Rhenier S.

Ilado, RN, MNc

 Aka. “adrenergic system”
 Neurotransmitter: “Norepinephrine”
 Adrenergic receptor organ cells – alpha1, alpha2,
beta1 and beta2
 Aka. “cholinergic system”
 Neurotransmitter: “acetylcholine”
 Cholinergic receptors organ cells – Nicotinic and
Muscarinic (stimulated by alkaloid nicotine and
muscarine)
 “Acetylcholinesterase” – enzyme that inactivates
acetylcholine before reaching receptor cell
Drugs that mimics SNS and PNS
Sympathetic Stimulants Parasympathetic Stimulants

A. Sympathomimetics A.Parasympathomimetics
(adrenergic or adrenergic (cholinergic or cholinergic
agonists) agonists)
1. Increase BP 1. Decrease BP
2. Increase PR 2. Decrease PR
3. Relax bronchioles 3. Constricts bronchioles
4. Dilate pupils 4. Constrict pupils
5. Relax uterine muscles 5. Increase urinary
contraction
6. Increase blood sugar 6. Increase peristalsis
Sympathetic Depressants Parasympathetic Depressants

B. Sympatholytics (adrenergic B. Parasympatholytics

blocker or adrenergic (anticholinergics or
antagonists) cholinergic antagonists, or
antispasmodics)
1. Decrease PR 1. Increase PR

2. Decrease BP 2. Decrease mucus secretions

3. Constrict bronchioles 3. Decrease GIT motility

4. Increase urinary retention

5. Dilates pupils
 Adrenergics (Sympathomimetics)
 Adrenergic blockers (Sympatholytics)
 Aka.
1. Adrenergic agonists – stimulates SNS
2. sympathomimetics – mimics the SNS
neurotransmitters
 Act on adrenergic receptor sites – heart, bronchiole
walls, GIT, urinary bladder and ciliary muscles of the
eye
 Adrenergic receptor sites – alpha 1, alpha2, beta1
and beta2
Site and Effects of Adrenergic
receptors
Alpha1
 Vasoconstriction (Increases
blood pressure)
 Primarily located in the blood
vessels

Alpha2
 Located on the sympathetic
nerve endings
 Inhibits release of
norepinephrine
 Dilates blood vessels
(hypotension)
Beta1
 Located primarily on the
heart
 Increases heart rate/force of
contraction

Beta2
 Located on the smooth
muscles of lungs, arterioles of
skeletal muscle and uterine
muscle
 Dilates bronchioles
 Increase blood flow to the
skeletal muscles
 Decrease uterine contraction
Inactivation of
Neurotransmitters
 Action of NT must be stopped
to prevent prolonging the effect
Inactivated through:
1. Reuptake of the transmitter
back into the neuron
2. Enzymatic transformation or
degradation – e.g. Monoamine
oxidase (MAO) for NE,
acetylcholinesterase for
acetylcholine
3. Diffusion away from the
receptor
Mode of action: acts on adrenergic
sites(alpha 1, beta 1 & beta2),
promotes CNS/cardiac stimulation
and bronchodilation
Pharmacokinetics
 ROUTE: SQ, IV, topical,
inhalation, intracardiac,
instillation
 Not given orally (rapidly
metabolized in the GI tract/liver)
 Metabolized in the liver and
excreted in the urine
Pharmacodynamics
 Frequently used in emergencies to treat
anaphylaxis
 A potent inotropic drug (strengthen myocardial
contraction)

EFFECTS of Epinephrine:
1. Increases CO
2. Vasoconstriction
3. Elevates SBP
4. Increases HR
5. bronchodilation
 High doses can result in – cardiac dysrhythmias
(monitor ECG)
 Onset/peak concentration times are rapid
 Epinephrine with digoxin – cardiac dysrhythmias
 Drugs that decreases the action of epinephrine:
1. beta-blockers
2. tricyclic antidepressants (TCA)
Therapeutic use/effects
 Treats
1. allergic reaction
2. anaphylaxis
3. bronchospasm
4. cardiac arrest

