Drug Mechanisms Flashcards

1
Q

Acetaminophen

A

Acetaminophen inhibits prostaglandin synthetase in the central nervous system, reducing pain and pyrexia.

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2
Q

ASA

A

ASA inhibits the formation of thromboxane A2, which is a potent platelet aggregator and vasoconstrictor. The platelet effects are irreversible, and last for the life of the platelet

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3
Q

Amiodarone

A

Amiodarone is a Class III antiarrhythmic, but also possesses characteristics of all four Vaughn-Williams classes of medications. It blocks sodium channels in the heart, antagonizes beta adrenoreceptors to inhibit some sympathetic activity, produces negative chronotropic effects in nodal tissues, lengthens the cardiac action potential, and also slows conduction and prolongs refractoriness by blocking potassium channels.

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4
Q

Atropine

A

Atropine competitively antagonizes acetylcholine at muscarinic (M2) receptors, producing parasympatholytic and vagolytic effects.

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5
Q

Calcium Chloride

A

Calcium is essential for a wide range of biological processes, including nerve conduction, muscle contraction, renal function, and coagulation. Administration of calcium in the out-of-hospital context is intended to improve myocardial contractility and ventricular automaticity.

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6
Q

Deminhydrinate

A

Inhibits cholinergic vestibular and reticular stimulation from motion.

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7
Q

Epinephrine

A

EPINEPHrine acts on alpha and beta-adrenergic receptors. Alpha-adrenergic activity produces vasoconstriction and reduces vascular permeability; beta-adrenergic activity results in bronchial smooth muscle relaxation, increased heart rate, and increased force of cardiac contractility. EPINEPHrine also inhibits histamine release.

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8
Q

Fentanyl

A

Inhibits ascending pain pathways in the central nervous system, altering pain perception by binding to selective Mu-opioid receptors, producing analgesia and euphoria.

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9
Q

Glucagon

A

Glucagon accelerates the conversion of glycogen to glucose in the liver, elevating blood glucose levels. It is only effective in treating hypoglycemia if liver glycogen is available.

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10
Q

Ibuprofen

A

Inhibits prostaglandin synthesis, reducing pain, inflammation, and pyrexia.

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11
Q

Ipratropium

A

Anticholinergic. Ipratropium antagonizes the activity of acetylcholine in the muscarinic (M3) receptors in bronchial smooth muscle, producing bronchodilation and muscle relaxation.

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12
Q

Ketamine

A

Ketamine is a non-competitive NMDA receptor antagonist that blocks glutamate. Low doses produce analgesia and modulate central sensitization, hyperalgesia, and opioid tolerance. Reduces polysynaptic spinal reflexes.

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13
Q

Lidocaine

A

Blocks voltage-gated sodium channels leading to a reversible block of the action potential.

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14
Q

Midazolam

A

Like other benzodiazepines, MIDAZOLam intensifies the activity of gamma aminobutyric acid, the major inhibitory neurotransmitter in the central nervous system. This action is believed to result in hyperpolarization of neuronal cells, which then take longer to reach threshold and depolarize.

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15
Q

Morphine

A

Acts on opioid receptors (primarily mu receptors) in the central nervous system to produce analgesia, euphoria, and sedation. Interaction with receptors in the spinal cord depresses pain transmission. Produces venodilation, reducing cardiac preload

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16
Q

Nitro

A

Nitroglycerin forms free radical nitric oxide (NO) which activates guanylate cyclase, resulting in an increase of guanosine 3’5’ monophosphate (cyclic GMP) in smooth muscle and other tissues
Relaxes smooth muscle in vasculature. Nitroglycerin works primarily as a venodilator, but can also produce coronary and systemic arterial vasodilation, decreasing preload and lowering myocardial oxygen demand.

17
Q

Phenylephrine

A

Agonizes alpha-adrenergic receptors producing arterial vasoconstriction.

18
Q

Salbutamol

A

Salbutamol is a selective beta-2 adrenergic agonist that produces bronchodilation and some degree of vasodilation. Some beta-1 effects can be seen, particularly at higher doses.

19
Q

Sodium Bicarbonate

A

Buffers or neutralizes excess acid (specifically, excess hydrogen ions) raising overall pH. In Hyper K this can cause extracellular potassium to shift into the cells.

20
Q

TXA

A

Prevents clot degradation by competitively binding to plasminogen, preventing plasmin from binding and ultimately stabilizing fibrin matrix.