Paramedic Pharmacology Flashcards
MOA: Activate adrenergic receptors by binding directly to the alpha 1 receptors (located in the eye, blood vessels, male sex organs and neck of the bladder), alpha 2 receptors (located at nerve terminals), beta 1 receptors (located in the heart and kidneys) and beta 2 receptors (located in the lungs, uterus, muscles and liver).
Classification: Adrenergic agonist
Effects: Used to treat cardiac arrest, bradycardia, asthma, COPD, anaphylaxis and croup.
EPINEPHRINE
MOA: Converts nitric oxide, used as a vasodilator to treat angina and CHF. Rapidly relaxes smooth muscle and dilates peripheral arteries and veins.
Class: Nitrate, vasodilator, angina agent
Effects: Decreases preload, after load, and myocardial oxygen demand.
NITROGLYCERINE
MOA: Effects stages 1, 2, and 3 of the action potential, and the repolarization of the cell. Slows down how fast calcium leaves the cell.
Class: Potassium Channel Blocker, Class III
Effects: Dangerous due to long half life. Used to treat V-fib and V-tach.
AMIODARONE
MOA: Local anesthetic, decrease rate of depolarization, inhibit sodium influx through sodium voltage gated channels. Effects stage 0 of the action potential.
Class: Local anesthesia, sodium channel blocker, arrhythmia
Effects: Used to treat pain, influx of sodium into the cell.
LIDOCAINE
MOA: Inhibits the acetylcholine enzyme , then attaches to the site where acetylcholine has attached. Removes organophosphates.
Class: Cholinergic, toxicity antidote
Effects: Reduces parasympathetic effects of organophosphate poisoning.
2-PAM or PRALIDOXIME
MOA: Produce their effects by activating adrenergic receptors with direct receptor binding.
Class: Non-selective beta agonist, adrenergic agonist
Effect: Produces bronchodilation by relaxing bronchial smooth muscle through beta 2 receptors in the lungs.
ALBUTEROL
MOA: Prevents conversion of angiotensin I to angiotensin II by blocking ACE inhibitors. Prevents release of aldosterone from the adrenal gland.
Class: ACE inhibitor, anti-hypertensive, thiazide diuretic
Effects: Decreases BP
LISINOPRIL
MOA: Decreases excitability of the cells by blocking Na++ channels in the CNS decreasing the irritability of the neuron while also decreasing the action potential threshold.
Class: Anti-epileptic
Effects: Treats seizures
DILANTIN
MOA: Selective adrenergic receptor blocking agent. Blocks beta 1 adrenergic receptors in the heart.
Class: Adrenergic antagonist, anti-arrhythmic
Effects: Decreases BP
ESMOLOL
MOA: Produces a blockade at the muscarinic acetylcholine receptors.
Class: Muscarinic antagonist
Effects: Used to treat bradycardia , dry secretions and organophosphate poisonings.
ATROVENT
MOA: Blocks voltage dependent calcium channels or calcium ion influx inhibitor by changing calcium ions across cell membranes of arterial smooth muscle in conductile/contractile myocardial cells. Effects phase 4 (slow) and phase 2 of the action potential.
Class: Calcium channel blocker, class IV Vaughn Williams, anti-dysrhythmic.
Effects: Treats angina pectorals, hypertension, SV node, atrial flutter/fibrillation
VERAPAMIL
MOA: Blocks the propagation of the action potential beginning at the nociceptors passed by glutamate at the synapse by inhibiting calcium influx. Effects both the mu and kappa receptors.
Class: Analgesic, opiate antagonist/antagonist (antagonizes mu receptors: analgesia, respiratory depression, sedation, euphoria, decreased GI motility; agonist to kappa receptors: analgesia, sedation, decreased GI motility)
Effects: Removes mu effects and enhances kappa effects
NUBAIN
MOA: Blocks propagation of action potential beginning at the nociceptors passed by glutamate at the synapse by inhibiting calcium influx. Mu/kappa receptors.
Class: Pure agonist ( agonizes both mu and kappa receptors), opiate, analgesia
Effects: Mu and kappa effects on the CNS. Used to treat break-through pain. 100x more potent than morphine.
FENTANYL
MOA: Used to treat pain. Blocks propagation of action potential at nociceptors passed by glutamate at the synapse by inhibiting calcium influx. Mu/kappa receptors.
Class: Opioid analgesic, opioid agonist
Effects: Effects both mu and kappa receptors on the CNS as a pure agonist.
MORPHINE SULFATE
MOA: Receptors have a chloride- channel, when GABA is activated the chloride- channel opens which allows chloride- to enter the neuron decreasing its intracellular voltage. Enhances GABA effects.
Class: Benzodiazepine
Effects: CNS anti-epileptic, reduces anxiety, promotes sleep (hypnotic/sedative) RAS, muscle relaxation, amnesia, depresses vasomotor and respiratory centers in the medulla.
VERSED
MOA: Binds to GABA receptors which open chloride- channels in the receptor allowing influx of chloride- and causing hyper-polarization of the neuron. Decreases intracellular voltage. Enhances normal GABA effects.
Class: Benzodiazepine
Effect: Preanesthetic agent, hypnotic, anti-convulsive sedative for treating anxiety
ATIVAN
MOA: In the presence of hydrogen+ ions, sodium bicarbonate disassociates to sodium and carbonic acid, the carbonic acid picks up a hydrogen+ ion changing to bicarbonate then disassociates into H2O and CO2, functioning as a buffer and alkalinizing the blood.
Class: Alkalinizing agent, buffering compound
Effects: Given to patients to improve pH levels
SODIUM BICARBONATE
MOA: Responsible for regulating the body’s retention of water by acting to increase H2O absorption in the collecting ducts of the kidney’s nephrons. Increases H2O permeability of collecting duct and distal convoluted tubule.
Class: Anti-Diuretic Hormone (ADH)
Effect: Increases peripheral vascular resistance, increases arterial blood pressure, fluid retention.
VASOPRESSIN