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PBL PY2 Fall > Dyslipidemia Therapeutics > Flashcards

Dyslipidemia Therapeutics Flashcards

1
Q

dyslipidemia is a disorder of ____

A

lipoprotein metabolism

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2
Q

what are the primary causes of dyslipidemia?

A

due to genetic defects and often result in heart disease in early life

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3
Q

when dyslipidemia is caused by primary causes, what is the typical LDL?

A

often much higher, >5mmol/L

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4
Q

what are some of the secondary causes of dyslipidemia?

A

excessive alcohol, chronic renal failure, diabetes or metabolic syndrome, obeisity, hypothyroidism, nephrotic syndrome, obstructive liver disease, pregnancy, B blockers, corticosteroids, hormone replacement therapy, OCP, thiazide diuretics highly active antiretroviral therapy

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5
Q

% of Canadians 18-79 with dyslipidemia

A

28%

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6
Q

% of canadians 60-79 with DysLipid

A

60%

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7
Q

% of Canadians 40-59 with dyslipid

A

35%

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8
Q

what % of Canadians have dyslip and dont know?

A

25%

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9
Q

___% of diagnosed males are controlled and ___% of diagnosed females

A

52% of males, 35% of females

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10
Q

what are chylomicrons?

A

lipoprotein rich in triglycerides

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11
Q

what is the function of chylomicrons?

A

delivers to muscle and adipose tissue and liver

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12
Q

where is VLDL produced?

A

liver

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13
Q

VLDL is delivered to ___

A

target muscle and adipose tissue

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14
Q

VLDL is a precursor for ___

A

LDL

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15
Q

IDL is created by ___ from what 2 other lipoproteins?

A

LPL; VLDL and chylomicrons

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16
Q

LDL is converted from ____

A

VLDL

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17
Q

how does LDL get taken up by cells?

A

LDL receptors

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18
Q

how does LDL lead to atherosclerosis?

A

when there is a high amount of LDL in the blood, they can stick to the walls of the blood vessels, attracting WBCs and causinf inflammation and forming a plaque that leads to atherosclerosis

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19
Q

what are the functions of LPL?

A

convert VLDL to IDL then LDL and breaks down chylomicrons

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20
Q

what is the role of HDL?

A

take excess cholesterol back to the liver to be removed

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21
Q

triglycerides are transported in the blood via ___

A

VLDL

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22
Q

triglycerides are associated with low ___

A

HDL

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23
Q

dietary cholesterol is absorbed through the intestines as ___ and transported to the liver

A

chylomicrons

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24
Q

what organ is responsible for cholesterol homeostasis?

A

liver

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25
Q

when cells remove cholesterol from the blood, what do they use it for?

A

making cell membranes and steroid hormone production

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26
Q

what lifestyle changes can be implemented to lower cholesterol?

A

avoid smoking
healthy diet like mediterranean, DASH etc.
avoid trans fats and reduce saturated fats
get lots of fruit & veg, fibre, olive oil, legumes, nuts, whole grains
healthy weight
physical activity
moderate alcohol intake

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27
Q

list 5 complications of dyslipidemia

A
  1. CVD (acute coronary syndrome, MI, angina, arrhythmias
  2. cerebrovascular disease (stroke, transient ischemic attack)
  3. pancreatitis
  4. peripheral vascular disease
  5. abdominal aortic aneuryssm
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28
Q

what are the many patient populations that need to be tested for dyslipid?

A
  1. Men 40+
  2. women 40+ or postmenopausal
  3. south Asian and Indigenous at younger age
  4. evidence of atherosclerosis
  5. abnormal aortic aneurysm
  6. diabetes
  7. arterial hypertension
  8. smokers
  9. physical findings (xanthomas, arcus cornea, xanthelasmas)
  10. family history of premature CVD
  11. CKD
  12. obesity (BMI 30+)
  13. IBS
  14. HIV
  15. erectile dysfunction
  16. COPD
  17. hypertension during pregnancy
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29
Q

pregnant people with what conditions need to be screened for dyslipidemia

A
  1. pre-eclampsia
  2. HTN
  3. gestational diabetes
  4. gestational diabetes
  5. preterm birth
  6. stillbirth
  7. low birth weight
  8. placental abruption
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30
Q

women who have CV complications during pregnancy, how long do these risks last?

