cardiac medication Flashcards

1
Q

Dyslipidemia screening

A

Men and women ≥ 40 yrs. of age (or post menopausal women)

Ethnicity: South Asian and First Nations people are at increased risk (consider earlier screening)

Patients with the following conditions (regardless of age):
DM
Obesity (BMI ≧ 30)
Chronic kidney disease (eGFR ≦ 60 mL/min)
FHx of premature CAD (Men < 55 yrs., Women < 65 yrs. in a 1st degree relative) & those that have a family hx. of dyslipidemia
Known atherosclerosis: CAD, MI, PCI/CABG, PVD, CVA/TIA, carotid arterial disease, AAA
Stigmata of dyslipidemia (arcus cornea, xanthelasma)
Inflammatory disease (RA, SLE, IBD)
HIV (Rx: HARRT)
Current tobacco use
HTN (includes hypertensive diseases in pregnancy i.e. preeclampsia)
Erectile dysfunction, COPD

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2
Q

screening of dyslipidemia

A

Lipid profile (non-fasting state)
TC (total cholesterol)
LDL-C (low density lipoprotein)
HDL-C (high density lipoprotein)
non-HDL-C (non-HDL-cholesterol)
TG
FBG, HbA1C level
Electrolytes (eGFR)
Lipoprotein (a) – once in a person’s lifetime at initial screening

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3
Q

non-HDL-C =

A

TC minus HDL-C

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4
Q

Apolipoprotein B (ApoB)

A

main component of LDL and VLDL (very low density lipoprotein)

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5
Q

Framingham Risk Score

A

High Risk: FRS of ≥ 20%
Intermediate Risk: 10%-19.9%
Low Risk: < 10%

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6
Q

Statin Indications

A

Atherosclerotic Cardiovascular Disease (ASCVD)
Most people with DM
- Age ≥ 40 yr.; Age ≥ 30 yr. + DM x 15 yrs.
- Microvascular disease
CKD: Age ≥ 50 yr. and eGFR < 60 mL/min
LDL ≥ 5.0 mmol/L

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7
Q

MOA of statin

A

Competitively block HMG-CoA reductase, a key rate limiting enzyme in cholesterol synthesis
Block the conversion of HMG-CoA to mevalonic acid
Reduce hepatic cholesterol synthesis
Upregulation of LDL receptors, increases hepatic uptake of LDL-C from circulation

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8
Q

Pleiotropic effects of statins

A

Improve endothelial function
Increase NO bioavailability
Inhibit inflammatory response
Stabilize atherosclerotic plaques

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9
Q

Contraindications to Prescribing Statins

A

Active or Chronic Liver Disease
Pregnancy and during breastfeeding

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10
Q

side effects of statins

A

Myalgia
Myositis (inflammation of skeletal muscles)
Rhabdomyolysis

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11
Q

Baseline Testing before initiating statins

A

TSH (hypothyroidism is a risk factor for statin intolerance)
Liver function
Renal function/creatinine: (CKD are at higher risk of statin)

Monitor labs at minimum every 6 months, with any changes in therapy, or if suspected adverse effects

Repeat a lipid profile in 4-6 weeks to reassess if at target

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12
Q

Primary prevention treatment threshold

A

IF non-HDL-C > 2.6 mmol/L or LDL-C ≥ 2.0 mmol/L or ApoB ≥ 0.8 g/L and on maximally tolerated statin dose, the next step is to discuss add-on therapy
First line add on therapy in primary prevention is Ezetimibe
Note that PCSK9 inhibitors are not recommended in primary prevention

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13
Q

Secondary prevention treatment threshold

A

IF the non-HDL-C ≥ 2.4 mmol/L or LDL-C ≥ 1.8 mmol/L or ApoB ≥ 0.7g/L, the next step is to intensity therapy with addition of ezetimibe and/or PCSK9 inhibitor

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14
Q

Ezetimibe

A

Inhibits absorption of dietary cholesterol in the small intestine
Metabolized in both the small intestine and liver but not by CYP450 enzyme system

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15
Q

PCSK9 Inhibitors

A

Monoclonal antibody that inhibits PCSK9, a protein that targets LDL receptors, and clears LDL from the blood

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16
Q

PCSK9 Inhibitors side effects

A

urticaria, rash, angioedema

17
Q

Hypertriglyceridemia medication

A

Fibric Acids (fenofibrate)

contraindication: Severe Renal or Hepatic Disease

*Can increase serum Cr

18
Q

ASA MOA

A

COX inhibitor - Irreversibly inhibits platelet aggregation

19
Q

ASA side effects

A

GI bleeding, dyspepsia, thrombocytopenia, allergic RXN (aspirin induced asthma)

20
Q

ASA is indicated for

A

ASA is indicated for the secondary prevention of CV disease

21
Q

Antiplatelet Therapy (APT)

A

Selectively inhibit ADP (adenosine diphosphate) induced platelet aggregation

Platelet P2Y12 receptor antagonists: Clopidogrel, Ticagrelor, Prasugrel

22
Q

ACE Inhibitors MOA

A

Prevent the conversion of angiotensin I to II; Angiotensin II is a potent vasoconstrictor
ACEi cause arterial and venous vasodilation
Block the breakdown of bradykinin

e.g. ramipril, perindopril

23
Q

Adverse effects of ACEi

A

Angioedema (life threatening)
ACE induced cough (ARBs can be used in patients with ACE induced cough)
Renal dysfunction, hyperkalemia
Hypotension

Cautious use in patients with RAS, single kidney, CKD (contraindicated in bilateral RAS)

Contraindicated in pregnancy (fetal malformations/death)

24
Q

Beta-Blockers MOA

A

↓myocardial oxygen demand, ↓ HR, ↓contractility

25
Q

adverse effects of beta-blockers

A

Bradycardia (contraindicated in heart 2nd/3rd degree heart block)
Hypotension
Fatigue, Sleep disturbance, Nausea
Sexual dysfunction
Bronchospasm
Worsen claudication symptoms

26
Q

nitrates MOA

A

↑ myocardial oxygen via vasodilation of coronary arteries (release of NO)

27
Q

MOA of calcium channel blockers

A

CCBs ↑ myocardial oxygen by vasodilation of coronary arteries

28
Q

Amlodipine is used to treat

A

angina & HTN (no arrhythmic action)

29
Q

side effects of amlodipine

A

HA, ↓BP, peripheral edema

30
Q

Non-dihydropyridines: Diltiazem, Verapamil

A

control HR by prolonging the refractory period of AV node; Arrhythmic use – i.e. managing SVT/tachyarrhythmia’s

31
Q

side effects of Non-dihydropyridines (Diltiazem, Verapamil)

A

↓ HR, ↓ BP, AV block
↓ HR and contractility - worsen HF