DRUGS ACTING ON AUTONOMIC NERVOUS SYSTEM

INTRODUCTION Responses
2 Systems Responsible for controlling-regulating, ·Decrease Blood Pressure

maintaining all body activities

1. Nervous System-moment to moment activities 2.Symphatetic (SANS)- Flight or Fight

2.Endocrine System-long term regulation Responses

·Increase Blood Pressure

A. NERVOUS SYSTEM ·Increase Heart Rate

1. Central Nervous System (CNS)

·Brain-Responsible for interpretation and

assessing impulses B. NEUROHORMONAL FUNCTION

·Spinal Cord-Conduct or Transport impulses from `Functional Unit: Neuron- capable of generating and
environment to specific organ system transmitting impulse because of structure

`Neurohormone-substance

TYPE OF IMPULSE `Transmission of impulse from one neuron to another

organ
1. External Impulse
-nerve to nerve
·Received by 5
-nerve to organ
Senses ·Red light
-Neurohormone or Neurotransmitter
·Brain --Impulse--> Spinal Cord

2. Internal Impulse
Sequence of Events in Transmission of Impulses
Urinary Bladder --Full--> Brain --> Spinal Cord --->
Urinary Bladder A. Biosynthesis of Neurohormones

Neurotransmitter-endogenous substances

2. Peripheral Nervous System (PNS) 1. Acetylcholine (Ach)

·Responsible for impulses, sending to the brain and 2. Epinephrine (Epi) or Norepinephrine (NE)
receiving impulse for desired action

E.g. Full Bladder A.1 Synthesis of Acetylcholine

·SOMATIC NERVOUS SYSTEM-controlled by will, ‘The first identified neurotransmitter by Otto Loewi
voluntary; movement or ambulation; movement from working on vagus nerve
one area to another
Synthesis:
·AUTONOMIC NERVOUS SYSTEM- not controlled by will,
involuntary; most action of visceral organs • one enzymatic step involving choline acetyltransferase

Acetyl-CoA + Choline –Choline Acetyltransferase- CoA +
Acetylcholine
AUTONOMIC NERVOUS SYSTEM
•Site of Synthesis: Parasympathetic Nerve Endings
1.Parasympathetic (PANS)- Rest and Digest

HOKSON.LEANO 1
•Storage: Vesicle on Parasympathetic -Ca goes in and destabilize the vesicles membrane or
making it unstable resulting to release of neurotransmitter
• Choline is derived primarily from the diet and
is transported across the BBB. -Higher Neurotransmitter: Interact with receptors

A.2 Synthesis of Norepinephrine


•Tyrosine –Tyrosine Hydroxylase .L-Dopa –Dopa D. Interactions of Neurotransmitter with Receptors

Decarboxylase Dopamine –Dopamine
 1. Acetylcholine bind to
B-Hydroxylase Epinephrine
•Site of Synthesis: Adrenal medulla (Kidney) by Chromaffin ·Nicotinic Receptor which is found in skeletal muscles
Cells
·Muscarinic Receptors which is found in visceral organs
•Storage: Terminal Nerves like heart, eyes, GIT, lungs, urinary bladder

B. Storage of Neurotransmitter 2. Acetylcholine bind to

`Neurohormone - body synthesize excess of ·Alpha receptor which is found in eyes, blood vessels
Neurotransmitter incase of emergency (surplus)
·Beta receptor which is found in heart, lungs, liver, uterus,
C. Release of Neurotransmitter kidneys

1. Depolarization

2. Exchange of ions (Na, K,) Neurotransmitter interaction with receptors result to

cholinergic or adrenergic activity
3. Entry of Ca ion

E. Inactivation of Neurotransmitter

1.1. Acetylcholine: Acetylcholinesterase (Achase)

The products are not excreted but are recycled in the body

Products of Inactivation by acetylcholinesterase:

·acetate- interact with CoA

·choline- recycled in the body

1. Nerve receives impulse

1.2. Epinephrine: Monoamine oxidase (MAO), Catechol-
2. Stimulation of Nerves wherein there is the opening of o-methlytransferase (COMT)
channels Epinephrine when inactivated:
3. Depolarization 
1.2 Epinephrine --MAO, COMT vanillylmandelic (VMA)

Urine (detected in urine and to athletes using enhancing
-Exchange of Charges drugs). ‘VMA- metabolic by-product of norepinephrine and
epinephrine can be used to detect neuroblastoma and other
-Sodium goes in (influx) and Potassium goes out (efflux) tumors of neural crest origin.
-( + in and – out)

-3Na:2K 1.3 Up taken by terminal nerve where it is released

-Negative charge make membrane more permeable (recycled and use again)