A

A lifetime. CVD and stroke 10-15 years after delivery

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31
Q

what values should be collected in a lipid panel?

A
  1. total cholesterol (TC)
  2. LDL
  3. triglycerides (TG)
  4. HDL
  5. non-HDL (when TG >1.5)
  6. ApoB (when TG >1.5)
  7. Lipoprotein (a)
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32
Q

when should a lipid panel be done fasting?

A

if patient has a history of TG >4.5 mmol/L

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33
Q

when should non-HDL be included in lipid panel?

A

when TG >1.5

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34
Q

when should ApoB be included in a lipid panel?

A

when TG >1.5

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35
Q

what are 2 benefits of including Lipoprotein (a) in a lipid panel?

A

not affected by age, lifestyle, fasting, or inflammation. Only needs to be measured once during screening

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36
Q

t/f there is no RCTs yet that show Lp(a) improved CV outcomes

A

t

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37
Q

what drugs help to lower Lp(a)?

A

PCSK9 inhibitors and niacin

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38
Q

what is the recommended action if Lp(a) is greater than 50mg/dL?

A

control CVD risk factors and implement intensive lifestyle modifications

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39
Q

hypertriglyceridemia is defined as TG above ___

A

1.7 mmol/L

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40
Q

risk of pancreatitis increases when TG are above ____, but is more significant when TG above ____

A

5.6 mmol/L; 11.3 mmol/L

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41
Q

therapy to treat hyperttriglyceridemia generally starts if TG are above ___

A

10 mmol/L

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42
Q

t/f the lifestyle modifications to lower TG are similar to those for lowering cholesterol

A

t

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43
Q

what 5 things should be included in a patient work-up for suspected dyslipidemia?

A
  1. patient and family hx (rule out secondary causes, premautiure CVD)
  2. physical exam
  3. lipid panel
  4. glucose levels
  5. eGFR
  6. albumin creatinine ration is optional
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44
Q

what are the conditions where statins are indicated?

A
  1. clinical atherosclerosis
  2. abdominal aortic aneurysm
  3. diabetes and (age 40+ or 15 year duration for peopled aged 30+, or microvascular disease)
  4. CKD (age 50+, eGFR <60mL/min, or ACR >3 mg/mmol)
  5. LDL 5.0+ mmol/L
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45
Q

t/f medication treatment for dyslipidemia should be considered in patient has a high FRS score (20%+)

A

t

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46
Q

under what conditions should a patient with an intermediate (10-19%) FRS be given mediaction management?

A
  1. LDL 3.5 mmol/L or
  2. non-HDL 4.3+ mmol/L or
  3. ApoB 1.2+g/L or
  4. men 50+ and women 60+ who have 1 additional risk factor for CVD (low HDL, increased weight circumference, impaired fasting glucise, smoking, HTN)
  5. elevated highly sensitive C reactive protein, family Hx of premature CVD, high Lp(a) and coronary artery calcium score >0
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47
Q

what is the recommendation if patient has a <10% FRS?

A

dont need statin therapy

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48
Q

high dose statins are slighly more effective than moderate doses in ____ (primary or secondary) prevention for reduction of nonfatal MI and stroke

A

secondary

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49
Q

the benefit of statin therapy depends on patients ____ score

A

10 year risk score (if its highm the NNT is lower)

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50
Q

for every 1 mmol/L reduction in cholesterol, there is a __% reduction in risk for all cause mortality

A

10

51
Q

for every 1 mmol/L reduction in cholesterol, there is a ____% reduction in risk for death from CVD

A

20

52
Q

for every 1 mmol/L reduction in cholesterol, there is a ___% reduction in non-fatal MI

A

27

53
Q

for every 1mmol/L reduction in cholesterol, there is a ___% reduction in risk for coronary revascularization

A

25%

54
Q

for every 1 mmol/L reduction in cholesterol, there is a ___% reduction in ischemic stroke

A

21

55
Q

what is the goal LDL?

A

<2.0mmol?l or a 50% reduction in LDL

56
Q

what is the target ApoB?

