Ner voussys drugs

Cholinergic Drugs

Cholinergic Drugs

Describe the cholinergic drug effects on major body systems.

Discuss the nursing process related to the care of patients receiving cholinergic drugs for select problems.

Cholinergic Drugs Drugs that stimulate the

parasympathetic nervous system (PSNS) opposing system to the SNS Known as: cholinergic agonists or

parasympathomimetics Mimic the effects of the PSNS neurotransmitter:

acetylcholine (Ach) Two types of Receptors:

determined by: Location & Action once stimulated Muscarinic receptors – recommended doses with

desired effect Nicotinic receptors – higher doses with undesirable

effects

Cholinergic DrugsMechanism of Action

Direct-acting cholinergic agonists Bind to cholinergic receptors, activating them

Indirect-acting cholinergic agonists Inhibit the enzyme acetylcholinesterase -

preventing, which breaks down ACh - more ACh is available at the receptors

Reversible - Bind to cholinesterase for a period of minutes to hours

Irreversible - Bind to cholinesterase and form a permanent covalent bond The body must make new cholinesterase to

break these bonds

Cholinergic Drugs“rest and digest” system

“SLUDGE”

Salivation Lacrimation Urinary incontinence Diarrhea Gastrointestinal cramps Emesis

Cholinergic DrugsDrug Effects

Stimulate intestine and bladder Increased gastric secretions Increased gastrointestinal motility Increased urinary frequency

Stimulate pupils Constriction (miosis) Reduced intraocular pressure

Increased salivation and sweating Cardiovascular effects

Decreased heart rate Vasodilation

Respiratory effects Bronchial constriction, narrowed airways

Cholinergic DrugsDrugs

Bethanechol (Urecholine) – urinary retention

Cevimeline (Evoxac) – Xerostomia Memantine (Namenda) – Alzheimer’s

dementia Physostigmine (Antilirium) – reversal

of anticholinergic drugs effects Pyridostigmine (Mestinon) –

Myasthenia gravis

Cholinergic DrugsIndications

Direct-acting drugs Reduce intraocular pressure

Topical useful for glaucoma and intraocular surgery pilocarpine


Direct-acting drug—bethanechol (Urecholine)

Increases tone and motility of bladder and GI tract

Relaxes sphincters in bladder and GI tract, allowing them to empty

Used to reverse postsurgical atony of the bladder and GI tract

Oral dose or SC injection


Indirect-acting drugs

Cause skeletal muscle contractions

Used for diagnosis and treatment of myasthenia gravis Pyridostigmine (Mestinon) – Myasthenia gravis

Used to reverse neuromuscular blocking drugs/anesthesia

Used to reverse anticholinergic poisoning (antidote) Examples: physostigmine (Antilirium)


Indirect-acting drugs—cevimeline (Evoxac)

Used to treat xerostomia (dry mouth) resulting from Sjögren’s syndrome

Cholinergic DrugsAdverse Effects

Adverse effects are a result of overstimulation of the PSNS

Cardiovascular Bradycardia, hypotension, conduction abnormalities (AV

block and cardiac arrest) CNS

Headache, dizziness, convulsions Gastrointestinal

Abdominal cramps, increased secretions, nausea, vomiting Respiratory

Increased bronchial secretions, bronchospasm Other

Lacrimation, sweating, salivation, loss of binocular accommodation, miosis

Cholinergic DrugsInteractions

Anticholinergics, antihistamines, sympathomimetics Antagonize cholinergic drugs, resulting

in decreased responses Other cholinergic drugs

Additive effects

Cholinergic DrugsNursing Implications

Assess for allergies, presence of GI or GU obstructions, asthma, peptic ulcer disease, or coronary artery disease

Perform baseline assessment of vital signs and systems overview

Medications should be taken as ordered and not abruptly stopped

The doses should be spread evenly apart to optimize the effects of the medication

Overdosing can cause life-threatening problems. Only physicians should adjust the dosages


Encourage patients with myasthenia gravis to take medication 30 minutes before eating to help improve chewing and swallowing

When cholinergic drugs are prescribed for Alzheimer’s disease, be honest with caregivers and patients that the drugs are for management of symptoms, not a cure

Therapeutic effects of anti-Alzheimer’s drugs may not occur for up to 6 weeks


Monitor for therapeutic effects Alleviated signs and symptoms of myasthenia

gravis In postoperative patients with decreased GI

peristalsis, look for: Increased bowel sounds Passage of flatus Occurrence of bowel movements

In patients with urinary retention/hypotonic bladder, urination should occur within 60 minutes of bethanechol administration

ALSO monitor for adverse effects

Drugs Affecting the Parasympathetic Nervous System

Parasympathetic Nervous System

Neurotransmitter is ACH

The receptors are called cholinergic receptors.

