-
Pseudoephedrine/phenylephrine
INDICATIONS
- ·
- Acute and chronic rhinitis
PHARMACODYNAMICS
- Sympathetic
- amines, they agonise alpha adrenoreceptors on vascular smooth muscle in the
- respiratory tract causing vasoconstriction of dilated nasal vessels. They
- result in reduced tissue hyperaemia, oedema and nasal congestion.
- ·
- Pseudoephedrine: Acts directly
- on both alpha and (to a lesser degree) beta adrenergic receptors. Through a
- direct action on alpha adrenergic receptors in the mucosa of the respiratory
- tract it causes vasoconstriction. It also relaxes bronchial smooth muscle by
- stimulating the beta20adrenergic receptors.
- ·
- Phenylephrine: Phenylephrine is
- a postsynaptic alpha1 receptor agonist.
- It causes vasoconstriction in the mucosa of the respiratory tract leading
- to decreased oedema and increased drainage of sinus cavities.
PHARMACOKINETICS
ADVERSE DRUG INTERACTIONS
CONTRAINDICSTION
- ·
- Coronary artery disease
-
Guaifenesin, Ammonium salts, Senega, Liquoirce
and Sodium
Linctus
Acetylcysteine, Brohexine
Anti-Tussives
INDICATIONS
- ·
- Dry cough- Opioid Derivatives
- ·
- Productive Cough- Expectorants,
- Demulcents, Mucolytics
PHARMACODYNAMICS
- ·
- Opioid derivatives: activate
- neuronal G-protein coupled opioid receptors, inhibiting adenylate cyclase,
- reducing cAMP levels and activating potassium channels resulting in
- hyperpolarization of the neuron. This reduces the release of substance P, which
- is a neurokinin binding NK-1 which activates the cough centre in the medulla.
- This results in a reduction in the frequency of dry, irritating cough.
- ·
- Expectorants: are thought to
- promote bronchial secretions, ciliary action and productive coughing by
- irritant action on mucous membranes. This increases mucous production and
- movement.
- ·
- Demulcents though to suppress
- coughs by forming a protective layer over sensory receptors in the pharynx. This
- suppresses coughing.
- ·
- Mucolytics: acetylcysteine:
- reduces mucous viscosity by splitting disulfide bonds in mucoproteins:
- Brohexine: is thought to improve mucous flow by enhancing hydrolyzing activity
- of lysosomal enzymes This results in a reduction of mucous viscosity and aids
- in expectoration
ADVERSE DRUG INTERACTIONS
CONTRAINDICATIONS
-
Promethazine, Cetirizine, Loratadine
Anti- Histamines
INDICATIONS
PHARMACODYNAMICS
- ·
- Selectively antagonise the
- action of histamine at H1 receptors in both CNS and periphery. Histamine
- released from mast cells and basophils causes local inflammation, smooth muscle
- contraction and blood vessel dilation. Older ‘drowsy’ drugs penetrate the blood
- brain barriers as well and so cause CNS sedation, cognitive impairment and
- motor retardation. Newer, less sedating drugs do not penetrate the blood brain
- barrier.
PHARMACOKINETICS
Promethazine, Cetirizine, Loratadine
CONTRAINDICATIONS
· Children <2
· Hyperthyroidism
· Heart disease
· Liver/Kidney disease
· Bladder obstruction
· Diabetes
-
Oral Glucocorticoids
Prednisolone, Prednisone
Inhaled Glucocorticoids (preventers)
Becolmethasone, Budesonide, Fluticasone
INDICATIONS
- ·
- Severe CODP (questionable)
PHARMACODYNAMICS
- ·
- Steroids cross the nuclear
- membrane and bind to transcription factors. Inhibit production of vasodilators
- by inhibiting COX-2. By inducing annexin (lipocortin-1) they inhibit production
- of leukotrienes and other inflammatory mediators. Also inhibits IL-5 which activates
- eosinophils, and IL-3 which activates mast cells. Also decrease neutrophil, macrophage
- movement, decrease T-helper cell action, impairs fibroblast function and
- atrophy of the thymus gland. Ultimately inhibits both the early and late phases
- of inflammation.
