AUTONOMIC NERVOUS SYSTEM & THE AUTONOMIC DRUGS

the CNS thru the the CNS thru the intestine

NERVOUS SYSTEM thoracic and cranio and sacral
lumbar region of area of the spinal
the spinal cord cord → ganglia
→ ganglia
Sympathetic Parasympathetic
postganglionic postganglionic
neurons – neurons –
Extends from the extends from the
ganglia → ganglia →
effector organ effector organs
fight or flight Rest & digest
response – response -
response to maintain
stressful homeostasis e.g.
situations e.g. digestive process
exercise and elimination
of waste.

Characteristics of SNS & PNS

2 anatomical division of the nervous system SNS PNS
1. CENTRAL NERVOUS SYSTEM Site of origin Thoracic and Brain and sacral
a. Brain lumbar region of area of the spinal
b. Spinal cord the spinal cord cord
2. PERIPHERAL NERVOUS SYSTEM Length of S- preganglionic L-preganglionic
a. Neurons outside the brain and spinal cord fibers L- postganglionic S-postganglionic
Location of Close to spinal Within or near the
2 Subdivisions of the Peripheral Nervous System ganglia cord effector organ
a. AFFERENT division – neurons that bring Preganglionic Extensive Minimal
information from the periphery TOWARDS the fiber
brain and spinal cord. branching
b. EFFERENT division – neurons that carry Distribution Wide Limited
signals AWAY from the brain and the spinal Type of Diffuse Discrete
cord. response
2 subdivisions of the efferent portion of the PNS
a. Somatic efferent neurons – involved in Actions of the SNS & PNS on effector organs
VOLUNTARY functions Effector organ SNS PNS
- Consists of single neuron that connects the Eye
CNS to the skeletal muscle fiber. -iris sphincter - dilation - constriction
- Response is faster than the ANS -ciliary muscle -relaxation - contraction
- Innervates skeletal muscles Trachea and Dilation Constriction, ↑
b. Autonomic efferent neurons – involved in bronchioles secretions
INVOLUNTARY functions Lacrimal glands No effect Stimulation of
- Consists of 2 neurons tears
- Innervates the organs Salivary gland Thick viscous Copious watery
secretion secretions
2 types of efferent neurons that carries nerve impulses Heart ↑HR, ↑CO ↓HR, ↓CO
from the CNS → effector organ Kidney Renin secretion no effect
a. Preganglionic neurons GIT ↓ GI motility and ↑ GI motility and
- CB originate in the CNS tone tone
- Emerge from the brainstem or spinal cord →
ganglia Ureter & bladder R-detrusor C- detrusor
Ganglia C-trigone R- trigone &
- Serve as relay station between the &sphincter sphincter
preganglionic neuron and postganglionic Female Genitalia Uterus
neuron Relaxation
b. Postganglionic neurons
Male Genitalia Ejaculation Erection
- CB originate in the ganglia
Blood vessels Constriction No effect
- Emerge from the ganglia → effector organs
(skin mucous
membrane)
3 subdivision of the efferent ANS
Blood vessels Dilation No effect
SNS PNS ENS
(muscle)
(Thoracolumbar (Craniosacral
Liver Glycogenolysis No effect
division) division)
Gluconeogenesis
Sympathetic Parasympathetic Neurons can be
Adrenal medulla Secretion of No effect
preganglionic preganglionic found in the
epinephrine
neurons – leaves neurons – leaves wall of the
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 AUTONOMIC NERVOUS SYSTEM & THE AUTONOMIC DRUGS
&norepinephrine
SYMPATHETIC/ADRENERGIC