MOA: Promotion of CNS and cardiac stimulation and

bronchodilation

Side effects
 Anorexia, nausea, vomiting, nervousness, tremors,
agitation, headache, pallor, insomnia, syncope,
dizziness
Adverse reaction
 Palpitations
 Tachycardia
 Dyspnea
 Life-threatening – Ventricular fibrillation,
pulmonary edema

Contraindication
 Cardiac dysrhythmias
 Pregnancy
 Cardiogenic shock
 Hypertension
 Hyperthyroidism
 DM
 Trade names: Levarterenol,
Levophed
 Acts on alpha1 and beta1
 Given IV incorporated in D5W
 Increases BP and CO

Therapeutic use
 Shock (Potent vasoconstrictor)

Nursing consideration
 BP monitoring every 2-5 min
during infusion
 Trade name: Intropin
 Acts on alpha1 and beta1
 Given PO and IV

Therapeutic use
 Correct hypotension
 Trade name: Neo-Synephrine
 Nasal decongestant
 Given via nasal instillation
 Acts on alpha1

Therapeutic use
 Nasal congestion
 Common colds
 Sinusitis and allergic rhinitis

Nursing consideration
 Have the client blow the nose before
administration
 Trade name: Sudafed, Actifed,
Co-Tylenol, Pediacare
 acts on alpha and beta1
 Nasal decongestant
 Given PO

Therapeutic use
 Nasal congestion

Nursing consideration
 Avoid taking with hx of
hypertension, cardiac disease,
DM
 Trade name: Alupent, Metaprel
 Acts on beta1 (increased heart rate) and beta2
(bronchodilation)
 Given PO/inhalation

Therapeutic use
 Bronchospasm
 Trade name: Dobutrex
 Acts on beta1
 Given IV

Therapeutic use
 Cardiac
decompensation/Cardiogenic
shock (enhance cardiac
contractility, SV & CO)
 Trade name: Brethine, Brethaire,
Bricanyl
 Acts on beta2
 Given PO and inhalation

Therapeutic use
 Bronchospasm (primary use)
 Prevents premature birth during
pregnancy
 Trade name: Yutopar
 Acts on beta2 and some beta1
 Given PO and IV

Therapeutic use
 Decrease/stop uterine
contraction
 Beta2 adrenergic agonist
 Mode of action: stimulates
beta2 adrenergic receptors
in the lungs – relaxation of
bronchial smooth muscles
 Trade name: Proventil,
Salbutamol, Ventolin,
Novo-Salmol
 Response – bronchodilation
 Given for asthmatic
patient
 High doses may affect
beta1 receptors – increase
HR
Side effects
 tremors, restleness and nervousness

Adverse reactions
 Palpitations, reflex tachycardia, hallucinations
 Life-threatening: cardiac dysrhythmias

Therapeutic Use
 Treats bronchospasm, asthma, bronchitis and other
COPD
 Record client VS
 Report signs of increasing BP and HR
 Monitor BP every 3-5 minutes when giving alpha
Adrenergics IV
 Report side effects:
tachycardia, palpitations, tremors, dizziness
and increased blood pressure
 Check urinary output and assess bladder distension
(urinary retention)
 For cardiac resuscitation,
epinephrine given 1mg/ml
diluted in 10 ml of saline solution
 Monitor IV site frequently when
administering norepinephrine
bitartrate (Levarterenol) or
dopamine (Intropin) – because
infiltration from these cause
tissue necrosis
 ANTIDOTE for norepinephrine
(Levophed) and dopamine is
phentolamine mesylate
(Regitine) 5-10mg, diluted in 10-
15ml of saline
 Offerfood to avoid nausea and vomiting
 Evaluate blood glucose levels (hypeglycemia)
 Aka. Adrenergic antagonist or
sympatholytics
 Blocks the effect of the
adrenergic neurotransmitters
either by
1. directly occupying the
alpha or beta receptors or
2. inhibiting the release
the release of the
neurotransmitters
(norepinephrine and
epinephrine)
Alpha 1
 Vasodilation (decrease BP)
 Miosis
 Reflex tachycardia
 Reduces contraction of smooth muscle in bladder

