Treatment of common cold
By
Dr.Mohamed Abd AlMoneim Attia
A. Nasal Decongestants
• This group of drugs is used to treat the initial
symptoms of irritation of the nasal mucosa (e.g.
nasal Stuffiness, runny nose).
• Agents that stimulate sympathetic responses or
block parasympathetic responses are useful in
treating nasal congestion.
• Agents that block the action of histamine
(Antihistaminics) are useful in preventing nasal
discomfort caused by release of histamine in allergic
disorders.
1. Sympathomimetics
• The sympathomimetics stimulate 1-adrenoceptor
lead to vasoconstriction in the inflamed mucous
membranes
• Used for symptomatic relief
A. Systemically used :
• Pseudoephedrine, Phenylpropanolamine Hcl
• Its alpha stimulant action may raise blood pressure
especially in patients given MAO inhibitors.
• It has C.N.S stimulant action like amphetamine.
B. Topically used:
• Imidazoline derivatives: oxymetazoline
• The imidazoline compounds activate alpha adrenergic
and imidazoline receptors and causes vasoconstriction.
• Some imidazolines are administered by topical ocular
or nasal administration to produce local decongestants,
while others are administered by systemic routs.
Adverse reactions and precautions:
Topical application:
• Burning and dryness of the mucosa which interfere with
the ciliary action.
• Rebound phenomena and tolerance: repeated and
frequent use of topical decongestants can produce
chronic swelling of the nasal mucosa similar to that of
chronic rhinitis. (It is reversible on stopping the drug).
• Chronic use may lead to atrophic rhinitis.
• Systemic reactions when absorbed especially in infants
and small children (tachycardia, palpitation,
hypertension, arrhythmias).
Oral administration:
• This route may produce systemic effects if larger
doses are given, especially in infants and children or
diseased patients.
• Orally administered drugs may produce dangerous
rise in blood pressure.
2. Antihistamine
• There are three types of histamine receptors:
– H1 receptors: present in different tissue mediate
inflammation
– H2 receptors: present in gastric parietal cells, heart
and mast cells
– H3 receptors: present at presynaptic sites-Nerve
endings & Brain, inhibit the release of
neurotransmitters.
– H4 Highly expressed in bone morrow and white
blood cells. Mediate mast cell chemotaxis.
Pharmacological Effects:
• Extravascular smooth muscles :
– Histamine increases permeability of blood vessels,
which results in edema.
• Cardiovascular system
– Histamine decreases both systolic and diastolic
blood pressure
– Histamine produces positive inotropic and
chronotropic effects
• Exocrine glands
– Histamine increase the release of gastric acid.
– Histamine can also stimulate pancreatic, bronchiolar,
lacrimal and salivary secretions. ( H1 receptors
stimulation).
• Nerve endings:
– H1 stimulates various nerve ending causing pain and
itching
Physiologic and Pathologic Roles
• Gastric secretion
• Allergic reactions and anaphylactic shock
• Tissue repair and growth.
Therapeutic Uses
• Histamine and its analogs have no wellestablished therapeutic uses, however it can be
used in diagnoses of pernicious anemia and to
test gastric acid secretion.
Antihistamine
 Physiological antagonists e.g. adrenaline
 Blockers of histamine receptors:
 H1 blockers (antihistamines)
 H2 blockers. (antiulcer)
 H3 blockers (still not approved for clinical use).
 Histamine release inhibitors (mast cell
stabilizers) e.g. ketotifen and cromoglycate.
 Desensitization Therapy
Classification of antihistamines
1st generation
2nd generation
Group
Example (Trade name)
I- Ethanolamines
Diphenhydramine
Dimenhydrinate
(Dramamine)
Clemastine
II-Ethylinediamines
Antazoline
III-Alkylamines
Chlorpheniramine maleate
IV- Phenothiazines
Promethazine
V- Piperazines
Cyclizine
Meclizine
VI- Others
Cyproheptadine
-Loratidine
Terfenadine
Pharmacological Actions
• The term antihistaminics still restricted to the drugs
blocking H1 receptors.
• Competitive block of H1 histaminic receptors and thus
could prevent or reverse all effects of histamine
produced by stimulation of H1 receptor at different
tissues:
 Smooth muscle of bronchi, small blood vessels and
intestine.
 Sensory impulses for itching.
 Capillary endothelium.
 Exocrine glands, except the stomach
• CNS effects:
 Sedation
 Antiemetic effect (Decrease CRTZ).
 Antimotion sickness (Decrease vestibular activity).
 Muscarinic receptor blocking action (share in
antimotion sickness activity).
 Competitive block of other monoamine receptors
e.g. Alpha adrenergic receptors. 5-HT receptors.
 Block of sodium channel of excitable membrane
(membrane stabilizing effect) e.g. Antazoline
Additional effects of the first
generation
• Anticholinergic effect → dry mouth, urinary
retention, tachycardia
• α- blocking effect →postural hypotension,
reflex tachycardia.
• Antiserotonin effect → ↑appetite
Therapeutic Uses
• Prophylaxis and treatment of different allergic
disorders
• Treatment of vomiting of pregnancy e.g. cyclizine &
promethazine.
• Prophylaxis of motion sickness e.g. promethazine,
dimenhydrinate and vertigo.
• Treatment of carcinoid tumor (cyproheptadine)
• Promotion of appetite (cyproheptadine)
The use of first generation H1
antihistamines is
contraindicated in treatment of
individuals working in jobs
where wakefulness is critical
Differences between the old
antihistaminics and the newer
ones
1st generation
Anticholinergic effects Present
2nd generation
(non sedative group)
Absent
Sedative effect
All of them have sedative Almost absent due to poor
effect with variable degrees
penetration to blood brain barrier
Antiemetic effect
Present
Absent
-blocking effect
Present
Absent
Local anaesthetic
effect
Present
Absent
Duration of action
Short
Most of them have long duration
of action.
Side effects
1-Sedation with impaired
concentration
2-Atropine-like side effects
3- Postural hypotension
4-Drug allergy is relatively
common.
1-Cardiac arrhythmias (prolong
QT interval)
2-Interaction
with
enzyme
inhibitors e.g. macrolid antibiotic
and ketoconazol leading to lethal
ventricular arrhythmia.