Medical/Trauma Meds Class & MOA Flashcards

Class:

Carbohydrate, hypertonic solution.

Mechanism of Action:

Rapidly increases serum glucose levels.

Class:

Benzodiazepine, anticonvulsant, sedative-hypnotic

Mechanism of Action:

Potentates' effects of inhibitory neurotransmitters.
Raises seizure threshold.
Induces amnesia and sedation.

Class:

Antihistamine

Mechanism of Action:

• Blocks cellular histamine receptors; decreases vasodilatation.
• Reverses extrapyramidal reactions.

Class:

Sympathomimetic.

Mechanism of Action:

Direct acting alpha and beta agonist

• Alpha: vascular bronchial, cutaneous, renal and visceral arteriolar vasoconstriction.
• Beta 1: positive inotropic, chronotropic and dromotropic actions, increases automaticity.
• Beta 2: bronchial smooth muscle relaxation and dilation of skeletal vasculature
• Blocks histamine release.

Class:

Narcotic Analgesic

Mechanism of Action:

A dose of 100 mcg (0.1 mg) (2 mL) is approximately equivalent in analgesic activity to 10 mg of morphine.

Class:

Hyperglycemic agent, pancreatic hormone.

Mechanism of Action:

• Increases blood glucose by stimulating glycolysis.
• Unknown mechanism of stabilizing cardiac rhythm in beta-blocker overdose.
• Minimal positive inotropic and chronotropic.

Class:

Corticosteroid

Mechanism of Action:

• Suppresses acute and chronic inflammation.
• Replaces absent glucocorticoids.
• Immunosuppressive effects.

Class:

Water soluble Vitamin

Mechanism of Action:

• Cyanide is an extremely toxic poison. In the absence of rapid and adequate treatment, exposure to a high dose of cyanide can result in death within minutes due to the inhibition of cytochrome oxidase resulting in arrest of cellular respiration.
• Specifically, cyanide binds rapidly with cytochrome a3, a component of the cytochrome c oxidase complex in mitochondria. Inhibition of cytochrome a3 prevents the cell from using oxygen and forces anaerobic metabolism, resulting in lactate production, cellular hypoxia and metabolic acidosis.
• In massive acute cyanide poisoning, the mechanism of toxicity may involve other enzyme systems as well. Signs and symptoms of acute systemic cyanide poisoning may develop rapidly within minutes, depending on the route and extent of cyanide exposure. The action of hydroxocobalamin in the treatment of cyanide poisoning is based on its ability to bind cyanide ions. Each hydroxocobalamin molecule can bind one cyanide ion by substituting it for the hydroxo ligand linked to the trivalent cobalt ion, to form cyanocobalamin, which is then excreted in the urine.

Class:

Sedative, analgesic, dissociative anesthetic.

Mechanism of Action:

Blocks pain receptors and minimizes spinal cord activity, affecting the association pathways of the brain between the thalamus and the limbic system.

Class:

Benzodiazepine, sedative, anticonvulsant.

Mechanism of Action:

Anxiolytic, anticonvulsant and sedative effects; suppresses propagation of seizure activity produced by foci in cortex, thalamus and limbic areas.

Class:

Corticosteroid.

• Mechanism of Action:
• Suppresses acute and chronic inflammation.
• Replaces absent glucocorticoids.
• Immunosuppressive effects.

Class:

Short-acting benzodiazepine CNS depressant.

Mechanism of Action:

• Increased production of GABA, an inhibitory neurotransmitter, causing procedural amnesia; anesthesia; skeletal muscle relaxation.
• Anxiolytic and sedative / hypnotic properties similar to other benzodiazepines.

Class:

Narcotic antagonist.

Mechanism of Action:

• Competitive inhibition at narcotic receptor sites.
• Reverse respiratory depression secondary to depressant drugs.
• Completely inhibits the effect of morphine.

Class:

Antiemetic

Mechanism of Action:

Selective 5-HT receptor antagonist, blocking serotonin, both peripherally on vagal nerve terminals and centrally in the CNS chemoreceptor trigger zone.

Class:

Cholinesterase reactivator.

Mechanism of Action:

• Reactivation of cholinesterase to effectively act as an antidote to organophosphate pesticide poisoning.
• This action allows for destruction of accumulated acetylcholine at the neuromuscular junction.

Class:

Hemostatic agent, antifibrinolytic, plasminogen inactivator

Mechanism of Action:

Reduces plasminogen activation, mitigating conversion to plasmin.