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70 Cards in this Set

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what is the postganglionic neurotransmitter in the parasympathetic nervous system
Acetylcholine (ACh)
what is the preganglionic neurotransmitter for the sympathetic nervous system?
Acetylcholine (ACh)
what is the preganglionic neurotransmitter for the parasympathetic nervous system?
Acetylcholine (ACh)
Which ACh receptor is located in in tissues innervated by postganglionic parasympathetic neurons?
Muscarinic
which ACh receptor is located in presynaptic noradrenergic and cholinergic nerve terminals?
Muscarinic
Which ACh receptor is located in non-innervated sites in vascular endothelium?
Muscarinic receptor
Where are Nicotinic receptors located? 4
· in sympathetic and parasympathetic ganglia

· in the adrenal medulla

· in the neuromuscular junction of the skeletal muscle

· in the central nervous system.
Where are muscarinic receptors located? 4
· in tissues innervated by postganglionic parasympathetic neurons

· in presynaptic noradrenergic and cholinergic nerve terminals

· in non-innervated sites in vascular endothelium

· in the central nervous system.
Which ACh receptor is located in sympathetic and parasympathetic ganglia?
Nicotinic
Which ACh receptor is located in the adrenal medulla?
nicotinic
Which ACh receptor is located in the neuromuscular junction of skeletal muscle?
Nicotinic
What cellular change induced by binding of ACh to nicotinic receptor?
Nicotinic receptors are ligand-gated ion channels whose activation results in a rapid increase in cellular permeability to sodium and calcium.
Mechanism of bethanechol
Cholinergic w/ high muscarinic (vs nicotinic) specificity.
What are the three classes of indirect acting cholinergic drugs? how different?
Organophosphates (very long acting)

Carbamates (long acting)

Edrophonium (short acting)
The three ACh congeners with resistance to hydrolosis
methacholine, carbachol, and bethanechol
Muscarinic effect upon iris sphincter muscle
Contraction (miosis)
Muscarinic effect upon ciliary muscle
Contraction (near vision)
Muscarinic effect upon SA node
Bradycardia
Muscarinic effect upon AV node
Reduced conduction velocity
Muscarinic effect upon bronchial muscle
Contraction
Muscarinic effect upon Gastrointestinal motility
Increased
Muscarinic effect upon gastrointestinal secretion
Increased
Muscarinic effect uppon bladder detrusser
Contraction
Muscarinic effect upon bladder trigone, sphincter
Relaxation
Clinical uses of Bethanechol
(Urecholine®)
improvement in gastric emptying

to treat urinary retention if physical obstruction (e.g., prostate enlargement) is not the cause.
Pilocarpine clinical uses
treat open-angle glaucoma (topically)

to induce salivation
Methacholine clinical uses
to provoke bronchoconstriction during diagnostic testing of pulmonary function (methacholine challenge )
*for the diagnosis of asthma
methacholine mechanism
cholinergic
carbachol mechanism
cholinergic
deadly nightshade, mechanism and active ingredient
muscarinic antagonists
atropine
Jimson weed mechanism
muscarinic antagonists
Side effects of muscarinic antagonists
constipation, xerostomia (dry mouth), hypohidrosis (decreased sweating), mydriasis (dilated pupils), urinary retention, precipitation of glaucoma, decreased lacrimation, tachycardia, and decreased respiratory secretions.
clinical use of atropine
raising heart rate during situations where vagal activity is pronounced (for example, vasovagal syncope).

pupil dilation

preanesthetic preparation of patients (facilitates intubation thru reduced respiratory secretions)
inhaled ipratropium clinical use
maintenance therapy in chronic obstructive pulmonary disease (COPD). **muscarinic antagonist, has a long half-life.
atropine mechanism
muscarinic antagonist
prinzepine mechanism
selective M1 muscarinic antagonist
Prienzepine clinical use
reduce gastric acid secretion (other drugs more widely used)
the Bezold-Jarisch reflex
bradycardia, hypotension, nausea

