Coronary Artery Disease & Dyslipidemia Flashcards

1
Q

What pregnancy category are HMG-CoA reductase inhibitors (statins)?

A

Category X

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2
Q

Define angina

A

sudden pain beneath sternum caused by mismatch of oxygen supply and demand

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3
Q

Define chronic stable angina

A

caused by coronary artery disease plaques with PARTIAL occlusion of the vessel

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4
Q

Define non-ST segment elevation myocardial infarction (NSTEMI)

A

clot formed against plaque that partially occludes the vessel

INCOMPLETE BLOCK

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5
Q

Define ST segment elevation myocardial infarction (STEMI)

A

clot formed against plaque that completely occludes the vessel

COMPLETE BLOCK

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6
Q

Define unstable angina

A

CAD vasospasm leads to plaque rupture that partially occludes the vessel

More high risk than stable angina

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7
Q

Define variant (Prinzmetal’s) angina

A

cause by vasospasm which decreased blood flow and oxygen supply

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8
Q

Nitrates

A

Mech of action: converted into nitric acid which acts on vascular smooth muscle (VSM)

Physiology: vasodilations, more effective on veins than arteries

** Nitroglycerin is the oldest and most commonly used

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9
Q

Nitroglycerin (nitrate)

A

Mech in stable angina: vasodilates veins to improve venous return of blood to the heart

Mech in variant angina: relaxes spasms in the coronary arteries to improve blood flow

Adverse Effects: headache, orthostatic hypotension, reflex tachycardia

Drug Ints: anti-hypertensive agents, Phosphodiesterase-5 (PDE5) (Sildenafil, Tadalafil, Vardenafil), beta-blockers, non-dihydropyridine calcium channel blockers

Tolerance: develops quickly in 24 hours, so given at LOWEST EFFECTIVE DOSES with ‘drug-free’ period of at least 8 hours

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10
Q

3 formulations for nitroglycerin

A

patch, sublingual tablet, intravenous

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11
Q

Isosorbide (nitrate)

A

Mech of action: identical to nitro

Isosorbide mononitrate (ER): given twice daily

Isosorbide dinitrate (IR): given three times daily

**Tolerance develops quickly, so implement 10-12 hr ‘drug-free’ period

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12
Q

Ranolazine (non-nitrate)

A

Mech: not well understood, may have to do with accumulation of Na and Ca in myocardial cells to increase heartbeat efficiency

Adverse Effects: QT prolongation, elevation in BP , constipation, nausea, dizziness, headache

Drug Interactions: CYP3A4 inhibitors, QT prolonging drugs, calcium channel blockers (EXCEPT amlodipine)

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13
Q

Beta blockers

A

Indication: angina of effort

Physiology: decrease myocardial oxygen demand by decreasing HR, improve oxygen supply by slowing heart rate which increases the heart’s time in diastole

Counseling Points: do not discontinue abruptly or you may experience rebound tachycardia

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14
Q

Calcium channel blockers

A

Indications: stable angina, variant angina

Physiologic Effects: increase oxygen supply by decreasing vasospasm, decrease afterload which decreases myocardial oxygen demand

Counseling Points: Avoid combining with beta-blockers

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15
Q

Preload

A

the initial stretching of the heart to allow blood in (systolic pressure)

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16
Q

Afterload

A

the final contraction of the heart to push blood out of the heart (diastolic pressure)

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17
Q

What is the general order of Managing a STEMI?

A
  1. Initial ‘routine’ therapy (Ex: nitroglycerin)
  2. Reperfusion Therapy (Ex:fibrinolytics & primary percutaneous coronary intervention (PCI)
  3. Secondary prevention (Ex:)
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18
Q

What does initial MI therapy consist of? (Hint: MONAB acronym)

A

Morphine (relieve STEMI-related pain and vasodilate to decrease oxygen demand)

Oxygen (given when O2 sat <90% to increase supply to myocardium)

Nitroglycerin (vasodilator) (decrease preload, increase collateral blood flow to the heart, treat ischemia-related pain)

Aspirin (suppress platelet aggregation, given immediately upon symptom development)

Beta-blockers (decrease HR and contractility, decrease myocardial

** All of these therapies are implemented simultaneously

19
Q

What is Primary PCI?

A

Primary Percutaneous Coronary Intervention

Use of angioplasty to re-cannulate the occluded coronary artery (using a stent inflated by a balloon)

Goal: initiate within 90 mins of patient contact

20
Q

What is fibrinolytic therapy?

A

Drugs that dissolve clots by stimulating production of plasmin

Ex: Ateplase (tPA) and reteplase

Goal: use within 30 mins of presentation to ED

21
Q

Adjunct to Reperfusion Therapy (ANTICOAGULANTS)

A

Heparin (IV): anticoagulant

Fondaparinux (SQ): selective factor Xa inhibitor, can be used in patients with heparin allergy

Bivalirudin (IV): direct thrombin inhibitor, can be used in patients with heparin allergy or history of heparin-induced thrombocytopenia

22
Q

Adjunct Reperfusion Therapy: (ANTIPLATELETS)

A

Thienopyridines (p/o): Clopidogrel, prasugrel, ticagrelor

Glycoprotein IIb/IIIa Inhibitors (IV): antiplatelet agents, only given to patients undergoing PCI
(Tirofiban, Eptifibatide,
Abciximab)

Aspirin

23
Q

What type of medication is only given to patients undergoing PCI (primary percutaneous coronary intervention?