Beta 1
 Decreases HR
 Reduces force of contraction

Beta 2
 Constricts bronchioles
 Contracts uterus
 Decrease blood sugar (inhibits glycogenolysis)
 Block or inhibit a response at the alpha adrenergic
receptor sites
 2 groups
a. Selective alpha blockers – block alpha 1
b. Nonselective alpha blockers – blocks alpha 1
and alpha 2
 EFFECTS
1. Promotes vasodilation (decreasing BP/
Orthostatic hypotension)
2. increase PR (compensatory mechanism)
3. dizziness
 Therapeutic use
a. used to treat peripheral
vascular disease (promotes
vasodilation leading to increase
blood flow to the extremities)
e.g. Raynaud’s phenomenon,
Buerger’s disease
b. Used to treat mild to
moderate hypertension
 E.g. tolazoline (Priscoline),
phentolamine mesylate
(Regitine)
doxazoson mesylate (Cardura)
prazoson HCL (Minipress)
terazosin HCL (Hytrin)
 is excessively reduced blood flow in response
to cold or emotional stress, causing
discoloration of the fingers, toes, and
occasionally other areas
 pathophysiology includes hyperactivation of
the sympathetic nervous system causing
extreme vasoconstriction of the peripheral
blood vessels, leading to tissue hypoxia.
 Chronic, recurrent cases can result in
ulceration and ischemic gangrene.
Raynaud’s phenomenon
s a recurring progressive inflammation and
thrombosis (clotting) of small and medium
arteries and veins of the hands and feet.
 It is strongly associated with use of tobacco
products, primarily from smoking, but also from
smokeless tobacco
 Peripheral pulses are diminished or absent
 color changes in extremity may range from
cyanotic blue to reddish blue
 Ulcerations and gangrene in the extremities are
common complications, often resulting in the
need for amputation of the involved extremity
Buerger’s disease
 Aka. Beta-blockers
 Blocks beta adrenergic receptors sites
 Decreases HR and BP
 2 groups
a. Nonselective beta blockers – blocks both
beta 1 and beta 2 receptors (Use in extreme
caution in COPD or asthama)
b. Selective beta blockers - blocks beta 1
receptors
 Therapeutic use
1. cardiac dysrhythmias
2. mild hypertension
3. mild tachycardia
4. angina pectoris/Myocardial Infarction
 Side effects:
1. bradycardia
2. palpitations
3. hypotension
4. headache
5. dizziness
6. hyperglycemia
7. bronchospasm
 Nonselective beta blockers
Prototype drugs: carvedilol (Coreg), labetalol
(Normodyne, Trandate), carteolol (Cartrol),
penbutolol (Levatol), propanolol HCL (Inderal),
nadolol (Corgard), pindolol (Visken), sotalol
(Betapace), timolol maleate (Blocadren)
 Selective beta blockers
Prototype drugs: metoprolol (Lopressor), atenolol
(Tenormin), acebutol HCL (Secretal), Betaxolol
(Kerlone), bisoprolol fumarate (Zebeta), esmolol
HCL (Brevibloc)
 Obtain baseline vitals signs (bradycardia and
decrease in BP re common cardiac effects of
beta adrenergic blockers)
 Advise client to avoid abruptly Stopping a
beta blocker; rebound hypertension, rebound
tachycardia or angina could result
 Teach client and family how to take pulse
and blood pressure
 Encourage client to avoid orthostatic
(postural) hypotension by slowly rising from
supine or sitting positions to standing
 Aka. Cholinergic stimulants, cholinergic agonists
 Stimulate the parasympathetic nervous system by
mimicking the neurotransmitter acetylcholine
 Acetylcholine (Ach) – a neurotransmitter located at
the ganglions (group of nerve cells) and the
parasympathetic terminal nerve endings
Cholinergic receptors sites
1. Muscarinic receptors
 Stimulate smooth muscle (GIT, GUT, glands, heart)
and slow heart rate
2. Nicotinic receptors (neuromuscular) – which affect
skeletal muscles

