ST.

LUKE’S COLLEGE OF NURSING

1st Semester
School Year: 2020-2021

GENERAL DISCUSSION SCHEDULE

COURSE CODE : NCM 106

COURSE TITLE : Pharmacology
LESSON NUMBER : 03 – Autonomic Nervous System (ANS) Drugs
TIME ALLOTMENT : 3 Hours
PRESCRIBED FLO : Preferred: e-Learning (E1, E2)
Alternative: Modular (M2)

TOPIC LEARNING OUTCOMES:

After the end of the lesson, the student should be able to:

1. Review the anatomy and physiology of the autonomic nervous system

2. Discuss, distinguish and identify the various nursing responsibilities and patient education on adrenergic and cholinergic drug

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 LESSON/TOPIC DISCUSSION

Learning Resources:
1. E-Textbook
o Pharmacology & the Nursing Process, 8th ed. Lilley, Harrington, Synders
o Pharmacology: A Patient-Centered Nursing Process Approach (L) 9th ed, c2019 by Kee/Hayes
o Pharmacology for Nurses, A Pathophysiological Approach, 4th Edition by Michael Adams
2. eBook
o Focus on Nursing Pharmacology, eBook with thePoint Student Resources by Karch
o Focus on Nursing Pharmacology by Karch
o Lippincott NCLEX-RN Pharmacology Review by Hill
3. Scanned Reference Books
4. Online Resources
5. Mobile Apps and PC Software

LESSON 3 TOPICS:

A. The Autonomic Nervous System (ANS)

B. Adrenergic Agonists
C. Adrenergic Antagonists
D. Cholinergic Agonists
E. Cholinergic Antagonists

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 A. The Autonomic Nervous System (ANS)

• Autonomic Nervous System

o Controls involuntary body functions, glands, and organs
o Cardiac muscles, smooth muscles of blood vessels, eyes, stomach and intestines
• Sympathetic Nervous System
o Adrenergic* System
• Parasympathetic Nervous System
o Cholinergic* System
• Functions of Sympathetic System
o Helps body cope with external stimuli and stress
o Triggers fight-or-flight response
o Works to save energy
o Activates GI system, (aids in digestion)
o Supports restorative body functions
• ANS Neurotransmitters - endogenous chemicals that transmit signals from one neuron (nerve cell) to another "target" neuron, muscle cell, or gland cell.
o Acetylcholine, Norepinephrine
• Acetylcholine
o Released from the axons of the preganglionic neurons in response to stress
o Stimulates postganglionic neurons, causing release of epinephrine and norepinephrine
• Norepinephrine
o Released from postganglionic neurons
o Caused sympathetic stimulation by triggering the release of epinephrine and more norepinephrine
o Produces its effect by combining with adrenergic receptors in effector organs
• Receptors
o Specialized target macromolecule that binds a drug and mediates its pharmacological action.
o Ex. enzymes, nucleic acids, or specialized membrane-bound proteins.
o The formation of the drug-receptor complex leads to a biological response.
• Types of Receptor Drugs
o Agonist
o Antagonist
o Selective
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 o Non-Selective
• Receptor Site – Proteins that are on the surface of each cell that act as receivers of chemical messenger molecules in the intercellular fluid surrounding
every cell.
• Agonists – activate receptors to produce the desired response; drugs that produce a similar response
• Antagonists – prevent receptor activation; drugs that block a response
• Remember! The drug agonist that has an exact fit with a receptor is a strong agonist and is more biologically active
• ANS Drug Pathway
1. Stress triggers ANS
2. ANS releases acetylcholine from preganglionic neuron
3. Acetylcholine triggers release of epinephrine and norepinephrine (as neurotransmitters) from postganglionic neuron
4. Epinephrine and norepinephrine goes to effector organs and activates receptor - creating a drug-receptor complex
5. Drug-receptor complex triggers a biologic response
• Neurotransmitter Inactivation – After neurotransmitters have performed their function, their action must be stopped to prevent prolonged effect.
o Drugs halt termination of neurotransmitter
▪ By inhibiting norepinephrine reuptake
▪ By inhibiting norepinephrine degradation
• Neurotransmitter Inactivation
o Reuptake of transmitter back to the neuron
o Enzymatic transformation or degradation: MAO and COMT
▪ Monoamine oxidase (MAO) inside the neuron
▪ Catechol-O-methyltransferase (COMT) outside the neuron
o Diffusion away from the transmitter
• Remember! Certain drugs halt termination of neurotransmitters (MAO inhibitors)