NEUROTRANSMITTER • THE “FIGHT OR FLIGHT” RESPONSE

• There is no structural continuity exist between o Dec. Pulmonary secretion
neurons o Bronchodilation
• Communication between nerve cells and between o Inc. Heart rate & Contractility
nerve cells and effector organs occurs through the o Arteriolar constriction
release of specific chemical signals called o Glycogen & lipids breakdown and glucose is
NEUROTRANSMITTERS released by the nerve synthesized for energy
terminal o Dec. Gastrointestinal secretions & motility
• NTs are hydrophilic in nature → they cannot easily o Urine retention
penetrate the lipid bilayer of target-cell plasma • NT – NE
membranes. • Receptor – adrenergic receptors; adrenoceptors
• NTs convey their signal by binding to specific
receptors on the cell surface of the target organs SYMPATHETIC RECEPTORS
• NTs most commonly involved in the actions of Types Tissue Response
therapeutically useful drugs α1 Pupil Dilation
o Norepinephrine Arteriolar smooth Constriction
o Acetylcholine muscle
o Dopamine GI & GU sphincter Constriction
o Histamine Pilomotor Piloerection
o Serotonin Seminal vesicle Ejaculation
o GABA Liver Glycogenolysis &
gluconeogenesis
α2 Presynaptic nerve Inhibits the release of
terminal NE
Platelet Aggregation
Pancreatic β cell Inhibits the release of
insulin
β1 Heart Inc. HR & CO
Juxtaglomerular cell Stimulates renin
release
β2 Vascular smooth Dilation
muscle skeletal
muscle
Bronchiolar sm Bronchodilation
GI and urinary sm Inc. GI & GU motility
Uterine sm Relaxation
Liver Glycogenolysis
Gluconeogenesis
β3 Adipose tissue Lipolysis

SYNTHESIS OF NOREPINEPHRINE
Fibers that synthesize and release Ach as NT; called as
cholinergic fibers
• Preganglionic fiber terminating in the adrenal
medulla → nicotinic receptor
• Autonomic ganglia both in the sympathetic and
parasympathetic → nicotinic receptor
• Postganglionic fiber of the parasympathetic division
→ MUSCARINIC receptor
• Somatic division → nicotinic receptor

Acetylcholinesterase / Achase - Enzyme that

inactivates Ach → AcetATE + choline

Fibers that synthesize and release

Norepinephrine/Noradrenaline or Epinephrine as NT;
called as Adrenergic fibers
• Postganglionic fiber of the sympathetic division
• Released by adrenal medulla

COMT & MAO – enzymes that inactivates NE →

metanephrine, normetanephrine and vanillylmandelic
acid

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 AUTONOMIC NERVOUS SYSTEM & THE AUTONOMIC DRUGS
1. Synthesis of Norepinephrine
- Tyrosine is transported by a Na+ linked carrier into
the cytoplasm of the adrenergic neuron.
- Hydroxylation of tyrosine to DOPA by tyrosine
hydroxylase
o It is the rate limiting step in the formation of
NE
B. NON CATECHOLAMINES
- Decarboxylation of DOPA to DOPAMINE by dopa
- Phenylephrine, ephedrine, amphetamine
decarboxylase in the presynaptic neuron.
- Characteristics
2. Storage of NE in vesicle
o Less potent in activating the α & β receptors
- Dopamine is transported into vesicle by VMAT
o Longer half-lives
- Hydroxylation of dopamine to NE by the enzyme
o Increased lipid solubility – greater access to
dopamine B-hydroxylase.
the CNS.
- Methylation of NE to Epinephrine in the adrenal
medulla
3. Release of NE
- The increase in Ca++ causes vesicles inside the
neuron to fuse with the cell membrane and expel
their contents into the synapse.
4. Binding of NE to receptors
5. Removal of NE
- NE may be
o Diffused out of the synaptic space and enter
the general circulation
o Metabolized by COMT
▪ NE can be oxidized by MAO
present in the mitochondria in
o Recaptured by an uptake system that pumps Mechanism of action of ADRENERGIC AGONISTS
the NE back into the neuron.
1. DIRECT ACTING AGONISTS
- Binds directly on α & β receptors
- Epinephrine, NE, Isoproterenol, Phenylephrine,
DRUGS AFFECTING NE RELEASE/REUPTAKE Albuterol, Clonidine, Dobutamine, Dopamine,
Fenoldpam, Formoterol, Metaproterenol, Salmeterol
A. PROMOTES RELEASE OF NE & Terbutaline
1. Amphetamine
2. Metamphetamine 2. INDIRECT ACTING AGONISTS
3. Angiotensin II - Block the uptake of NE, causes NE release from
4. Tyramine presynaptic terminal
- They do not directly bind or affect the post synaptic
B. INHIBIT REUPTAKE OF NE receptors.
1. Tricyclic antidepressants - Amphetamine, cocaine
2. Cocaine 3. MIXED ACTION AGONISTS
- Have the capacity to stimulate adrenoceptors directly
C. BLOCK STEPS IN NE SYNTHESIS - Can also stimulate the release of NE from the
1. Metyrosine (rate limiting step) adrenergic neurons.
2. Reserpine (storage/entry into vesicles)
3. Guanethedine (release of NE)
4. Bretylium (release of NE)