2 types of Cholinergic drugs

1. Direct-acting cholinergic drugs – acts on receptors
to activate a tissue response
2. Indirect-acting cholinergic drugs (Cholinesterase
Inhibitors) – inhibit the action of the enzyme
“cholinesterase (ChE)/acetylcholinesterase(AChE)”
to permit acetylcholine to attach to the receptor
sites
 Cardiovascular: decrease HR, lower blood pressure
(vasodilation)
 GIT: increase peristalsis
 GUT: urinary bladder contraction
 Ocular: pupil constriction (miosis)
 Lung: bronchial constriction
 Salivary glands: increase salivation
 muscle: maintains muscle strength, increase
neuromuscular transmission
 Primarily selective to muscarinic receptors
but nonspecific (GIT, GUT, glands, heart)
 Prototype drugs:
1. betanechol (Urecholine)- used to treat
urinary retention; promotes urination by
causing bladder contraction, given PO &
SQ

2. metoclopromide (Reglan) – used to

treat GERD, increases gastric emptying
time, given PO, IM, IV

2. pilocarpine HCL (Pilocar) – reduce

fluid pressure for glaucoma by pupil
constriction (miosis)
 Sideeffects: gastric pain/cramping, diarrhea,
increase salivary and bronchial secretions, miosis,
bradycardia, orthostatic hypotension,
bronchoconstriction
 Aka. Cholinesterase inhibitors,
acetylcholinesterase inhibitors, anticholinesterase
 Do not act on receptors
 Binds with cholinesterase to allow acetylcholine to
activate muscarinic and nicotinic cholinergic
receptors
 inhibit or inactivate enzyme cholinesterase,
permitting acetylcholine to accumulate at the
receptor sites
 Permit skeletal muscle stimulation which increases
the force of muscular contraction
 Useful to increase muscle tone for clients with
myasthenia gravis (Neuromuscular disorder)
 Therapeutic use:
1. Primarily used to treat myasthenia gravis
(neuromuscular disorder that leads to fluctuating muscle
weakness and fatigue. In the most common cases, muscle
weakness is caused by circulating antibodies that block
acetylcholine receptors at the postsynaptic neuromuscular
junction)
2. glaucoma (is a term describing a group of ocular
(eye) disorders resulting in optic nerve damage or loss to the
field of vision, in many patients caused by a clinically
characterized pressure buildup in regards to the fluid of the
eye (intraocular pressure-associated optic neuropathy)
3. Alzheimer’s disease (chronic neurodegenerative
disease that usually starts slowly and gets worse over
time.[1][2] The most common early symptom is difficulty in
remembering recent events (short term memory loss)
 Side effects: increase GIT motility, bradycardia, miosis,
bronchial constriction and increase urination
Myasthenia gravis Alzheimer’s disease
Glaucoma
 Prototype drugs:
demecarium bromide (Humorsol), echothiophate
iodide (Phospholine iodide), isoflurophate
(Floropryl) – used to reduced Intraocular pressure
(IOP) in glaucoma

2 types of indirect acting:

1. Reversible Cholinesterase Inhibitors
 Binds with enzyme cholinesterase for several
minutes to hours
 Mode of action
1. Produce pupillary constriction
in the treatment of glaucoma
Prototype: physostigmine
salicylate (Eserine Salicylate)

2. Increase muscle strength in

client with myasthenia gravis
Prototype drugs:
Neostigmine (Prostigmin-short
acting),
pyridostigmine bromide (Mestinon-
moderate acting),
ambenonium chloride (Mytelase-
long acting),
edrophonium chloride (Tensilon-
short acting for diagnostic
purposes)
2.Irreversible Cholinesterase Inhibitors
 Bind with the enzyme permanently (long lasting
effect)
 Used to produce pupillary constriction
 ANTIDOTE: pralidoxime (Protopam)
 Monitor VS (HR/ BP)
 Record fluid intake and output
 Give cholinergics 1 hour before or 2 hours after
meals
 Observe for side effects: cramping, diarrhea,
increase salivation and bronchial secretions,
bradycardia, orthostatic hypotension
 Auscultate breath sounds for rales (crackling
sounds); cholinergic drugs can increase bronchial
secretions
 ANTIDOTE: atropine sulfate – for cholinergic
overdose
 Early signs of overdose: salivation, sweating,
abdominal cramps and flushing
 For indirect acting drugs: monitor for cholinergic
crisis (overdose) – muscular weakness and
increased salivation
 Aka. Cholinergic blocking agents, cholinergic
antagonists, antispasmodics, muscarinic antagonist

