Angina Flashcards
What is the primary cause of angina?
an imbalance between the oxygen requirement of the heart and the oxygen supplied to it via the coronary vessels
Initial drug therapy of angina involves the use of:
- Organic nitrates
- CCBs
- Beta blockers
What can be done to increase oxygen to ischemic tissue if reduction of oxygen demand does not control the symptoms of angina?
- Coronary bypass grafts
- Angioplasty
Name the Nitrate
Nitroglycerin
True or False: Nitroglycerin dilates both arteries and veins
True
What is the MOA of nitroglycerin?
Denitrated by glutathione S-transferase resulting in a free nitrite ion which is then converted to NO leading to activation of GC which will increase cGMP which causes vasodilation—the vasodilation decreases arterial pressure, venous return, and intracardiac volume
Name the toxicities of Nitroglycerin
- Orthostatic hypotension
- Reflex tachycardia
- Throbbing headache
Nitroglycerin is contraindicated if
cranial pressure is elevated
Dilation of the epicardial coronary arteries causes a(n) (increase or decrease?) in coronary artery spasm, platelet aggregation, and myocardial oxygen demand
decrease
What route of administration works the fastest but has a brief duration of action?
sublingual
Longer duration of action is achieved with:
- Oral
- Transdermal slow release preparations
- IV infusion
What drugs are contraindicated with the use of Nitrates?
PDE-5 inhibitors
Continuous exposure to nitrates causes ______
tolerance
True or False: Continuous exposure causes tolerance due to diminished NO release or systemic compensatory mechanisms
True
All CCBs tht are currently used in therapeutics are (R or L) type CCB?
L-type
What type of CCB is the dominant type in cardiac smooth muscle?
L-type
Although CCBs block calcium channels in most types of smooth muscle, _________ smooth muscle appears to be the most sensitive
vascular
Which CCB was the first clinically useful member of this class of drugs?
Verapamil
Which CCB is from the dihydropyridine family of CCBs?
Nifedipine
What is the MOA of CCBs?
Bind to the L-type calcium channel on the inside of the membrane reducing the frequency of opening in response to depolarization causing a marked decrease in transmembrane calcium influx
How does the MOA of CCBs affect vascular smooth muscle?
leads to a long-lasting relaxation of vascular smooth muscle, vasodilation, and reduction in BP
How does the MOA of CCBs affect cardiac muscle?
leads to a reduction in contractility, LV wall stress, SA node rate, and AV node conduction velocity leading to a reduction in myocardial oxygen requirements
Name the toxicities of CCBs
- Cardiac depression
- Cardiac arrest
- Bradycardia
- AV block
- Heart failure
Reflex tachycardia in response to hypotension occurs more often with
Nifedipine
Which CCBs cause significant myocardial depression and exhibit an antiarrhythmic effect?
Verapamil
Diltiazem
Patients who are taking ___________ are more sensitive to the cardiodepressant effects of CCBs
beta-blockers
What is the MOA of Beta-blockers in the management of angina?
decrease myocardial oxygen requirements, both at rest and during exercise, by decreasing heart rate, BP, and contractility
Are beta-blockers vasodilators?
no
Undesirable effects of the Beta-blockers in angina include a(n) (increase or decrease?) in diastolic volume, which is associated with a(n) (increase or decrease?) in myocardial oxygen requirements
increase; increase
What are some contraindications of beta-blockers?
- Asthma and other bronchospastic conditions
- Severe bradycardia
- AV blockade
- Severe left ventricular failure
The undesirable effects of the beta-blockers can be balanced by the concomitant use of
nitrates
What is the indication of Ranolazine?
treatment of chronic angina in patients who have not achieved an adequate response with other antianginal drugs and have no other treatment alternatives
Which drugs are contraindicated with the use of Ranolazine?
Diltiazem
Verapamil
What is the MOA of Ranolazine?
Inhibits the late inward sodium current leading to reduction in intracellular calcium sodium levels, reversal of calcium overload, restoration of ventricular pump function, and prevention of ischemia-induced arrhythmias
Name the toxicities of Ranolazine
- Prolonged QT interval
- Constipation
- Nausea
- Dizziness
Ranolazine is a substrate for
CYP3A4
Ranolazine should not be used with inhibitors of CYP3A4, which could (increase or decrease?) its serum concentrations and QTc interval prolongation
increase
True of False: Ranolazine is contraindicated in patients with QT prolongation or hepatic impairment?
True
What type of drugs are contraindicated with the use of Ranolazine?
drugs that prolong the QTc interval
