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68 Cards in this Set

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TNG, NitroStat, isosorbine dinitrate
Pharmacologic class of nitroglycerin
organic nitrate
Therapeutic class of nitroglycerin
antianginal, vasodilator, venodilator
Pharmacodynamics of nitroglycerin
reacts directly with nitrate receptor on SM cell

sulfhydryl groups in or on receptor reduce organic nitrate (R-NO3) to NO2 and then NO

NO crosses into SM cells and activates guanylate cyclase leading to production of cGMP from GTP

cGMP acits to relax SM cells (probably by dephosphorylation of myosin light chains, making them less likely to react with Actin)

then produces venodilation and vasodilation
cGMP with regards to NO
NO activates guanylate cyclase which produces cGMP from ATP

cGMP acts to relax SM cells (probably by dephosphorylation of myosin light chains, making them less likely to react with actin)
Pharmacokinetics of nitroglycerin
well absorbed by mouth, BUUUT very high first pass effect

prompt onset (1-2 minutes) when taken as a SL tablet or spray

can also be given transdermally or iv
Toxicity of Nitroglycerin
excessive hypotension, especially if the patient is volume depleted

throbbing headache, flushing
Interactions of Nitroglycerin with other drugs
excessive hypotension with other vasodilators

severe hypotension if taken with Viagra (sildenafil)
Special considerations of Nitroglycerin
remove transdermal patch BEFORE defibrillation

use only fresh TNG tablets

tolerance can develop quickly (give 8 hrs holiday qday...never take for 24 hours straight)

Tachyphylaxis (less response after repeated dose)

Take when sitting down, not driving (may get syncopic)

Angina goes away in several minutes by reducing preload and lowering afterload by decreasing BP...increased perfusion by coronary arteries by vasodilation of the coronaries
atenolol is a longer acting beta blocker
atenolol is a longer acting beta blocker
what should i NEVER do with beta blockers??
never withdrawal beta-blockers abruptly!!!

the abrupt increase in HR, BP, contractility, etc, can lead to abrupt increase in angina or even MI...REBOUND
Tenormin, propranolol, metoprolol
same class as Atenolol
Pharmacologic class of Atenolol (propranolol, metoprolol)
beta adrenoceptor blocker

beta 1 specific
Therapeutic class of Atenolol
antihypertensive, antiarrhythmic, primary and secondary prevention of MI, anti-anginal
Pharmacodynamics of Atenolol
binds directly to beta-receptors, with a preference for beta-1 over beta-2

leads to lower BP via several potential mechanisms

(less CO, less activation of RAA system)
Pharmacokinetics of Atenolol
available po or iv

variable oral F

onset 1-2 hours

duration: 12-24 hours

can be given once pre day

renally excreted (longer half-life)
Toxicity of Atenolol
excessive hypotension


heart block can worsen severe CHF (but indicated for mild to moderate CHF)

worsen bronchospasm in severe asthmatics
Interactions of atenolol with other drugs
additive effects with most other antihypertensives

additive AV block with CEB's
Special considerations for atenolol
may be especially useful in HTN patients with exertional angina, MI, atrial fibrillation

watch out for abrupt withdrawal

its generic, so its cheaper
Isoptin, Calan, similar to nifedipine, amlodipine, and diliazem
Pharmacologic class of Verapamil
calcium entry blocker
Therapeutic class of Verapamil
antihypertensive, antianginal, and antiarrythmic
Pharmacodynamics of verapamil
reduces BP by inhibiting the influx of calcium through "slow channels"

thereby dilating peripheral arterioles

produces negative inotropic effects as well

for angina: reduces afterload, thus decreasing oxygen consumption

inhibits spasm of coronary arteries in vasospastic angina

blocks re-entry paths through AV node in paroxysmal SVT
Pharmacokinetics of verapamil
absorbed rapidly, but F = 30%

available in SR tablets

cleared by kidney and liver (produces active metabolites)

onset 2 hours po

1-5 minutes iv

half life is 6-12 hours
Toxicity of verapamil
hypotension, AV block, worsening of CHF, and bradycardia
Interactions with other drugs and verapamil
additive effects with most other antihypertensives

additivie toxic effects on heart when given with beta-blockers
Special considerations of verapamil
used reduced doses in patients with both renal and hepatic disease

short acting nifedipine (and similar CEB's) can increase risk of MI (unclear why)

pregnancy C
For vasospastic angina
whether spontaneous or induced, can be dramatically reversed by intracoronary nitroglycerin (observed in cath lab)

BETA BLOCKERS ARE CONTRAINDICATED!!! (because if you give beta-blockers, alpha 1 vasoconstriction will be left unopposed...make it worse)

