Neuroscience Drugs

Inhibitors of Ach release

 Aminoglycosides, Magnesium
 Botulin Toxin, Β-Bungarotoxin
 Neurotoxins: Saxitoxin (red tide), Tertodotoxin, Ciguatoxin

Interferes with postsynaptic action of Ach (charged N groups, similar to Ach, very polar; causes skeletal
muscle paralysis: eye > mastication > limbs > abdominal > respiratory)

IM, IV (usually 0.3 – 1mg/kg BW by IV)

Onset < 5 mins

1st phase elimination involves removal from site

Non-depolarizing (competitive antagonist of nicotinic recptors, binds to receptors and prevents

action of Ach)

 d-turbocurarine
o Long Acting 30-120 mins
o 2nd phase elimination: Renal
 Pancuronium
o Long Acting 30-120 mins
o 2nd phase elimination: Renal
o Adverse effects: M2 muscarinic receptor blockade
 Vecuronium
o Medium acting 15-30 mins
o 2nd phase elimination: Hepatic
 Atracurium
o Medium acting 15-30 mins
o 2nd phase elimination: Hepatic
 Alcuronium
o Medium acting 15-30 mins
o 2nd phase elimination: blood (laudanosine metabolite produced)
 Mivacurium
o Short acting 5-15 mins

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 o 2nd phase elimination: blood - pseudocholinesterase

Depolarizing (agonist of nicotinic receptors, not metabolized by acetlycholinesterase, hence

persistent depolarization as it is degraded slower than acetylcholine causing blockage of voltage gated
sodium channel)

 Succinylcholine
o Short acting 5-15 mins
o 2nd phase elimination: blood – pseudocholinesterase
o Adverse effects:
 Malignant hyperthermia
 Increased intraocular pressure
 Post operative pain
 Increased K+ -> hyperkalemia

Other adverse effects

 Histamine release
 Ganglionic receptor binding

Uses:

Muscle relaxant

 With general anaesthetics

 During endotracheal intubation
 During orthopedic manipulation
 To alleviate peripheral symptoms of convulsion
 To provide controlled ventilation (obstructive airway disease)

Dimethphenyl-piperazinium – nicotinic ganglionic receptor agonist

Atropine – muscarinic receptor antagonist

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List of Drugs Affecting α-Adrenergic Receptors
α2 agonists
 Non-selective agents
o Norepinephrine
o Epinephrine
 Selective agents
o Clonidine
o Alpha-methylnoradrenaline

α1 agonists
 Non-selective agents
o Norepinephrine
o Epinerphrine
o Ephedrine
 Selective agents
o Phenylephrine

α1 antagonist
 Non-selective agents
o Phentolamine
o Phenoxybenzamine
 Selective Agents
o Prazosin
o Doxazosin
o Terazosin

β1 agonist
 selective
o Dobutamine

β2 agonist
 Non-selective agents
o Norepinephrine
o Epinephrine
o Isoproterenol
o Isoprenaline
 Selective agents
o Salbutamol
o Salmeterol
o Terbutaline

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 o Ritodrine
o Metoproterenol
o Pirbuterol
o Formoterol

β 1 antagonists
 nonselective
o alprenolol
o oxprenolol
 selective
o metoprolol
o atenolol

β2 antagonist
 Non-selective agents
o Propranolol
o Nadolol
o Sotalol
 Selective Agents
o timolol
o betaxolol

List of Drugs Affecting Muscarinic Receptors

Muscarinic Agonists

 Non-selective agents
o Acetylcholine
o Pilocarpine
o Bethanechol
o Methacholine
 Selective Agents
o Sildenafil/Viagra

Muscarinic Antagonist

 Non-selective agents
o Atropine(Lomotil)
o Scopolammine (hyoscine)
 Selective Agents
o Pirenzepine (M1)

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 o Ipratropium bromide (M3)
o Homatropine (M3)
o Tropicamide (M3)

Drugs acting in the CNS to alter ANS activity

α2 agonists (activate vagus nerve -> inhibit sympathetic nerve at medullary area of brain thus
reduction in heart rate and sympathetic activity on blood vessels)

