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58 Cards in this Set

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What drug blocks the transporter that takes up choline into the nerve terminal?
two types of Acetylcholinesterase?
1. True Acetylcholinesterase - NMJ, etc
2. butyrylcholiesterase - BuChE - in blood and liver
Natural inhibitor of muscarinic receptors?
Natural inhibitor of nicotinic receptors
Curare (tubocurarine)
Where are Nn receptors located?
All sympathetic and parasymp ganglia

Adrenal Medulla

sympathetic vasodilatory fibers

Some CNS neurons

Presynaptic membranes of some parasympathetic postganglionic neurons
These subtypes of muscarinic receptors work via a Gq11
M1, M3, M5 - -> PLC -> IP3 and DAG -> stimulate Ca++ and PKC
These subtypes of muscarinic receptors work via Gi or Go
M2, M4
Synthetic choline derivatives used as muscarinic agonists
Methacholine, Carbachol, Bethanechol
What should you administer if you get cholinergic ester toxicity?
Atropine and epinephrine
Don't give cholinergic esters to people with what conditions?
Asthma, hyperthyroidism (a-fib), coronary insufficiency, peptic ulcers
What are the 3 main types of cholinergic esters?
Bethanochol, Carbachol, Methacholine
3 types of cholinomimetic alkyloids
Muscarine (amantia mushroom)
Arecoline (betel nuts)
Pilocarpine (pilocarpus shrub)
These types of drugs increase skeletal muscle activity, cause phase I blocks, phase II blocks, cause cardiovascular changes, and increase ganglionic transmission
ACHE inhibitors
AchE inhibitors in the CNS cause what types of problems?
tremor, anxiety, restlessness, decreased ability to concentrate, memory loss, confusion, sleep disturbances, convulsions, coma, circulatory and respiratory depression, desynchronization of the EEG
What are the 3 classes of AChE inhibitors?
mono/bis quaternary amines
Name 2 quaternary amines that are AcHE inhibitors
Edrophonium and Ambenonium
Name 3 carbamates that are AcHE inhibitors
Physostigmine, Neostigmine, pyridostigmine
Clinical uses of AcHE inhibitors
Reverse blockade of NMJ by nondepolarizing muscle relaxants during anesthesia

Treating myasthenia gravis

Used to be used to treat open angle glaucoma


Smooth muscle atony

Anti-muscarinic toxicity - overdoses of atropine, scopolamine, tricyclic antidepressants, phenothizines, antihistamines

