Autonomic Pharmacology part 2 Flashcards
(39 cards)
Action of Neuromuscular blocking drugs
- Block cholinergic transmission at neuromuscular junctions
- Act as either:
- Antagonists (non-depolarizing)
- Agonists (depolarizing)
- Inhibit release of ACH
Neuromuscular blocking agents
- Tubocurarine (inhibits nicotinic receptors)
- Succinylcholine (depolarization)
- Botulinum toxin
What is the action of tubocurarine (Curare)
- Competitively and reversibly inhibits nicotinic receptors at neuromuscular junction; blocks action of ACH
- Depolarization of membrane is inhibited and muscle contraction is blocked
- Causes weakness of skeletal muscles; possible death due to asphyxiation from paralysis of diaphragm
Can the competitive blocker like tubocurarine be overcome?
Yes by administration of cholinesterase inhibitors
Action of succinylcholine
Attaches to nicotinic receptor and like ACH, results in depolarization
- Constant stimulation of receptor causes sodium channel to open, producing depolarization
T or F, With time, in succinylcholine drug, receptor cannot transmit any further impulses and repolarization occurs as the sodium channel closes
True
Succinylcholine can produce what result?
muscle fasciculations followed by paralysis
- Paralysis lasts only a few minutes because drug is broken down by plasma cholinesterase
Indications of Succinylcholine
- Endotracheal intubation
- relax skeletal muscles during surgery
- Reduce intensity of muscle contractions of convulsions
Action of Botulinum Toxin
Affects presynaptic membrane of neuromuscular junction in humans
- Prevents calcium-dependent release of ACH
- Produces state of denervation
- Muscle inactivation persists until new fibrils grow from nerve and form junction plates on new areas of muscle cell walls
- Muscle tics, muscle disorders, cosmetic procedures
Mechanism of action for Ganglionic Blocking Agents
Inhibit nicotinic receptors, so blocks neurotranmission in both PANS and SANS
3 ganglionic blocking agents
- Nicotine
- Trimethaphan (not used anymore)
- Hexamethonium
Which ganglionic blocking agent is so toxic that one drop on skin can be fatal?
Nicotine
Nicotine:
Low doses = result?
high doses: = result/
Low doses = produces stimulation due to depolarization
High doses = produces no response at nicotinic receptors but stimulates muscarine receptors
Pharmacologic effects of Nicotine
- Respiratory paralysis; increases BP, HR, GI motility and secretions
- Constricts blood vessels and reduces blood flow to extremities
Indication for Nicotine
tobacco cessation therapy
Also used as an insecticide
Action of Adrenergic drugs
Act at receptors of the sympathetic nervous system (SANS)
List the endogenous neurotransmitters considered adrenergic drugs
Catecholamines (synthesized in neural tissues)
- Epinephrine - released from adrenal medulla
- Norepinephrine - released at terminal nerve endings
- Dopamine - brain, splanchnic, renal vasculature
List the exogenous neurotransmitter considered adrenergic drugs
- isoproterenol
Different receptors in Adrenergic drugs
alpha
beta
Adrenergic drugs are classified how?
By their mechanism of action
- Direct acting
- Indirect acting (causes release of endogenous norepinephrine, which then produces the response)
- Mixed action
List the Adrenergic Drug classes
Alpha agonists
Beta agonists
Alpha antagonists (blockers) Beta antagonists (blockers)
Stimulation of alpha receptors causes what?
- Vasoconstriction of vessels in skin (look pale when scared)
- Protects you from bleeding if skin is damaged during trauma (fight response)
- Smooth muscle contraction
Action of beta 1 receptor stimulation
- Cardiac stimulation
- Increased rate and force of contraction
- Breakdown of glycogen to increase glucose (need energy during fight or flight
Action of beta 2 receptor stimulation
- Smooth muscle relaxation
- Vasodilation of vessels in skeletal muscle (need good blood flow to muscle to run away)
- Bronchodilation (relaxation of smooth muscles in bronchioles makes it easier to break)