 Clonidine
 Α-methylnoradrenaline

β-antagonists (inhibit sympathetic nerve activity area of brain)

 Propranolol

Drugs that affect ANS ganglionic transmission

 Stimulants (not used therapeutically) (increase blood pressure, heart rate, release
epinephrine, increase GIT motility)
o Acetylcholine
o Nicotine

 Blockers/Antagonists
o Trimethaphan
 Competitive antagonists at ganglionic nicotinic receptors
 Used occasionally to treat hypertensive crisis
 IV
o Pentolinium
 Competitive antagonists at ganglionic nicotinic receptors
o Hexamethonium

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Drugs that affect transmission at the sympathetic nerve terminals

 α-2 adrenergic agonists (Inhibit norepinephrine release and reduce sympathetic activity
to tissues, can be used to relieve hypertension)
o Non-selective agents
 Norepinephrine
 Epinephrine
o Selective Agents
 Clonidine
 α-methylnorepinephrine

 β2 – adrenergic antagonists (inhibit the facilitated release of norepinephrine by

blocking β2 receptors (which open calcium channels) on nerve terminals -> reduce sympathetic
nerve activity to tissues, also used for hypertension)
o Non-selective
 Propranolol
 Nadolol
 Sotalol

 Guanethidine (briefly blocks stimulating effect of action potential and temporarily inhibits
mobilization of neurotransmitter vesicles, causes brief reduction in sympathetic nerve activity)
o Taken up by active uptake 1 (competes with NE)
o Drug enters vesicles and displaces NE where some is metabolized by MAO (Monoamine
oxidases), remainder leaks into junction producing sympathetic effects
o Eventually NE is depleted leading to prolonged reduction of sympathetic activity
o Used when there is overstimulation of sympathetic activity (e.g. hypertensive crisis)

 Alkaloids (compete with NE for uptake-1, NE accumulates in junction and produces

prolonged effects)
o O, never IV
o Cocaine
 Release NE from vesicles
o Ampetamines
 Release NE from vesicles
o Ephedrine
 Release NE from vesicles
o Tyramine
 From dairy products

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  Release NE from vesicles

Drugs that affect transmission at parasympathetic nerve terminals

 Acetylcholine
 Vesamicol (inhibits transport of Ach from cytoplasm into vesicles, depletion of vesicles and
reduction in parasympathetic activity)
 Botulinum toxin (botox) (inhibits mobilization of Ach vesicles to nerve terminal membrane, also
reduces cholinergic transmission at the somatic nerve/skeletal muscle junction leading to
muscle relaxation)

 Acetylcholinesterase drugs (inhibit ache and degradation of ach at neuroeffector and

neuromuscular junction, ach effect is prolonged)
o Reversible Agents
 Neostigmine
 Physostigmine
 Pyridostigmine
 Edrophonium
o Irriversible Agents
 Malathion
 Parathion
 Sarin (nerve gas)

Autonomic drugs on salivary glands

 M3 Receptor Agonist(Stimulate secretion of aqueous saliva)

o Acetylcholine
o Pilocarpine
o Bethanechol
o Methacholine
 M3 Receptor Antagonist (inhibit salivary secretion induced by M3 agonists)
o Atropine
o Scopolammine (hyoscine)
 β adrenergic receptor agonist (stimulate viscous saliva rich with amylase)
o Norepinephrine

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 o Epinephrine
 Intense sympathetic nerve stimulation inhibits blood flow to salivary glands and reduce
secretion

Autonomic drugs on GIT

 M1 and M3 agonists (stimulate secretion of gastric acid, M3 also contract stomach

smooth muscle and relax pyloric sphincter which facilitates stomach emptying. Muscle
contraction increases peristalsis and may lead to diarrhea)
o Acetylcholine
o Pilocarpine
o Bethanechol

 M1 and M3 Antagonists (inhibit secretion of gastric acid)

o Non selective agents (also inhibit stomach muscle contraction, pyloric sphincter
relaxation -> delay gastric empting, inhibiting contraction may lead to constipation)
 Atropine
 Lomotil - Antidiarrheal drug containing atropine
 Scopolamine
o M1 antagonist
 Pirenzepine

