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1. UNIT IV
CHOLINERGIC & ANTI- CHOLINERGIC
DRUGS
By: Muhammad Aurangzeb
Lecturer-INS/KMU

2. Objectives
By the completion of this section the learners will be able to:
• List characteristics of Cholinergic & Anti-Cholinergic drugs
in terms of effects on body tissues, indications for use,
adverse effects, nursing process implications, principles of
therapy and observations of client‟s responses.
• Discuss antidotes for cholinergic drugs & Anti-Cholinergic
drugs.
• Describe signs and symptoms of cholinergic drugs & Anti-
Cholinergic drug overdose.
• Describe major nursing care needs of clients receiving
these classes of drugs.
• Discuss principles of therapy & nursing process for using
Cholinergic & Anti Cholinergic drugs.

5. Neurotransmitters
• Sympathetic: noradrenaline (norepinephrine)
• Parasympathetic : acetylcholine

7. Overview
• Drugs affecting the autonomic nervous system (ANS) are
divided into two groups according to the type of neuron
involved in their mechanism of action.
• The cholinergic drugs, act on receptors that are activated by
acetylcholine (ACh),
• The adrenergic drugs act on receptors stimulated by
norepinephrine or epinephrine.

8. Cholinergic system
• The cholinergic system is composed of nerve cells
that use the neurotransmitter acetylcholine.
• Acetylcholine esterase enzyme that catalyzes the
breakdown of acetylcholine

9. Acetlyecholinesterases
• ACh is degraded to choline + Acetic acid by
enzyme Acetylcholinesterase (AChE).
• There are two types of AChE:
a. True
b. Pseudo

10. Cholinergic Receptors
• Cholinergic receptors are of two types:
• Muscarinic
• Nicotinic.

11. Cholinergic Receptors
• Muscarinic receptors are of five subtypes, i.e. M1,
M2, M3, M4 and M5
• Nicotinic are of two subtypes, i.e. nicotinic neuronal
(Nn) and nicotinic muscle (Nm)
• M1 receptors are present in → autonomic ganglia,
gastric glands and central nervous system (CNS)
• M 2 receptors are present in → heart, smooth
muscles and nerves

12. Cholinergic Receptors
• M3 receptors are present in → exocrine glands,
smooth muscles and eye
• M4, M5 receptors are present in → CNS
• Nm receptors are present in neuromuscular junction
(NMJ)
• Nn receptors are present in autonomic ganglia,
adrenal medulla and CNS

14. Actions of Ach
Characteristics M1
(neuronal)
Location &
Function
•Ganglia –
impulse
transmissi
on
M2
(cardiac)
• SA node
-Decreased rate
of impulse
generation
•AV node –
decreased
conduction
velocity
•Atrium,
ventricle-
decreased
contractility
M3
(glandular)
•Exocrine
glands-
secretion
•Visceral
smooth Muscle
– contraction

15. Actions of Ach
Characteristics M1
Location &
Function
(neuronal)
•Ganglia,
gastric
cells –
impulse
transmissi
on, HCl
secretion
M2
(cardiac)
• SA node
-Decreased rate
of impulse
generation
•AV node –
decreased
conduction
velocity
•Atrium,
ventricle-
decreased
contractility
M3
(glandular)
•Exocrine
glands-
secretion
•Visceral
smooth Muscle
– contraction

16. Actions of Ach
Characteristics M1
Location &
Function
(neuronal)
•Ganglia,
gastric
cells –
impulse
transmissi
on, HCl
secretion
M2
(cardiac)
• SA node
-Decreased rate
of impulse
generation
•AV node –
decreased
conduction
velocity
•Atrium,
ventricle-
decreased
contractility
M3
(glandular)
•Exocrine
glands-
secretion
•Visceral
smooth Muscle
– contraction

17. Actions of Ach
Characteristics M1
Location &
Function
(neuronal)
•Ganglia,
gastric
cells –
impulse
transmissi
on, HCl
secretion
M2
(cardiac)
• SA node
-Decreased rate
of impulse
generation
•AV node –
decreased
conduction
velocity
•Atrium,
ventricle-
decreased
contractility
M3
(glandular)
•Exocrine
glands (salivary,
sweat)
-secretion
•Visceral
smooth Muscle
(bronchus,
bladder, GIT) –
contraction

