This document discusses drugs used to treat various respiratory diseases. It begins by introducing common respiratory diseases like asthma, COPD, cough, and lung infections. It then discusses the pathophysiology and treatment of asthma with drugs like bronchodilators, corticosteroids, leukotriene antagonists, and anti-IgE antibody. It also covers treatment of cough with expectorants, antitussives, and bronchodilators. Finally, it discusses drugs for COPD like bronchodilators, corticosteroids, antibiotics, and oxygen therapy.
Call Girls Jp Nagar Just Call 7001305949 Top Class Call Girl Service Available
Respiratory diseases drugs
1. Drugs used to treat
respiratory diseases
Presented by,
Dr.Adarsh Kumar Srivastav
M.P.T. Neuro
2. Introduction
• The most frequently encountered respiratory diseases in
a general medical setting are,
chronic obstructive pulmonary disease (COPD)
asthma
cough
respiratory tract infection
lung cancer
bronchiectasis
interstitial lung disease
pulmonary embolic disease.
3. Asthma
• Asthma is characterized by fluctuating
airways obstruction, with diurnal
variation and nocturnal
exacerbations.
• This manifests as the triad of wheeze,
cough and breathlessness.
• These symptoms are due to a
combination of constriction of
bronchial smooth muscle, oedema of
the mucosa lining the small bronchi,
and plugging of the bronchial lumen
with viscous mucus and inflammatory
4. • Asthma is broadly categorized into non-allergic
and allergic, but there is considerable overlap.
• In allergic asthma, which is usually of early onset,
extrinsic allergens produce a type I allergic
reaction in atopic subjects.
• Type I reactions are triggered via reaginic
antibodies (IgE) on the surface of mast cells and
other immune effector cells, especially activated
Th2 lymphocytes, which release cytokines that
recruit eosinophils and promote further IgE
synthesis and sensitivity.
5. • Patients with non-allergic (late-onset) asthma
do not appear to be sensitive to any single
well-defined antigen, although infection
(usually viral) often precipitates an attack.
7. C. Mast cell stabilizers
Sodium cromoglycate, Ketotifen.
D. Corticosteroids
1. Systemic: Hydrocortisone, Prednisolone and others.
2. Inhalational: Beclomethasone dipropionate,
Budesonide, Fluticasone propionate, Flunisolide,
Ciclesonide.
E. Anti-IgE antibody
Omalizumab.
8. Bronchodilators: β2-adrenoceptor
agonists
Pharmacokinetics-
• two groups of β2-adrenoceptor agonists, short-
acting β2-agonists (SABAs) and longacting β2-
agonists (LABAs). They are administered by the
inhaled route or, in acute exacerbations of asthma or
COPD, via nebuliser.
• Intravenous infusion of salbutamol can be used in
acute asthma. Onset of bronchodilation with SABAs
is within 1–2 minutes and sustained for 4–6 hours.
LABAs produce sustained bronchodilation over a 12
hour period.
• Formoterol also has a rapid onset of action, whilst
salmeterol,
9. • Adverse effects-
hypokalaemia
tachycardia and tremor.
• Clinical use -
used for symptom control both in asthma and COPD
SABAs should be used as required to relieve
symptoms, although they may be taken in advance of
exercise in those asthmatics prone to exercise-
induced bronchoconstriction.
• Dose-
Salbutamol: 200 μg inhaled as required.
Terbutaline: 250–500 μg inhaled as required.
Salmeterol: 50 μg inhaled bd.
Formoterol: 12/24 μg inhaled bd.
10. Bronchodilators: anticholinergics
• Pharmacokinetics-
• Ipratropium bromide produces bronchodilation over
4–6 hours and is usually administered by inhalers or
occasionally nebulisers.
• Tiotropium has a longer duration of action (18–24
hours) and is given once daily.
• Adverse effects-
• glaucoma or symptoms of bladder outflow
obstruction.
11. • Clinical use
Ipratropium bromide and tiotropium are used as
bronchodilators
ipratropium bromide is also used in the management
of acute asthma.
• Dose
Ipratropium bromide: inhaler 20–40 μg qds inhaled,
nebulised 250–500 μg up to four times daily.
Tiotropium: 10-18 μg inhaled once daily, depending
on device.
12. Bronchodilators: Cys leukotriene
receptor antagonists
Leukotriene D4 (LTD4) is the major bronchoconstrictor
mediator in the leukotriene synthesis pathway and
brings about airway smooth muscle contraction via
activation of the Cys leukotriene 1 receptor.