Autonomic drugs on blood vessels

 α1 adrenergic agonists (vasoconstriction, increase in BP decrease in HR [baroreceptor

reflex])
o Nonselective agents
 Norepinephrine
 Epinerphrine
o Selective Agent
 Phenylephrine
o Uses: Reversal of low blood pressue, nasal decongestant, combination with local
anaesthetic
o Transduction process: phospholipase C enzyme interacts with PIP2 to produce IP3 and
DAG. IP3 (the 2nd messenger) releases Ca2+ from SER which activates MLCK facilitating
contraction of vascular smooth muscle

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 α1 adrenergic antagonist (vasodilation, fall in BP, increase in HR)
o Nonselective agent
 Phentolamine
 Phenoxybenzamine
o Selective Agents
 Prazosin
 Doxazosin
 Terazosin
o Uses: hypertension (preferred with hypertensive male patients with benign prostate
hyperplasia (BPH))

 β2 adrenergic receptors agonists (vasodilation, fall in BP, increase in HR, not

exploited clinically but occur as side effect when treating bronchial asthma)
o Epinephrine
 Low doses
o Non Selective
 Isoproterenol
 Isoprenaline
o Selective
 Salbutamol
 Salmeterol
 Terbutaline
o Transduction process: activate adenylate cyclase enzyme, interacts with ATP to produce
cAMP (second messenger), cAMP inactivates MLCK via PKA preventing interaction
between actin and myosin leading to vasodilation

 β2 adrenergic receptors antagonists (reverse β 2 [vasoconstriction], facilitate

predominance of α1 mediated vasoconstriction of cutaneous blood vessels leading to cold
extremities as side effect, not exploited clinically)
o Nonselective agents
 Propranolol
 Nadolol

 M3 agonists (vasodilation through relaxation of smooth muscle, fall in BP increase in HR)

o Does not contribute to normal control but receptors are present (parasympathetic)
o Acetylcholine
o Bethanechol
o Pilocarpine
o Not exploited clinically, but occurs as SE

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 o Transduction same as α1 for 1st part, calcium released activates NO synthase which
converts arginine to NO and citrulline, NO (2 nd messenger) activates guanylate cyclase,
produces cGMP from GTP causing relaxation of vascular muscle -> vasodilation and fall
in BP

 M3 antagonists (inhibit effect of M3 agonists but have no effect alone, can alter blood
pressure through action on the heart. Na causes initial slow depolarization and Ca causes
subsequent depolarization at SA nodes)
o Atropine
 Large doses release histamines -> fall in BP
o Scopolamine
o Homatropine

Autonomic drugs on heart

 M2 receptor agonists (act on M2 receptors at SA and AV nodes, increase K+ outflow from

nodal cells, cells become hyperpolarized -> slow rate of AP generation -> reduction in HR
o M2 receptors linked to adenylate cyclase -> inhibit production of cAMP from ATP ->
reduced entry of Ca -> reduction in force of atrial muscle contraction
o Nonselective agents
 Acetylcholine

 M2 receptor antagonists (reverse actions increase HR and force of contraction)

 β receptor agonists (mainly β1 some small β2, opposite of M2, cAMP increases Ca inflow
by phosphorylating channels which cause them to become open)
o Nonselective agents
 Epinephrine
 Norepinephrine
 Isopoterenol
o Selective β1 agents
 Dobutamine
o DO NOT MIX DOBUTAMINE AND DOPAMINE
o Used in treatment of cardiovascular disease

 β 1 receptor antagonists (inhibit β agonists effect, reduction in HR and force of

contraction)
o Nonselective agents
 Propanolol

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  Nadolol
o Nonselective partial agents
 Alprenolol
 Oxprenolol
o Selective agents
 Metoprolol
 Atenolol
o Uses: hypertension, cardiac arrhythmias, angina pectoris