Drugs that bind to cholinergic receptors and produced effects similar to ACH are referred to as cholinergic drugs.


ACHACH

ACH

ACH

ACH

ACH ACH

ACH

ACH

ACH

ACH

ACH

ACH

ACH

Acetylcholinesterase


Nicotinic ReceptorsMuscarinic Receptors

Receptors

N-1 N-2


Nicotinic Receptors

Nicotinic-II Receptors

Found at ganglions of Sympathetic and Parasympathetic Post- ganglionic fibers

Found at Neuromuscular junction ofSkeletal muscles.

Nicotinic-I Receptors

Parasympathetic Fibers

Post-ganglionic Fiber

Sympathetic Fibers

Pre-ganglionic Fiber

Pre-ganglionic Fiber

Post-ganglionic FiberAdrenergic Receptor

Muscarinic Receptors


Nicotinic II Receptors

Ganglion, Nicotinic I receptor

Ganglion, Nicotinic I receptor

Somatic Fibers


Nicotine

Alkaloid obtained from tobacco.

Stimulate the NI receptors at low doses.

Block the NII receptors at high doses.

Drugs Affecting the Parasympathetic

Nervous System

GanglionicBlockers

GanglionicStimulants

Nicotinic I Drugs


Muscarinic Receptors

Found at the parasympathetic postganglionic nerve endings

Drugs that act like ACH at these receptors are referred to as cholinergic or muscarinic drugs.

Drugs that block ACH at the muscarinic receptors are referred to as anticholinergic or antimuscarinic drugs.


Anti-cholinergicDrugs

CholinergicDrugs

ParasympatheticDrugs


Direct ActingCholinergic Drugs

CholinergicDrugs

Indirect ActingCholinergic Drugs


Direct Acting Cholinergic Drugs

Bind to muscarinic receptors.

Produces ACH like effect.

Slowly inactivated by acetylcholinesterase.


Pharmocological Effects

Increase GI secretion and motility

Increase in genitourinary activity.

Bronchoconstriction


Pharmocological Effects

Miosis

Vasodilatation (lower BP)

Decrease heart rate.

Direct Acting Main Use

Acetylcholine Miotic

Bethanecol Nonobstructive urinary retention

Carbachol Treatment of glaucoma

Methacholine Miotic

Pilocarpine Treatment of glaucoma



IrreversibleInhibitors

ReversibleInhibitors

Indirect ActingCholinergic Drugs

(Anticholinesterases)


ACHACH

ACH

ACH

ACH

ACHACH

ACH

ACH

ACH

ACH

ACH

ACH

ACH

Acetylcholinesterase

Anticholinesterases


Reversible Inhibitors

Blocks cholinergic and nicotinic receptors.

Use in the diagnosis and treatment of myasthenia gravis.


Irreversible Inhibitors

Derivatives of organophosphate compounds.

Widely used as insecticides, pesticides and chemical warfare agents.

Long duration of action


Clinical Use

Topical use in glaucoma

Treatment of myasthenia gravis

Treatment of urinary retention and intestinal stasis


Clinical Use

Treatment of Alzheimer’s disease.

Antidote to skeletal muscle blockers.

Antidotes to anticholinergic drug poisoning.


Indirect-ActingCholinergic Drug

Reversible

AmbenoniumEdrophoniumNeostigmine

PhysostigminePyridostigmine

Irreversible

Isoflurophate


Adverse and Toxic Effect

Nausea

Vomiting

Diarrhea

Blurred vision



Excessive sweating

Muscular tremors

Bronchoconstriction

Bradycardia



Hypotension

Mucular paralysis

Respiratory arrest


Cholinergic Crisis

Excessive drug dosage in patients with myasthenia gravis.

High concentration of ACH causes excessive stimulation of the muscarinic receptors.

High concentration of ACH causes blockade of nicotinic receptor.


