Pharm Part 1 Flashcards
Verapamil
- Calcium channel blocker
- arrhythmia, for supraventricular tachyarrhythmias and paroxysmal tachycardia and atrial fibrillation
- Chronic stable angina stemming from AV node
Quinidine (Type 1A drugs)
arrhythmia, increases refractory period of cardiac muscle, for supraventricular tachyarrhythmias and atrial fibrillation
Phenytoin (Dilatin)
- arrhythmia, to reverse digitalis induced arrhythmias
- anti-epileptic
Lidocaine (Type 1B drugs)
- arrhythmia, decrease cardiac excitability, shortening action potention, for ventricular arrhythmias
Verapamil (angina)
angina, Ca2+ channel blocker, decrease oxygen demand by reducing afterload by reducing peripheral resistance via vasodilation
Propranolol (angina)
angina, reduces oxygen demand by preventing chronotropic responses to endogenous epinephrine
Nitroglycerin
angina, increases oxygen supply to heart by direct vasodilatory action on smooth muscle in coronary arteries
Captopril, lisinopril
HTN, ACE inhibitors
Spironolactone
HTN, diuretic, potassium sparing; antagonist for aldosterone in Collecting Tubes
Ethacrynic acid
HTN, loop or high ceiling diuretic, is associated with deafness/ototoxicity
Furosemide
HTN, diuretic, high-ceiling or loop acting; can cause deafness
Chlorothiazide
HTN, diuretic, thiazide, when administered with digitalis, will increase penetration of digitalis into myocardium
- most widely used
- Inhibits Na+ resorption causing excretion of Na+, K+ and water
What are the three thiazides
dyazide
metolazone
indapamide
Hydralazine
HTN, directly acts to vasodilate vascular smooth muscle
Metoprolol
HTN, selective beta1 blocker, reduced CO and BP
Propranolol (HTN)
HTN, nonselective beta blocker reducing CO, inhibits renin secretion from juxtaglomerular cells
Clonidine
HTN, stimulates alpha2 receptors in CNS, reduces sympathetic outflow to peripheral vessels resulting in VD
- decrease HR, decrease CO and TPR
Methyldopa
HTN, acts centrally as a false NT to stimulate alpha 2 receptors to reduce SNS outflow, resulting in VD
- best for renal damage patients
Prazosin
HTN, alpha1 blocker, inhibits NE binding –> VD
Digitalis
glycoside for arrhythmia, decreases rate of AV conduction, for atrial fibrillation and paroxysmal tachycardia
- alters Ca+ movement, increase in force of contraction of myocardial tissue (inotropic effect)
- inhibits Na+, K+ ATPase leading to calium influx, decrease HR
- Thiazides increase toxicity
Propranolol (arrhythmia)
arrhythmia, for paroxysmal tachycardia
Glycosides
CHF, ex: digitalis and digoxin, have positive inotropic effect, increasing force of contraction of myocardium by inhibiting Na+/K+ ATPase and thus increasing Ca2+ influx, reduces compensatory changes associated with CHF like heart size, rate, edema
Captopril
CHF and HTN, ACE inhibitor, blocks the enzyme that converts angiotensin I into angiotensin II
- angiotensin II causes casoconstriction and increase BP
guanethidine
- Enters the nerve and concentrated in transmitter vesicles, where it replaces norepinephrine
- reserved for severe hypertension
reserpine
depletes NE by inhibiting reuptake
atenolol
HTN, selective beta1 blocker
Doxazosin
HTN, alpha1 selective blocker
Timolol
HTN, non-selective beta blocker
Nadolol
HTN, non-selective beta blocker
Calcium Channel Blockers (antiangina)
decrease oxygen demand by reducing afterload by reducing peripheral resistance via vasodilation
Digitalis toxicity
- nausea and vomiting, yellow-green vision, extrasystole (heartbeat outside the normal rhythm), AV conduction block
- related to coadministration with chlorothiazide (potentiates toxicity)
Amide metabolized LA
in liver by p450 enzyme
- drug names with have 2 “i”
Ester metabolized LA
by esterases in plasma,
- drug names will have 1 “i”
- also a little in liver
prilocaine
causes methemoglobinemia
- Methemoglobin is a form of hemoglobin that contains the ferric [Fe3+] form of iron. The affinity for oxygen of ferric iron is impaired.
- oxygen–hemoglobin dissociation curve therefore shifted to the left
how does LA work
prevents generation of nerve impulses by interfering with sodium transport into the neurons resulting in depolarization (decrease Na+ uptake)
- no effect on K+ at nerve axon
How does LA enter membrane
only non-ionized (free base form) can penetrate tissues membranes and then becomes ionized once in neuron
How many mg of lidocaine are in one 2% capsule
36 mg
What happens when LA given at high dose
can lead to generalized state of CNS depression which can result in respiratory depression, myocardial depression and death
LA and Grave’s disease
could result in hypertensive crisis
Cocaine
only LA that doesn’t cause vasodilation
- VASOCONSTRICTION
- blocks reuptake of NE into adrenergic neurons
- produces powerful stimulation of cerebral cortex
Max dose of epi for cardiovascular disease patient
- 0.04 mg
- 1:100K epi capsule has 0.01 mg
Bisulfites
component of LA that causes an allergy (give mepivacaine)