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CPR Pharm > Stable and Vasospastic Angina Drugs > Flashcards

Stable and Vasospastic Angina Drugs Flashcards

1
Q

What is stable angina

A

occlusion of coronary arteries resulting from the formation of atherosclerotic plaque

􏰂 - Most common form of angina

􏰂 - Symptoms occur during exertion or stress

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2
Q

What’s vasospastic (variant angina?

A

episodes of vasoconstriction of coronary arteries

􏰂- Likely genetic in origin

􏰂 - Symptoms occur at rest

􏰂- Much less common than classic angina

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3
Q

What are approaches to angina tx?

A
  • DECREASE CARDIAC WORK –> reduce O2 demand

- INCREASE BLOOD FLOW THROUGH CORONARY ARTERIES –> increases O2 supply

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4
Q

How can coronary blood flow be increased/restored to treat angina?

A
  • Coronary artery bypass grafting
  • Percutaneous coronary intervention (PCI)
  • Stent – expandable tube used as scaffolding to keep vessel open

– Pharmacotherapy is not effective in increasing blood flow through the stenotic coronary artery into the ischemic area

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5
Q

What determines myocardial O2 demand?

A

– Heart rate

– Contractility

– Preload

– Afterload

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6
Q

What Drug classes are used to treat angina? (4)

A
  1. nitrates
  2. Calcium channel blockers
  3. Beta blockers
  4. Ranolazine
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7
Q

Nitrolgycerine is a …?

A

Nitrates (nitrovasodilators)

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8
Q

isosorbide dinitrate is a..?

A

Nitrates (nitrovasodilators)

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9
Q

Isosorbide mononitrate is a…?

A

Nitrates (nitrovasodilators)

  • isosorbide mononitrate is a poor substrate of nitrate
    reductase–> has higher Availability
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10
Q

Describe nitrate pharmacokinetics`

A

Significant first-pass metabolism – high nitrate reductase activity in the liver
􏰂
• Bioavailability with oral route is low

• Other routes that avoid first-pass metabolism are used

• Partially denitrated metabolites may still have activityand longer half-lives
•

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11
Q

What enzyme do nitrates target?

A

produce NO –> targets guanylyl cyclase to cause
-hyper polarization and reduce calcium entry

  • Smooth muscle relaxation
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12
Q

How do nitrates reduce O2 demand?

A

Nitrate-> NO-> Venous dilation-> reduced preload-> decreasedO2 demand

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13
Q

What depletes tissues of NO?

A

increased generation of superoxide anions

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14
Q

What are short acting Nitrates? Use?

A
  • sublingual Isosorbide dinitrate
  • sublingual Nitroglycerin

-Short-acting formulations are used to relieve the angina attack

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15
Q

What are long acting nitrates? Use?

A
  • Nitroglycerin - oral/ointment/patch
  • Isosorbide dinitrate - oral
  • Isosorbide mononitrate - oral
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16
Q

What are the adverse effects of nitrates

A
  • Headache (due to meningeal vasodilation) – Nitrates are contraindicated if intracranial pressure is elevated
  • Orthostatic hypotension
  • Increased sympathetic discharge (Tachycardia, Increased cardiac contractility)
  • Increased renal Na+ and H2O reabsorption
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17
Q

What drugs do nitrates interact with?

A 
ERECTILE DYSFUNCTION DRUGS
– Sildenafil  
- Vardenafil 
– Tadalafil
• Inhibit cGMP-> increase cGMP--> DRAMATIC BP DROP
- can cause acute MI
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18
Q

What are the 2 types so calcium channel blockers?

A
  1. Non-cardio active/dihydropyridines (don’t reduce HR)

2. Cardioactive (Reduce HR)

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19
Q

What are the dihydropyridines (non-cardioactive) CCBs?

A

• Nifedipine (Adalat) (short-acting, t1/2 4 h)

-Amlodipine (Norvasc) (long-acting, t1/2 30-50 h)

• Nicardipine (Cardene) (short-acting, t1/2 2-4 h)

**NAN cardioactive CCB

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20
Q

What are the cardioactive CCBs?

A
  • Diltiazem (Cardizem)

* Verapamil (Isoptin)

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21
Q

What are the targets of Dihyropyridines?

A

Non-cardioactive CCBs target vascular smooth muscle

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22
Q

What are the targets of cardio active CCBs?

A
  • Vascular smooth muscle
  • Cardiac muscle
  • Cardiac pacemakers cells
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23
Q

How do CCBs treat stable angina?

A

decreased myocardial O2 demand

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24
Q

How do CCBs decrease myocardial O2 demand in stable Angina?