• Pharmacokinetics-
• All of the currently used Cys leukotriene receptor
antagonists are administered by the oral route. There
are diff erences in rates of absorption and
metabolism between drugs in this class: montelukast
is used once daily whereas zafi rlukast is used twice
daily.
13. • Adverse effects-
• In general, Cys leukotriene receptor antagonists are
well tolerated. Initial concerns regarding increased
incidence of Churg Strauss syndrome have largely
resolved.
• Clinical use-
• Management of asthma
14. Bronchodilators: inhaled
corticosteroids
Pharmacokinetics-
• Corticosteroids should be administered wherever
possible by the inhaled route and via a device that
maximises lung distribution.
• The aim is to achieve the maximum anti-
inflammatory effect in the lung whilst minimising
absorption and unwanted systemic effects.
• Twice-daily administration is usual.
• Nebulised steroids have been used in a small number
of asthmatic patients although controlled trials are
few.
15. Adverse effects-
• Side effects are usually due to local deposition with
inhaled devices (hoarse voice, oral candidiasis).
• Adrenal suppression
• Osteoporosis
• Reduced growth rate in children
16. Clinical use-
• Management of asthma except for very mild
patients.
• Clinical use should be tailored to give the minimum
dose in the long term which controls disease: the
dose–response relationship for corticosteroids is
relatively flat and whilst some benefit may be
obtained by doubling the dose of inhaled steroids in
many patients, the benefit is relatively small
• There are a range of inhaled corticosteroids available
including beclomethasone, budesonide, fluticasone
and ciclesonide
17. Dose-
• Beclomethasone, budesonide: start at 200 μg bd,
increase to a maximum of 2000 μg per day if necessary.
• Fluticasone is twice as potent as beclomethasone
and is usually used at 125–250 μg bd.
• Chlorofluorocarbons (CFC)-free inhaled steroids
have different distribution characteristics and
beclomethasone administered through a CFC-free
inhaler can be given at half the dose to achieve the
same lung deposition.
• In practice CFC-free preparations are packaged so
that the same number of doses (one to two puff s
twice a day) can be administered as with CFC-
containing inhalers.
18. Anti-IgE therapy
• A humanised monoclonal antibody against IgE has
been approved for the management of chronic
persistent asthma.
• Administration is subcutaneously on a monthly basis.
• Use is limited by patient’s weight (dose to be
administered calculated in part from body weight
and in part by total IgE levels).
• Anti-IgE therapy is much more expensive than other
routinely used asthma medications, hence a cost –
benefit analysis should be considered in each patient
for whom therapy is suggested.
19. Cough
• Cough is a normal physiological reflex
that frees the respiratory tract of
accumulated secretions and removes
particulate matter.
• The reflex is usually initiated by
irritation of the mucous membrane of
the respiratory tract and is co-ordinated
by a centre in the medulla.
22. Bromhexine
• A derivative of the alkaloid vasicine obtained from
Adhatoda vasica (Vasaka), is a potent mucolytic and
mucokinetic, capable of inducing thin copious
bronchial secretion.
• It depolymerises mucopolysaccharides directly as
well as by liberating lysosomal enzymes—network of
fibres in tenacious sputum is broken.
• It is particularly useful if mucus plugs are present.
• Side effects are rhinorrhoea and lacrimation, nausea,
gastric irritation, hypersensitivity.
• Dose: adults 8 mg TDS, children 1–5 years 4 mg BD,
5–10 years 4 mg TDS.
23. Codeine
• An opium alkaloid, qualitatively similar to and less
potent than morphine, but is more selective for
cough centre.
• Codeine is regarded as the standard antitussive;
suppresses cough for about 6 hours.
• The antitussive action is blocked by naloxone
indicating that it is exerted through opioid receptors
in the brain.
24. • Abuse liability is low, but present; constipation is the
chief drawback.
• At higher doses respiratory depression and
drowsiness can occur, especially in children.
• Driving may be impaired. Like morphine, it is
contraindicated in asthmatics and in patients with
diminished respiratory reserve; should be avoided in
children.
• Dose: 10–30 mg; children 2–6 years 2.5–5 mg, 6–12
years 5–10 mg, frequently used as syrup codeine
phos. 4–8 ml.
25. Noscapine (Narcotine)
• An opium alkaloid of the benzoisoquinoline series.
• It depresses cough but has no narcotic, analgesic or
dependence inducing properties.
• It is nearly equipotent antitussive as codeine,
especially useful in spasmodic cough.
• Headache and nausea occur occasionally as side
effect.
• It can release histamine and produce
bronchoconstriction in asthmatics.
• Dose: 15–30 mg, children 2–6 years 7.5 mg, 6–12
years 15 mg.