Autonomic drugs on respiratory system

 Mainly parasympathetic but also by circulating epinephrine from adrenal medulla, secretion of
mucus controlled by both divisions
 M3 agonists (muscle contraction and secretion of mucous -> increased airway resistance)
o Acetylcholine
o Bethanechol

 M3 antagonists (reduction of airway resistance)

o Atropine
o Ipratropium bromide
o Scopolamine
o Treatment of bronchitis and bronchoconstriction
o IP3 and Ca2+ mediate effects

 β2 agonists (relax bronchial smooth muscle leading to bronchodilation and decreased airway
resistance)
o Production of cAMP mediates β2 agonist effect by inhibiting MLCK
o Nonselective agents
 epinephrine
 ephedrine
o Selective agents
 Salbutamol
 Salmeterol
 Terbutaline
o Uses: asthma

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  β2 antagonists (inhibit effects, precipitate asthmatic attack in susceptible subjects)
o propranolol

 α1 agonists (act on blood vessels supplying mucous glands, reduce blood flow to these
glands -> reduced production of mucous)
o IP3 and Ca2+ mediate effect
o Nonselective
 Epinephrine
 Ephedrine
o Selective agents
 Phenylephrine
o Uses: nasal congestion
o constant cutting off of blood flow to goblet cells causes necrosis

Autonomic drugs on urinogenital system

 Both divisions influence function

 M3 agonists (contract detusor muscle and relax the internal sphincter at the neck of
bladder)
o Acetylcholine
o Bethanechol
o Uses: non-obstructive urinary retention
 M3 antagonists (inhibit contraction of bladder)
o Atropine
o Scopolamine
o Uses: increased urinary frequency
 β2 agonists (relax detrusor muscle, minor effect)
o epinephrine
o salbutamol
 α1 agonists (contract internal sphincter)
o Norepinephrine
o Epinephrine
 α1 antagonists (inhibit effect)
o Prazosin
o Uses: Facilitate voiding of urine in male hypertensive patients with BPH

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Autonomic drugs on reproductive system

 α1 agonists (contract vas deferens to cause ejaculation)

o NE
o E
 M3 agonists (stimulate production of NO and cGMP to increase blood flow to penis causing
erection)
o Ach
o Uses: erectile dysfunction, given with agents which prevent cGMP degradation e.g.
Sildenafil/Viagra
 β2 agonists (relax uterine muscle)
o Salbutamol
o Ritodrine
o Uses: prevention of premature labour

Autonomic drugs on eye

 M3 agonists (sphincter papillae parasympathetically innervated, reduce amount of light

reaching retina)
o Ach
o Pilocarpine
o Anticholinesterase drugs (e.g. physiostigmine)
 M3 antagonists (inhibit pupil contraction leading to dilation)
o Atropine
o Homatropine
o Tropicamide
o Used for eye exams
 α1 agonists (dilator papillae innervated sympathetically, relaxes radial muscle leading to
mydriasis ie dilation of pupil)
o Epinephrine
o Phenylphrine
o Light entering eye causes both pupils to contract -> consensual pupil response
o Uses: asses brain damage in comatose and unconscious patients
 M3 agonists (cilliary muscles innervated parasympathetically, contract ciliary muscle
increasing curvature of lens and reduce focal length)
o Ach
o Pilocarpine
o M3 antagonists (atropine) – inhibit effect and interfere with focusing (cycloplegia)

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  β antagonists (IOP determined by net effect of production of aquesous humour from ciliary
body and outflow from anterior chamber of eye, increase rate of production but agonists not
used clinically, antagonists decrease pressure)
o Timolol
o Βxolol
o Uses: glaucoma
 α1 agonists (decrease rate of production of aqueous humour, constrict arteries reduce blood
flow to ciliary body)
o E
o Uses: glaucoma
 M3 agonists (increase rate of outflow of aqueous humour, reduce IOP, contract sphincter
papillae and ciliary muscles leading to increase in flitration angle and patency of trabecular
meshwork ath entrance of canal of Schlemm, this facilitates outflow into episcleral vein)
o Pilocarpine
o Anticholinesterase drugs
o Uses: glaucoma