4. The membrane of neuron becomes permeable to Ca

HOKSON.LEANO 2
1.4 Up taken by Glial cells of smooth muscles F.2 Return of Na, K
(recycled and use again)
F.3 Goes back to resting potential to receive another
F. Repolarization of the nerve/neuron impulse

F.1 Return of charges

C. COMPARISON BETWEEN PANS AND ANS

ANATOMICAL DIFFERENCE
Point of Comparison PANS SANS
1. Outflow from CNS Craniosacral Thoracolumbar
2. Ganglia Near or within the structure innervated Close to Spinal cord
3. Pre - ganglionic fiber Long and myelinated Short (since near to spinal cord) and
myelinated
4. Post – ganglionic fiber Short and non-myelinated (since localized Long and myelinated
effect) (since generalized effect)
5. Response to stimulation Localized to a restricted area Generalized and widespread
6. NT at all ganglia Acetylcholine Acetylcholine
7. NT at post ganglionic nerve Acetylcholine Norepinephrine
ending
HOKSON.LEANO 3
Terms:

Ganglia- a group of neurons

Ganglion- a structure containing a number of nerve cell bodies, typically linked by synapses, and often forming a swelling on a
nerve fiber

Impulse- signal that travels along the length of a nerve fiber and ends in the release of neurotransmitters

MUSCARINIC RECEPTORS

HOKSON.LEANO 4
 DRUGS ACTIONG ON PERIPHERAL NERVOUS SYSTEM

A. NUEORTRANSMITTER

A.1 ACETYLCHOLINE STRUCTURE

B. RECEPTORS

RECEPTOR LOCATION MECHANISM

M1 Nerve Endings Gq-coupled
M2 Heart, and some nerve endings Gi-coupled
M3 Effector cells : smooth muscle, glands, endothelium Gq coupled
NN ANS ganglia Na-K ion channel
NM Neuromuscular end plate Na-K ion channel

Muscarinic: G-receptors related to enzymes, stimulates further release of secondary messenger like DAG, IP

Nicotinic M- Ligand gated

C. ORGAN SYSTEM EFFECTS (ACETYLCHOLINE)

HOKSON.LEANO 5
1. EYES (PUPILS) 
c. Sweat Glands- M3 receptor: Stimulation Hydrosis,
 Sweating/ Diaphoresis
a. Ciliary Muscle- M3 receptor: Contraction Near Vision

 d. Nasopharyngeal- M3 receptor: Stimulation runny
b. Sphincter Muscle- M3 receptor: Contraction Miosis nose
2. LUNGS 6. SKELETAL MUSCLE

a. Smooth Muscle of Bronchioles- M3 receptor: Contraction 

-- Nicotinic N receptor: Contraction Movement
at presence of Acetylcholine that leads to Broncho
constriction that can result to dyspnea 7. CARDIOVASCULAR SYSTEM
 -Ach affects heart by vagus of vagal nerve
b. Bronchial glands-- M3 receptor: Stimulation

increasing mucus secretion dyspnea that can ppt a. heart- M2 receptor
asthma
3. GI TRACT b. blood vessels- M2 receptor:

a. Smooth Muscle of GI-- M3 receptor: contraction  

-Vagus nerve depresses HR, BP, DECREASE HR, BP
 ANTI-DUMBBELLS
peristalsis diarrhea

b. GI glands--- M3 receptor: stimulation HCl Secretion –
Hyperacidity Diarrhea
4. URINARY BLADDER Urination
a. Trigone and Sphincter Muscle-- M3 receptor: relaxation

Micturation or Urination Miosis/muscle weakness
 Bronchorrhea
b. Detrusor Muscle-- M3 receptor: contraction
Micturation or Urination Bradycardia
5. GLANDS
Emesis
 
a. Lacrimal- M3 receptor: Stimulation Lacrimation Lacrimation
Increase tears
 Salivation/sweating
b. Salivary- M3 receptor: Stimulation Salivation

D. DRUGS

D.1 AGONIST

1. NAMES: Cholinoreceptors Stimulants, Cholinomimetics, Cholinergic Agonist, Parasympathomimetic

RECEPTORS: Muscarinic Agonist or Nicotinic Agonist

2.MOA: AGONIST 1

Drugs occupy same receptor site as endogenous Ach to produce same or enhanced activity or action