18. Actions of Ach
Characteristics NM
(muscle type)
NN
(neuronal type)
Location &
Function
Skeletal
neuromuscular
junction (NMJ) –
contraction
•Autonomic
ganglia– impulse
transmission

20. Acetylcholine
ACh has both muscarinic and nicotinic activity.
Action on cardiovascular system:
• Heart: acetylcholine causes decrease in heart rate and cardiac
output (negative chronotropy) and negative ionotrophy) M2
Receptors
• Blood vessels: acetylcholine causes vasodilation and lowering
of blood pressure. acetylcholine activates M3 receptors found
on endothelial cells lining the smooth muscles of blood
vessels causing vasodilation
• Gastrointestinal (GI) tract: acetylcholine increases salivary
secretion and stimulates intestinal secretions and motility

22. Actions of ACh
• Respiratory system: acetylcholine enhances bronchiolar
secretions and cause bronchoconstriction(M3)
• Urinary system: acetylcholine increases the tone of the
detrusor muscle, causing urination(M3)
• Exocrine Glands: In Sweat, sebaceous and lacrimal glands ach
increase their secretion
Eye:
• Circular muscle of iris (M3)- contraction- miosis
• Ciliary muscle (M3) – contraction- eye’s focus is
accommodated for near vision –
• Better drainage of aqueous humor – reduced intraocular
pressure
• Lacrimal glands (M3)- lacrimation

23. Acetylcholine
No therapeutic use because
I. Ultra short action: rapidly hydrolyzed by
cholinesterases
II. Widespread and nonselective activity: act on all
receptors

24. Cholinergic Drugs
• Act at same site, i.e. ACh.
• Mimic actions of ACh.
• Therefore called ‘Cholinomimetics’ or
‘Parasympathomimetics’.

25. DIRECT ACTING Indirect acting
(irreversible inhibitors
of acetylcholinesterase
Indirect acting (reversible
inhibitors of
acetylcholinesterase)
Acetylcholine Echothiophate Neostigmine
Pilocarpine Physostigmine
Carbachol Pyridostigmine
Bethanechol Galantamine
Classification of cholinergic
drugs( parasympathomimetics)
A parasympathomimetic drug or cholinomimetic drug, is a
substance that stimulates the parasympathetic nervous system.

26. 1). Directly acting
1. Directly acting
• Methacholine, bethanechol, pilocarpine, Carbachol
• Act on muscarinic receptors

27. Therapeutic uses
• Ophthalmic use :
i) Glaucoma
ii) To counteract the effects of mydriatics
iii)To break adhesions between the iris and lens or iris
and cornea

28. Therapeutic uses
• Carbachol/Bethanechol resistant to metabolism by both cholinesterases,
hence long duration of action.
1. Carbachol—it has both muscarinic and nicotinic actions used in glaucoma.
2. Bethanechol: it has only muscarinic activity. It is used in post operative
urinary retention and paralytic ileus: Bethanechol has more pronounced
effects on smooth muscles
3. Pilocarpine is an example of a nonselective muscarinic agonist used in
clinical practice to treat xerostomia and glaucoma.
4. Neostigmine: it is used to improve muscle strength in patients with a
certain muscle disease (myasthenia gravis).
5. Physostigmine has FDA approval for use in the treatment of glaucoma and
the treatment of anticholinergic toxicity. In case of Belladona (Atropine)
poisoning Physostigmine is specific antidote

29. Adverse Reactions of Cholinomimetics
(Mnemonic SLUDGE’)
• S: Salivation
• L: Lacrimation
• U: Urination
• D: Diarrhea
• G: GI/GU cramps
• E: Emesis/Eye (miosis).