AUTONOMIC DRUGS
I. ADRENERGIC AGONISTS/
SYMPATHOMIMETICS
A. CATECHOLAMINES
- Epinephrine, NE, isoproterenol, dopamine,
dobutamine
- Characteristics
o High potency in directly activating the α & β
receptors – with –OH groups in the 3rd and
4th positions on the benzene ring
o Rapidly inactivated by COMT and MAO
o Poor penetration into the CNS

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 AUTONOMIC NERVOUS SYSTEM & THE AUTONOMIC DRUGS
- Ephedrine, pseudoephedrine

CATECHOLAMINES
DRUG RECEPTOR THERAPEUTIC USE
SPECIFICITY
1. Epinephrine α1, α2, β1, β2 1. Acute asthma/Bronchospasm
- Metanephrine & - Epinephrine causes powerful bronchodilation
vanellylmandelic acid – 2. Anaphylactic shock/anaphylaxis
metabolite present in - Severe allergic reaction characterized by a sharp drop in
urine blood pressure, urticarial and DOB.
- IM, IV, SQ, ET tube, 3. Cardiac arrest
inhalation – route of - 1mg IV push q3 minutes.
administration 4. In local anesthetic agent to increase duration of action
- Oral administration is - Local anesthetic agent usually 1:100,000 parts of
ineffective epinephrine
- Produce vasoconstriction at the site of injection
- Topical preparation of this can also be used to control
oozing of capillary blood.
2. Norepinephrine α1, α2, β1 1. Treatment of anaphylactic shock
- Normetanephrine – - Causes greater vasoconstriction than epinephrine
metabolite present in - Not used for treatment of asthma
urine
- IV – route of admin
- SQ & oral route – is
ineffective
3. Isoproterenol β1, β2 1. As cardiac stimulant
4. Dopamine Dopamine 1. Treatment of shock
- Immediate metabolic receptor, α1,β1
2. Treatment of heart failure
precursor of NE - By stimulating the β receptor → increase CO
5. Dobutamine β1 1. Treatment of acute congestive heart failure
NON CATECHOLAMINES
DRUG RECEPTOR THERAPEUTIC USE
SPECIFICITY
1. Oxymetazoline α1 1. As nasal decongestant
2. Ophthalmic drops for the relief of redness of the eyes
associated with swimming, colds and contact lenses
- Direct stimulation of the α receptors on BVs supplying
the nasal mucosa and the conjunctiva to reduce blood
flow and decrease congestion.
- S/E: rebound congestion and dependence
2. Phenylephrine α1 1. Nasal decongestant
2. It can increase BP
3. Treatment of supraventricular tachycardia (SVT) – a
rapid heart action arising from the AV junction and atria.
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 AUTONOMIC NERVOUS SYSTEM & THE AUTONOMIC DRUGS
4. Methoxamine α1 1. Treatment of SVT
5. Clonidine α2 1. Treatment of essential hypertension
- Act centrally to produce inhibition of sympathetic
response
- Abrupt discontinuance must be avoided to prevent
rebound hypertension
6. Albuterol, Terbutaline β2 1. Treatment of bronchospasm
- Short acting β2 agonist 2. Terbutaline – used as uterine relaxant to suppress
- Administered orally, premature labor
MDI
7. Salmeterol, Formoterol β2 1. Treatment of bronchospasm
- Long acting β2 agonist - Not recommended as mono
- Administered as MDI therapy but are highly efficacious when combined with
corticosteroid
- Seretide® (Fluticasone + Salmetrol), Symbicort
(Budesonide + Formoterol)
2. Amphetamine α, β, CNS 1. Treatment of ADHD, narcolepsy (brief attack of deep
- Dextroamphetamine, sleep occurring with cataplexy (sudden loss of muscle
methamphetamine, power) and hypnagogic (period of drowsiness
methylphenidate, immediately preceding sleeP) hallucination) and appetite
dexmethylphenidate control
3. Tyramine - Not clinically useful drug
- Normal byproduct of tyrosine metabolism → oxidized by
MAO in the GIT
- Found in fermented food such as aged cheese and wine
- It can enter the nerve terminal and displaced NE and act
on adrenoceptors.
- Tyramine rich food + MAOIs = Hypertensive crisis
4. Ephedrine, α, β, CNS 1. Nasal decongestant
Pseudoephedrine (plant 2. Increase in BP
alkaloids)

