PHAR 300 Study Guide - Final Guide: Ethylene Glycol Poisoning, Central Nervous System Depression, Receptor Antagonist

• School: McGill University
• Department: Pharmacology and Therapeutics
• Course: PHAR 300
• Professor: Edith Zorychta

Document Summary

Death (the respiratory centre stops doing its job) Chronic use will lead to rebound excitation in the case of sudden stopping. An alcoholic will have adverse withdrawal effect which can be very dangerous. 0-0. 05%: loss of inhibition, excitement, incoordination, impaired judgement, slurred speech, body sway. 0. 05-0. 1%: impaired rx time, further impaired judgement, impaired driving, ataxia. 0. 2-0. 3%: respiratory depression, danger of death in present of other cns depressants, blackouts. Facilitates gaba receptors, leading to initial increase in excitation (disinhibition) Opens gaba-a to increase inhibition: gaba-a has subsites for many other drugs, ethanol has many binding sites, facilitates gabaurgic inhibition. There are tonically active extrasynaptic receptors: ethanol acts on both types of receptors. Ethanol can lead to the release of glycine, which enhances post-synaptic inhibition responses in cns. Blocks excitatory channels, leading to decrease in excitation. Sodium, potassium and calcium-mediated excitation is hindered.