Drugs used in ACS/Stable Angina Flashcards

1
Q

How can surgery be used to treat stable Angina?

A


Surgery and interventional cardiology approaches are effective
•Coronary artery bypass grafting
•Percutaneous coronary intervention (PCI)
•Stent expandable tube used as scaffolding to keep vessel open
–Reocclusion
–Drug eluting stents ( antiproliferative drugs

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

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2
Q

what is the approach to treat stable angina

A

Reduce myocardial oxygen demand

  • HR
  • COntractility
  • Preload
  • Afterload
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3
Q

what are the 3 Nitrates?

A
–
Nitroglycerin (generic, Nitro Dur , Nitro Time)
–
Isosorbide dinitrate 
–
Isosorbide mononitrate
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4
Q

MOA of Nitrates

A

activate cGMP that will activate protein kinase G that causes Myosin LC dephosphorylation that causes Smooth muscle relaxation

also opens potassium chanels that causes hyperpolarization and reduced calcium entry

all helps to reduce Preload

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5
Q

what is the sensitivity of vasculature to nitrate induced vasodilation

A

Veins
Large arteries
Small arteries and arteioles

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6
Q

Adverse effects and contradictions 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 H 2 O reabsorption

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7
Q

what are 3 drug interactions with Nitrates?

A

All three drugs used in erectile dysfunction
–Sildenafil
–Vardenafil
–Tadalafil
•Inhibit cGMP phosphodiesterase 5, increase cGMP
•Minimal effects on hemodynamics when administered alone in men with coronary artery
disease
•Combination with nitrates causes severe increase in cGMP and a dramatic drop in BP
•Acute myocardial infarctions have been reported

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8
Q

what are the 3 Non cardioactive Calcium channel blockers

A

(Dihydropyridines)

  • Amlodine long acting
  • Nifedipine (short acting)
  • Nicardipine (short acting)
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9
Q

what are 2 Cardioactive Dihydropyridines?

A

Diltiazem

Verapamil

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10
Q

how does dihydropyridines and Cardioactive CCBs affect the heart

A
–Dihydropyridines
•Vascular smooth muscle
-decrease PVR and afterloadd
-arteries affected more than veins
-more effective vasodilaters than cardioactive CCBs

–Cardioactive CCBs
•Vascular smooth muscle
•Cardiac muscle (decreased contractillity)
•Cardiac pacemakers cells (reduced HR)

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11
Q

Major 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)

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12
Q

what are the 4 Beta blockers used in stable angina

A

Propranolol
Nadolol
Metoprolol
Atenolol

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13
Q

Mechanism of Action of Beta blockers?

A

Decreased Myocardial oxygen demand
-Decrease in HR leads to improved myocardial perfusion
and reduced oxygen demand at rest and during exercise
–Decrease in cardiac contractility
–Decrease in blood pressure leads to reduced afterload

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14
Q

Advese effects of Beta Blockers

A

–Reduced cardiac output
–Bronchoconstriction
–Impaired liver glucose mobilization
–Produce an unfavorable blood lipoprotein profile (increase VLDL and
decrease HDL)
–Sedation, depression
–Withdrawal syndrome associated with sympathetic hyperresponsiveness

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15
Q

Contraindictions of Beta Blockers

A
–Asthma
–Peripheral vascular disease
–Type 1 diabetics on insulin
–Bradyarrhythmias and AV conduction abnormalities
–Severe depression of cardiac function
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16
Q

Ranolazine MOA

A

Inhibits Late Na+ current in Cardiomyocytes

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

17
Q

Best form of therapy for Stable Angina?

A

Combination therapy of Nitrates with either a Calcium channel blocker or a Beta blocker

18
Q

Approaches to treating Vasospastic Angina?