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 AUTONOMIC NERVOUS SYSTEM & THE AUTONOMIC DRUGS

Adrenergic antagonist / Adrenergic Blockers / a. Propranolol

Sympatholytics a. Hypertension
o ↓ CO
- Binds to the adrenoceptors but do not result into its o Inhibits renin release from the kidney
activation; b. Reduce migraine episodes
- It prevents receptor activation by endogenous - Prophylactic only
catecholamine. c. Hyperthyroidism
- Tachycardia is one of the signs and symptoms of
I. α-ADRENERGIC BLOCKING AGENTS/α- hyperthyroidism → serious cardiac arrhythmia
BLOCKERS d. Angina pectoris
- ↓ oxygen demand of the heart muscle → reduced
a. Phenoxybenzamine (Dibezyline) chest pain and exertion
- non-selective, irreversible, long acting, non- e. Myocardial infarction
competitive - Has protective effect on the myocardium → protect
- EFFECTS: __________________of BV → patient against a second heart attack
__________; _____________ NE release → ______ - Reduce infarct size and hastens recovery
CO. - Mechanism: reducing the action of circulating
- THERAPEUTIC USE: treatment of catecholamine which can increase the oxygen
pheochromocytoma demand in an already ischemic heart muscle
- S/E:
b. Phentolamine (Oraverse) ADVERSE EFFECT OF PROPRANOLOL
- Non-selective, reversible, short-acting, competitive a. Bronchoconstriction – PROPRANOLOL IS
(approximately 4 hours) CONTRAINDICATED IN PATIENT WITH
- THERAPEUTIC USE: diagnosis of ASTHMA & COPD
pheochromocytoma - use β1 selective blockers
c. –ZOSIN (Prazosin, Terazosin, Doxazosin, b. Arrhythmia
Tamsulosin, Alfusozosin) - Occurs during abrupt discontinuation after long term
- Selective, competitive α1 blockers use
- Effects: lower the TPR → ______ BP, minimal - must be tapered off gradually for at least a few
changes in CO; decrease tone in the smooth muscle weeks
of the bladder and prostate → _______urine flow c. Hypoglycemia
- THERAPEUTIC USE: Treatment of hypertension - Due to decreased glycogenolysis and decreased
(Prazosin, Terazosin, Doxazosin); Management of glucagon secretion
BPH (Tamsulosin (α1A selectivity), Alfusozosin) - It masks the hypoglycemic symptoms such as tremor
- S/E: first dose syncope; postural hypotension – how tachycardia and nervous ness
to minimize: adjusting the first dose to one-third - Monitoring of blood sugar is necessary or better use
or one-fourth of the normal dose and by giving β1 selective blockers for diabetic patient
the drug at bedtime. d. CNS effects
d. Yohimbine - Depression (manifested by insomnia), dizziness,
- Selective competitive α2 blocker fatigue, weakness, visual disturbance, short-term
- Used to relieve vasoconstriction associated with memory loss.
Raynaud’s disease
2. Timolol and Nadolol
II. β-ADRENERGIC BLOCKING AGENTS - More potent than propranolol; longer duration of
- competitive antagonist action
- -OLOL except Labetalol & Carvedilol a. Glaucoma – Timolol reduces the production of
- Selectivity aqueous humor in the eye → diminished IOP.
SELECTIVE (β1 blocker) NON-SELECTIVE (β1 & β2
blockers 3. Acebutolol, Atenolol, Metoprolol, Bisoprolol,
Betaxolol Propranolol Betaxolol, Nebivolol, and Esmolol - β1 selective
Bisoprolol Penbutolol antagonist/blocker
Esmolol Carteolol - Esmolol – very short acting; given only thru IV
Atenolol Carvedilol - USE: Treatment of hypertension in patient with
Acebutolol Labetalol impaired pulmonary function and diabetes.
Metoprolol Timolol
Celiprolol Nadolol 4. Pindolol, Acebutolol, Carteolol and Penbutolol –
Nebivolol antagonist with partial agonist activity; intrinsic
- Therapeutic uses sympathomimetic activity
o Hypertension - They are not pure antagonist, they also have the
o Angina ability to weakly stimulate both β1 and β2 receptors
o Cardia arrhythmias - They are capable of releasing catecholamine
o Myocardial infarction - Can be used in treating hypertensive patient with
o CHF MODERATE BRADYCARDIA; can also be used
o Hyperthyroidism for hypertensive diabetic patients.
o Glaucoma 5. Labetalol and Carvedilol – antagonist of both α and
β receptor