Treatment of Myasthenia Gravis

Increasing Ach concentration

 Acetylcholinesterases (reversible inhibition of ach-ase -> accumulation of ach)
o Increase ach at NMJ and autonomic junction
o inhibition of pseudocholinesterases in blood
o No dosage schedule fits all patients, need for will vary from day to day
o Different muscles respond differently
o Potential for cholinergic crisis -> emesis, diarrhea, excess salivation, miosis, lacrimation,
increased bronchial secretion, brady/tachycardia
o Edrophonium
 short acting (2 – 10 mins)
 Used to diagnose myasthenia crisis vs cholinergic crisis
 IV
 MC – improved muscle strength
 CC - worsening
o Neostigmine
 SC, IM, O
 R
 onset: IV (4-30mins), O (45-75mins)
 Duration: 3-4 hrs
 T½: 2hrs

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  SE: salivation, anorexia, emesis, abdominal cramps, diarrhea, muscle cramps,
fasciculation, weakness, cholinergic crisis
o Pyridostigmine
 O (well absorbed)
 R
 T½: 4hrs
 SE same as neostigmine

Immunosuppression
 Glucococorticoid (Immunsuppression of thymus gland -> inhibition of nicotinic receptor
antibodies)
o Prednisolone
 1st choice immunosuppressant, marked improvement in 75% of patients
o Prednisone
 prodrug of prednisolone
 small dose gradually increasing
 Onset: 2 – 3 weeks, max: 6 – 8 week
 If improvement after 4 weeks, alternate day dosing done -> 3-4 months at lower
dose
o SE – initial muscle weakness, cushing’s syndrome, water retention, interferes with
glucose use, negative calcium balance, obesity, suppression of adrenal glands (decreases
CRF and ACTH)

 Azathioprine (inhibits lymphocyte proliferation via inhibition of DNA synthesis -> inhibition of
production nicotinic receptor antibodies)
o converted in liver to 6-mercaptopurine, converted in cells to 6-thioguanine triphosphate
o Used alone of in combination with prednisone
o O
o Onset: 3 – 12 months, maximum effect: 12 – 24 months
o SE: hepatotoxicity, emesis, flu-like, bone marrow suppression, teratogenic
 Cyclosporine (prevents activation of T cells)
o O (slow absorption), IV
o gradually increase dose
o Onset: 2 – 12 weeks, max effect: 7 months
o accumulates in tissues, no depression of bone marrow
o T½: 24hrs
o SE: nephrotoxicity, hepatotoxicity, hypertension

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Treatment of Spasticity (cerebral palsy, multiple sclerosis, stroke, dystonia (e.g.
blepharospasm)

 Dantrolene (inhibits ca release from SR -> prevents skeletal muscle excitation contraction
coupling)
o Reserved for traumatic cord lesions, advanced ms, cerebral palsy, malignant
hyperthermia
o O
o H
o T½: 9hrs
o SE: hepatoxic

 GABA effects
o Baclofen (Agonist at GABA-B receptors in spinal cord [pre and post synaptic],
 presynaptic -> reduces nocioceptive inputs, preduce substance P + glutamate
release in spinal cord -> reduced pain)
 postsynaptic -> causes hyperpolarization (increase K+, decrease adenylate
cyclase activity -> increase slow IPSP
 O (good)
 R
 T½: 3 – 4hrs
 SE: minimal sedation, taper withdrawl [sudden anxiety, hallucination
 Uses – lesions of spinal cord
o Diazepam (potentiates action at GABA-A receptors [mostly postsynaptic] -> decreases
AP, acts at spinal and suprapinal lvl to decrease output to moto fibers)
 O, IV
 H
 T½: 60hrs
 Active metabolites – nordiazepam
 Intrathecal baclofen pump -> pump SC with catheter line, pump stores and
releases prescribed amt, pump refilled 6-8 wks by needle through skin
 Botulinum Toxin (Botox, binds to presynaptic nicotinic receptors, inhibits ach release by
preventing synaptic vesicle fusion)
o Uses – significantly in dystonia e.g. blepharospasm (involuntary contraction of eye
muscles)
o IM – affected muscle
o Onset: days, 4 weeks to peaks