 Inhibitsthe action of acetylcholine by occupying

the acetylcholine receptors - Blocking the PS
nerves producing SNS-like effects
 Organs affected by the anticholinergic group of
drugs are heart, respiratory tract, GI tract, urinary
bladder, eyes and glands
 Major responses to Anticholinergics
1. decrease GIT motility
2. decrease salivation
3. mydriasis
4. increase pulse rate
5. decrease bladder contraction
6. decrease muscle rigidity and tremors
7. dilates bronchial airway
 Antidotefor Cholinesterase inhibitors
 Prototype drugs:

- Propantheline bromide (Pro-

Banthine) – antispasmodic for peptic
ulcer, used for the treatment of
excessive cramps or spasms of the
stomach, intestines (gut) or bladder,
and involuntary urination
- Scopolamine hydrobromide –
preanesthetic, used in the treatment
of motion sickness; postoperative
nausea and vomiting
- Cyclopentolate HCL (Cyclogyl) -
causes mydriasis to dilate pupil
before an eye examination
 Classic anticholinergic
 Act on muscarinic receptor, but have
little effect on nicotinic receptor
 Main use:
1. preoperative medication-
decrease salivary secretions
2. antispasmodic drug – peptic
ulcers, relaxes smooth muscles of
the GIT/decreasing peristalsis
3. increases heart rate for
bradycardic patient
4. antidote for cholinesterase
inhibitor or muscarinic drug i.e.
bethanechol
Side effects/Adverse reactions
 Dry mouth
 Decrease perspiration
 Blurred vision
 Tachycardia
 Constipation
 Urinary retention
 Nausea
 Headache
 Dry skin
 Abdominal distention
 Photophobia
 coma
Nursing Responsibilities: ATROPINE SULFATE
 Obtain baseline vital sign. Tachycardia is a side
effect in large doses
 Assess urine output. Urinary retention may occur
 Encourage client to void before taking the
medication (urinary retention)
 Determine fluid intake and output. Encourage
client to void before taking the medication
(anticholinergic can cause urinary retention)
 Check for constipation caused by decrease in GI
motility
 Provide mouth care. Atropine decreases oral
secretions and can cause dryness
 Advice patient that atropine is Contraindicated in
glaucoma
Major group of CNS Stimulants:
 Amphetamines –that is used in the treatment of
attention deficit hyperactivity disorder (ADHD),
narcolepsy, and obesity
 Caffeine - ingested to relieve or prevent
drowsiness and to improve performance.
 Analeptics – act on brainstem and medulla to
stimulate respiration
 Anorexiants – acts on cerebral cortex and
hypothalamus to suppress appetite
Note:
 Long term use of amphetamines can produce
psychological dependence or tolerance
 Abruptly stopping of the drug may result in
depression and withdrawal symptoms (set of
symptoms occurring in discontinuation or
dosage reduction of some types of
medications)
 extracted from alpha
methylphenethylamine; potent central
nervous system (CNS) stimulant
 Stimulates release of the neurotransmitters –
norepinephrine and dopamine – from the
brain and the SNS.
 Improve cerebral cortex activity resulted in:
1. high performance on working memory
2. increase motivation to perform task
3. increase wakefulness
 Causes euphoria and alertness; but causes
sleeplessness, restlessness, tremors and
irritability.
 Continuous use may results to cardiovascular
problems - increased HR, palpitations,
cardiac dysrhythmias, and increased BP
 Half-lifevaries from 4 to 30 hours
 Given for narcolepsy, and in some cases for
ADHD(Attention deficit hyperactivity disorder),
depression, obesity and nasal congestion