B. Adrenergic Agonists

• Adrenergic Agonists
o AKA sympathomimetic, catecholamines
o Drugs that stimulate the adrenergic receptors to mimic sympathetic effect
o Stimulation: Alpha Adrenergic Receptors
o Alpha1
▪ ↑ cardiac contractility, vasoconstriction
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 ▪ Dilate pupils, ↓ salivary gland secretion
▪ ↑ bladder and prostate contraction
o Alpha2
▪ ↓ norepinephrine release: ↑ vasodilation
▪ ↓ GI motility and tone
o Stimulation: Beta Adrenergic Receptors
o Beta1
▪ ↑ cardiac contractility, ↑ HR
▪ ↑ renin secretion, ↑BP
o Beta2
▪ ↓ GI tone and motility
▪ Bronchodilation
▪ ↑ blood flow in skeletal muscles
▪ ↓ uterine tone
▪ Activates liver glycogenolysis*: ↑ blood glucose
o Simulation: Dopamine Receptors - Vasodilation

• Indication:
o Bradycardia, heart blocks, and ↓CO
o Acute and chronic asthma
o Acute drug-induced allergic reaction
o Mild renal failure
o Stimulates heart in cardiac arrest
o Acute hypotension and shock
o Heart failure
• Drug interaction:
o +alpha adrenergic blockers = hypotension
o +epinephrine on DM = may need to increase dose
o +other adrenergics = ↑effect
o +trycyclic antidepressants* = hypertension
• Side Effects/Adverse Effects:
o Arrhythmias

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 o Tachycardia
o angina*
o restlessness
o anxiety
o dizziness
o headache
o HPN
o Stroke
o hyperglycemia

Table 3.1: Adrenergic Agonists:

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 Photo from: Pharmacology for Nurses, A Pathophysiological Approach, 4th Edition by Michael Adams

• Contraindication/Precaution:
o C: AMI, tachyarrhymias, pregnancy
o P: DM, artherosclerosis**, Reynaud’s disease***, cardiac insufficiency
• Nsx. Action:

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 o Monitor ECG, VS, and I/O
o Correct hypovolemia prior to administration
o Administer via large-bore needle to prevent extravasation*
o Antidote: Phentolamine (Regitine) and NSS
o Administer with infusion pump
o Monitor sudden hypotension post-administration
o Epinephrine reversal agent: phentolamine

C. Adrenergics Antagonists
• Adrenergics Antagonists
o AKA symphatolytics, adrenergic blockers
o Action: drugs that block effects of neurotransmitters in adrenergic receptor sites
o Directly: by occupying receptors
o Indirectly: by inhibiting release of neurotransmitters epinephrine and norepinephrine
o Depression: Alpha Adrenergic Receptors
▪ Alpha1
• Vasodilation, ↓BP, reflex tachycardia*
• Pupil constriction
• Suppresses ejaculation
• Reduces contraction of smooth muscles in bladder neck and prostate
o Depression: Beta Adrenergic Receptors
▪ Beta1
• ↓Cardiac contractility, ↓BP
• ↓HR
▪ Beta2
• Bronchoconstriction
• Contracts uterus
• Inhibits glycogenolysis
• Indication:
o Alpha Adrenergic Antagonists
▪ PVD, Reynauld’s disease, HPN, adrenergic excess (ex. Pheochromocytoma*)
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 ▪ Vascular headache
o Beta Adrenergic Antagonists
▪ HPN, angina, tachyarrhythmia, open-angle glaucoma*, pheochromocytoma, hypertrophic cardiomyopathy**
▪ Mild to severe heart failure, left ventricular dysfunction after MI
▪ Prevent migraine headache, MI and acute anxiety reaction
• Side Effects/Adverse Reactions:
o Alpha Blockers
▪ Orthostatic hypotension
▪ Vertigo
▪ Palpitation
▪ sexual dysfunction
o Beta Blockers
▪ Bradycardia
▪ Hypotension
▪ Dysrhythmias
▪ Headaches
▪ Dizziness
▪ Fainting
▪ Fatigue
▪ Mental depression
▪ Nausea, vomiting
▪ Diarrhea
▪ Blood dyscrasias
▪ Hypoglycemia

Table 3.2: Adrenergic Antagonists

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 Photo from: Pharmacology for Nurses, A Pathophysiological Approach, 4th Edition by Michael Adams

• Drug Interaction:
o Alpha-Blockers:
▪ +AntiHPN drugs = ↑effect
▪ Prazosin*+diuretics, propranolol, or other beta-blockers = ↑syncope**
o Beta-blockers:
▪ +Digoxin, Ca channel blockers, cimetidine = ↑effect and toxicity
▪ +Antacid, Ca salts, barbiturates, anti-inflammatories, rifampin = ↓effect
▪ Non-selective Beta-blockers may ↓effect of theophylline as bronchodilator