Treatment

Stop anticholinesterase drug administration.

Give atropine to block the effect of excess muscarinic stimulation


Cholinergic Crisis

Excessive exposure to sprays containing derivatives of irreversible anticholinesterase.

High concentration of ACH causes excessive stimulation of the muscarinic receptors.

High concentration of ACH causes blockade of nicotinic receptor.


Treatment

Remove person from the exposure.

Give Pralidoxime to reactivate the anticholinesterase enzyme.

Give atropine to block the effect of excess muscarinic stimulation


Anticholinergic Drugs

Binds to muscarinic receptors.

Act by competitive antagonism of ACH.

Prototype drugs: Belladonna alkaloids, atropine and scopolamine


Pharmacological Action

Increase heart rate.

Increase the secretions of the respiratory tract and may cause bronchoconstriction.

Reduce salivary and GI tract.

Inhibit urinary peristalsis and voiding of urine.


Pharmacological Action

Depressant effects on the CNS causing drowsiness and sedation.

At high doses cause both stimulation and depression of the CNS

At toxic doses excitation, delirium, hallucination and profound CNS depression leading to respiratory arrest and death.


Ocular Effect

Mydriasis

Cycloplegia

Increases Intraocular pressure.



Cause by excessive blockage of the Parasympathetic Nervous System.

Dry mouth.

Visual disturbances

Urinary retention

Constipation.



Dryness of the skin

Flushing

Hyperpyrexia

CNS stimulation and depression


Anticholinergic Drugs

Belladonna Alkaloids

AtropineScopolamineHyoscyamine

Semisynthetic Drug

Homatropine

Synthetic Drugs

DiclyclomineIsopropamidePropanthelineMethantheline

Drugs Affecting the Sympathetic Nervous System

NE

NE

NE

NE

NE NE

Involuntary MuscleMembrane

Adrenergic nerve ending

Release

Metabolism Reuptake

MAO

Adrenergic Receptor


AlphaReceptors

Beta 2 Receptors

Beta 1Receptors

Adrenergic Receptors

BetaReceptors


Alpha-adrenergic Receptors

Found predominantly on smooth muscle membrane.

When stimulated by NE or EPI produce contraction.

Produces vasoconstriction of most blood vessels.


Beta-adrenergic Receptors

Found on both cardiac and some smooth muscle membranes.

In the heart, beta 1 receptors predominates.

When stimulated by NE or EPI, they increase heart rate and force of contraction.



Found on smooth muscle in the bronchus and smooth muscles of blood vessels supplying muscle and the heart.

Stimulated with EPI result in relaxation.



In smooth muscle, beta 2 receptors predominates.

When stimulated by EPI, they produces muscle relaxation.

Found in smooth muscles of blood vessels supplying skeletal muscle and the coronary arteries.

Found on smooth muscle in the bronchial tree.


Beta 1Receptors

Found on smooth muscle in the heart

Increase heart rate and force of contraction.


Beta 2 Receptors

Found on smooth muscleof blood vessels supplyingskeletal muscle and the heart.

Found on smoothmuscle in the bronchial tree.

Vasodilatation. Bronchodilation.


SympatholyticDrugs

SympathomimeticDrugs

SympatheticDrugs


SympathomimeticDrugs

Alpha-adrenergic Beta- adrenergic

Selective Beta 1Adrenergic.

Selective Beta 2Adrenergic.


Alpha-adrenergic Drugs

NE prototype

Most important clinical effect is contraction of smooth muscles.

Vasoconstriction of most blood vessels leading to increase in blood pressure.

Contraction of sphincter muscles.


Contraction of Sphincter Muscles

GI tract Urinary Tract Eyes

Inhibits movement ofintestinal contents

Restricts passage of urine.

Mydriasis


Alpha-adrenergic Drugs

Clinical Indications

Hypotensive states

Decongestion

Pupillary dilation


Adverse Effects

Hypertensive crisis

Cerebral hemorrhage

Cardiac arrhythmias

Irritation of the nasal sinuses or eye.


Drug Main Use

Epinephrine To increase BP

Norepinephrine To increase BP

Pseudoephedrine Nasal decongestion

Tetrahydrozoline Ophthalmic decongestion


Beta-adrenergic Drugs

Stimulation of the heart

Bronchodilation

Relaxes uterine smooth muscle


Drugs Classification Main Use

Epinephrine Alpha, Beta-1 and Beta-2

Vasopressor, Cardiac stimulant, bronchodilator.