30. 2. Indirectly acting (Anticholinesterases)
A. Reversible :
• Physostigmine,
• neostigmine,
• pyridostigmine,
• edrophonium,
• Galantamine
B. Irreversible:
• Echothiophate
• Organophosphates: Parathion, Malathion

31. Mechanism of action of Anticholinesterases
Inhibit acetylcholinesterase (AChE) enzyme
Ach ----------- Choline + acetate AChE
_
_
Neostigmine
Accumulation of Ach: enhances its Action

32. Irreversible AChE inhibitors
• Mainly used as insecticides and pesticides
• Irreversible AntiChE i.e. Echothiophate eye drops for
glaucoma

33. Irreversible Anti-ChE (Organophosphorus
Compounds)
• Organophosphorus, compounds.
• They are powerful, irreversible inhibitors of AChE.
• Binding is covalent, Hence, binding is stable and irreversible.
• All OP compounds (except echothiophate) are highly lipid
soluble.
• Hence, can be absorbed from all routes, including intact skin.
• Thus, OP poisoning can also occur by spraying of agricultural
pesticides/insecticides.

34. Organophosphorus Poisoning
• OP compounds are used as agricultural insecticides/ pesticides. Hence, poisoning
is frequent.
• Signs/Symptoms:
a. Similar to cholinergic (muscarinic, nicotinic, CNS) hyperactivity.
b. For example, SLUDGE
c. Sweating, increased tracheobronchial secretions, increased GI secretions,
bronchospasm, hypotension, convulsions and coma.
d. Respiratory paralysis can cause death.
• Treatment:
a. Poisoning via skin:
i. Remove clothing.
ii. Wash skin with soap and water.
b. Poisoning via oral route.
i. Gastric lavage.
c. Maintain BP and airway patency.
d. Atropine IV 2 mg every 10 minutes. Till pupil dilates/ dryness of mouth (drug of
choice).

35. Cont..
• Reactivation of acetylcholinesterase
• Pralidoxime can reactivate inhibited AChE. However,
it is unable to penetrate into the CNS and therefore is
not useful in treating the CNS effects of
organophosphates.

36. Adverse effects of anticholinesterases
• Diarrhea, urination, bronchoconstriction,
lacrimation, salivation, sweating, bradycardia,
fasciculation of skeletal muscle
• Organophosphorus poisoning: treated with an
anticholinergic, atropine

37. Anticholinergics
• Also called antimuscarinics, parasympatholytics or
cholinergic blocking drugs.
• They block the effects of ACh on muscarinic
receptors.
• Drugs that block nicotinic receptors are ganglionic
blockers or neuromuscular blockers.

38. Cholinergic Antagonists
Those drugs which antagonize the effect of acetylcholine.
 Atropine
 Scopolamine(hyoscine)
 Ipratropium bromide (atem inahalor)
 Tropicamide
 Glycopyrolate
 Propantheline
 Pirenzepine (M1 selective antagonist)
 Clidinium (M1 selective antagonist)(Librax)
 Dicyclomine
 Oxybutynin (Ditropan)
atropa belladona

39. Mechanism of Action
• Anticholinergic drugs combine reversibly with
muscarinic cholinergic receptors thus
preventing access of neurotransmitter
acetylcholine.

40. Classification
Natural alkaloids :
•Atropine* (prototype), Scopolamine
(Hyoscine)
Semisynthetic derivatives :
• Homatropine*, ipratropium bromide,
tiotropium bromide
Synthetic compounds :
i) Mydriatics – Cyclopentolate*, tropicamide
ii) Antiparkinsonian – Benzhexol, Biperiden,
Benztropine

41. Cont…
iii) Antisecretory- antispasmodics – Dicyclomine
Pirenzepine Glycopyrrolate
• Semisynthetic and synthetic anticholinergics
- Atropine substitutes

42. Atropine
• Eye: Atropine blocks muscarinic activity in the eye, resulting in mydriasis
(dilation of the pupil)
• Atropine use as antidote for organic phosphate poisoining.
• Gastrointestinal (GI): Atropine reduce activity of the GI tract. can be used
as an antispasmodic.
• Secretions: Atropine blocks muscarinic receptors in the salivary glands,
producing dryness of the mouth (xerostomia). The salivary glands are
exquisitely sensitive to atropine. Sweat and lacrimal glands are similarly
affected.
• Cardiovascular: Atropine produces diverse effects on the cardiovascular
system, depending on the dose At low doses, atropine causes decrease
in heart rate. Higher doses of atropine cause a progressive increase in
heart rate by blocking the M2 receptors on the sinoatrial node.