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 ▪ Non-selective Beta-blockers + sympathomimetics = HPN and reflex bradycardia

• Nsx Action:
o Monitor BP for signs of orthostatic hypotension
o When taking ergotamine for vascular headache, client should lie down in a dark, quiet room

D. Cholinergic Agonists

• Cholinergic Agonists
o AKA parasympathomimetics, cholinomimetics, cholinergic stimulants
o Drugs that stimulate cholinergic receptors, mimicking the action of acetylcholine
• Stimulation: Cholinergic Receptors
o Muscarinic receptors - Affect smooth muscles
o Nicotinic receptors - Affect skeletal muscles
o Acetylcholinesterase - Breaks down ACh = acetic acid + choline
• Stimulation: Cholinergic Receptors
o CV:↓HR and BP, vasodilation, slows conduction of AV node
o GI:↑tone and motility, ↑peristalsis, relax sphincter muscles
o GU: Contract bladder, ↑ureter tone, relax sphincter muscles, stimulate urination
o Eyes: pupil constriction, increase accommodation
o Lungs: Bronchial constriction, increase secretions
o Glands: ↑salivation, perspiration, tears
o Striated muscle: ↑neuromuscular transmission
• Indications:
o Glaucoma
o Atonic bladder*
o Post-op and postpartum urine retention
o Abdominal distension and GI atony
o Salivary gland hypofunction

Table 3.3: Cholinergic Agonists

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 Photo from: Pharmacology for Nurses, A Pathophysiological Approach, 4th Edition by Michael Adams

• Side-effects/Adverse Effects:
o HPN
o headache
o sweating
o ↑salivation
o abdominal cramps
o nausea
o vomiting
o diarrhea
o blurred vision
o urinary frequency
o ↓HR
o SOB
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 • Contraindication/Precaution:
o Prostate enlargement
o Urinary / GI obstruction
o Hyperthyroidism
o Bradycardia or AV conduction defects
o Asthma
o CAD

• Drug Interactions:
o +anticholinergic drugs = ↓effect
o +anticholinesterase drugs = ↑effect and risk for toxicity
o +quinidine* =↓effect
• Nsx. Action:
o Monitor I/O
o Assess bowel sounds and abdomen for paralytic ileus*
o Give bethanechol PO and SQ only
o WOF drug toxicity: urinary urgency, excessive secretions, resp. depression or spasm, bradycardia, abd cramping and involuntary defecation
o Antidote: atropine

E. Cholinergic Antagonists

• Cholinergic Antagonists
o AKA parasympatholytics, anticholinergics, cholinergic blockers
o Action: Inhibit action of ACh by occupying ACh receptors
• Action:
o ↓ GI motility, ↓ salivation, mydriasis, ↑HR, urinary retention, decrease rigidity and tremors
o Antidote to organophosphate ingestion or cholinomimetics
• Indication:
o Reverse heart blocks
o Paralyzes ciliary muscles
o Parkinson’s disease, GI spasm, motion sickness, and enuresis
o Symptomatic bradycardia (atropine)
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 o Reduces oral, gastric and respiratory secretions
o Biliary colic*
o Antidote to cholinergic drugs
o Prevents nausea and vomiting from motion sickness (scopolamine)

• Drug Interactions:
o +Trycyclic antidepressants, antidyskinetics, antiemetics, antipsychotics, cyclobenzaprine, or orphenadrine = ↑risk for AE
o Cholinergic agonists / anticholinesterase drugs = ↑effects
o NTG patch ↓effect when taken with anticholinergics
• Side Effects/Adverse Effects:
o Mydriasis
o Photophobia
o blurred vision
o confusion
o dry mouth
o restlessness
o agitation
o dizziness
o N/V
o constipation
o tachycardia
o palpitation
o ↓secretions

Table 3.4: Cholinergic Antagonists

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 Photo from: Pharmacology for Nurses, A Pathophysiological Approach, 4th Edition by Michael Adams

• Contraindications/Precautions:
o C: Angle-closure glaucoma, uncontrolled tachycardia, urinary of GI tract obstructions, COPD, severe ulcerative colitis*, MG, acute or severe
hemorrhage, and unstable CV status
o P: breastfeeding women
• Nsx Action:
o Administer before meals
o Monitor I/O and for adverse reactions
o Measures for dry mouth and constipation
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 Prepared by: Reviewed by: Approved by:

Dr. Tristan Jourdan C. Dela Cruz, RN Dennis Luis D. Abellera, RN MAN Dr. John Michael O. Lorena, RN
Lecturer, Pharmacology Academic Head Dean

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