elicited by high doses of nicotine
NM nicotinic receptor
mediates skeletal muscle stimulation
NN nicotinic receptor
mediates stimulation of the ganglia of the autonomic nervous system
arterioles:
Predominant System Ganglionic Blockade Effect
Sympathetic Vasodilation
Veins:
Predominant System Ganglionic Blockade Effect
Sympathetic Vasodilation
Heart:
Predominant System Ganglionic Blockade Effect
Parasympathetic Tachycardia
Iris:
Predominant System Ganglionic Blockade Effect
Parasympathetic Mydriasis
Ciliary muscle:
Predominant System Ganglionic Blockade Effect
Parasympathetic Cycloplegia
Gastrointestinal tract
Predominant System Ganglionic Blockade Effect
Hypomotility
Urinary bladder
Predominant System Ganglionic Blockade Effect
Salivary glands
Predominant System Ganglionic Blockade Effect
Parasympathetic Xerostomia
Sweat glands Predominant System Ganglionic Blockade Effect
Sympathetic cholinergic Anhidrosis
"Reversible" cholinesterase inhibitors. 1 which enters CNS, 2 which do not
physostigmine that enters the CNS

neostigmine and edrophonium that do not
Neostigmine clinical use
stimulate motor activity of the small intestine and colon

treating atony of the detrusor muscle of the urinary bladder

myasthenia gravis

glaucoma, sometimes
Neostigme mechanism
"reversible" cholinesterase inhibitor which does not enter CNS
Edrophonium clinical use
"tensilon test' of myasthenia gravis
side effects of physostigmine, 4

treatment
nausea, pallor, sweating and bradycardia

anticholinergic drugs which are quaternary amines do not enter CNS
drug for treatment of anticholinergic syndrome
Physostigmine
new cholinesterase inhibitors for treating alzheimers
(Aricept®) and rivastigmine (Exelon®) have little hepatotoxicity and have replaced tacrine
drug to counteract intoxication by cholinesterase inhibitor
pralidoxime
Clinical Manifestations of Cholinesterase Inhibitor Intoxication: Muscarinic
13
· Miosis

· Blurred vision (spasm of accommodation)

· Lacrimation

· Sweating

· Excessive respiratory secretions

· Dyspnea (bronchoconstriction)

· Bradycardia

· Hypotension

· Salivation

· Nausea

· Cramping (gastrointestinal spasm)

· Diarrhea

· Urgency (urinary incontinence)
Clinical Manifestations of Cholinesterase Inhibitor Intoxication: Nicotinic

3
· Fasciculations (early)

· Weakness (late)

· Adrenomedullary (sympathetic) discharge (early and transient)
Clinical Manifestations of Cholinesterase Inhibitor Intoxication: CNS
9
· Anxiety

· Insomnia

· Nightmares

· Confusion

· Hypertension (rare)

· Tremors

· Convulsions

· Respiratory depression

· Circulatory collapse
Therapy of Cholinesterase Inhibitor Intoxication, mild poisoning
4
· Atropine sulfate, 1-2 mg intravenously, as necessary

· Termination of exposure

· Pralidoxime, 1 g infused slowly, or 1-3 orally (if no GI symptoms)

· Supportive care
Therapy of Cholinesterase Inhibitor Intoxication
severe poisoning, 7
· Artificial respiration

· Atropine sulfate, 2-4 mg intravenously at 5 minute intervals until abatement of symptoms occurs or signs of atropinization (tachycardia, dilated pupil, drug skin) appear

· Pralidoxime, 1 g infused slowly

· Termination of exposure

· If convulsion, diazepam 5-10 mg intravenously

· Supportive care

· Hospitalization for 2-3 days
effect of cholinesterase inhibitor on depolarizing vs nondepolarizing neuromuscular blocking druges
can overcome non depolarizing
Tubocuranine mechanism
Nondepolarizing neuromuscular blocking
Succinylcholine mechanism
Depolarizing neuromuscular blocking
order of muscel parayzation by muscle blocker
extraocular muscles are affected first, then the muscles of the hands and feet, head and neck, abdomen and limbs, and finally the muscles of ventilation
Dantrolene mechanism
reduces the release of activator calcium from the sarcoplasmic reticulum
dantrolene clinical use
treat the muscle contractures associated with malignant hyperthermia

*not usefull for acute muscle spasm
Baclofen mechanism
partial GABA agonist, probably in the spinal cord.

muscle relaxant
strychnine mechanism
enhances glycine inhibitory effects