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 AUTONOMIC NERVOUS SYSTEM & THE AUTONOMIC DRUGS
OTHERS GI smooth Increase GI motility
1. Midodrine muscle and tone
- An α1 receptor selective agonist Urinary smooth Contraction →
- A prodrug; hydrolyzed to desglymidodrine muscle urination
- Used for the treatment of postural hypotension Bronchiolar Bronchoconstriction
2. Ephedrine smooth muscle
- An alkaloid found in Ma-Huang Secretory Increased secretions
glands
PARASYMPATHETIC / CHOLINERGIC NICOTINIC RECEPTORS
• Cholinergic neurons SUBTYPES TISSUE RESPONSE
o Preganglionic fibers terminating in the adrenal NM Muscle type Contraction of muscle
medulla. NN Neuronal type Depolarization of
o Autonomic ganglia (both sympathetic and neurons
parasympathetic)
o Post ganglionic fiber of the parasympathetic
division
o Muscles of the somatic system

• The REST and DIGEST response

o ___________of pupil / miosis
o ___________ bronchial secretions
o Stimulation of tears
o Copious watery secretions
o ___________ HR & CO
o ___________ GI motility and tone
o ___________ urine flow Synthesis of acetylcholine
o Erection of male genitalia 1. Entry of choline from the extracellular fluid into the
cytoplasm of the cholinergic neuron with the aid of
• NT – acetylcholine sodium dependent choline transporter (CHT)
- Choline is the precursor of acetylcholine
• CHOLINERGIC RECEPTOR/ - The uptake of choline is the rate limiting step in the
CHOLINOCEPTORS synthesis of ACh.
o MUSCARINIC – when MUSCARINE - This entry of choline inside the cytoplasm is
alkaloid is applied in the ganglia and inhibited by _________________________
autonomic parasympathetic effector cells,
autonomic effector cells mimics the 2. With the aid of choline acetyltranferase (ChAT),
parasympathetic reaction while the ganglia choline reacts with acetyl coenzyme A (AcCoa)
showed no effect; forming acetylcholine in the cytosol
o NICOTINIC – LOW level of NICOTINE A. Storage of acetylcholine
can stimulate the autonomic ganglia and the - Acetylcholine is then transported into the storage
skeletal muscle neuromuscular junction: vesicle with the aid of vesicle associated transporter
high level of nicotine can block the nicotinic (VAT)
receptors. - Transport of Ach inside the vesicle is inhibited by
___________________.
CHOLINOCEPTORS / CHOLINERGIC RECEPTORS B. Release of Ach
MUSCARINIC RECEPTORS - Occurs when voltage sensitive calcium channel are
SUBTYPES TISSUE RESPONSE opened allowing the influx of calcium which will
M1 Nerve Depolarization result into the fusion of vesicles with the surface
M2 Cardiac cells Decrease HR membrane.
smooth Decrease contractility - This process is blocked by ___________________
muscles - Spider venom causes the release of Ach.
M3 Pupil Contraction / miosis C. Binding of the Ach to the receptor
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 AUTONOMIC NERVOUS SYSTEM & THE AUTONOMIC DRUGS
- binding either to the muscarinic or nicotinic receptor
D. Deg radation of acetylcholine
- Acetylcholine is rapidly hydrolyzed by
acetylcholinesterase forming ACETATE and
CHOLINE
E. Recycling of choline
- Choline is taken up by the neuron.

