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Chapter 3 Pharm

Pharmacolgy

TermDefinition
Nervous system is divided into Central Nervous System and Peripheral Nervous system
Motor efferent section is divided into Autonomic nervous system (involuntary) and Somatic nervous system (conscious activities)
Nervous system Sends signals through neurons or ganglion cells Uses neurotransmitters to cross synapses Somatic nervous system -nerve cell body originates in CNS Autonomic nervous system -interruption between CNS and innervation site
Neurons and Ganglia Preganglionic neurons- lead from vertebrae to synapse Postganglionic neurons- lead from synapse to organ or gland Multiple synapses occur in ganglia- drugs can have effect here
Function and Anatomy of the ANS Controls generally involuntary physiologic functions Two main divisions: parasympathetic and sympathetic Synapses occur in autonomic ganglia -sympathetic: most located near spinal cord -parasympathetic: most located near effector site
Where is sympathetic located near spinal cord
Where is parasympathetic located near the effector site
Sympathetic division Preganglionic neurons short Postganglionic neurons long
Parasympathetic division Preganglionic neurons very long Postganglionic neurons short
Parasympathetic division Branches Branches through cranial and sacral segments
Sympathetic division Branches Through thoracic and lumbar segments
Multiple synapses occur in ganglia Drugs can have effect here
Neurotransmitters Stored in nerve terminal Released with nerve impulse Diffuse across cleft, interact with receptors Either: Leads to production of electrical signals Causes physiologic changes in neuroeffector organ
Acetylcholine (ACH) Ganglionic synapse and neuroeffector site in parasympathetic system Ganglionic synapse in sympathetic system
Norepinephrine (NE) Neuroeffector site in sympathetic system
Cholinergic agents Affect ganglion, parasympathetic neuroeffector site, or muscular junction by stimulating ACH release
Anticholinergic agents Block ACH receptor or prevent ACH release
Adrenergic agents Stimulate receptor to release NE (adrenaline)
Antiadrenergic agents Block NE receptor from having effect
General Physiologic Functions Controlled by the ANS Parasympathetic and sympathetic divisions -innervate most organs (dual innervation) -usually have opposite effects
The Sympathetic Nervous System Generally dominant system when under stress Prominent when body in danger - fight or flight response -prolonged state can lead to death Adrenergic drugs -mimic sympathetic action, stimulate NE release
The sympathetic nerve ending Neurotransmitter is NE -synthesized in nerve ending -packaged in vesicles -released when impulse reaches nerve ending -combines with type of receptor present
Methods of terminating physiologic effects of NE Transport NE back into nerve terminal -repackaged into vesicles Diffuse NE away from site -ultimately metabolized by: monoamine oxidase catechol-0-methyl-transferase
Presynaptic site in nerve ending create false transmitters, block reuptake of NE, deplete NE from storage vesicles, increase NE release from nerve endings, block NE release from nerve terminals
Postjunctional site where receptors are located stimulate a-receptors, b-receptors, or both block a-receptors, or b-receptors
Alpha-adrenergic drugs stimulate a-receptor sites
Beta-adrenergic drugs stimulate b-receptor sites
Neuronal activators increase NE levels in nerve ending
Alpha blockers block a receptors
Beta blockers block b receptors
Neuronal blockers inhibit NE levels in nerve ending
Alpha-Adrenergic Drugs stimulate a receptor sites, include NE, epinephrine, and phenylephrine, vasoconstriction most dominant clinical effect, often administered intravenously, commonly referred to as vasopressors
Alpha-Blocking Drugs Block a receptor sites, create generalized, nonselective vasodilation, considered second-line antihypertensive, some specifically target bladder, prostate gland
Beta-adrenergic drugs Mainly stimulate B1-B2 receptors Used to treat: bradycardia by increasing heart rate/ heart failure by stimulating cardiac contractions
Beta-Blocking drugs Commonly used in clinical practice Many available: some affect b1 and b2 receptors, some relatively selective for b1-receptors Block effects of NE and epinephrine -decrease heart rate, force of heart contraction
Adrenergic neuronal activators and blockers decrease adrenergic nerve function. affect all sites where NE released, tend to influence a- and b-receptors, agents include reserpine, methyldopa, and clonidine
Methylodopa causes activation of receptor site by metabolite, stimulates centrally acting a2-receptors
Clonidine reduces sympathetic tone, and acts on cardiovascular center in brain stem
Overall effects of the parasympathetic division Dominant when body at rest Controls and stimulates: -digestion -waste elimination -genitourinary system Cardiovascular system generally decreased
ACH synthesized nerve ending, packaged in vesicles, nerve impulse stimulates combination with receptor
Acetylcholinesterase (ACHE) Enzyme that metabolizes excess ACH
Cholinergic Receptors Five muscarinic receptors (M1-M5) -throughout body Nicotinic-1 (N1) -All ANS ganglion sites Nicotinic-2 (N2) -neuromuscular junctions in somatic nervous system
Mechanism of action of cholinergic drugs Broader spectrum of unwanted side effects Possible drug-receptor interactions: -stimulate muscarinic receptor, producing cholinergic effect -block cholinergic receptors, prevent ACH interaction -block ACHE, enhancing duration of parasympathetic impul
Choline esters Stimulate muscarinic receptors
Anticholinesterases Block the ACHE enzyme
Anticholinergics Block ACH receptor sites
Antimuscarinics Block muscarinic receptor sites
Anticholinesterase Drugs/ Cholinesterase Inhibitors inhibit ACHE effects/ cause prolonged, intensified ACH effects/ Long-term use may cause: muscle weakness, diarrhea, excess salivation, excess bronchial secretions/ limited therapeutic use
Anticholinergic Drugs block muscarinic receptors, high doses can affect nicotinic receptors, indication depends on specific receptors
Created by: cassiemartin
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