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What is the major ADR of ranolazine?
QT prolongation
What is the MOA of ranolazine?
not fully understood
inhibit late Na channels
What are the 3 parameters of oxygen demand?
HR
Contractility
Ventricular wall stress
What are the main components of ventricular wall stress? Which one is dependent on veins, which on arteries?
preload and afterload
preload- veins
afterload- arteries
What is the most common cause of ischemia?
atherosclerosis
Which angina is not associated with atherosclerotic plaques?
variant angina
What is preload and afterload?
preload- stretch on the walls of the ventricles at the end of diastole
afterload- pressure ventricles have to overcome to push blood out of the heart
What group of antianginals must be first converted into NO?
nitrates
Which enzyme is stimulated by nitric oxide? What molecule is produced?
Enzyme- Guanylyl Cyclase
molecule- cGMP
What is the MAJOR effect produced by nitrates?
Decrease preload and decrease myocardial oxygen demand
Does nitroglycerin have good oral bioavailability?
no!
we usually go for NTG sublingual (sometimes transdermal)
What are the ADRs of nitrates? What are the causes associated w/ each ADR?
Flushing
dilation of blood vessels
Orthostatic Hypotension
dilation of veins
Reflex tachycardia
response from arteriolar dilation
HA
dilation of meningeal artery
N/V, dizzy
What are the 2 MECHANISMS of tolerance of nitroglycerin?
reduced # of sulfhydryl groups (-SH) = can’t turn nitrates into NO
presence of peroxynitrate (from making NO) = inhibits guanylyl cyclase
Nitrates should NOT be used with what class of drugs? Why?
Nitrates should not be used with PDE5 Inhibitors (-afil) because of the risk of refractory hypotension.
basically nitrates make more cGMP and are metabolized by PDE
PDE Inhibitors would lead to an increase in cGMP because it would inhibit the metabolism of nitrates
B1 agonism leads to what effects?
increased myocardial oxygen demand
increase HR
increase contractility
increase renin release
Should beta-blockers w/ ISA or b2 blocking effects be used in IHD?
no
How do beta-blockers work do decrease cardiac muscle contraction?
inhibit cardiac muscle contraction by
inhibiting Gs, and inhibiting the adenylyl cyclase pathway
How do beta-blockers effect the APs in nodal cells?
decrease phase 4 depolarization
prolong repolarization
What is the major effect of beta-blockers in IHD?
DECREASE myocardial oxygen demand
What specific beta-blockers are used in IHD?
b1 selective w/ no ISA
metoprolol, atenolol, bisoprolol
What is the boxed warning of beta-blockers?
avoid abrupt D/C
What are the ADRs of beta-blockers?
hypotension
bradycardia
hypoglycemia
dizzy, sedation
bronchospasm (in non-selective)
Why should beta-blockers not be used in variant angina?
beta receptors deal with vasodilation in the coronary arteries
a beta blocker will inhibit this vasodilation and lead to vasoconstriction in the coronary arteries
will result in decreased blood flow
What are the structural requirements for beta-blocking activity?
aryloxypropanolamine
What group should be added to a beta-blocker for b1 selectivity?
para (4’) group with H bond acceptor
Which CCBs are vasoactive and cardioactive?
Vasoactive- DHPs
Cardioactive- non-DHPs
Where are L-type Calcium channels located at in the cell?
cell membrane
What is the MAIN effect of CCBs?
increase myocardial oxygen supply
What is the MOA of aspirin?
Covalently (irreversibly) bind to COX 1 and COX 2 enzymes
How does aspirin inhibit platelet aggregation?
COX 1 enzyme functions to make TxA2. TxA2 deals with platelet activation and aggregation. Therefore, if COX 1 is inhibited, platelets can’t aggregate.
What is clopidogrel and how is it activated?
Clopidogrel is a P2Y12 ADP receptor pathway inhibitor.
Clopidogrel is a PRODRUG and must be activated through CYP2C19.
Why should PPIs not be used with clopidogrel?
PPIs are CYP2C19 inhibitors. Clopidogrel needs CYP2C19 to be activated, so use of a PPI would be pointless.
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