Physio Drugs Flashcards
class of drugs that prevents choline reuptake
hemicholinium
class of drugs that prevents vesicular storage of ACh
vesamicol
class of drugs that degrades synaptobrevin (SNARE) and prevents vesicle fusion/exocytosis
botulinum toxin (botox)
class of drugs used clinically to paralyze selected muscles with excessive tone
botox
what clinical syndrome is botox used to unmask
lambert eaton syndrome
used to treat focal dystonia
dystonia is a state of abnormal muscle tone resulting in muscular spasm and abnormal posture
botox
class of drug that increases ACh in the synaptic cleft thereby enhancing postsynaptic effects of ACh
AChE inhibitors
parasympathomimetics
5 types of anticholinesterase
edrophonium, neostigmine, physostigmine, parathion, malathion
used for diagnosing myasthenia gravis (MG) and eaton lambert
edrophonium (simple alcohol)
duration of edrophonium
short duration of action
used to treat myasthenia gravis (MG) and also used for reversal of neuromuscular blocker
neostigmine and physostigmine
used to treat atropine poisoning
physostigmine (can cross BBB)
duration of neostigmine and physostigmine
long duration of action
how does neostigmine and physostigmine work
it increases the duration of time that ACh is in the synaptic cleft by increasing half life of AChE inhibitors hence increasing the chances it will bind to a receptor
strong pesticide and is irreversible
malathion and parathion
have to make new receptors to overcome
what happens when there is increased stimulation of ACh receptors
muscle paralysis then death
A boy ate some berries. He became tachycardic, his temperature increased, and his eye were dilated. what drug do you use to treat?
physostigmine
atropine poisoning
responsible for vasodilating the vascular smooth muscle of the splanchnics
remove your sympathetics
autoimmune disease that blocks calcium reuptake hence reducing ACh release
Lambert Eaton
autoimmune disease that produces antibodies that bind to nicotinic receptors hence reducing neuromuscular junction transmission
myasthenia gravis
how do you tell difference between lambert eaton blocking of the calcium reuptake and botox
with blocking of Ca - there is still a little vesicular release
with botox - there is no vesicular release at all
advantages of acetocholinesterase inhibitors
increase parasympathetic tone, increase central cholinergic neurotransmission in dementia, reversal of paralysis from non depolarizing neuromuscular blockers
disadvantages of acetocholinesterase inhibitors
excessive muscarinic stimulation, excessive nicotinic stimulation, chemical warfare
what happens if muscarinic over stimulated
SLuM BoD
salivation, lacrimation, miosis, bradycardia, diarrhea
A woman is prescribed neostigmine. She returns complaining of diarrhea, abdominal cramps, and salivation. what would alleviate her side effects?
muscarinic antagonist
increase GI motility, salivation, and miosis
muscarinic agonist
what are the 5 muscarinic agonists
carbachol, pilocarpine, methacholine, bethanecol, acetylcholine
used to treat glaucoma by activating miosis, decreases intraocular pressure, and sjogren syndrome
pilocarpine
used to diagnose asthma and has little affinity for nicotinic receptors
methacholine
selective for muscarinic receptors and used to treat urine retention and GI and urinary motility
bethanecol
muscarinic antagonist allows what type of response to dominate
sympathetics
how do muscarinic antagonists work
they bind to muscarinic receptors and prevent ACh from binding
actions of muscarinic antagonists
pupil dilation, tachycardia, decreased salivary, GIT, and bronchial secretions
what does atropine reduce
SLUDGE
salivation, lacrimation, urination, diaphoresis (sweating), GIT motility, emesis(vomiting)
used to treat muscarinic poisoning and anticholinesterase poisoning
atropine
depolarizing neuromuscular blocker
succinylcholine
side effects of nicotinic receptor depolarizing blockades
K release, bradycardia, prolonged muscle paralysis, malignant hyperthermia
what does succinylcholine do
keeps muscle from contracting by keeping it in a constant depolarized state
what happens when nicotinic receptors have prolonged activation or there is an overload of ACh
they become desensitized and eventually muscle paralysis