Isoproterenol Beta-1 and Beta-2

Cardiac stimulant, bronchodilator.

Albuterol Beta-2 Bronchodilator.

Ritodrine Beta-2 Arrest preterm labor.


Epinephrine

DOC for allergic reactions

Use in combination with local anesthetics.

Used as a cardiac stimulant in emergencies.

Use in the treatment of asthma.


Adverse Effects

CNS stimulation – tremor, restlessness, anxiety (beta effect)

Over-stimulation of the heart (beta 1 effect)

Lower blood pressure (beta 2 effect)


Dopamine

Neurotransmitter in the brain.

Precursor in the synthesis of NE

Stimulates dopaminergic, beta-1 and alpha-receptors.

Use as a drug.

Dobutamine similar to dopamine but with more Beta-1 effect.


NE

NE

NE

NE

Tyrosine

NE

DopamineDOPA

MAO


DOPAMINE DOSE

RECEPTORS

STIMULATED

EFFECTS

Low dose Stimulate dopaminergic receptors in the renal and mesenteric blood vessels.

Increased renal blood flow and vasodilatation.

Moderate dose Stimulates beta-1 receptors in the heart.

Increase myocardial contractility.

Higher dose Stimulate alpha-receptors Produces vasoconstriction.


Alpha-adrenergic blocking drugs

Binds to Alpha receptors

Antagonizes the effects of NE and EPI

Leads to a decrease in sympathetic response

Resulting in vasodilatation and thus decrease in BP.


Alpha-adrenergic blocking drugs.

Clinical Indications

Treatment of hypertension.

Vasodilator in treatment of Raynaud’s disease.

Diagnosis of Pheochromocytoma.


Alpha-adrenergic blocking drugs.

Adverse Effects

Constriction of pupils

Increased GI activity

Nasal congestion

Reflex tachycardia ( if BP is lowered too much).


Drugs Main Use

Doxazosin Treatment of Hypertension

Prazosin Treatment of Hypertension

Phentolamine Diagnosis of pheochromocytoma.

Treatment of vascular disease.


Beta-adrenergic blocking drugs.

Binds to beta receptors

Antagonizes the effects of NE and EPI

Leads to a decrease in sympathetic response.

Resulting in decrease heart rate and force of contraction.


Selective Beta-1Non-selective

Beta-blockingDrugs


Nonselective Blockers Main Use

Labetalol Hypertension

Nadolol Hypertension, Angina Pectoris

Pindolol Hypertension

Propanolol Hypertension, Angina Pectoris, arrhythmhias, migraine

Timolol Hypertension, post myocardial infarction.


Selective Blockers Main Use

Acebutolol Hypertension, ventricular arrhythmias.

Atenolol Hypertension, Angina Pectoris

Bisoprolol Hypertension

Esmolol Supraventricular tachycardia

Metoprolol Hypertension, Angina Pectoris


Propranolol

Decrease heart rate

Decrease force of contraction

Decrease rate of conduction

Resulting decrease in effort and work of the heart causes a decrease in oxygen consumption.

Drugs Affecting the Sympathetic Nervous System Oral and iv preparation

Drug is carried directly to the liver by the portal system.

Significant first pass metabolism.

Lipid soluble and passes into the brain.

Causes CNS sedation, depression and decreased central sympathetic activity.


Used in the treatment of angina, and various cardiac arrhythmia.

Adverse effects include nausea, vomiting and diarrhea, bradycardia with resulting reduced cardiac function, bronchoconstriction.

Most serious drug interactions involve therapy of beta blockers with other drugs that decrease cardiac function (cardiac glycosides, anti-arrhythmic drugs and calcium blockers).


Adrenergic neuronal blockers

Drugs that interfere with the formation and or storage of NE

Alpha-methyl dopa

Reserpine

Guanethidine


NE

NE

NE

NE

Tyrosine

NE

DopamineDOPA

Alpha-methyl dopa

MAO

Reserpine

Guanethidine


Drugs Mechanism of Action Main Use

Alpha-methyl dopa Blocks formation of Dopamine

Treatment of hypertension

Reserpine Depletes NE storage granule


Guanethidine Block release of NE and depletes NE storage granule


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