3. DRUGS

3.1 ALKALOIDS:

DRUG BRAND NAME MOA USES

Muscarine Activates muscarinic (M) Glaucoma
receptors
• increases IP3 and DAG
Nicotine Nicoderm CQ®, Nicotrol®, Activates all nicotinic (N) CNS Stimulant
HOKSON.LEANO
6
 Commit®, Nicorette receptors •
opens Na+-K+ channels in
ganglia and
neuromuscular end plates
Lobeline clozaprexin® inhibits nicotine-evoked Smoking cessation
dopamine release
Cevimeline Evoxac® Smoking cessation; dry
mouth
Varenicline Chantix® A partial agonist at N receptors Smoking cessation, txt of
nicotine addiction
3.2 SYNTHETIC

DRUG BRAND NAME MOA USESGlaucoma

Betanechol Urecholine® Activates muscarinic (M) Increase Smooth Muscle
receptors tone for abdominal
• increases IP3 and DAG surgery
Metacholine Provocholine® Diagnose bronchial
hyperactivity

D.2 INDIRECLY ACTING DRUGS

1. NAMES: Acetyl CoA cholinesterase inhibitor


2. MOA: Inhibit activity of Achase thus prolonging the binding of Ach to Nicotinic or Muscarinic receptor: Achase + Drugs Prolong

3. DRUGS

Drug Brand Name Uses

Physostigmine Eserin® Anti-glaucoma
Ambenonium Mytelase For Myasthenia gravis
Edrophonium Tensilon® Diagnose Myasthenia Gravis
Neostigmine Prostigmin® Anti-glaucoma
Pyridostigmine Mestinon® Regonol® Anti-glaucoma
Echothiophate Phospholine® For Chronic Glaucoma
Donepezil Aricept® Anti-dementia
Galantamine Reminyl® Razadyne® Anti-dementia
Rivastigmine Exelon® Anti-dementia and anti-parkinson
Tacrine Cognex® Anti-dementia
Carbachol Miostat® Anti-glaucoma
Malathion Carbophos® Maldison®, Mercaptothion® Pesticide
Parathion Bladan M® Dalf® Pesticide

3.1 BOTANICAL SOURCES

Drug Common Name Scientific Name Family Name

Nicotine Tobacco Nicotiana tabacum Solanaceae
Muscarine Fly Agaric Amanita muscaria Amanitaceae
Pilocarpine Jaborandi Pilocarpus jaborandi Rutaceae
Lobeline Indian tobacco Lobelia inflata Campanulaceae
Physostigmine Calabar bean Physostigma venenosum Fabaceae

HOKSON.LEANO 7
E. CLINICAL APPLICATION OF CHOLINERGIC AGONIST
1) MYASTHENIA GRAVIS

comes from the Greek and Latin words meaning "grave muscular weakness”

disease of neuromuscular junction, progressive disease

chronic autoimmune neuromuscular disorder that is characterized by fluctuating weakness of the voluntary muscle groups, ptosis,
difficulty in speaking and swallowing thus there is salivation and drooling, extremity weakness, diplopia

PATHOPHYSIOLOGY: Acetylcholine travels across the space to the muscle fiber side of the neuromuscular junction where it attaches to
many receptor sites. The muscle contracts when enough of the receptor sites have been activated by the acetylcholine. In MG, there can
be as much as an 80% reduction in the number of these receptor sites. The reduction in the number of receptor sites is caused by an
antibody that destroys or blocks the receptor site. These antibodies attack the
nicotinic receptor.
Antibodies are proteins that play an important role in the immune system. They are normally directed at foreign proteins called
antigens that attack the body. Such foreign proteins include bacteria and viruses. Antibodies help the body to protect itself
from these foreign proteins. For reasons not well understood, the immune system of the person with MG makes antibodies
against the receptor sites of the neuromuscular junction. Abnormal antibodies can be measured in the blood of many
people with MG. The antibodies destroy the receptor sites more rapidly than the body can replace them. Muscle weakness
occurs when acetylcholine cannot activate enough receptor sites at the neuromuscular junction. This event result to
paralysis. In myasthenia gravis, small muscles such as muscles in fingers and face are attack first then large muscle such
as respiratory muscle is attacked. This result to respiratory prolapse and since there is no contraction this will result to death

SIGNS AND SYMPTOMS
1) Droopy eyelids
2) Double vision
3) Difficulty of swallowing
4) Change in the quality of voice
5) Difficulty in breathing

DIAGNOSIS OF MG:
a) EDROPHONIUM TEST: Injection of the chemical Edrophonium chloride (Tensilon) may result in a sudden, although
temporary, improvement in your muscle strength. This is an indication that you may have myasthenia gravis.
It is administered intravenously
Get Muscle strength
Inject 2mg of Edrophonium
Wait for 45 seconds, get Muscle strength
If there is an increase in Muscle Strength, then the patient is positive to Myasthenia Gravis
If there is no improvement, repeat the test by administering 3mg then 5 mg or give 8mg once, if there is still no
improvement, then the patient is negative to Myasthenia Gravis and there might be presence of other Muscle
diseases
Edrophonium chloride blocks an enzyme that breaks down acetylcholine, the chemical that transmits signals from your
nerve endings to your muscle receptor sites. Used because of its short duration of action.
b) ICE PACK TEST
If you have a droopy eyelid, your doctor may conduct an ice pack test. In this test, a doctor places a bag filled with ice on
your eyelid. After two minutes, your doctor removes the bag and analyzes your droopy eyelid for signs of improvement.
Doctors may conduct this test instead of the edrophonium test.