PHARMACOKINETICS
ADVERSE DRUG REACTIONS
CONTRAINDICATIONS
·
-
Relievers: short acting Beta agonists (SABAs)
Salbutamol (ventolin), Terbutaline (Bricanyl)
Symptom Controllers: Long acting Beta agonists
(LABAs)
Salmeterol (serevent)
Eformeterol (Oxis)
BETA-Agonist
INDICATIONS
PHARMACODYNAMICS
- Agonise B2
- receptors on bronchial smooth muscle, upregulating PKA which inhibits MLCK and
- thus prevents phosphorylation and contraction of smooth muscle. Also inhibit
- mediator release from mast cells and macrophages, and increase ciliary mucous
- clearance. Results in bronchial smooth muscle, increasing FEV1, reducing
- residual volume and delaying onset of dynamic hyperinflation during exercise.
ADVERSE DRUG REACTIONS
-
Relievers: Muscarinic Antagonist
Ipratropium Bromide
Symptom Controllers: Muscarinic Antagonists
Tiotropium Bromide
- Muscarinic Antagonists-relievers
- + symptom controllers
INDICATIONS
PHARMACODYNAMICS
- Anticholinergic non-discriminatory
- muscarinic antagonist that competitively inhibits M3 receptors. In smooth
- muscle cells prevents production of IP3 and DAG, reducing Ca2+ and inhibiting
- contraction. In glandular and mast cells, decreases cGMP and IP3 reducing
- mucous secretion and release of mediators. This results in an attenuating vagal
- tone that reduces bronchospasm and mucous production, increasing exercise
- tolerance.
ADVERSE DRUG REACTIONS
-
Montelukast and
Zafirlukast
- Leukotriene Receptor
- antagonists
INDICATIONS
PHARMACODYNAMICS
- Leukotriene-
- receptor antagonists block binding of leukotrienes to the cysteinyl leukotriene
- receptor CysLT1 (found in the respiratory mucosa and inflammatory cells)
- preventing bronchospasm and inflammation.
ADVERSE DRUG REACTIONS
-
Sodium cromoglycate and
Nedocromil sodium
Mast Cell Stabilisers
INDICATIONS
PHARMACODYNAMICS
- Mast cell
- stabilisers prevent histamine release from mast cells by blocking calcium
- channels. They also suppress activation of sensory nerves, desensitise neuronal
- reflexes and inhibit release of T-cell cytokines.
PHARMACOKINETICS
ADVERSE DRUG REACTIONS
- ·
- Pharyngeal and tracheal
- irritation
-
Theophylline and Aminophylline
Xanthine Bronchodilator
INDICATIONS
PHARMACODYNAMICS
- This is unclear;
- it is thought that it inhibits phosphodiesterase resulting in the smooth muscle
- dilation in addition to some anti-inflammatory effects; antagonizing adenosine
- may be responsible for its side effects.
- PHARMACOKINETICS
ADVERSE DRUG REACTIONS
-
Aspirin, Ibuprofen, Diclofenac, Naproxen,
Indomethacin, Paracetamol
- Non-Steroidal
- Anti-inflammatory drugs
INDICATIONS
- PHARMACODYNAMICS
- Anti-inflammatory action due to decrease in PGE2
- and prostacyclin production causing reduced vasodilation and oedema. Analgesic
- effect due to decreased prostaglandin production and thus less sensitization of
- nociceptive nerve endings to inflammatory mediators such as bradykinin.
- Antipyretic actions as NSAIDs prevent IL-1 activating COXs in the CNS, which
- produce prostaglandins that raise the hypothalamic set point.
PHARMACOKINETICS
- ·
- Half Life; 1-6 hours (naproxen
- 14 hours)
ADVERSE DRUG REACTIONS
- ·
- Gastrointestinal bleeding (due
- to inhibition of COX1 which normally provides prostaglandins to maintain the
- mucosal lining of the stomach N.B
- Ibuprofen is gentlest on the stomach and Misoprostol is a stable analogue of
- PGE1 and can as such be used with NSAIDs to protect against GI bleeding)
CONTRAINDICATIONS
- ·
- (ASPIRIN) Children <12 (due
- to risk of Reye’s syndrome)
- ·
- Beware ‘triple whammy’ drug
- combination of NSAID+ ACEI/ARB+ Diuretic, which can cause acute renal failure.
- ·
- Used with caution in IBD
-
Celecoxib, Rofecoxib
Selective COX2 Inhibitors
INDICATIONS
PHARMACODYNAMICS
- ·
- Selectively inhibit COX2
- enzymes. COX2 is thought to be responsible for most inflammation, pain and
- fever; while adverse effects are though to be mostly due to inhibition of COX1
- (housekeeping enzyme)
PHARMACOKINETICS
ADVERSE DRUG REACTIONS
- ·
- Cardiovascular events: due to
- inhibition of COX2
CONTRAINDICATIONS
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