26. Chlophedianol
• It is a centrally acting antitussive with slow onset
and longer duration of action.
• Side effect: Dryness of mouth, vertigo, irritability.
• Dose: 20–40 mg;
27. Bronchodilators
• Bronchospasm can induce or aggravate cough.
• Stimulation of pulmonary receptors can trigger both
cough and bronchoconstriction, especially in
individuals with bronchial hyperreactivity.
• Bronchodilators relieve cough in such individuals and
improve the effectiveness of cough in clearing
secretions by increasing surface velocity of airflow
during the act of coughing.
28. • They should be used only when an element of
bronchoconstriction is present and not routinely.
• Their fixed dose combinations with antitussives are
not satisfactory because of differences in time course
of action of the components and liability for
indiscriminate use.
30. ACUTE BRONCHITIS
• Acute bronchitis is common.
• There is little convincing evidence
that antibiotics confer benefit in
otherwise fit patients presenting
with cough and purulent sputum,
and usually the most important step
is to stop smoking.
• In the absence of fever or evidence
of pneumonia, it seems appropriate
to avoid antibiotics for this self-
limiting condition.
31. CHRONIC BRONCHITIS AND
EMPHYSEMA
• Chronic bronchitis is associated with a chronic or
recurrent increase in the volume of mucoid bronchial
secretions sufficient to cause expectoration.
• At this stage, there need be no disability and measures
such as giving up smoking (which may be aided by the
use of nicotine replacment; and avoidance of air
pollution improve the prognosis.
32. • Simple hypersecretion may be complicated by
infection or the development of airways obstruction.
• Bacterial infection is usually due to mixed infections
including organisms such as Haemophilus influenzae,
although pneumococci, staphylococci or occasionally
Branhamella may also be responsible.
• The commonly encountered acute bronchitic
exacerbation is due to bacterial infection in only
about one-third of cases.
• In the rest, other factors – such as increased air
pollution, environmental temperature changes or
viruses – are presumably responsible.
33. • Mycoplasma pneumoniae infections may be
responsible for some cases and these respond to
macrolides.
• Antibiotic therapy is considered when there is
increased breathlessness, increased sputum volume
and, in particular, increased sputum purulence.
• Rational antibiotic choice is based on adequate
sputum penetration and the suspected organisms.
34. • The decision is seldom assisted by sputum culture or
Gram stain, in contrast to the treatment of
pneumonia.
• It is appropriate to vary the antibiotic used for
different attacks, since effectiveness presumably
reflects the sensitivity of organisms resident in the
respiratory tract.
• Commonly used antibacterials include:
• azithromycin or clarithromycin;
• amoxicillin or co-amoxiclav;
• oral cephalosporin, e.g. cefadroxil;
• fluoroquinolone, e.g. ciprofloxacin.
35. • Long-term oxygen therapy (LTOT), usually at least 15
hours daily, in severely disabled bronchitis patients
with pulmonary hypertension decreases mortality
and morbidity.
• The mortality of such patients is related to
pulmonary hypertension, which is increased by
chronic hypoxia.
• Relief of hypoxia on a long-term basis by increasing
the concentration of inspired oxygen reverses the
vasoconstriction in the pulmonary arteries and
decreases pulmonary hypertension.
• Long-term oxygen therapy cannot be safely offered
to patients who continue to smoke because of the
hazards of fire and explosion.
36. Therapy of chronic obstructive
airways disease
Acute exacerbation
• Controlled oxygen therapy (e.g. FiO2 24–28%);
• Nebulized β2-agonists (salbutamol every 2–4 hours,
if needed) or intravenously if refractory;
• Nebulized anticholinergics, such as ipratropium
bromide;
• Antibiotics (e.g. clarithromycin, co-amoxiclav,
levofloxacin).
• Short-term oral prednisolone.
37. Chronic disease-
• Stop smoking cigarettes.
• Optimize inhaled bronchodilators
(salbutamol/ipratropium bromide) and their
administration.
• Consider oral theophylline and/or inhaled
glucocorticosteroids.
• Treat infection early and aggressively with antibiotics.
• Offer long-term oxygen therapy (LTOT) for at least 15
hours per day for cor pulmonale.
• Diuretics should be used for peripheral oedema.
• Consider venesection for severe secondary
polycythaemia.
• Exercise, within limits of tolerance.
38. • REFERENCES-
• Ch-33,pg no.233-243 therapy of asthma, COPD, and other respiratory
disorders;james m ritter; a textbook of clinical pharmacology and
therapeutics.
• Ch-6,pg no.71-80 Drugs used to treatrespiratory disease, Gerard A. McKay
• Matthew R. Walters
• K.D. tripathi