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Cholinergics.docx

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Department
Nursing
Course
NURS 2050
Professor
Cynthia Barkhouse Mckeen
Semester
Fall

Description
CHOLINERGICS: (AUTONOMICS II) ** Acts on Parasympathetic and Sweating Drugs: 1. Direct acting •agonists •antagonists 2. Indirect acting •Cholinesterase inhibitors Muscarinic Agonists: CI for ppl with Asthma Therapeutic Uses: 1. Urinary Retention (relaxes most muscles/ increases voiding pressure by contracting one of the muscles in the bladder wall) 2. Xerostomia (dry mouth, by increasing salivation) 3. Connective tissue disease (like RA) 4. Increases tear production 5. Glaucoma 6. Miosis (pupil constriction) Muscarinic Antagonists Atropine- Muscarinic antagonist- blocks the action of acetylcholine @ muscarinic receptors (competitive) ∆ Para + sweat blocker  Parasympatholytic o Antimuscarinic- blocks at muscarinic o Anticholinergic – blocks ACh  At therapeutic doses it will be selective for muscarinic receptors o Higher doses will produce blockade at nicotinic receptors too Muscarinic Agonist Muscarinic Antagonist - Atropine Heart ↓ HR Heart ↑ HR Exocrine Glands ↑ Secretion (salivary, Exocrine Glands ↓ Secretion bronchial, sweat, stomach) Smooth muscles Constriction of bronchi Smooth muscles Relaxation of bronchi ↑ Tone of urinary muscle ↓ Tone of urinary muscle ↑ Tone/Motility of GI ↓ Tone/Motility of GI Eye Miosis (contraction of pupEye Mydraiasis (dilation of pupil) Contraction of ciliary Cycloplegia (relaxation of muscle—near vision) ciliary muscle—far vision) CNS CNS Excitation high doses- delirium/coma Therapeutic Uses (atropine) 1. Preanesthetic medication 2. Eye disorders 3. Bradycardia 4. Intestinal Hypertonicity/ Hypermotility 5. Muscarinic Agonist poisoning 6. Peptic ulcer disease 7. Athma Adverse Effects (atropine)  Dry Mouth  Blurred Vision Physostigmine & Neostigmine – reversible cholinesterase inhibitors  Urinary Retention  Constipation  Tachycardia  Anhidrosis (lack of sweat)  Lung (promotes bronchial dilation) Cholinesterase inhibitors - indirect acting cholinergic agonists  Prevent ACh breakdown by inhibiting acetylcholinersterases (or cholinesterase)  Can have effects at ALL cholinergic junctions- ―nonselective‖ as it can inhibit all enzymes  Two basic categories of cholinesterase inhibitors  Reversible – moderate duration  Irreversible – prolonged effects – a source of poisoning Neuromuscular Blocking (NMB) Agents: 1. Prevent ACH from activating nicotinic m receptors on skeletal muscles Mechanism of Action of NMBs 1. Nondepolarizing neuromuscular blocker (bind competitively) • Turbocurarine, Pancuronium (Pavulon®),Rocuronium (Zemuron®), Vecuronium (Norcuron®) 2. Depolarizing neuromuscular blocker (used in the ICU for incubation, surgery) – mimic ACh at NMJ • Succinylcholine (sole ultra-short acting agent) Depolarizing Agent – Succinylcholine (mimics ACH) TQ example in class: - 14 year old in emerg, ate magic mushrooms (from a species with muscarine) - Excessive tearing, salivation, diarrhea, difficulty breathing, dizzy - BP= 80/40 - EKG= sinus bradycardia (rate ~50 beats per minute, too slow) - They use atropine to increase HR (because that manages bradycardia) ∆ mushrooms activate a muscarine receptor. Muscarinic receptors cause PARA + sweating activation ∆ Atropine a muscarinic antagonist helps manage symptoms After giving the medication he has: Head/neck Mydrasis Cycloplegia (blurred vision) Xerostomia (dry mouth) CVS Increased HR Lung Relaxtion of bronchi GI Decrease in diarrhea GU Decreased urine output MSK/ Skin Skin is dry to touch They gave too much Atropine So they give Physostigmine which is a Reversible Cholinesterase Inhibitor, which prevents the Ach breakdown. ADRENERGICS (AUTONOMICS III) Acts on Sympathetic Adrenergic Receptors: mediated by NE, E 1. Alpha 1 and Alpha 2 (on eyes, blood vessels, penis, prostatic capsule, bladder) - Alpha 1: (on eyes, blood vessels, penis, prostatic capsule, bladder) - Vasoconstriction - ejaculation - contraction of the bladder, neck & prostate - Alpha 2: (less clinical significance) (located on nerve terminals, but not ANS) - located in the pre-synaptic junction, regulate transmitter release 2. Beta 1 and Beta 2 Beta 1: - Heart: increases HR, force of contraction, velocity of conduction in AV node - Kidney: Renin release (end effect- increase in BP) Beta 2: (has the most impact) - Lungs: Broncial dilation - Uterus: Relaxation of uterine muscles - Blood vessels: Vasodilation - Liver + Skeletal: Glycogenolysis (leads to hyperglycemia) 3. Dopamine: dilates renal blood vessel, ↑ renal perfusion Drug Actions: ***Direct Receptor Binding (most common) 1. Adrenergic Agonists (affects receptor binding directly) 2. Adrenergic Antagonists (affects receptor binding directly) 3. Indirect-acting Agents (affects re-up take, releases & inactivation of neurotransmitters) Indirect ways: (ex. NE) 1. Promotes release- can have effects in the periphery which explains side effects. E.g. cardiac, HTN 2. Blocks reuptake o Net Effect – High NE in the Cleft o Reuptake – major mechanism of terminating adrenergic transmission (ex. Tricyclic antidepressants) 3. Inhibits inactivation o Monoamine oxidase inhibitors (MAO is in adrenergic neurons, liver, intestinal wall Adrenergic Agonists: Catecholamines & Non-Catecholamines - Receptors and agents – differ in select
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