CHOLINERGIC AGONIST /
CHOLINOMIMETICS /
PARASYMPATHOMIMETICS
- Act on receptors activated by acetylcholine
4. Cevimeline
A. Direct acting cholinergic agonist - Promote salivation and lacrimation in patient with
1. Acetylcholine Sjogren’s syndrome – an autoimmune disease which
- A quarternary ammonium compound that cannot destroys the exocrine glands
penetrate the membranes 5. Pilocarpine
- It lacks therapeutic importance because of - Wide angle glaucoma
multiplicity of actions & rapid inactivation by the - Most potent stimulator of secretions
acetylcholinesterase.
2. Bethanechol B. Indirect acting cholinergic agonist:
- Structurally related to Ach but resistant to Achase Acetylcholinesterase
inactivation; inactivated by hydrolysis inhibitors/Antiacetylcholinesterase (Reversible)
- Indication - These drugs act by inhibiting Achase thereby
o Enhance normal functioning of GIT and prolonging the lifetime of Ach.
bladder post operatively 1. Endrophonium (Tensilon)
3. Carbachol - Short acting; IV route
- Miotic agent to decrease IOP in patient with - Used in the DIAGNOSIS of myasthenia gravis
glaucoma (MG) – an autoimmune disorder caused by
circulating antibodies that blocks the acetylcholine
GLAUCOMA receptors → fluctuating muscle weakness and
- ↑ IOP → damage to retina and optic nerve, fatigue
restriction of visual fields, blindness 2. Physostigmine
- 2 major forms of glaucoma - Used as miotic in managing wide angle glaucoma
o Open angle (wide-angle) - Antidote for atropine, phenothiazine and TCA
▪ Can be treated pharmacologically toxicity
• Reduce aqueous humor - 3. Neostigmine(Prostigmin) (30 min-2 hrs DA)
beta blockers - DOC of choice for paralytic ileus and atony of the
• Contraction of ciliary bladder because of surgery.
muscle → opening of - Used in symptomatic treatment of MG
trabecular mesh → increase - Antidote for NM blocker toxicity (tubocurarine)
outflow – cholinomimetic 4. Ambenonium (4-8 hrs DA), Pyridostigmine
• Increase outflow – (Mestinon) (3-6 hrs DA)
latanoprost - Used for chronic management of MG
• Decrease secretion – 5. Tacrine, Donepezil (Aricept), Galantamine
brimonidine and diuretics (Reminyl), Rivastigmine (Exelon)
- Used for the management of Alzheimer’s disease

C. Indirect acting cholinergic agonist (Irreversible)

o Closed angle (narrow-angle)
▪ Acute & painful increase in IOP
▪ Controlled on an emergency basis or
by surgical removal of part of iris
(iridectomy)
- Covalently binds to Achase → permanent
inactivation → prolonging the action of
acetylcholine
1. Echothiophate
- Used as alternative treatment for chronic open angle
glaucoma
- 1 week DA
2. Malathion – component of insecticide
3. Parathion - component of insecticide
4. Soman – nerve agent
5. Sarin – nerve agent
6. Isoflurophate
D. Reactivator of acetylcholinesterase
1. Pralidoxime (PAM)
- Used to reverse the action of echothiophate.

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 AUTONOMIC NERVOUS SYSTEM & THE AUTONOMIC DRUGS
PARASYMPATHETIC SIDE EFFECTS - Low dose – it stimulates the ganglia; resulting to
Diarrhea __________ BP, CO, peristalsis and secretions
Urination - High dose – it blocks the ganglia; resulting to
Miosis __________ BP and GI and bladder activity
Bronchoconstriction - Used for smoking cessation
Emesis
Lacrimation
2. Mecamylamine
Sweating - Used for short term treatment of hypertension
Salivation 3. Trimethaphan
- Used for treatment hypertension
Cholinergic blockers / Parasympatholytics /
Anticholinergics
Neuromuscular blockers