Treatment: Cholinesterase Inhibitor but it should be titrated first and slowly increase the dose to determine the dose the patient can
tolerate

Cholinesterase Inhibitor: Rivastigmine, Neostigmine, Ambenomium, Pyridostigmine

MOA: Indirectly acting- inhibit activity of Acetylcholinesterase; since there is limited number of nicotinic receptor, there is only limited
number of Acetylcholine that will bind. If Acetylcholinesterase is activated then the number of Acetycholine that will bind will also
decrease. Inhibiting activity of Acetylcholinesterase will let the binding of Acetylcholine to Nicotinic receptor thus there will be contraction
or there will be a prolong cholinergic effect.


Increasing the dose/ titrating the dose of drugs for the management of Myasthenia Gravis Cholinergic Crisis (excess of anticholinesterase
drug; EFFECTS: miosis, cannot breath, diarrhea, & salivation)

2) GI ATONY

HOKSON.LEANO 8
 
Atony “no tone” in the stomach and failure to contract normally, causing a delay in movement of food out of the stomach

Commonly due to post anesthesia specifically general anesthesia thus decrease in muscle contraction or relaxation of muscles;
also due to trauma of spine

Note: After surgery or administering anesthesia, flatulence indicates that there is muscle contraction

DOC: Betanechol (Urocholine®): induce peristalsis

PRECAUTION FOR CHOLINERGIC DRUGS: There should be no obstruction present in the sphincter that will cause perforation
and exacerbate the condition

The obstruction is due to urinary stones. Cholinergic drugs induce urination. Stones might be brushed to the urinary bladder. It will cause
high pressure in the urinary bladder so it might burst and worsen the condition. The physician should be sure about the absence of stones
before giving the cholinergic drug.
3) GLAUCOMA

Disease where there’s an increase intraocular pressure due to the accumulation of aqueous humor (which is normally drained or
outflow behind the eye) that causes pain and blindness.

ANTERIOR CHAMBER: place where the aqueous humor is drained.

CANAL OF SCHLEMM: where aqueous humor drains out

AQUEOUS HUMOR: flow in the anterior chamber and carries nutrients in the eye

ACUTE ANGLE GLAUCOMA: the fluid pressure inside the eye rises quickly; requires surgery because it is an emergency OPEN
ANGLE GLAUCOMA: progressive and acute condition; use drugs for its management

TREATMENT: ADRENERGIC AND CHOLINERGIC DRUGS: cause constriction of radial muscle and sphincter
   
muscle widen the schlemm canal draining of aqueous humor decrease IOP increase outflow of aqueous humor

INSTRUMENT USED TO MEASURE IOP: Tonometer
4) ALZHEIMER’S DISEASE

Disease generally seen in elderly which is dementia which is characterized by forgetfulness, memory loss and decrease in cognitive
function.

Usually diagnose when too late; response to drug is decreased

Due to decrease in Acetylcholine


Use Cholinergic agonist that prolong the reaction of M5 and Acetylcholine by inhibition of Acetylchonisterase prolonging function of brain

TREATMENT: Tacrine, Donepezil, Rivastigmine, Galantamine
5) URINARY RETENTION

Due to post anesthesia or trauma of spine

Urinary bladder is relaxed thus there is accumulation of urine

Muscarinic receptor is inactivated thus the patient cannot urinate

TREATMENT: Betanechol- it contracts detrusor muscle and relaxes the sphincter and trigone muscle resulting to contraction
of Urinary Bladder thus the person can urinate

Precaution: there should be no mechanical obstruction such as kidney stones since if the detrusor contracts the urinary bladder will
brushed to stones that can exacerbate and perforate the condition or there will be accumulation of urine that could lead to bursting

Check for obstruction by X-ray
6) OTHER USES
a) SUPRAVENTRICULAR TACHYRHYTHMIAS
Drug: Decreases heart rate via vagus nerve but cholinergic drugs are not first line therapy
b) ATROPINE POISONING: Use of Physostigmine as antidote