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 o Duration: 3 -4 months
o SE: muscle weakness, difficulty swallowing, flu-like, pain and soreness at site, antibody
formation

Respiratory drugs
Asthma Drugs

 Bronchiodilators
o β2agonists (stimulation of β2 receptors on bronchial muscle Þ activation of
adenylate cyclase Þ levels of cAMP Þ relaxation of bronchial muscles. May also inhibit
TNFα release from monocytes and other inflammatory mediators from mast cells)
 Salbutamol /albuterol (Ventolin®)
 short acting
 Duration 4-6 hrs, max effect 30 mins
 Terbutaline
 short acting
 Duration 4-6 hrs, max effect 30 mins
 Salmeterol
 slow onset, long lasting
 not used for acute attacks
 Duration up to 12hrs
 Metoproterenol
 Pirbuterol
 Formoterol
 long lasting
 Duration up to 12 hrs
 Inhalation (less side effects), O, Injection
 SE: tremors, tachycardia, relaxation of pregnant uterus
 Contraindications: Pregnancy, hypertension, arrhythmias

o Xanthine derivatives (Methylxanthines) (Inhibit phosphodiesterase Þ

accumulation of cAMP Þ relaxation of bronchial muscle via increased rate of
inactivation of myosin light chain kinase (MLCK))
 Theophylline
 Aminophylline
 Bronchodilation, improved mucocilliary clearance, increased contractility of
diaphragm
 O, injection

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  CP450
 SE: emesis, increased gastric secretion, tremors, nervousness, seizures,
vasodilation, increased rate of contractions, dieresis, allergic reactions
o Anticholinergic agents (Non-selective inhibition of acetylcholine at M receptors
on bronchial muscles Þ relaxation of muscles, May also: mucociliary clearance, ↓
bronchial secretions)
 Ipratropium Bromide
 Oxitropium
 Uses: Bronchial asthma, COPD
 Inhalation
 Poor absorption in circulation
 Max effect: 30 – 45 mins
 Duration: 4hrs
 SE: very little effect

 Anti-inflammatory
o Glucocorticoids (↓ formation of cytokines (Þ ↓ IgE production)
Inhibition of Phospholipase A2 Þ ↓ arachidonic acid release Þ ↓ leukotriene synthesis
↓ synthesis of PG I2 Þ ↓ vascular permeability Þ ↓ oedema
↓ mucosal hypersecretion
Inhibition of allergen-induced migration of eosinophils
Sensitize smooth muscle to action of b-agonists))
 Oral
 Prednisone
 Methylprednisolone
 Inhalation
 Beclomethasone
 Triamcinolone
 Flunisolide
 Budesonide
 Fluticasone
 Maintenance therapy (± b-agonists or anti-leukotrienes)
 Inhalation
 Status asthmaticus
 IV steroids
 Inhalation SE: sore throat, hoarse voice, oropharyngeal candidasis
 Oral SE: peptic ulcer, osteoporosis, adrenal suppression, immune suppression,
hyperglycemia, growth retardation in children, cataract formation

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 o Mast Cell Stabilizers (inhibition of mast cell degranulation -> inhibition of release
of mediators from mast cells)
 Cromolyn/cromoglycate
 Nedocromil
 Uses: inhalation as prophylaxis in allergen-induced, irritant-induced and
exercise-induced asthma (Children usually have better response), Allergic rhinitis
 N.B. Not useful as bronchodilator in acute asthma attack
 SE: hypersensitivity -> bronchoconstriction, dermatitis, irritation of upper
respiratory tract

o Leukotriene Pathway Inhibitors

 Antileukotrienes (reduced production by inhibition of 5-lipoxyoxygenase)
 Zileuton
 Leukotriene antagonist (reversibly block LK receptors on airways)
 Zafirlukast
 Montelukast
 Improves respiratory function, ↓ mucus secretions, ↓ dose of b-agonists and
corticosteroids required
 Uses: prophylaxis of exercise/allergen-induced, aspirin-sensitive asthma +
inhaled corticosteroids in mild asthma not sufficiently controlled by b-agonists
 SE: Headache, GI distress
 Omalizumab (binds to IgE in blood, ↓ IgE binding to mast cells Þ ↓ release of histamine, LKs,
other mediators from mast cells)
o SC every 2 – 4 weeks
o SE: potentially fatal anaphylactic reaction