A

•To relieve coronary spasm and increase blood flow into
the affected area using vasodilators

Management is primarily focused on prevention of
episodes
•CCBs are the first choice drugs
–Diltiazem or amlodipine are often used

If CCBs are contraindicated (low BP, bradycardia, AV
block), long acting nitrates are used
–Are effective but less desirable due to occurrence of
tolerance
–Can be added to CCBs to improve efficacy

19
Q

When to use Antiplatelet drugs?

A

Acute Coronary syndromes

Inhibit platelet function
-primarily used to prevent clots from forming in arteries (white thrombi

20
Q

when to use anticoagulants

A

regulate the function and synthesis of clotting factors

-primarily used to prevent clots from forming in the venous system (red thrombi)

21
Q

When to use Thrombolytics

A

Destroy blood clots after they are formed

-Reestablish blood flow through vessels once the clots have formed

22
Q

What are the 3 types of Antiplatelet drugs?

A

Inhibitors of thromboxane A 2 synthesis

P2Y 12 (ADP) Receptor Blockers

Platelet glycoprotein receptor blockers

23
Q

what are the drugs in the inhibitors of thromboxane A2 synthesis?

A

Aspirin (acetylsalicylic

antiplatelet drug

24
Q

what are the drugs in the P2Y12(ADP) receptor blockers

A
  • Clopidogrel
  • Prasugrel
  • Ticagrelor

all antiplatelet drugs

25
Q

what are the names in the Platelet glycoprotein receptor blockers?

A
  • Abciximab
  • Eptifibatide
  • Tirofiban
26
Q

MOA of asprin

A


Irreversible inhibition of cyclooxygenase to block TxA 2
production (via acetylation of the enzyme’s active site)
•TxA2 is a potent inducer of platelet aggregation

27
Q

what is the adverse effects of aspirin

A


Gastrointestinal bleeding

Aspirin hypersensitivity

28
Q

MOA of P2Y12 (ADP) Receptor blockers

A
Mechanism
of action
•cAMP prevents platelet aggregation
•ADP activates P2Y 12 receptor, a GPCR
coupled to Gi protein, to inhibit adenylyl
cyclase and reduce cellular cAMP level
•Blocking these receptors will increase
adenylyl cyclase activity and cellular
cAMP levels
29
Q

what is the thing to monitor with Clopidogrel?

A

Clopidogrel resistance

  • CYP2C19 isoenzyme
  • high in asian
30
Q

what is the MOA for GLycoprotein (GP) IIB/IIIA inhibitors

Clinical Use?
Adverse effects?

A

GP IIa IIIb inhibitors prevent binding of ligands to the GP IIb IIIa receptor to inhibit platelet
aggregation

Clinical use has declined in the past several years
•Used during PCI in high risk patients

Adverse effects:
Bleeding (especially in patients with chronic kidney disease)
•Thrombocytopenia (more often seen with abciximab

31
Q

what are the two types of THrombolytic drugs and what are the drugs among the two types?

A


Tissue type Plasminogen Activator drugs
•Alteplaserecombinant human protein
•Reteplase recombinant modified human protein
•Tenecteplase recombinant mutated human protein

Streptokinase preparation
•Streptokinase: purified from bacteria

32
Q

MOA of Thrombolytic drugs?

A

Lyse fibrin after the thrombi has formed

Activate endogenous fibrinolytic system by converting plasminogen into plasmin
-streptokinase is a protein produced by streptococci that binds to plasminogen to activate it

33
Q

when are thrombolytics used? and what are their adverse effects

A

used if PCI cannot be used since it is by far more superior

Adverse effects:
-Bleeding
allergic reaction (streptokinase)

34
Q

What are some ANticoagulant drugs?

A

–Unfractionated heparin (UFH)
–Enoxaparin
–Bivalirudin
–Fondaparinux

35
Q

Other drug classes used in Acute coronary Syndrome

A
–Nitrates
–Beta blockers
–Calcium channel blockers (in patients with contraindications or intolerance
to beta blockers)
–ACE inhibitors
–Angiotensin receptor blockers
–Aldosterone antagonists
–Morphine sulfate