A.ADVERSE EFFECTS OF CHOLINERGIC DRUGS

1) Miosis 3) Diarrhea
2) Blurred vision 4) Dyspnea

HOKSON.LEANO 9
5) Hyperacidity 11) Salivation (Ptyalism)
6) Sweating 12) Bradycardia
7) Abdominal cramps 13) Lacrimation
8) Polyurea or Frequent urination or Urinary 14) Urinary urgency
Urgency 15) Decreased of visual activity (Myopia)
9) Hypotension 16) Muscle ramps, pain
10) Rhinorrhea (runny nose)

B. CONTRAINDICATIONS/ PRECAUTIONS
CONTRAINDICATIONS: absolutely should not be used
PRECAUTIONS: used but with monitoring
1) Asthma- CI due to bronchoconstriction
2) PUD- CI
3) Bladder obstruction- CI
4) Hypertension- Precaution
5) Elderly- Precaution

ANTICHOLINERGICS

A. MECHANISM OF ACTION (Antagonist I): These drug occupy the same receptor site (muscarinic,
adrenergic) of acetylcholine of the cholinergic drug thus inhibition of its binding that results to no
cholinergic activity B. ORGAN SYSTEM EFFECTS
ORGAN EFFECTOR RECEPTOR ACTION EFFECT
EYES (PUPILS) CILIARY MUSCLE M3 Relaxation Far vision
SPHINCTER MUSCLE Relaxation Mydriasis, Cycloplegia
RESPIRATORY SMOOTH M3 Relaxation Ease in breathing,

TRACT (LUNGS) MUSCLES BRONCHIOLES Bronchodilation and
MUCOUS/BRONCHIAL Decrease in stimulation decrease secretion of
GLANDS of mucus mucous
GIT SMOOTH MUSCLE OF GI M3 Relaxation Decrease in
peristalsis=constipation
GI GLANDS Decrease stimulation Deccrease in HCl
secretion
URINARY TRIGONE and SPHINCTER M3 Contraction Urinary retention
BLADDER MUSCLE
DETRUSOR MUSCLE Relaxation
GLANDS LACRIMALGLANDS Decrease Xerostomia (dry mouth)
M3 secretion/stimulation
SALIVARY GLANDS Decrease Sandy eyes
secretion/stimulation
SWEAT GLANDS Decrease Anhidrosis, decrease
secretion/stimulation sweating
NASOPHARYNGEAL Decrease Dry nose
secretion/stimulation
SKELETAL NN Relaxation No Movement
MUSCLES
CARDIOVASCULAR HEART M2 Depression of Vagus Hypertension

SYSTEM: not nerve Increase in
directly affected by heart

Ach rate Vasoconstriction

VAGUS NERVE: of BV Increase BP
contains M2 BLOOD VESSELS
receptor that cause

HOKSON.LEANO 10
depression of the
heart when it is
stimulated

CNS Depress the CNS Lethargy
(reactive in the presence Hallucination
of anti-cholinergic drug) Disorientation
Drowsiness
C. DRUGS
a) PROTOTYPE: Tropane Alkaloids (Tertiary amines)

DRUGS SOURCES EFFECTS

Scopolamine Flower tops of Hyoscyamus niger, Motion sickness, Irritable bowel syndrome, GIT
Solanaceae spasm, depresses the CNS
Atropine Seed pods of Atropa belladonna, Stimulate the CNS,Irritable Bowel Syndrome,
Solanaceae Enteric colitis
b) OTHER NAMES
 Anticholinergic drugs
 Cholinergic antagonist
 Parasympathetic Antagonist

Anti-nicotinic drug

Anti-muscarinic Drug
DRUGS

ATROPINE AND CONGENERS

HOMATROPINE Equipin; Isopto Hematropine Mydriatic
ANISOTROPINE/OCTATROPINE Valpin; Endovalpin Antispasmodic
METHYLBROMIDE
BENZTROPINE Cogentin Parkinson’s Disease
HYOSCYAMINE Symax, Hyomax PUD and IBS
HYOSCINE Buscopan (HNBB) Motion Sickness; Antispasmodic
IPRATROPIUM Atrovent COPD
TROSPIUM/CHLORDIAZEPOXIDE Librium, Sanctura Anxiolytic
SCOPOLAMINE AND CONGENERS
SCOPOLAMINE Isopto Hyoscine, Transderm-Scop Mydriatic
METHSCOPOLAMINE Pamine PUD adjunct
OTHERS
BIPERIDEN Akineton Parkinson’s Disease
CYCLOPENTOLATE Cyclogyl Mydriatic
GLYCOPYRROLATE/GLYCOPYRRONIUM Cuvposa, Robinul Anaesthetic
BROMIDE
DICYCLOVERINE Byclomine Antispasmodic
MEPENZOLATE Cantil PUD adjunct
OXYBUTYNIN Ditropan XL Urinary Antispasmodic
PROPANTHELLINE Pro-Banthine Antispasmodic
TRIHEXYPHENIDYL Artane; Trihex Parkinson’s Disease
TRIDIHEXETHYL Pathilon PUD
TROPICAMIDE Mydriacyl; Tropicacyl Mydriatic
METHANTHELINE Asabaine, Banthine Antispasmodic
DARIFENICIN Enablex TXT overactive bladder
FESOTERODINE Toviaz Urinary Antispasmodic
FLAVOXATE Urispas Urinary Antispasmodic
SOLIFENACIN Vesicare Urinary Antispasmodic

