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Autonomic Nervous System Drugs

Autonomic Nervous System
-Automatic functions
-Controls cardiac & smooth muscles
-Glandular secretion
-Divided into sympathetic and parasympathetic systems
-Fight or flight response
-Expends energy
-Increases HR
-Dilates pupiles
-Dilates bronchi
-Decreases secretions
-Main ending NT is norepinephrine
-Input to all organs
-Initial nerve shorter, second nerve longer
-Dominates at rest
-Conserves energy
-Decreases HR
-Increases GI tract functions
-Constricts pupils
-Main end NT is aceytylcholine
-Input to all organs
-Initial nerver longer, second nerve shorter
Neurotransmission Processes
-Synthesis of neurotransmitters (NTs)
-Packaging of NTs in presynaptic terminals
-Stimulation of presynaptic nerve/release of NT
-Diffusion of NT across synaptic cleft & binding to post-synaptic membrane
-Activation of the post-synaptic cell
-Degradation/reuptake of the NT
Alpha 1 Receptor
-SNS receptor
-Decrease of secretions
-Pupil dilation
-Increased GI motility
-Urinary retention
Alpha 2 Receptor
-SNS receptor
-Overload switch; decreases sympathetic tone if too great
-Decreased CNS sympathetic outflow (post-synaptic)
-Decreased norepinephrine release (pre-synaptic)
-Decreased insulin release
Beta 1 Receptor
-SNS receptor
-Increased HR
-Increased cardiac output
-Automaticity (number of heart beats per min)
-Increased renin secretion (retains salt/water)
-Majority in heart
Beta 2 Receptor
-SNS receptor
-Bronchial relaxation/dilation (easier to breathe)
-Uterine relaxation (supresses labor)
-Vasodilation in skeletal muscle, brain, and kidney (attracts more blood to area)
-Majority in respiratory system
Dopamine Receptor
-Increased HR
-Increased BP
-Increased blood flow in kidney
-Sympathetic agonist
-Increased HR
-Increased glucose
-Increased lipolysis
-Increased GI relaxation
-Used as cardiac stimulant
-Used for anaphylaxis, combined w/local anesthetics
-Alpha and Beta agonist
-Can work on all receptors
-Sympathetic agonist
-Increased vasoconstriction so intense it causes a reflex decrease in HR
-Used for septic shock (usually blood-borne)
-Sympathetic agonist
-Works at dopamine receptor
-Low doses maintain good renal blood flow
-Higher doses increase BP
-Increase cardiac contractility
-Used for shock (usually traumatic injury)
-Given by continuous IV infusion
-Sympathetic agonist
-Increase efficiency of heart beat
-Beta 1 agonist
-Increase HR
-Increase contractility
-A DOC (drug of choice) for cardiac stimulation for cardiac arrests
-IV infusion
-Sympathetic agonist
-Works on Alpha 1 receptors
-Produces vasoconstriction
-Used in cold meds, also used to dilate pupil
-Sympathetic agonist
-Beta 2 agonist
-Causes bronchiolar and uterine relaxation
-Used to prevent asthma
-Used for premature labor and delivery
-Heightened mood
-Decreased appetite
-Used for ADD and narcolepsy
-Vasoconstriction at Alpha 1 receptor
-Fewer CNS effects
-Used for nasal congestion
Sympathetic Nervous System Neurotransmitters
Parasympathetic Nervous System Neurotransmitter
Indirect-Acting Stimulus
-Stimulates release of vessel that binds with receptor
Direct-Acting Stimulus
-Interacts with receptor
Trade Names of Epinephrine
Crystal Meth
-Sympathomimitec; synthetic derivative of CNS stimulant
-Elevated mood, insomnia, decreased appetite, high BP, high HR
-Paranoia, schizophrenia, seizures
-Longer high
-Severe withdrawal
-Acute violent behavior
-Long-term Parkinson-like effect
Phenoxybenzamine (Dibenzyline)
-Sympathetic antagonist
-Blocks Alpha 1 and Alpha 2 receptors
-Causes vasodilation
-Long-acting, po q day dosing
-Used for pheocromocytoma
-Mimics sympathetic response
-Increased Epi and NE in urine
-Very high BP
Phentalomine (Regitine)
-Sympathetic antagonist
-Blocks Alpha 1 and Alpha 2 receptors
-Causes vasodilation
-Used for pheocromocytoma
-Reduces necrosis in tissues
