mmol/L?

A
  1. current clinical trials do not indicate what the target should be
  2. we do not know the magnitude of additional ASCVD risk reduction that would be achieved with one target lower than another
  3. It does not take into account potential adverse effects from multi drug therapy that might be needed to achieve a specific goal
31
Q

What was concluded in the TOP 2015 study?

A
  • do NOT target specific lipid levels
  • do NOT repeat lipid level testing for a patient on a statin
  • we do not know what level we need to get to in terms of LDL— therefore we do NOT care at all about targets. The statin is lowering the targets by about 25% and also lowers the CV risk so this is all we care about
32
Q

What are the general SE of statins?

A
  • muscle aches, GI upset (diarrhea and nausea), sleep disturbances, new onset of diabetes (not significant enough)
33
Q

Are aminotransferases important to keep track of when someone is on a statin?

A
  • liver failure is RARE so testing is not totally necessary
  • unless there are concerning sx such as dark urine, upper abdominal pain, n/v, yellowing of the skin or the eyes, general itchiness, pale stools
34
Q

What is the main characteristics of the muscle complaints associated with statins?

A
  • muscle discomfort (dull, weakness, cramps)
  • described as heaviness, stiffness or cramping along with weakness with exertion
  • may be worsened by exercise or may occur in sedentary patients
  • starts in larger muscles (shoulders, upper arms, pelvic girdle, thigh, calves)
  • diffuse, often intermittent of variable duration
  • onset after 1-12 months of therapy (or after dose increase)
35
Q

Myalgia is caused by no significant increase in _______

A

creatinine kinase

36
Q

How should myalgia be managed with a statin?

A
  • obtain CK level +/- hold statin (no need to stop a statin if there is low suspicion of myopathy - timing doesn’t fit, inconsistent symptoms, few risk factors. Continue for 1-2 weeks without monitoring)
    -if myalgia is consistent with statin use- hold for 1-2 weeks, or until sx resolve and then rechallenge)
    -
37
Q

What is the evidence between using a trial of coenzyme Q10 or vitamin D?

A
  • limited evidence in treating myalgia
38
Q

What does it take to be diagnosed with myositis?

A
  • CK levels of 28-110 U/L in women and 52-175 U/L in men
  • inflammation of the skeletal muscle and muscle discomfort
  • myalgia plus plasma CK levels > 2-4 x ULN but < 10 x ULN
  • may be caused by strenuous exercise
  • potentially serious
39
Q

What is used to manage myositis?

A

> 2-4x ULN but <10x ULN: D/C statins

  • consider precipitating factors (thyroid, exercise, drug interactions)
  • reassess risk vs benefit of restarting statin (very limited evidence of this)
  • change stain and/or reduce dose and titrate up slowly (q2-4 wks)
40
Q

What is rhabdomyolysis?

A
  • severe, prgressive muscles aches, weakness and pain with a CK ?3-10 ULN and marked serum creatinine election or myoglobinuria (there is a protein that is binding to the muscle and comes out in the urine- comes out in the urine as an orange colour)
  • muscle damage, myoglobinuria and high risk of acute renal failure - medical emergency
    (this is VERY RARE and requires hospitalization is it is diagnosed!)
41
Q

When should we be retesting patients that are not on a statin?

A
  • recommend for a CV risk assessment to be completed every 5 years for mean and women over 40 (unless other risk factors develop in the interim)
42
Q

Repeat testing of lipids in _____ for low risk patients that are not on a statin

A

8-10 years

43
Q

What is considered to be high risk?

A
  • FRS >20%
  • clinical vascular disease
  • abdominal aortic aneurysm
  • diabetes and age >40 years or > 15 years duration and age >30 years or microvascular disease
  • chronic kidney disease
  • high risk hypertension
44
Q

What do statin do for patients who have CAD?

A
  • CHD or death: ~25% RRR

- mortality: ~3% ARR (NNT !30 x 5-6 years)

45
Q

What is the advantage of high doses of statins?

A

-high doses of statins add an additional 10% RRR (1% ARR) in CHD events or death
(more important in those that are high risk and are using the statin for secondary prevention)

46
Q

What are some of the common drug interactions associated with statins?

A
  • cyt p450 3A4 - grapefruit affects this system
  • azole antifungals, cyclosporine, macrolide antibiotics, amiodarone, verapamil and diltiazem, warfarin, fibrates, HIV protease inhibitors and nicotinic acid
47
Q

What are some major characteristics of statin related myopathy?

A
  • does not get better- it either stays the same or gets worse
  • usually bilateral
48
Q

Do fibrates or niacin add any benefit when added onto a statin?

A
  • NO
49
Q

What are the effects of adding ezetimibe to a statin?

A
  • decreases LDL by 15-20%
  • decreases CV events by a RRR of 6%
  • there are no big differences in safety here

(bottom line: if they’ve had an MI and can only tolerate half a dose of a statin - then it may be reasonable to add ezetimibe)

50
Q

What are the effects of using a PCSK-9 inhibitor?

A

decrease LDL by 50-70%

- BUT costs a lot and does not decrease mortality

51
Q

What are the effects of taking niacin on TGs?

A

decreasing triglycerides by 20-35%

52
Q

What are the effects of taking fibrates on TGs?

A

decreases by 20-50%

- decrease of non-fatal MI by ~10% (RRR), no difference in overall CVD

53
Q

What are the effects of taking omega-3 fatty acids on triglycerides?

A
  • decreases TGs by 25-30%

- —- no benefit of any CV outcome

54
Q

Statins _____ pancreatitis

Fibrates_____ pancreatitis

A

decrease

increase

Clinical Pharmacy 2 (18 decks)

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