HOKSON.LEANO 11
 TOLTERODINE Detrol Urinary Antispasmodic
CLIDINIUM Librax PUD adjunct; IBS; Enterocolitis
BELLADONA TINCTURE Barbidonna IBS
CLINICAL APPLICATIONS

1. OPTHALMIC EXAMINATION: the drug fully dilates the eyes to be examined properly; for refraction of the eyes; dilates
the pupil
DRUG USED: Atropine, Cyclopentolate
2. PRE-OPERATIVE MEDICATIONS

Used before surgical procedure
 

ATROPINE: produce Xerostomia (throat) intubation that aid in respiration the tube is considered as a
foreign body thus, the body releases saliva to fight the foreign body and expectoration as an effect
  
SCOPOLAMINE: depress the CNS (groggy) sedating unconcious

ATROPINE
·Decreases Heart
·Used specially for nervous patient since it depresses the vagus
nerve ·Not DOC (DOC: B-Blocker)
3. GI TRACT
a. Aid in the treatment of PUD: decreases HCl secretion that serves as adjunct in the treatment of PUD together
with H2 blockers or PPI
 

Precaution: Anticholinergic drug decreases peristalsis the food stays in the GIT induces the
secretion HCl thus worsen the PUD

Solution: give the DOC first but not immediately the adjunct
b. Treatment of Diarrhea (due from the increase in peristalsis)

Action: drug will decrease peristalsis to treat diarrhea but should not cause by certain microorganisms

Use Antibiotics for Diarrhea caused by bacteria like Erceflora®
c. Biliary colic/ Gallstone attack

Contraction of gallbladder

Drug relax the smooth muscle of the GI tract thus decreasing the pain
d. Dysmenorrhea

 
Pain due to the contraction of GI muscles D relax the GI muscle relieve pain/spasms
4. ASTHMA
   
Relaxes the bronchial muscle decrease in mucus secretions bronchodilation asthma relief
5. Motion Sickness

Dizziness when traveling

Normal Physiology: Inner ear and Vestibular Apparatus together with Cerebellum work together to maintain
proprioception (maintenance of posture/position) and balance

Pathophysiology: Miscommunication of inner ear and vestibular apparatus thus wrong interpretation of
cerebellum

Txt: Scopolamine (Transderm-Scop®) Patch- given behind the ear, sedative effect since it depresses CNS

*Note: Motion Sickness is treated when you sleep
6. Enuresis a.k.a "Bed Wetting"
Involuntary micturation

Pathophysiology: Sphincter is not close properly due to poor control thus sensitive to stimulation

Common in elderly

Txt:

Solifenacin- Vesicare®

Darifenacin- Enablex®

MOA of Txt: Contraction of Sphincter Muscle thus no pressure that provide temporary relief
7. Parkinson's Disease
 an autoimmune disease characterized by tremors, bradykinesia, dyskinesia, postural imbalance

HOKSON.LEANO 12
 
Normal Physiology: Acetylcholine and Dopamine are homostatically present in basal ganglia that works together for
muscle movement, dopamine depresses CNS thus exerting inhibitory effect while Acetylcholine exert an excitatory
effect

Pathophysiology: There is decrease dopamine since the dopamine receptors will be occupied by Antibodies

S/sx due to imbalance of NT

Tremors due to excess Acetylcholine that occupy basal ganglia; pill rolling action of hands

Bradykinesia due to lack of dopamine thus slow movement

Akinesia is difficulty in initiating movement

Dyskinesia is difficulty in movement

Postural Imbalance where in patient can fall anytime

Salivation

Txt: Supply dopamine to counteract acetylcholine by using anticholinergic drug

Trinex® - Triclabendazole

Tridine®- Tricholine citrate
8. Twilight Sleep

Characterized by insensitivity to pain but without loss of consciousness

Produced by scopolamine that depresses the CNS and Morphine to manage pain

Used in Dilatation and Curefllage/ RASPA/ Obstetrics
9. Bronchial Asthma

Decreases mucus secretion because of bronchodilation

10. Mushroom Poisoning


2 Types

a. Rapid Onset: caused by A. marita sp containing muscarine


Onset of action: 15-20 mins after ingestion

S/Sx: Cholinergic in Nature

Txt: Atropine and other Anticholinergic Drug

b. Delayed Onset: caused by Inocybe sp. (colored, wild type) also contains muscarine