Terazosin (Hytrin), Doxazosin (Cardura), Tamsulosin (Flomax), Alfozosin (Uroxatral)
-Sympathetic antagonists
-Alpha 1 blocker
-Relaxes bladder, not effective for HTN
-Used for benign prostatic hyperplasia (BPH) and sometimes HTN
Labetolol (Trandate), Carvedilol (Coreg)
-Sympathetic antagonist
-Blocks Alpha 1, Beta 1, Beta 2 receptors
-Decreases BP
-Decreases HR
-Used for HTN, especially post-MI (protective measures)
Propranolol (Inderal), Sotalol (Betapace), Timolol (Biocadren), Carteolol (Cartrol), Penbutolol (Levatol)
-Sympathetic antagonist
-Blocks Beta 1 and Beta 2 receptors
-Decreases HR
-Caution with asthmatics, diabetics
-Used for HTN
*Will decrease exercise tolerance
Timolol (Blokadren)
-Sympathetic antagonist
-Blocks Beta 1 and Beta 2 receptors
-Decreases HR
-Used for eye surgery (pupil constriction)
Metoprolol (Lopressor) and Atenolol (Tenormin)
-Sympathetic antagonist
-Blocks Beta 1 receptor
-Used for HTN, less bronchospasm
-PNS mediator
Nicotinic (ganglia, muscles) and Muscarinic (organs)
-PNS receptors
PNS Stimulation
-Decrease HR
-Increase gastric secretion, motility, emptying
-Increase urination
-Miosis (pupil constriction)
-Increase sweating, salivation, nasal secretions
-Increase bronchial secretions
Two Ways Drugs Mimic PNS Actions
-Directly binding to acetylcholine receptors
-Inhibiting the enzyme that breaks down acetylcholine (acetylcholinesterase, AChE)
Cevimeline (Evoxac)
-Parasympathetic agonist
-Muscarinic agonist
-Used for dry mouth in Sjogren's
-Do not use in asthma; can promote asthma attacks
Pilocarpine (Pilocar, OcusertPilo)
-Parasympathetic agonist
-Muscarinic agonist
-Used for glaucoma
-Oral treatment for Sjogren's
Bethanechol (Urecholine)
-Parasympathetic agonist
-Muscarinic agonist.
-Treats urinary retention and GI atony
-Voids bladder and GI tract
Edrophonium (Tensilon)
-Parasympathetic agonist
-AChE inhibitor
-Diagnosis of myasthenia gravis
Physostigmine (Antilirium)
-Parasympathetic agonist
-AChE inhibitor
-Used for glaucoma and anticholinergic tox
Atropine (Atropisol)
-Parasympathetic antagonist (anticholinergic)
-ACh antagonist; dose-dependent blockade of muscarinic receptors
-Used for diarrhea, bronchospasms, anesthesia, urinary incontinence, ER codes (blocks PNS response)
-Decreases secretions
Scopolamine (Transdermscop)
-Parasympathetic antagonist (anticholinergic)
-ACh antagonist
-Treats motion sickness (dermal patch)
Dicyclomine (Bentyl)
-Parasympathetic antagonist (anticholinergic)
-ACh antagonist
-Treats irritable bowels
Trihexyphenidyl (Artane) and Benztropine (Cogentin)
-Parasympathetic antagonist (anticholinergic)
-ACh antagonist
-Treats Parkinson's disease
Darifenacin (Enablex), Oxybutynin (Ditropan), Solifenacin (VESIcare), Tolteridine (Detrol), Trospium (Sanctura), Fesoterodine (Toviaz)
-Parasympathetic antagonist (anticholinergic)
-Treats overactive bladders
-Block muscarinic receptors on the bladder detrusor muscle to decrease bladder contractions
-Dry mouth is most bothersome SE
-Due to a decrease in ACh in parts of brain
-Affects speech, cognition, memory, activities of daily living (ADL)
Treatments for Dementia
-Increasing ACh in the brain
-Decreasing rate of degeneration of ACh-rich neurons
Cholinesterase Inhibitor
-Drugs that inchrease ACh in the brain by decreasing its rate of breakdown
-Not very effective
-Modest improvements in behavior, cognition, and function
-Recommended for all patients with mild to moderate AD
Cholinesterase Inhibitor
-Only 25-30% respond
-NOT curative, only palliative
-SEs include GI distress, headache, dizziness, bronchoconstriction, increased urine/fecal output
-Pills or patch form
Donepezil (Aricept)
-Cholinesterase inhibitor
-Increases ACh levels
-Treatment for AD
-Causes GI side effects and bradycardia
Rivastigmine (Exelon)
-Cholinesterase inhibitor
-Increases ACh levels
-Treatment for AD