Side Effects & Adverse Reactions

 Restlessness, insomnia, tachycardia,
hypertension, heart palpitations, dry mouth,
anorexia, weight loss, diarrhea, or
constipation, and impotence
 caused by a dysregulation of the neurotransmitters
– serotonin, norepinephrine, and dopamine
 Occurs primarily in children usually before 7 years
old
 3-7 times more common in boys than girls
 Characteristic behaviors include
1. Inattentiveness,
2. inability to concentrate,
3. restlessness,
4. hyperactivity,
5. inability to complete tasks, and
6. impulsive,
7. poor coordination
 a chronic neurologic
disorder due to inability
to regulate sleep wake
cycle characterized by
falling asleep during the
normal waking activities
such as driving a car or
talking with someone
 Characterized by
frequent, brief and
uncontrolled bouts of
sleep, sometimes
accompanied by
hallucinations and
inability to move (Sleep
paralysis)
 amphetamine-like drugs
 MOA: Given to increase the child’s
attention-span and cognitive
performance (memory, reading)
and decrease impulsiveness,
hyperactivity and restlessness
 Methylphenidate(Ritalin) – most
commonly prescribed to treat
ADHD and also used to treat
narcolepsy
 Given 10 mg, 2-3 times a day, 30
mins before meals
Pharmacokinetics
 well absorbed in the GI mucosa
 Usually administered twice a day before
breakfast and lunch
 given 30-45 minutes before meals for
better absorption
 not be given within 6 hours before sleep
because it may cause insomnia
Side effects/Adverse reactions
Insomnia, restlessness, nervousness,
tremors, irritability
tachycardia, palpitations, elevated
blood pressure
Growth suppression
Transient loss of weight in children
Pharmacodynamics
 Corrects ADHD by decreasing hyperactivity and
improving attention span
 Amphetamines are generally avoided because
of higher potential for abuse, habituation, and
tolerance
 sympathomimetics enhance the actions of
methylphenidate
 Antihypertensives and barbiturates can
decrease the action of these drugs
 Foods that contain caffeine should be avoided
because they increase drug action
 Amphetamine sulfate (Adderall) CSS
II
Narcolepsy – PO5-20mg daily TID
ADHD – PO 2-5mg/day
 Amphetamine HCL (Desoxyn) CSS II
ADHD – PO 2-5mg daily
Nursing Responsibilities:
METHYPHENIDATE (Ritalin)
Monitor VS
Record height, weight and growth of
children
Observe client for withdrawal
symptoms e.g. nausea, vomiting,
weakness, headache
Monitor for side effects
a new drug for
narcolepsy
 Increases the amount of
time that clients with
narcolepsy feel awake
 Does not disrupt night
time sleep
 Given PO, 200mg/day
 Side effects: headaches,
nausea, diarrhea and
nervousness
 Appetite suppressants usually for
obesity
 Given PO

Side effects:
 Nervousness, restlessness, irritability,
insomnia, palpitations, hypertension
(for long term use)
Prototype drugs:
1. Amphetamines
 Considered once as anorexiants for
short-term use (4-12 weeks)
 Not recommended due tolerance,
psychologic dependence and abuse
2. Benzphetamine HCL (Didrex)
 Similar to amphetamines

 Potential for abuse

 PO 25-50mg daily TID

3. Dextroamphetamine (Dexedrine)
 Treat obesity
 Causes restlessness and insomnia
 For short term use

4. Diethylpropion HCL (Dospan, Tenuate,

Tepanil)
 For appetite suppression by stimulating
the appetite control in the hypothalamus
 Take 1 hours before meals
 For short term use

5. Mazindol (Mazanor, Sanorex)

 Treat obesity
 Give with meals to avoid GI discomfort

6.orlistat (Xenical)
 For long term weight loss and weight
maintenance by reducing fat absorption in
the GIT
 Given PO 60-120mg tid during meals
containing fat
 CNS stimulants that mostly affect the
brainstem and spinal cord but also
affect the cerebral cortex
 Primary use is to stimulate respiration

