Coronary Artery Disease & Dyslipidemia Flashcards

1
Q

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

A

Category X

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Define angina

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Define chronic stable angina

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Define non-ST segment elevation myocardial infarction (NSTEMI)

A

clot formed against plaque that partially occludes the vessel

INCOMPLETE BLOCK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Define ST segment elevation myocardial infarction (STEMI)

A

clot formed against plaque that completely occludes the vessel

COMPLETE BLOCK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Define unstable angina

A

CAD vasospasm leads to plaque rupture that partially occludes the vessel

More high risk than stable angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Define variant (Prinzmetal’s) angina

A

cause by vasospasm which decreased blood flow and oxygen supply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

3 formulations for nitroglycerin

A

patch, sublingual tablet, intravenous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Preload

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Afterload

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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:)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

Calcium Channel Blockers

A
  • not recommended for routine use
  • no effect on mortality
  • if necessary for arrhythmia control, consider verapamil or diltiazem
26
Q

What is the main difference between nitroglycerin and isosorbide?

A

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
Q

What is the main difference between beta blockers and calcium channel blockers?

A

B-Blockers decrease HR to increase oxygen supply

CC-Blockers decrease vasospasms to increase oxygen supply

28
Q

Define atherosclerosis

A

thickening of coronary arteries that may lead to MI or stroke

29
Q

Where does blood cholesterol come from?

patho

A

Synthesized by our own liver AND from diet (animal products)

30
Q

What is the general process for atherosclerosis?

patho

A

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
Q

HMG-CoA Reductase Inhibitors (oral)

A

*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
Q

What lab test would a patient on a statin need every few months?

A

LFT (liver function test) because this medication is metabolized in the liver and is inhibiting an enzyme of the liver

33
Q

Bile Acid Sequestrants (oral)

A

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
Q

What is the main difference between statins and bile acid sequestrants?

A

statins inhibit an enzyme, bile acid inhibit reuptake

Statins are also generally more effective than bile acid sequestrants

35
Q

What effect do cholestyramine and colestipol have on fat soluble vitamins?

A

Decrease absorption

36
Q

Why are patients instructed to take statins at night?

A

They are more effective at night because the cholesterol-making enzyme (HMG-CoA) is more effective at night.

37
Q

Is ezetimibe a bile acid sequestrant?

A

No, but it works similarly in that is decreases absorption of cholesterol.

38
Q

Ezetimibe (oral)

A

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
Q

Are statins contraindicated in pregnancy?

A

Yes.

40
Q

Fibric Acid Derivatives or “fibrates” (oral)

A

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
Q

Which drugs are most effective for lowering triglyceride levels?

A

fibric acid derivatives

42
Q

Proprotein Convertase Subtilism/Kexin Type 9 (PCSK9 Inhibitors)

(SQ monoclonal antibodies)

A

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
Q

Niacin (B2 vitamin)

A

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
Q

Fish Oil (oral)

A

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