• These drugs block the cholinergic

transmission between motor nerve endings
and nicotinic receptors on the NM endplate
of skeletal muscle.
• NM blockers are structural analog of
Acetylcholine.
• They can act as either AGONIST
(depolarizing) or ANTAGONIST (non-
depolarizing) at the receptors on the
endplate of the NMJ.
• Clinical use:
A. Anti-muscarinic agents o Adjunct to surgery to produce
1. Atropine complete muscle relaxation.
- An alkaloid from Atropa belladonna ▪ NMB should not be used to
- Mydriatic - __________ of pupils substitute for inadequate
- DA when administered topically in the eyes – 7- depth of anesthesia
14 days o To facilitate tracheal intubation.
- C/I: narrow angle glaucoma
NON – DEPOLARIZING NMB
- Used as antispasmodic (atropine – active isomer
• Tubocurarine – prototype
of l-hyoscyamine)
• Replaced by other agents because of its adverse
- Used as antidote mushroom poisoning and
effects.
cholinesterase inhibitor poisoning and
• MOA at low doses
cholinergic agonist poisoning o competitive blocker
- Used as anti-secretory agent to block secretions o How to overcome its action?
in the upper and lower respiratory tract prior to • MOA at high doses
surgery o it can block the ion channel of the
2. Tropicamide (6 hrs), Cyclopentolate (24 hrs) endplate → reduce the ability of the
- Mydriatic AChase inhibitors to reverse its action.
- Preferred over atropine due to its shorter o
duration of action
- Used for ophthalmic examinations
3. Scopolamine
- Used for prevention of motion sickness
4. Ipratropium (QID dosing) and Tiotropium (OD
dosing)
- Given via inhalation used as bronchodilator in
patient with asthma and COPD.
5. Benztropine and Trihexyphenidyl
- Centrally acting anti-muscarinic agents used for
the treatment of Parkinson’s disease.
6. Darifenacin, Fesoterodine, Oxybutynin,
Solifenacin, Tolterodine, Trospium
- Used for the treatment of overactive urinary
bladder. • not all muscles are equally sensitive to its
blockade:
B. Ganglionic blockers • Order of paralysis: Face, eyes → fingers →
1. Nicotine limb, neck trunck → intercostal muscles →
- Active ingredient in tobacco diaphragm muscle.

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 AUTONOMIC NERVOUS SYSTEM & THE AUTONOMIC DRUGS
• Order of recovery: reverse manner of paralysis and hyperpyrexia. Occur when it is
• Pharmacokinetic profile: given with Halothane
o Route: IV ▪ management
• examples: • cooling blanket
o Pancuronium • Dantrolene → blocks
o Atracurium → release histamine and is the release of calcium
metabolized to Laudanosine → provoke from sarcoplasmic
seizure. reticulum of muscle
o Cisatracurium – same property to cells thereby reducing
atracurium but less likely to cause heat production and
seizure. relaxing muscle tone
o Vecuronium – prolonged clearance in o apnea - paralysis of the diaphragm
patient with liver disease ▪ possible causes
o Rocuronium – same as vecuronium • genetic deficient of
Achase
• Drug interaction • Rapid release of K in
o antagonistic effect with cholinesterase intracellular store -
inhibitor caution to patient
o additive effect with halogenated taking digoxin and
hydrocarbon diuretics.
o synergistic effect with aminoglycoside o hyperkalemia
antibiotics ▪ CI to burn patients
o additive effect with CCBs

DEPOLARIZING NMB
• Act like acetylcholine. It depolarizes the plasma
membrane of the muscle fiber
• More resistant to AChase degradation
• EXAMPLE: succinylcholine

MOA
• succinylcholine binds to the nicotinic receptor
and act like Acetylcholine to depolarize the
muscle → sodium channel opens resulting to
transient twitching of the muscle (fasciculation)
→ gradual repolarization as the sodium channel
closes → flaccid paralysis

• pharmacokinetics
o given thru IV
o Continuous infusion is needed to
maintain longer duration of effect.
• adverse effect
o malignant hyperthermia – genetic
abnormality manifested as muscular
rigidity, metabolic acidosis, tachycardia

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