43. Cont…
• Respiratory system : Bronchodilatation Decreased secretions
• CNS: Atropine has CNS stimulant action at high dose. High
doses cause cortical excitation, restlessness, disorientation,
hallucination & delirium followed by respiratory depression &
coma. It suppresses tremor & rigidity of parkinsonism.
• Smooth muscles: All visceral smooth muscles that receive
parasympathetic motor innervation are relaxed by atropine
due to M3 blockade
• Glands: Atropine decreases sweat, salivary, bronchial &
lacrimal secretions by M3 blockade
• Body temperature : - Rise in body temperature occur at high
doses due to both inhibition of sweating as well as stimulation
of temperature regulating centre in the hypothalamus

44. Cont…
Genitourinary tract :
• Relaxation of ureter and urinary bladder – urinary
retention
Glands :
• Decreases sweat, salivary, tracheobronchial and
lacrimal secretion

45. Uses ofatropine
• Preanaesthetic medication: to decrease secretion
• Oraganophosphorous poisoning

46. Therapeutic uses of anticholinergics
• Pre-anesthetic medication : reduces excessive
salivation(Sialorrhea ) & respiratory secretions. (glycopyrrolate
and scopolamine)
• Peptic ulcer : decreases gastric secretions (clidinium)& provide
symptomatic relief in peptic ulcer now been superseded by H2
blockers & PPIs.
• As anti-spasmodic: intestinal & renal colic, abdominal cramps
• To relive urinary frequency & urgency or involuntary
urination (enuresis)(Oxybutynin, Propantheline)
• Bronchial Asthma (ipratropium)
• As mydiatric & cycloplegic.
• As cardiac vagolytic
• Organophosphates Poisoning and mushroom poisoning.
• Antidote for cholinergic agonists: Atropine is used for the
treatment of organophosphate (insecticides, nerve gases)
• Treatment of excessive sweating (hyperhidrosis)

47. Therapeutic uses
• Motion sickness : Scopolamine
• Parkinson’s disease :benzhexol, benztropine etc.
• Bronchial asthma: ipratropium and tiotropium
bromide
• Preanaesthetic medication : glycopyrrolate ,
• As mydriatic during fundoscopy and testing of
refractive error – Tropicamide, cyclopentolate

48. Side effects
• Belladona poisoning
– Dry mouth, difficulty in swallowing and talking.
– Dry flushed and hot skin.
– Dilated pupil
– Fever,
– Difficulty in micturition,
– Excitement, ataxia, delirium, hallucination.
– Convulsion and coma may occur in severe poisoning.
• Treatment of 3Ds : Physostigmine 15- 60 micro gram / kg IV
every 1- 2 hourly.
cycloplegia : paralysis of the ciliary muscle of the eye.

49. Side effects of atropine :
• Dry mouth
• Blurred vision and photophobia
• Urinary retention
• Constipation
• Dry, hot skin
• Precipitation of glaucoma
• Decreased sweating

50. Nursing Consideration
• Assess for contraindications or cautions (e.g., history of allergy to drug, GI
obstruction, hepato-renal dysfunction, etc.) to avoid adverse effects.
• Establish baseline physical assessment to monitor for any potential
adverse effects.
• Assess neurological status (e.g., orientation, affect, reflexes) to evaluate
any CNS effects.
• Assess abdomen (e.g., bowel sounds, bowel and bladder patterns, urinary
output) to evaluate for GI and GU adverse effects.
• Ensure proper administration of the drug to ensure effective use and
decrease the risk of adverse effects.
• Provide comfort measures (e.g., sugarless lozenges, lighting control, small
and frequent meals) to help patient cope with drug effects.
• Provide patient education about drug effects and warning signs to report
to enhance knowledge about drug therapy and promote compliance.

51. References
• Karch, A. M., & Karch. (2011). Focus on nursing pharmacology.
Wolters Kluwer Health/Lippincott Williams & Wilkins. [Link]
• Katzung, B. G. (2017). Basic and clinical pharmacology.
McGraw-Hill Education.
• Lehne, R. A., Moore, L. A., Crosby, L. J., & Hamilton, D. B.
(2004). Pharmacology for nursing care.
• Smeltzer, S. C., & Bare, B. G. (1992). Brunner & Suddarth’s
textbook of medical-surgical nursing. Philadelphia: JB
Lippincott