Xanthines (methylxanthines)
1. Caffeine
 Stimulates CNS, large doses stimulate
respiration
 Used for newborns with apnea and
respiratory distress to stimulate
respiration
 Increases HR and BP
 Given PO, IM, IV (5-10mg/kg/day)
2. Theophylline
 Used mostly to relax bronchioles
but also used to increased
respiration in newborns with apnea
 Used to relax the bronchioles
(Bronchodilation)
 Given 5mg/kg on day 1, then
2mg/kg/day
Side Effects & Adverse Reactions
 nervousness, restlessness, tremors,
twitching, palpitations, and
insomnia
 Other side effects include diuresis,
GI irritation, and rarely tinnitus
(ringing in the ear)
 High doses can cause psychologic
dependence
Respiratory Central Nervous
System Stimulant
Doxapram HCL (Dopram)
 CNS and respiratory stimulant
 Used to treat respiratory
depression caused by drug
overdose, pre- and post-
anesthetic respiratory
depression, and COPD
 Administered intravenously (0.5
– 1mg/kg), and its onset of
action is within 20-40 seconds
with a peak action of 2 minutes
 Overdose can cause
hypertension, tachycardia,
trembling and convulsions
 “pain on one side of the head”
 neurological disease characterized by
recurrent moderate to severe
headaches
 Characterized by a unilateral throbbing
(pulsating) head pain, accompanied by
nausea, vomiting, and photophobia
worsen with physical activity
 Symptoms frequently persist for 4 to 24
hours and for several days in some
cases
 Preceded with an aura (visual/sensory
disturbance)
 3 times more common in women than
man
Pathophysiology
 caused by inflammation and dilation of the
blood vessels in the cranium
 Etiology is unknown but some theories suggest
that an imbalance in serotonin – (causes
vasoconstriction and suppresses migraine
headaches)
 foods such as cheese, chocolate, and red wine
can trigger an attack
 Familial tendency
2 types
1. Classic migraine – associated with aura that
occurs minutes to hours before onset
2. Common migraine – not associated with aura
a neurological disorder characterized by
recurrent, severe headaches on one side of the
head, typically around the eye
 accompanying autonomic symptoms includes
eye watering, nasal congestion and swelling
around the eye, typically confined to the side
of the head with the pain.
 Occurs in a series of cluster attacks – one or
more attacks everyday for several weeks
 Not associated with aura and do not cause
nausea and vomiting
 men are more commonly affected than women
s the most common type of primary
headache
 pain is frequently present on both
sides of the head at the same time;
typically mild to moderate, but may
be severe.
 pain can radiate from the lower
back of the head, the neck, eyes, or
other muscle groups in the body
typically affecting both sides of the
head
 more common in women than men
Preventive treatment
includes
 Beta adrenergic blockers like
propanolol (Inderal),
atenolol (Tenormin), and
metoprolol (Lopressor)
 Calcium channel blockers
like verapamil (Calan), and
nifedepine (Procardia)
 Tricyclic antidepresants like
triptyline (Elavil) and
imipramine (Tofranil)
Treatment depends on the
intensity of pain
mild migraine attacks
1. Nonseroidal antiinflammatory
drugs (NSAIDs)
 Aspirin, acetaminophen, ibuprofen,
naproxen (Aleve)

2. Opioid analgesics
 Meperidine (Demerol)
For moderate to severe attacks
Ergot Alkaloids
1. Ergotamine tartrate
 nonspecific serotonin agonist and
vasoconstrictor
 Antimigraine drug
 taken early during an attack
 N&V may occur
 Available in SL and PO tablets

2. Dihydroergotamine mesylate
 An ergot alkaloid
 Can be administered SQ, IM, IV, or
nasal spray
 Prevent or abort migraine attacks
Selective serotonin receptor agonists
(triptans)
1. Sumatriptan (Imitrex)
 Anti-migraine drug
 5-HT1 receptor agonist
 Latest drug developed for treatment of
migraine
 More effective than ergotamine in treating
acute migraine attacks
 Treat acute migraine attacks and cluster
headaches
 MOA: Promotes vasoconstriction of cranial
arteries to relieve migraine attacks
 Given PO (25-50 mg for 1 dose), SQ (6mg)
and intranasal