Onset of action: 12-16 hours after eating

S/Sx: Circulatory collapse, kidney problems, due to organ failure

Txt: Symptomatic
11. Insecticide Poisoning

Pathophysiology: Malathion and Parathion bind to Acetylcholinesterase for more than 100 hours due to their high
affinity, prolonging now the binding of Acetylcholine to receptor site manifesting cholinergic effects

S/sx: Manifestation of DUMBBELLS

Insecticide Poisoning Txt:

a. Enzyme Regenerator

Pralidoxime (PAM- 2-pyridine aldoxime methyl chloride) interact with Malathion and Parathion releasing
Acetylcholinesterase thus the Acetylcholine binding to receptor will be metabolized

b. Anticholinergic (Atropine)

since bond (oxygen and sulfur --> double bond) between Acetylcholineaterase and Malathion & Parathion
become stronger when more than 12 hours (aging)

Atropine counteract action of Acetylcholine

HOKSON.LEANO 13
ADVERSE DRUG REACTIONS
1. Cycloplegia- muscles become fixedly dilated 10. Feeling of Fullness

2.
Tachycardia 11. Hallucinations
3.
Constipation 12. Drowsiness
4.
Dry Mouth 13. Mydriasis
5.
Hyperthermia since BV is constricted, heat 14. Palpitations
cannot be dissipated; can cause death to 15. Delirium
children 16. Lethargy
6. Hypertension 17. Agitation
7. Sandy Eyes "sandy feeling" due to decrease 18. Achlorhydria
lacrimal fluid 19. Disorientation
8. Urinary Retention 20. Euphoria
9. Hot and Flushed Skin

CONTRAINDICATIONS/PRECAUTIONS

 Elderly  Peptic Ulcer Disease

 Glaucoma  Coronary Artery Disease

Myasthenia Gravis

GANGLIONIC BLOCKING DRUGS

`Ganglionic-group of neurons

Block skeletal muscle (specifically in depolarizing)

MOA: Decreases depolarization of Skeletal Muscle resulting to decrease movement (contraction and relaxation)

Used for skeletal muscle relaxation

Mecamylamine- used in surgical procedure to relax muscle

SYMPATHETIC AUTONOMC NERVOUS SYSTEM

A. NEUROTRANSMITTER

Epinephrine- major

Norepinephrine- minor

Dopamine- minor than norepinephrine

B. RECEPTORS

Alpha 1- smooth muscle particularly blood vessels, papillary muscle

Alpha 2- platelets and fat cells

Beta 1- heart

Beta 2- Lungs, Uterus, Kidneys, Liver

Beta 3- Urinary Bladder

Dopamine 1- smooth muscles

Dopamine 2- nerve endings
HOKSON.LEANO 14
`Life Cycle of Epinephrine

Synthesis

Release: depolarization of Caions

Binding to receptor site specifically alpha for Inhibition and contraction, beta for stimulation and relaxation

Inactivation: MAO/COMT -->VMA, Reuptake to site of release and glial cells

C ORGAN SYSTEM EFFECTS

ORGAN EFFECTOR RECEPTOR ACTION EFFECT

EYES CILIARY MUSCLE B1 Relaxation Mydriasis but no Cycloplegia
RADIAL MUSCLE A1 Contrcation Mydriasis but no Cycloplegia
BRONCHIAL UPPER A1 Decrease in secretion Decongestion
SYSTEM RESPIRATORY of mucus
TRACT (Nasal
Mucosa)
LOWER B2 Relaxation Bronchodilation; txt of asthma
RESPIRATORY
TRACT (Smooth
muscle of bronchial
trees)
GIT SMOOTH MUSCLE OF B Relaxation Decrease in
GI RECEPTORS peristalsis=constipation

UTERUS B2 Relaxation when

uterus is gravid
(pregnant)
LIVER Increase Increase concentration of glucose
B2 glycogenolysis-
breakdown of
glycogen to produce
glucose
Increase
gluconeogenesis-
synthesis of glucose
from protein or fats
PANCREAS A Decrease insulin Increase glucose concentration
secretion
CARDIOVASCULAR HEART B1 All function is Tachycardia; Increase Blood
SYSTEM SA NODE increased pressure
(PACEMAKER OF THE + Inotropy- force of
HEART S1 LUB S2 contraction
 