A

Glycoprotein IIb/IIIa Inhibitors
(Tirofiban, Eptifibatide,
Abciximab)

24
Q

ACE Inhibitors as Adjuncts to Reperfusion Therapy

A
  • decrease short-term mortality post-MI
  • decrease remodeling of the ventricle
  • recommended for all STEMI patients
25
Calcium Channel Blockers
- not recommended for routine use - no effect on mortality - if necessary for arrhythmia control, consider verapamil or diltiazem
26
What is the main difference between nitroglycerin and isosorbide?
Isosorbide comes in mononitrate (ER) form and dinitrate (IR) form which are given 2 and 3x daily respectively, whereas nitro is taken when patient is actively experiencing angina.
27
What is the main difference between beta blockers and calcium channel blockers?
B-Blockers decrease HR to increase oxygen supply CC-Blockers decrease vasospasms to increase oxygen supply
28
Define atherosclerosis
thickening of coronary arteries that may lead to MI or stroke
29
Where does blood cholesterol come from? | patho
Synthesized by our own liver AND from diet (animal products)
30
What is the general process for atherosclerosis? | patho
LDL is deposited in the endothelium, leading to inflammation and the recruitment of immune cells. LDL is ingested by immune cells, lipid accumulates into a "fatty streak" and the inflammation recruits platelets Activated platelets deposit on top of the fatty streak, creating a prothrombotic environment that results in a fibrous plaque. Some cells may die, releasing cell debris and lipid, as well as creating a necrotic core. If there is destabilization, the plaque may rupture completely
31
HMG-CoA Reductase Inhibitors (oral)
*Most effective drugs for lowering cholesterol, typically the first-line therapy. Commonly know as "statins" ``` Atorvastatin Rovustatin Lovastatin Pravastatin Simvastatin ``` Mech: Inhibit HMG-CoA reductase enzyme which is needed for cholesterol synthesis Indications: - hypercholesterolemia - Primary and secondary prevention - Post-MI therapy - Diabetes DDI's: other lipid lowering drugs, drugs that inhibit CYP3A4 (this drug is metabolized by that enzyme, so a lack of it may lead to toxicity) Adverse Reactions: headache, rash, GI upset, hepatotoxicity Counseling points: take medication in evening at bedtime, max effects seen in 4-6 weeks, lifelong treatment,
32
What lab test would a patient on a statin need every few months?
LFT (liver function test) because this medication is metabolized in the liver and is inhibiting an enzyme of the liver
33
Bile Acid Sequestrants (oral)
Mech: bind to bile acids to lessen cholesterol reuptake into the blood Colesevelam Cholestyramine Colestipol Indication: decrease LDL Adverse Effects: constipation, nausea, bloating Counseling Points: take 4 hours before other drugs, so that they do not bind. Take with food and water to lessen GI symptoms
34
What is the main difference between statins and bile acid sequestrants?
statins inhibit an enzyme, bile acid inhibit reuptake Statins are also generally more effective than bile acid sequestrants
35
What effect do cholestyramine and colestipol have on fat soluble vitamins?
Decrease absorption
36
Why are patients instructed to take statins at night?
They are more effective at night because the cholesterol-making enzyme (HMG-CoA) is more effective at night.
37
Is ezetimibe a bile acid sequestrant?
No, but it works similarly in that is decreases absorption of cholesterol.
38
Ezetimibe (oral)
Mech: decreases absorption of cholesterol in the small intestine Indication: decrease LDL Adverse Effects: typically well-tolerate, but may cause myopathy, rhabdomyolysis, hepatitis DDI's: statins, fibrates (increased risk of gallstones), bile acid sequestrants
39
Are statins contraindicated in pregnancy?
Yes.
40
Fibric Acid Derivatives or "fibrates" (oral)
Third line agent for lowering lipid levels Gembibrozil Fenofibrate Fenofibric Acid Mech: stimulate lipoprotein lipase via activation of PPAR-alpha Indication: adjunct therapy for patients with significant LDL, primary hypertryglicidemia Adverse Effects: GI upset, gallstones, myopathy, livery injury DDI's: increased risk of myopathy when combined with a statin
41
Which drugs are most effective for lowering triglyceride levels?
fibric acid derivatives
42
Proprotein Convertase Subtilism/Kexin Type 9 (PCSK9 Inhibitors) (SQ monoclonal antibodies)
Mech: prevent the binding of PCSK9 to LDLR and enhances clearance of LDL Alirocumab Evolocumab Adverse Effects: hypersensitivity reactions, immunogenicity (body developing antibodies against drug itself)
43
Niacin (B2 vitamin)
Vitamin = not regulated by FDA Previously thought to decrease LDL and TG levels, but this has not been shown. *OUTDATED THERAPY Adverse Effects: flushing
44
Fish Oil (oral)
Goal: have 1 gram/day min. of beneficial oils to maintain healthy heart ``` Docosahexaenoic acid (DHA) Eicosapentaeonic acid (EPA) ``` Brand Names: Vascepa an Lovaza Effective for lowering TG levels, 20-50% Counseling points: freeze to prevent fishy burps