Asthma combination treatment

 Mild asthma - inhaled β-agonists as needed
 Chronic asthma - prophylaxis, inhaled corticosteroids or mast cell stabilizer + β-agonists as
needed or salmeterol prophylactically
 Severe prolonged asthma – oral corticosteroids + β-agonists
 Asthma crisis – IV corticosteroid + inhaled β-agonists

Asthma Combination Agents

 Combivent = Ipratropium + Salbutamol (M-antagonist + β-agonist)
 Symbicort = Formoterol + Budenoside (β-agonists + steroid)
 Seretide = Salmeterol + Fluticasone (β-agonists + steroid)

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COPD
 Chronic bronchitis – inflammation and scarring of bronchial tuebes Þ ↓ airflow + heavy mucus +
chronic cough + shortness of breath
 Emphysema - irreversible damage to alveoli Þ ↓ oxygen to blood Þ shortness of breath, Þ lungs
lose elasticity Þ difficulty exhaling

Treatment COPD
 Bronchodilators (1st choice)
 Glucocorticoids (for acute exacerbation of symptoms)
 Antibiotics (for infections)
 Oxygen therapy (if necessary)
 Lifestyle changes (exercise, avoid smoking and air pollutants)

Other Agents
 Decongestants (Stimulate α-adrenergic receptors, Þ vasoconstriction of nasal vessels Þ ↓
capillary blood flow in the mucosa and ↓ volume of nasal mucosa Þ opening of airways , ↓
capillary blood flow in the mucosa of bronchioles Þ ↓ edema and ↓ secretions )
o Epinephrine
o Phenylephrine
o Pseudoephedrine
o Ephedrine
o SE: hypertension, tachyarrhythmias, rebound nasal congestion (down regulation of
receptors)

 Cough Relievers
o Antitussives
 Opoids (stimulate opoid receptors and suppress cough reflex -> depressing
medullary cough center)
 Codeine
 Hydrocodone
 Butorphanol
 Dextromethorphan
o low efficacy
 Uses: control of non-productive cough -> reduce exhaustion and loss of
sleep associated with coughing at night
 Productive cough should not be suppressed except for good reason
 SE: very few, constipation, emesis, tolerance, slight CNS depression
 Demulcents
 Honey

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  Glycerine
 Licorice
 Uses: coughs originating above larynx, form protective coating over
irritated pharyngeal mucosa
 Humidifiers
 Act as demulcent by decreasing viscosity of bronchial secretions
 Water inhaled as aerosol or steam + medicaments (e.g. eucalyptus,
NaCl)

o Expectorants (stimulate gastric mucosa -> increase glandular secretion of

respiratory epithelium -> coating of mucosa, may also loosen phlegm and relieve chest
congestion)
 Saline Expectorants
 Potassium Iodide
 Ammonium chloride
 glycerol iodide
 menthol
 Guaifenesin (robitussin)
 Asmasol
 NB adequate hydration is important to encourage expectoration
 SE: emesis, gastric ulceration; iodides – unpleasant taste, skin eruptions,
swelling of salivary glands, hypothyroidism, high dose guaifenesin – skeletal
muscle relazation

 Mucolytics (disrupts the structure of acid mucopolysaccharide fibres in mucoid sputum Þ ↓

viscosity of mucus Þ easier expulsion of sputum)
o Bromhexine
o significant 1st pass metabolism
o Binds plasma protein, no real drug interaction
o Hepatic metabolism
o SE: rare, emesis, diarrhea, indigestion, transient rise in serum aminotransferase values,
headache, vertigo, sweating
o Allergic reactions: rashes, swelling of mouth and face, difficulty breathing

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