DUB) AV NODE + Chronotropy- rate

PURKINJI FIBERS of contraction
HEART BEAT IN + Bathmotropy-
SYNC excitability of heart
NORMAL HEART + Dromotropy-
BEATS: 60-100 conduction of impulse
BLOOD VESSELS A1 Contraction Vasoconstriction; Increase Blood
BP=CO (Cardiac Pressure
Output) X
PVR(Peripheral
Vascular Resistance)
BV NARROWER=
HOKSON.LEANO 15
 INCREASE IN PVR
AND BP
CNS B Brain Stimulation Wakefulness, alertness, insomnia,
RECEPTORS confusion, delirium, disorientation
KIDNEYS B2 Secretion of Increase Blood pressure

RENIN recruit

RAAS Increase
BP
Renin-enzyme that
breakdown
Angiotensin to
Angiotensin 1
)vasoconstrictor) –

ACE Angiotensin 2

–ACE Aldosterone

Increase cardiac

output Increase
BP
SKIN Pilomotor Muscle A Contraction Gooseflesh

DRUGS

a. Other Names

Sympathomimetic

Adrenergic agonist

“Catecholamine”

Adrenoceptor Agonist

b. MOA: Agonist 1: occupy the same receptor site as Epinephrine and Norepinephrine to produce same effect or a more
intense effect

c. Catecholamine- the 1st identified substances or drugs acting on adrenergic receptor (ALPHA AND BETA RECEPTOR)

d. DRUGS that have CATECHOL STRUCTURE

CATHECHOL STRUCTURE

HOKSON.LEANO 16
Epinephrine
Norepinephrine

Isoproterenol Dopamine
E.Specific Drugs

GENERIC NAME BRAND NAME USE/CATEGORY

Epinephrine Epipen, Adrenalin Cl, CNS Stimulant
Auvi-Q

Norepinephrine Levophed CNS Stimulant

Dipivefrin/e Propine Glaucoma
Isoproterenol Isuprel Txt of Bradycardia
Metaproterenol Alupent Bronchodilator
Amphetamine Adderall ADHD
Methamphetamine Desoxyn CNS Stimulant
Dobutamine Dobutrex Inotropic Agent; CHF
Mephentermine Termin Cardiac Stimulant
Metaraminol Aramine Vasoconstrictor; for
Hypotension
Methoxamine Vasoxyl Vasoconstrictor; for
Hypotension
Desoxyephedrine/ Desoxyn CNS Stimulant
Methamphetamine

Ephedrine Akovaz, Corphedra Asthma

Naphazoline Privine, Vasocon Decongestant
Oxymetazoline Afrin, Visine LR Topical Decongestant
Phenylephrine Neo-Synephrine Decongestant

HOKSON.LEANO 17
Phenylpropanolamine Accutrim, Dexatrim Decongestant & Appetite
Suppressant

Pseudoephedrine Sudafed Decongestant

Cocaine Cocaine Roxane CNS Stimulant
Dextromethamphetamine/ Dexedrine CNS Stimulant; ADHD
Dextroamphetamine

Dexmethylphenidate Focalin ADHD

Methylphenidate Ritalin CNS Stimulant; ADHD
Tetrahydrozoline Visine Decongestant; for Eye
irritation
Xylometazoline Otrivin Nasal Vasoconstriction
decongestant

Hydroxymethamphetamine Norveritol, Pulsoton Eye drops; Causes mydriasis

Albuterol (Salbutamol) Ventolin, Proventil B2 Agonist; Asthma
Salbutamol (Albuterol) Ventolin Bronchodilator; Asthma
Clenbuterol Dilaterol, Spiropent, Decongestant; Asthma; for
Ventipulmin veterinary use

Bitolterol Tornalate Bronchodilator; Asthma; COPD

Isoetharine Bronkosol, Dilabron Bronchodilator; Asthma
Terbutaline Brethaire, Brethine Bronchodilator; Asthma; COPD
Formoterol Perforomist Asthma; COPD
Salmeterol Serevent Salmeterol
Isoxsuprine Vasodilan Vasodilator; Uterine relaxation
Nylidrin Arlidin Inotropic agent; Vasodilator
Ritodrine Yutopar Tocolytic; Control premature
labor

Procaterol Ventpro B2 agonist; Asthma

Pirbuterol Maxair B2 agonist; Bronchodilator;
Asthma

Tulobuterol Breton B2 agonist; Asthma; Patch

Bambuterol Bambec B2 agonist; Asthma

HOKSON.LEANO 18