Use CEB's because of their direct vasodilating action
What is vasospastic angina
primarily caused by sudden vasospasm of a major coronary artery (which may also be involved with atherosclerosis)

may also be related (or induced) by catecholamines, etc.
Do NOT use beta blockers for what?
vasospastic angina
Unstable angina
this is a crescendo angina, preinfarction angina...all phrases that describe angina that is rapidly worsening in terms on intensity of pain, frequency, timing, trigger, duration, response to treatment, etc

most often involves a chronically narrowed artery WITH THE ACUTE DEVELOPMENT OF A RUPTURED PLAQUE

must treat with suppression of platelet adhesion and aggregation

(other names)
Bayer, Acriptin, Halfprin, many others
Pharm class of Aspirin
Therapeutic class of Aspirin
analgesic, anti-inflammatory, antiplatelet, antipyretic
Pharmacodynamics of Aspirin
at low doses (below 325 mg/day) tends to irreversibly inhibit COX in platelets, leading to decreased formation of thromboxane A2 (vasoconstrictor and platelet aggregator) and transiently inhibits COX in endothelium, leading to transient decreased formation of prostacyclin (PGI2...vasodilator, inhibitor of platelet aggregation)
Thromboxane A2
vasoconstrictor, platelet aggregator


inhibitor of platelet aggregation
Pharmacokinetics of Aspirin
F = 60%

T max is variable

Metabolized to salicylate

half life 3-4 hours

duration 4-24 hours

90% excreted as salicylate metabolites in urine
Toxicity of aspirin
especially at high doses can cause ulceration of GI tract, bleeding disorders, and tinnitus
Interactions of aspirin with other drugs
inhibits tubular secretion of methotrexate, potentiate bleeding from warfarin
Special considerations of Aspirin
avoid in patients with nasal polyps and asthma

regular, buffered, enteric coated
COX 2 inhibitors
selectively inhibits the production of PGI2 (which we said was a vasodilator, inhibitor of platelet aggregation)

this causes worse platelet aggregation

patients had excess strokes and heart attacks

(common name)
Therapeutic class of clopidogrel
platelet aggregation inhibitor
Pharmacodynamics of Clopidogrel
blocks ADP receptors, which then helps prevent aggregation mediated by ADP released by an activated platelet from recruiting other platelets

useful in primary or secondary prevention of TIA, stroke, angina, MI, PCTA, ACS, stent procedures, etc.
Pharmacokinetics of Clopidogrel
well absorbed

onset 1-2 hours after oral dose

hepatic metabolism

half life -8 hours
Toxicity of Clopidogrel
hemorrhage at virtually any site
Interactions of Clopidogrel with other drugs
may inhibit CYP 3A4
Special considerations of Clopidogrel
careful risk/benefit assessment in each patient


(other names)


Pharm class of abciximab
Fab fragment chimeric monoclonal antibody
Therapeutic class of abciximab
adjuct to PCL to prevent ischemic complications

Treatment of MI
Pharmacodynamics of Abciximab
noncompetitive inhibitor of the GP IIb/IIIa receptor

prevents binding of fibrinogen, vWF, and other adhesive ligands to the receptor on activated platelets

need to block > 80% of these receptors to maximally inhibit platelet
Pharmacokinetics of Abciximab
IV bolus followed by IV infusion

half life about 30 minutes

bleeding time declines to <12 minutes with 12 hours of stopping infusion
Toxicity of Abciximab
contraindicated in presence of aneurysm, AV malformation, bleeding, coagulopathy, GI bleed, intracranial mass, retinal bleeding, stroke, surgery, low platelet, trauma, and fasculitis
Interactions of Abciximab
additive effects with aspirin, clopidogrel heparin, low dose t-PA
Special considerations of Abciximab
exact role is still being defined, and evolves over time

cost is a big factor
More about NO...its an EDRF
endothelium derived relaxing factor
Produce NO directly
NO and nitroprusside
Drugs that encourage the production of NO from endothelial cells
Acetylcholine, histamine, bradykinin, serotonin, substance P
Other effects of NO
inhibition of platelet aggregation, phagocytosis, excitatory neurotransmission in CNS
Propranolol is NOT

Thus, other beta-blockers like metoprolol, acebutolol, or atenolol are preferred

important for asthmatics
Pindolol has...
intrinsic sympathomimetic activity

less effective in anti-angina endeavors and should be avoided
Beta blockers have been shown to...
prolong survival
Beta blockers are contraindicated in...
patients with asthma, diabetes, severe bradycardia, peripheral vascular disease, or COPD
Make sure to do what with Beta blockers??
do NOT discontinue abruptly

gradual tapering of the dose over 5-10 days to avoid rebound angina or hypertension
Calcium channel blockers
decrease the inward current carried by calcium, resulting in a decreased rate of Phase 4 spontaneous depolarization

slow conduction in tissues that are dependent on calcium currents, such as the AV node


all calcium channel blockers are therefore vasodilators that cause a decrease in SM tone and vascular resistance

used for vasospastic angina: NOT beta blockers (because if beta blockers were used, alpha 1 vasoconstriction would go about unopposed)
Verpamil mainly affects:

Nifidepine mainly affects:

Diltiazem mainly affects:
Verapamil: myocardium (greater inotropic decreasing effects, but worse vasodilator..greatly metabolized in the liver)

Nifedipine: more effect of SM in peripheral vasculature

Diltiazem: somewhere in between; cardio effects similar to diltiazem, but not as potent...can releive coronary artery spasm...extensively metabolized in the liver)