-Causes significant GI side effects including weight loss
-PO or patch
-Slowed HR
Galantamine (Razadyne)
-Cholinesterase inhibitor
-Increases ACh levels
-Treatment for AD
-GI side effects and bronchoconstriction
Memantine (Namenda)
-NMDA receptor antagonist
-Modulates the effect of the glutamate at NMDA receptors, reducing the destructive effect of this NT in the brain
-Reserved for moderate to severe AD
-Well-tolerated when taken PO
-May cause dizziness, headache, confusion
Ginkgo Biloba
-May show some promise in improving cognitive performance and behavior
Parkinson's Disease
-Caused by a decrease of dopamine in the nerves of the substantia nigra in the brain
-Depigmentation of substantia nigra
-Decreased dopamine levels allow excessive ACh activity
-Increased ACh activity causes tremor, bradykinesia, rigidity, blank faces, postural instability
-No cure, palliative treatment
-Can't treat disease
-Manages symptoms
-Focuses on comfort of patient
Drug Holiday
-Time off from medications
-Lets nerves rest and recover
-Requires hospitalization
-Prevents nerve burn out
Levodopa (L-dopa)
-Treatment for Parkinson's disease
-Precursor to dopamine (building block)
-Crosses BBB and is converted to dopamine
-Most effective for Parkinson's; first-line
Carbidopa (Lodosyn)
-Treatment for Parkinson's disease
-Inhibits dopa decarboxylase in the periphery
-May cause nausea, gait abnormalities, postural hypotension, arrhythmias
-Treatment for Parkinson's disease
-Combination of L-dopa and carbidopa
-Treatment for Parkinson's disease
-Combination of L-dopa and carbidopa; dissolved on tongue
Amantadine (Symmetrel)
-Treatment for Parkinson's disease
-Initially a flu drug
-Increases dopamine release from nerve terminals
-Helps to titrate dopamine
-Used for L-dopa dyskinesias
-May cause livedo reticularis (rose-colored mottling of skin) and othostatic hypotension
Selegiline (Eldepryl)
-Treatment for Parkinson's disease
-First-line drug for Parkinson's
-Prevents dopamine breakdown by blocking MAO-B (enzyme that breaks down dopamine)
-Causes agitation and insomnia
Trihexyphenidyl (Artane) and Benztropine (Cogentin)
-Treatment for Parkinson's disease
-Anticholinergic; decreases ACh levels
-Causes tachycardia, mydriasis
Wearing Off
-Drug loses effect earlier than expected (e.g. 8hrs instead of 12 hrs)
-Sign of drug tolerance or disease progression
-Dosing intervals should be decreased or add an agonist
-Requires compliance and/or increased care oversight
Off Time
-Drug should be working but stops at random intervals
-Indicates drug tolerance and/or disease progression
-Another drug should be added to regimen
Ropinirole (Requip)
-Treatment for Parkinson's disease
-Also used for restless leg syndrome
-Combination of L-dopa/carbidopa/entacapone
Dopamine Agonist
-Cause nausea, psychosis, effects on movement
Neuromuscular Blocker
-Anticholinergic specific to the ACh receptor on skeletal muscle
-Causes temporary paralysis, loss of muscle tone
-Muscle relaxant
-Facilitates intubation
-Controls ventilation
-Vary in onset and duration
Succinylcholine (Anectine)
-Neuromuscular blocker
-Onset within 30 seconds to 1 minute, duration of 5 minutes
-Used for intubation or endoscopy
Curare (Atracurium, Cisatracurium, Pancuronium, Rocuronium, Vecuronium)
-Neuromuscular blocker
-Work for about 20-40 min; recovery may take an hour, given IV
-Used for surgical procedures in addition to anesthesia
Malignant Hyperthermia
-Allergic reaction to neuromuscular blocker
-Presents as muscle rigidity, tremors, and high fever
-Treatment requires d/c of causative drug, fever reduction, and Dantrolene for muscle spasms
Benzodiazepine, Baclofen (Lioresal), Carisoprodol (Soma), Cyclobenzaprine (Flexeril)
-Skeletal muscle relaxants
-Work centrally to relieve muscle spasms or cramping
-Biggest side effect is exhaustion
Carisoprodol (Soma)
-Muscle relaxant banned in Europe