Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
22 Cards in this Set
- Front
- Back
|
Organophosphorus Compounds
Irreversible AChE Inhibitors Therapeutic Agents |
Echothiophate
Diisoprophyl |
|
|
Irreversible AChE Inhibitors
Insecticides |
Tetraethyl pyrophosate
Parathion Malathion |
|
|
Irreversible AChE Inhibitors
Nerve Gases |
Sarin
Soman Tabun |
|
|
Irreversible AChE Inhibitors MOA
|
Irreversibly phophorylate (hence inactivate) AChE
|
|
|
If we irreversibly inactivate AChE, what effect will that have on ACh?
|
ACh will stay too long --> adverwe effects whih will be lethal
|
|
|
Diisopropyl Fluorophosphate
|
DFP
High lipid solubility Volatile |
|
|
Echothiophate
|
Positively charged
not volatile Preferred over DFP |
|
|
what are the therapeutic uses of DFP and echothiophate?
|
Miotic
Glaucoma These are drugs of last resort |
|
|
What is important about insecticides?
|
Most of organophosphates are well aborbed from the skin, gut, and conjuctiva --> dangerous to humans
Limited half life when dissolved in water |
|
|
What is Parathion?
|
Insecticide
Not used clinically Major problem with accidental poisoning. |
|
|
What is Malathion?
|
Insecticide
Low dermal absorption Detoxified by plasma carboxylesterases more rapidly in mammals and birds than in insects Used clinically to treat head lice |
|
|
What is the range of toxicity in the irreversible AChE inhibitors?
|
Malathion < Parathion <<<< Sarin
|
|
|
What are the adverse effects of AChE inhibitors?
|
Lens opacities (echothiophate)
Chronic neurotoxicity Cholinergic overstimulation Cholinergic crisis |
|
|
How does triorthocresylphosphate (an additive in lubricating oils) causes chronic neurotoxicity?
|
Triorthocresylphosphate --> inhibits neurotoxic esterase --> axonal swelling & demylenation --> sensory disturbances, ataxia, weakness, tendon reflexes, muscle twitching, reduced tenderness
|
|
|
What can ACh do?
|
Stimulate M receptors at effector organs.
Stimulate cholinergic receptors in the CNS Produce stimulation followed by depression or paralysis of autonomic ganglia and skeletal muscle |
|
|
What is the difference between neostigmine, physostigmine, and the organophosphates?
|
Neo--reversible, doesn't cross BBB
Physostigmine--reversible, crosses BBB Organophosphates--irreversible, crosses BBB |
|
|
What effects will be caused by cholinergic overstimulation/crisis?
|
Miosis
spasm of accommodation Extreme salivation Sweating Bronchoconstriction Vomiting Diarrhea Bradycardia Hypotension Urinary urgency |
|
|
What are the CNS effects of cholinergic overstimulation/crisis?
|
Confusion
Ataxia Slurred speech Loss of reflexes Convulsions Coma Central respiratory paralysis |
|
|
What are the skeletal muscle effects of cholinergic overstimulation/crisis?
|
Involuntary twitching
Severe weakness Paralysis |
|
|
What is the cause of death in the cholinergic overstimulation/crisis?
|
Respiratory failure and cardiovascular collapse
|
|
|
What is the treatment of cholinergic crisis?
|
Sarin --> excessive activation of M/N receptors (both central and peripheral)--> central (muscarinic blocker--atropine) and peripheral (cholinesterase reactivator--2-PAM)
|
|
|
What is cholinesterase reactivator?
|
Pralidoxime (2-PAM)
NMJ Autonomic ganglia peripheral effector sites Used only for organophosphate poisoning |