A

<0.8 g/L

57
Q

what is the target non-HDL?

A

<2.6 mmol/L

58
Q

which drugs have the greatest impact on lowering LDL?

A

PCSK9 inhibitors, then statins

59
Q

which drugs have the greatest impact on raising HDL?

A

fibrates & niacin

60
Q

which drugs have the greatest impact on lowering TG?

A

fibrates and niacin

61
Q

list the 6 statins mentioned in lecture

A

rosuvastatin, atorvastatin, simvastatin, pravastatin, lovastatin, fluvastatin

62
Q

what are the common side effects of statins?

A

transient GI upset, headache, rash, muscle apin

63
Q

statins are contraindicated in what conditions?

A

active liver disease, increased alcohol intake, pregnancy

64
Q

which statins interact with CYP3A4?

A

atorvastatin, lovastatin, simvastatin

65
Q

what are the statins that interact with CYP2C9 and 2C19?

A

fluvastatin, rosuvastatin

66
Q

what are some common interactions with statins?

A

clarithromycin, erythromycin, gemfibrozil, amiodarone, digoxin, warfarin, GFJ

67
Q

which 2 statins have fewer drug interactions compared to the others>

A

rosuvastatin, pravastatin

68
Q

there is some question around whether statins elevate ____ and cause ___ issues

A

glucose; memory

69
Q

what monitoring shouldd be done for statins?

A
  1. lipids 4-12 weeks after starting, then q 3-12 months
  2. baseline liver enzyme (ALT) repeat if signs of hepatotoxicity
  3. baseline CK and repeat if muscl symptoms
70
Q

define myopathy

A

broad term referring to muscle disease/disorder

71
Q

define myalgia

A

symptoms of muscle aches

72
Q

define myositis

A

symptoms along with CK elevations

73
Q

what is rhabdoylosis?

A

muscle aches or weakness with CK > 20x ULN

74
Q

what is hyperCKemia?

A

elevated CK withiut symptoms

75
Q

what is done if the CK levels are <5x the upper limit of normal?

A

continue statin therapy with monitoring

76
Q

what is done if the CK levels are greater >5x the upper limit of normal?

A

hold the statin and monitor and potentially trial other statins and or lower doses

77
Q

if a patient is unable to tolerate a statin after trying multiple types and doses, what drugs can be used instead?

A

ezetimibe, PCSK9 inhibitors

78
Q

is ezetimibe typically given as monotherapy?

A

usually an adjunct unless statins are not tolerated

79
Q

t/f ezetimibe is well-tolerated

A

t

80
Q

what is the general MOA of exetimibe?

A

decreases intestinal cholesterol absorption

81
Q

does ezetimibe have many drug interactions?

A

not really

82
Q

what is the dose of ezetimibe?

A

10mg PO UID

83
Q

there has been a trial hich showed that patient whith CKD when taking a combo of simvastatin & ezetimibe, what was the result?

A

reduced incidence of CV events (SHARP)

84
Q

a trial showed that after ACS, the combination of ezetimibe and simvastatin showed what results?

A

positive CV and cerebrovascular outcomes and can be considered if a potent statin is not tolerated

85
Q

give 3 examples of fibrates

A

bezafibrate, fenofibrate, gemfibrozil

86
Q

what are some of the ADRs of fibrates?

A

GI upset, rash, abdominal pain

87
Q

what are some of teh C\I for fibrates?

A

severe hepatic impairment, gallbladder dx and renal dx

88
Q

fibrates are most effective for lowering ___, but can also lower ___ and raise ___

A

TG; LDL; HDL

89
Q

dosing for bezafibrate

A

400mg SR daily (max 600mg/day)

90
Q

feno-micro dosing

A

200mg UID

91
Q

feno-supra dosing

A

160mg UID

92
Q

gemfibrozil dosing

A

300mg BID (1500mg/day) not really used anymore

93
Q

gemfibrozil is contraindicated if patient is already taking what class of drug?

A

statin

94
Q

what monitoring needs to be done for fibrates?

A

liver function tests, TG, CBC, renal function, lipid parameters

95
Q

give 3 examples of bile acid sequestrants (resins) given in lecture

A
  1. cholestyramine granules
  2. colestipol granules or tablets
  3. colesvelam granules or tablets
96
Q

what is a special administration instruction for the resin granules?