A
  1. Dilation of peripheral arterioles (Decreased PVR and afterload, decreased blood pressure)
    – Arterioles affected more than veins (less orthostatic hypotension)
    – Both cardioactive CCbs and dihydropyridines are effective but dihydropyridines are more effective vasodilators
  2. Decreased cardiac contractility
    – Observed with cardioactive CCBs only
  3. Reduced heart rate
    – Observed with cardioactive CCBs only
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25
Q

What are the adverse effects of CCBs?

A

• Major
– Cardiac depression, cardiac arrest, and acute heart failure (cardioactive CCBs)

 – Bradyarrhythmias, atrioventricular block (cardioactive CCBs)

   – Severe hypotension

   – Short acting dihydropyridine CCBs – vasodilation triggers reflex sympathetic activation

– Nifedipine (immediate release) increases the risk of MI in patients with hypertension – slow-release and long-acting dihydropyridines are better tolerated

• Minor
– Flushing, headache, anorexia, dizziness
– Peripheral edema
– Constipation (verapamil) 23

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26
Q

What beta blockers are used to treat stable angina?

A

– Propranolol (Inderal)
– Nadolol (Corgard)
– Metoprolol (Toprol)
– Atenolol (Tenormin)

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27
Q

How do beta blockers treat stable angina?

A

decreased myocardial oxygen demand

28
Q

How do beta blockers decrease myocardial O2 demand?

A
  1. Decrease in HR l–>improved myocardial perfusion and reduced oxygen demand at rest and during exercise
  2. Decrease in cardiac contractility
  3. Decrease in blood pressure —>reduced afterload
29
Q

What are the adverse reactions of beta blockers?

A
  1. Reduced cardiac output
  2. Bronchoconstriction
  3. Impaired liver glucose mobilization
  4. Produce an unfavorable blood lipoprotein profile (increase VLDL and decrease HDL)
  5. Sedation, depression
  6. Withdrawal syndrome associated with sympathetic hyperresponsiveness
30
Q

What are the contraindications of Beta Blockers?

A
  1. Asthma
  2. Peripheral vascular disease
  3. Type 1 diabetics on insulin
  4. Bradyarrhythmias and AV conduction abnormalities
  5. Severe depression of cardiac function
31
Q

How does Ranolazine work?

A

Inhibits late Na+ current in cardiomyocytes

- late Na+ current is enhanced in ischemic myocardium and can cause Ca2+ overload and depolarization abnormalities

32
Q

How is Ranolazine used to treat angina?

A

Ranolazine normalizes repolarization of cardiac myocytes and reduces mechanical dysfunction

– May reduce diastolic tension and compression of coronary vessels in diastole

– May reduce cardiac contractility and oxygen demand

• Ranolazine does not affect heart rate and peripheral hemodynamics

33
Q

What is the clinical use of Ranolazine?

A

Stable angina which is refractory to standard medications

• Decreases angina episodes and improves exercise tolerance in patients taking
nitrates, or amlodipine, or atenolol

34
Q

What are the 4 first lines to treat chronic atherosclerotic Angina?

A
  1. Lipid lowering therapy
  2. Lifestyle modifications
  3. infrequently use immediate release nitrates
  4. anti- platelet therapy like aspirin
35
Q

What is the second line Tx for Chronic Angina

A

Beta blocker or Alternative CCB or long acting nitrate

36
Q

What is the 3rd line tx for chronic angina?

A
  • Add a CCB or BB if not using

- If they have low BP use a long acting nitrate or ranolazine

37
Q

What is the 4th line tx for stable angina

A

Triple therapy

  • BB
  • CCB
  • long acting nitrate or ranolazine
38
Q

What is 5th line Tx?

A

Consider CABG

39
Q

What are adverse effects of nitrates alone?

A
  • HR reflex increase
  • Contractility reflex increase

(pro for using combined with BB or CCB)

40
Q

What are the Adverse effects of BB or CCB alone?

A
  • increase EDV
  • Increase ejection time
    (pro for using combined with BB or CCB)
41
Q

What is first line to treat vasospasitc angina?

A

CCB –> Diltiazem or amlodipine

- if CCB is contraindicated from Low BP, Bradycardia, or AV block, use LA nitrates (can develop tolerance)

42
Q

What is a red thrombus?

A
  • fibrin-rich with trapped RBCs
  • 􏰁 Forms in low-pressure veins and in the heart; result of platelet binding and aggregation followed by formation of bulky fibrin tails in which red blood cells become enmeshed
  • 􏰁 Pathologic conditions associated with red thrombi: pain and severe swelling, embolism and distant pathology (embolic stroke)
43
Q

What is a white thrombus?

A

-platelet-rich thrombus

􏰁- Forms in high-pressure arteries and is the result of platelet binding to the damaged endothelium and aggregation with little involvement of fibrin

􏰁 -Pathologic condition associated with white thrombi: local ischemia due to arterial occlusion (in coronary arteries: acute coronary syndromes)

44
Q

What are the drug categories to treat thromboembolic disorders? What do they do?

