Pharmacology Exam 1 Medication Mechanisms

Mechanism of Opiods Act on the CNS to alter pain perception Binds to receptors on the presynaptic neuron and inhibit transmission of neurotransmitter across the synaptic terminal Binds to receptors on the postsynaptic neuron and decreases excitation of neurotransmitter receptors on the membrane Mechanism of NSAIDs (anti-inflammatory) Inhibits the action of prostaglandins by directly inhibiting a precursor enzyme called cyclooxygenase Mechanism of COX-2 Selective drugs (anti-inflammatory and anti-pain) Inhibits synthesis of only COX-2 enzymes Spare production of beneficial prostaglandins Mechanism of Diazepam (muscle relaxant) Acts on the polysynaptic reflex arc in the spinal cord Decreases excitability of the alpha motor neuron This then decreases activity of those reflex arcs and the muscles supplied by that motor neuron Mechanism of Baclofen (muscle relaxant) Directly by stimulating GABA receptors in the spinal cord Decreases excitation of the alpha motor neurons, optimizing muscle relaxation and decreasing sedation Mechanism of Alpha-2 Agonists (muscle relaxant) Bind to alpha 2 receptors (receptors that are located in interneurons in the CNS, especially at the cord and brainstem level) and stimulate those receptors This decreases excitatory input onto the alpha motor neuron, causing muscle relaxation Mechanism of Dantroline (muscle relaxant) inhibits the release of calcium from the sarcoplasmic reticulum in skeletal muscle and thus decreases the strength of muscle contraction Mechanism of Botulinum Toxin (muscle relaxant) Muscle paralytic that is injected locally to control severe muscle spasms. It works by inhibiting acetylcholine release at the neuromuscular junction A connectin protein is one that allows the acetylcholine filled vesicles to bind with the cell membrane in order to be released via exoctyosis into the synaptic cleft Botulinum toxin destroys these connectin proteins so that Ach vesicles cannot fuse with the cell membrane Mechanism of Dilantin (anti-seizure) Decreases Na+ entry into rapidly firing neurons (stops action potential)

Mechanism of L-Dopa Therapy (Parkinsons) L-dopa, a precursor for dopamine, CAN in fact cross the blood brain barrier Once this occurs, the brain converts L-dopa into dopamine This will increase the dopamine content in the basal ganglia Mechanism of Caridopa (Parkinsons) Prevents the L-dopa from being converted into dopamine until it can reach the brain (so it will still be able to cross the blood brain barrier) by inhibiting dopa decarboxylase, the enzyme that powers L-dopa conversion to dopamine Mechanism of COMT (Parkinsons) COMT is an enzyme that breaks down L-dopa in peripheral tissues before it crosses the blood brain barrier. The COMT inhibitor prevents this from occurring so that the L-dopa can get to the brain unaltered Mechanism of Dopamine Agonists (Parkinsons) Synthetic drugs that directly stimulate the same receptors as dopamine in the basal ganglia Mechanism of Selegiline/Eldepryl (Parkinsons) Inhibits MAOs (the enzyme that breaks down dopamine in the brain) and thus prolongs dopamine effects