A

mix with juice, milk, water, applesauce before ingesting

97
Q

how do the doses start when starting a resin?

A

start low and titrate up for tolerability

98
Q

what are some of the ADRs of resins?

A

constipation, nausea, bloating

99
Q

what are some of the C/I for resins?

A

biliary obstruction, TG>4.6 and use caution if they are >2.3

100
Q

what are some drug interactions with resins?

A

lots of things, especially fat-soluble vitamins. Should space out all medications by 2-4hrs from resins

101
Q

resins have been shown to have positive CV outcomes as monotherapy, but what limits their use?

A

drug interactions and tolerability

102
Q

are resins safe in pregnancy and in children?

A

yes

103
Q

at high doses, Niacin may lower ___ and ____ and raise ____

A

LDL & TG; HDL

104
Q

how does the dosing start with niacin?

A

start low and titrate up

105
Q

which form of Niacin may cause less fluching?

A

Niaspan (rx version of Niacin)

106
Q

what are some of the ADRs of Niacin?

A

GI upset, flushing, increased LFTs with doses >2g or the SR formulation

107
Q

Niacin is c/i in what conditions?

A

severe PUD, chronic liver dx, sevre gout, caution in diabetes

108
Q

is there research evidence to back up the use of Niacin?

A

not really. No CV benefit found when combined with statins and one study was stopped due to increase in stroke

109
Q

what needs to be monitored if Niacin is being used?

A

liver function tests, blood glucose if diabetic, lipid panels

110
Q

give 2 examples of PCSK9 inhibitors

A
  1. evolocumab

2. alirocumab

111
Q

dosing of evolucumab

A

140mg q 2 weeks or 420mg q 4 weeks

112
Q

dosing of alirocumab

A

75-150mg q 2 weeks, or 300mg q 4 weeks

113
Q

what is an important factor to consider when thinking about using a PCSK9 inhibitor?

A

they are injections and they are very expensive

114
Q

in which patients are PCSK9 inhibitors used?

A

high risk patients who have not reached targets with the max tolerated doses of other agenst like statins or statins and ezetimibe. Also may be useful in patients with familial hypercholesterolemia or in secondary prevention

115
Q

what are some of the side effects of PCSK9 inhibitors?

A

pharyngitis, injection site rxns, allergic rxns

116
Q

PCSK9 inhibitors have shown positive CV outcomes in patients with ____

A

ASCVD

117
Q

what is the 1st line for secondary prevention?

A

high dose statin or max toleated dose

118
Q

in secondary prevention, if LDL is greater or equal to ___, or non-HDL is greater or equal to ____ or ApoB is greater or equal to ____, adding a PCSK9 inhibitor or ezetimibe is recommended

A

1.8mmol/L; 2.4mmol/L, 0.7g/L

119
Q

which secondary prevention patients get the most benefit from the addition of a PCSK9 inhibitor?

A
  1. recent acute coronary event (ACS) w/i last year
  2. clinical evidence of ASCVD and any of the following: diabetes or metabolic syndrome, polyvascular disease, symptomatic PAD, recurrent MI, MI in past 2 years, previous CABG surgery, LDL 2.6+ or heterozygous FH, lipoprotein a 60mg/dl+ or 120mmol/L+
120
Q

what is the current evidence around omega 3 fatty acids?

A

no CV outcome data, but useful in decreasing TG, which can reduce risk of pancreatitis (2-4g per day)

121
Q

omega 3 should be used with caution in patients with increased risk of ____

A

bleeding

122
Q

what is Icosapent ethyl and what is the evidence for its use in dyslipidemia?

A

an Rx grade EPA ethyl (Vascepa). Showed benefit in secondary prevention and in patients with diabetes and 1 or more CV risk factors with elevated TG (1.5-5.6) who were already on a statin (REDUCE IT trial)

123
Q

what is the dosing of Vascepa?

A

2000mg daily

124
Q

how much physical activity is recommended to reduce lipids>

A

150 min of moderate to vigorous aerobic exercise (weekly?)

PBL PY2 Fall (21 decks)

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