Alzheimers Disease
3 drugs used to reverse NMJ blockade of anesthesia
Neostigmine, pyridostigmine, edrophonium
What drug is used to test for myasthenia gravis?
Edrophonium chloride - monoquaternary amine, ACHE inhibitor
What drugs are used to treat myasthenia gravis?
Neostigmine and pyridostigmine
3 ACHE inhibitors used to treat strabismus
Isoflourphate, echothiophate, demecarium (organophosphates)
What should you use to treat smooth muscle atony in the GI or urinary tract?
In 25% of these patients, physostigmine and rivastigmine, as well as Aricept, have shown promising results
It has been suggested that administering this drug during a nerve gas attack will provide a reversible blockade to prevent an irreversible one
This antimuscarinic also affects nicotinic receptors
Name 3 naturally occuring muscarinic antagonists
Atropine - belladonna and jimsom weed
Scopolamine - henbane
Homatropine (semisynthetic with tropine and mandelic acid)
3 synthetic quaternary ammonium muscarinic antagonists
Tiotropium bromide
Ipratropium bromide (Atrovent)
Propantheline bromide (probathin)
4 synthetic tertiary amine msucarinic antagonists
Cyclopentolate, tropicamide, dicyclomine, triphenamil
What is the pirenzepine analog selective for M2 receptors that has cardiac effects and is being investigated for treating arrhythmias associated with decreased heart rates
What is the best way to use scopolamine to treat motion sickness?
transdermally, in the postauricular mastoid region 4 hrs prior to motion
What affect does atropine or scopolamine have on the heart?
Transient bradycardia as it blocks muscarinic receptors that decrease AcH. Then with greater doses it casues a progressive increase in HR blocking M2 receptors in SA node. There is age-dependent effects - most marked in young adults with significant vagal tone. Infants and elderly are less likely to respond to atropine
What medication is used to combat ACHE inhibitor toxicity / mushroom poisoning?
Atropine - counters cholinomimetics like neostigmine and ACHE inhibitors. Also treats organophosphat insecticide poisoning and as an antidote for mushroom poisoning from muscarine
High doses of this drug can cause decreased concentration and memory, sedation, excitation, ataxia, asynergy, EEG drowsy state, disorientation, hallucination, and coma - a condition known as CENTRAL ANTICHOLINERGIC SYNDROME
Diagnosis of this is confirmed with physostigmine 1mg IM injection - if there is no response by salivation, sweating, or increased GI activity, an antimuscarinic agent is present
Atropine (antimuscarinic) poisoning
Do not ever use this drug to treat antimuscarinic poisoning, as it has significant antimuscarinic activity
These have been replaced by nitroprusside and adrenergic blockers because they produce more predictable responses
Ganglionic blocking agents
What are the 3 main ganglionic blocking agents?
Hexamethonium, Tremthapan, and Mecamylamine HCL
Nicotine, lobeline, trimethylammonium, dimethyl-4-phenylpiperazne, and DMPP are all used as what?
Agents to stimulate autonomic ganglia - Nn --> fast EPSPs. Of little therapeutic use, but good experimentally.
This is a relaxant that works directly upon muscle and can prevent hyperthermia and spasticity
Dantrolene - prevents Ca++ release from SR
What do these drugs do? Baclofen, Meprobamate, benzodiapepines
Centrally acting muscle relaxants and anti-spasmodic agents. They lessen muscle activity but are not as effective as neuromuscular blocking agents.
What are neuromuscular blocking agents typically used for?
They exert no CNS effects, and are generally used to make surgical maneuvers safer and more efficient. The permit use of lower levels of anesthesia, permit endotracheal intubation, decrease fasciculations at site of surgery, and help maintain ventailation. THEY HAVE NO ANALGESIC OR ANESTHETIC ACTIVITY. Also prevent bone fractures during EST.
What is the structure of neuromuscular blocking agents and what does this help accomplish?
2-3 quaternary ammonium ions that are positively charged make it remain in extracellular space and not cross BBB
What are the three classes of neuromuscular blockers?
Competative (nondepolarizing)
AcH release blockers
Name some competative NM blockers
tubocurarine, pancuronium, popecuronium, atrcurium, doxacurium, mivacurium gallamine, vecuronium
What is the only depolarizing NM blocker currently used
Succinyl Choline, cannot be reversed with more Acetylcholine. Has a 3 minute half life and is metabolized 100%. Short half life and is used for INTUBATION.
Name the ACH release NM blocker
Botulinum toxin - inactivates proteins involved in docking and fusion of transmitter containing vesicles.
pseudo ACHE in the plasma metabolizes these two NM blockers
Succinycholine and mivacurium. PseudoACHE actions can be greatly reduced (and thus succinylcholine and mivacurium effects are increaed) with liver damage, because it is made there. Also patients can be homo or heterozygous for messed up pseudo-ACHE. Making succinylcholines effects last a lot longer.
Patients with diminished renal function shouldn't use what particular NM blockers?
Pancuronium, metocuring, tubocurarine, or gallamine
The effects of NM blockers can be potentiated by what?
Anesthetic agents
The effects of competitive NM blockers can be potentiated by low electrolyte levels. What electrolytes?
Ca++ and K+
Burns, denervated muscles, spinal cord injuries require how much greater NM blockers?
2-3x greater doses
What are the side effects of NM blockers?
BP changes, heart rate changes, stimulation of histamine release
Pancuronium can block muscarinic receptors and lead to what?
Increased heart rate
These 3 NM blockers can cause cardiac arrythmias thru muscarinic receptor mediated effects
Pancuronium, succinylcholine, and gallamine
Succinylcholine can cause life-thretening effects in electrical discturbance and alter effectiveness of drugs in what types of patients?
Those with soft-tissue damage. Depolarization caused by succinylchline results in increased K+ efflucs from muscle.
Histamine release is a problem with this particular NM blocker.
What are the particular drug interactions with NM blockers?
Anesthetics - increase action of competative NM blockers

Malignant hyperthermia - succinyl choline or any inhalation anesthetic. Must be genetically predisposed.

Antibiotics can increase effects of NM blockers (aminoglycosides, tetracyclines, polymyxin, clindamycin)

Phenytoin/carbamazepine decreases duration of mivacurium