Respiratory Drugs for placement

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Respiratory Drugs for placement
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2013-09-20 17:17:21
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  1. Pseudoephedrine/phenylephrine
    • 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.
  2. Guaifenesin, Ammonium salts, Senega, Liquoirce
    and Sodium Citrate
    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

    • ·     
    • Opioid

    • o  
    • Dependence

    • o  
    • Lethargy

    • o  
    • Stupor

     

    • ·     
    • Expectorants

    • o  
    • Nausea

    • o  
    • Vomiting

    • o  
    • Abdominal pain

    • o  
    • Constipation

     

    CONTRAINDICATIONS

    • ·     
    • Opioids

    • o  
    • Respiratory failure

    • o  
    • Asthma

    • o  
    • COPD

    • o  
    • Children <2
  3. Promethazine,
    Cetirizine, Loratadine
    • ·     
    • 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.
  4. Oral Glucocorticoids


    Prednisolone, Prednisone




    Inhaled Glucocorticoids (preventers)


    Becolmethasone, Budesonide, Fluticasone
    INDICATIONS

    • ·     
    • Asthma

    • ·     
    • 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

    • ·     
    • Half life; 2-3 hours

    • ·     
    • Vd: N/A

    ADVERSE DRUG REACTIONS

    • ·     
    • Oral thrush

    • ·     
    • Sore throat

    • ·     
    • Adrenal suppression

    • ·     
    • Immunodeficiency

    • ·     
    • Hyperglycemia
  5. Relievers: short acting Beta agonists (SABAs)


    Salbutamol (ventolin), Terbutaline (Bricanyl)




    Symptom Controllers: Long acting Beta agonists
    (LABAs)


    Salmeterol (serevent)
    Eformeterol (Oxis)
    BETA-Agonist

    INDICATIONS

    • ·     
    • Acute Asthma

    • ·     
    • COPD

    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

    • ·     
    • Tremor

    • ·     
    • Tachycardia

    • ·     
    • Cardiac dysrhythmias
  6. Ipratropium Bromide


















    Tiotropium Bromide
    • Muscarinic Antagonists-relievers
    • + symptom controllers

    INDICATIONS

    • ·     
    • Acute asthma

    • ·     
    • COPD

    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

    • ·     
    • Dry Mouth

    • ·     
    • Cough

    • ·     
    • Throat Irritation

    • ·     
    • Urinary Retention

    • ·     
    • Glaucoma
  7. Montelukast and

    Zafirlukast
    INDICATIONS

    • ·     
    • Asthma

    • ·     
    • COPD

    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

    • ·     
    • Headache

    • ·     
    • Abdominal pain

    • ·     
    • Diarrhoea

    • ·     
    • Hepatitis
  8. Sodium cromoglycate and

    Nedocromil sodium
    Mast Cell Stabilisers

    INDICATIONS

    • ·     
    • Asthma

    • ·     
    • COPD

    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

    • ·     
    • Half Life;

    • ·     
    • Vd;

    ADVERSE DRUG REACTIONS

    • ·     
    • Pharyngeal and tracheal
    • irritation

    • ·     
    • Cough

    • ·     
    • Wheezing

    • ·     
    • Bronchospasm

    • ·     
    • Headache
  9. Theophylline and Aminophylline
    Xanthine Bronchodilator

    INDICATIONS

    • ·     
    • Asthma

    • ·     
    • COPD

    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

    • ·     
    • Half Life;

    • ·     
    • Vd;

    ADVERSE DRUG REACTIONS

    • ·     
    • Insomnia

    • ·     
    • Nervousness

    • ·     
    • Nausea

    • ·     
    • Headache

    • ·     
    • Seizure

    • ·     
    • Arrhythmia
  10. Aspirin, Ibuprofen, Diclofenac, Naproxen,
    Indomethacin, Paracetamol
    INDICATIONS

    • ·     
    • Pain

    • ·     
    • Fever

    • ·     
    • Inflammation

    • 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)

    • ·     
    • Vd;

    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)

    • ·     
    • Nausea/Vomiting

    • ·     
    • Dyspepsia

    • ·     
    • Gastric ulceration

    • ·     
    • Diarrhoea

    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

    • ·     
    • Pregnancy
  11. Celecoxib, Rofecoxib
    Selective COX2 Inhibitors

    INDICATIONS

    • ·     
    • Long term pain relief

    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

    • ·     
    • Half Life; 11 hours

    • ·     
    • Vd;

    ADVERSE DRUG REACTIONS

    • ·     
    • Cardiovascular events: due to
    • inhibition of COX2

    CONTRAINDICATIONS

    • ·     
    • Any CVD history

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