Moa

Front 1

ABCIXIMAB

Back 1

 Binds with Glycoprotein (GP) IIb/IIIa receptors on the surface of platelets inhibiting thefinal common pathway for platelet aggregation.

 Binding with GP IIb/IIIa receptors produces a blockade that interferes with fibrinogen,von Willebrand factor and other platelet aggregation modulators.

 Binding with GP IIb/IIIa receptors effectively prevents the formation of intravascularthrombus and may contribute to the resolution of pre-existing thrombus.

Front 2

ACETYLSALICYLIC ACID, ASPIRIN, ASA

Back 2

In small doses aspirin blocks thromboxane A2, a potent platelet aggregate andvasoconstrictor.This property has led to its use in the acute phase of management of the myocardialinfarction.Decreased platelet aggregation.

Front 3

ACETYLSALICYLIC ACID, ASPIRIN, ASA (EMT Administration)

Back 3

In small doses aspirin blocks thromboxane A2, a potent platelet aggregate andvasoconstrictor.This property has led to its use in the acute phase of management of the myocardialinfarction.Decreased platelet aggregation.

Front 4

ADENOSINE

Back 4

 Slows conduction time through AV node; can interrupt re-entrant pathways through theAV node.

 Slows sinus rate.

 Larger doses decrease BP by decreasing peripheral resistance.

Front 5

ALBUMIN, normal serum 5% / 25%

Back 5

Exerts oncotic pressure, which expands volume of circulating blood and maintainscardiac output.

Front 6

ALUTEROL SULFATE

Generic: ALBUTEROL SULFATE

Back 6

ß agonist (primarily ß2); relaxes bronchial smooth muscle, resulting in bronchodilation;also relaxes vascular and uterine smooth muscle; decreases airway resistance

Front 7

AMIODARONE

Back 7

 Multiple effects on sodium, potassium and calcium channels.

 Prolongs action potential, refractory period. Ventricular automaticity (potassium channel blockade).

 Slows membrane depolarization and impulse conduction (sodium channel blockade).

 Negative chronotropic activity in nodal tissue, rate reduction, and antisympathetic activity (calcium channel and B-blockade).

 Dilates coronary arteries due to calcium and alpha-adrenergic blocking action.

Front 8

ATROPINE SULFATE

Back 8

Pharmacological: Blocks the action of acetylcholine as a competitive antagonist atmuscarinic receptor sites in smooth muscle, secretory glands, and the CNS. It works byblocking parasympathetic response and allowing sympathetic response to take over,resulting in an increase in cardiac output and the drying of secretions. Atropine reversesthe muscarinic effects of cholinergic poisoning by primarily reversing bronchorrhea andbronchoconstriction. At high enough doses, atropine may have an effect on nicotinicreceptors responsible for restlessness, hallucinations, disorientation, and/or delirium.Clinical:

CV: Increased heart rate (positive chronotropic effect); increased conductionvelocity; increased force of contraction (slight), increase cardiac output.

Resp: Decreased mucus production; increased bronchial smooth musclerelaxation (bronchodilation).

GI: Decreased GI secretion and motility.

GU: Decreased urinary bladder tone.

Misc: Mydriasis (pupillary dilation); decreased sweat production.