A

􏰀- Antiplatelet drugs–>􏰁 inhibit platelet function (prevent clots from forming in
the arteries white thrombi)

􏰀 -Anticoagulants–> 􏰁 regulate the function and synthesis of clotting factors (used to prevent clots from forming in the venous system (red thrombi)

-Thrombolytics 􏰁–>destroy blood clots after they are formed,􏰁 Re-establish blood flow through vessels once clots have formed

45
Q

What are the antiplatlet drug categories?

A
  1. Thromboxane A2 synthesis inhibitors
  2. P2Y12 Receptor blockers
  3. Platelet glycoprotein receptor blocker
46
Q

What kind of drug is Aspirin

A

Anti platelet that inhibits thromboxane A2 synthesis

47
Q

How does Aspirin work?

A
  • Irreversible inhibition of cyclooxygenase to block TxA2 production
  • 􏰀 TxA2 is a potent inducer of platelet aggregation
48
Q

What is the clinical use of aspirin?

A
  • Started as soon as possible in acute coronary events

-usually part of dual
antiplatelet therapy: aspirin and a P2Y12 blocker)

-􏰁 prevent of coronary events with low dose aspirin

49
Q

Are adverse effects of Aspirin common? What are they?

A
  • Not common

-􏰁 Gastrointestinal bleeding
􏰁
-Aspirin hypersensitivity

50
Q

What is clopidogrel?

A

Antiplatlet P2Y12 (ADP) RECEPTOR BLOCKERS

51
Q

What is prasugrel?

A

Antiplatelet- P2Y12 (ADP) RECEPTOR BLOCKERS

52
Q

What is Ticagrelor?

A

Antiplatelet- P2Y12 (ADP) RECEPTOR BLOCKERS

53
Q

How do P2Y12 (ADP) RECEPTOR BLOCKERS work?

A

Blocks P2Y12 –> increase in cAMP

  • P2Y12 is activated by ADP and inhibits adenylate cyclase to inhibit cAMP which prevents platelet aggregation
  • P2Y12 receptor blockers allow cAMP to increase and prevent platelet aggregation
54
Q

What allele is nonfunctional in Clopidogrel resistance?

A

CYP2C19

55
Q

What is the clinical use of clopidogrel?

A
  • Started as soon as possible in acute coronary events (usually as part of dual antiplatelet therapy with aspirin)

􏰀 -Used alone in patients with aspirin hypersensitivity

􏰀- Secondary prevention in patients with history of acute coronary events

56
Q

What are the adverse side effects of P2Y12 (ADP) RECEPTOR BLOCKERS

A

Major/minor bleeding

57
Q

Abciximab is a?

A

GLYCOPROTEIN (GP) IIB/IIIA INHIBITORS

- antiplatelet

58
Q

Eptifibatide is a?

A

GLYCOPROTEIN (GP) IIB/IIIA INHIBITORS

- anti platelet

59
Q

Tirofiban is a?

A

GLYCOPROTEIN (GP) IIB/IIIA INHIBITORS

- antiplatlet

60
Q

How do GLYCOPROTEIN (GP) IIB/IIIA INHIBITORS work?

A

Block platelet aggregation

61
Q

What is the clinical use of GLYCOPROTEIN (GP) IIB/IIIA INHIBITORS?

A
  • Clinical use has declined in the past several years

- 􏰀 Used during percutaneous coronary intervention (PCI) in high-risk patients

62
Q

What are adverse effects of GLYCOPROTEIN (GP) IIB/IIIA INHIBITORS?

A
  • 􏰀 Bleeding (especially in patients with chronic kidney disease)
    􏰀
  • Thrombocytopenia (more often seen with abciximab)
63
Q

What are the types of Thrombolytic drugs?

A
  • Tissue plasminogen activator

- Streptokinase

64
Q

How do thrombolytic fibrinolytic drugs work?

A
  • Induce fibrinolysis (lyse fibrin after thrombi have formed)
    􏰀
  • Activate endogenous fibrinolytic system by converting plasminogen into plasmin
65
Q

What is streptokinase?

A

is a protein produced by Streptococci that binds to plasminogen to activate it

66
Q

What are the clinical uses of PCI?

A
  • used when percutaneous coronary intervention can’t be performed quickly enough
  • used in STEMI (or NSTEMI within 12 hrs, not common)
67
Q

What are adverse effects of Thrombolytic Drugs?

A
  • Bleeding (especially with streptokinase causing systemic fibrinogenolysis) 􏰁
  • Allergic reactions (streptokinase)

CPR Pharm (5 decks)

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