PPT for Allied health sciences

1. Bronchodilators &
Xanthines
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Dr.R.Rao Prethendhira Singh.
BDS., Msc Med.Pharmacology.PGDCR
Dept.of Pharmacology.

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4. PHYSIOLOGY OF RESPIRATION
• Respiration is the exchange of gases between the tissue of the body and
to outside environment.
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Breathing in of an air Respiratory tract
Uptake of oxygen from the lungs
Transport of oxygen through the body in
the blood stream
Utilization of oxygen in the metabolic
activities
Removal of carbon dioxide from the body.

5. Innervation of respiratory system
 Parasympathetic supply
M3 receptors in smooth muscles and glands.
 Bronchoconstriction
 Increase mucus secretion
 No sympathetic supply but B2 receptors in smooth muscles and
glands.
 Bronchodilation
 Decrease mucus secretion

7. Pulmonary Diseases
•Bronchial Asthma
•Acute Severe Asthma
•Chronic Asthma
•Acute bronchitis
•Chronic bronchitis and emphysema
•Chronic obstructive pulmonary disease
•Respiratory failure
•Cough
•α1-Antitrypsin deficiency
•Drug-induced pulmonary disease
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8. Asthma
Asthma is a chronic inflammatory disorder
of airways that result in airway
obstruction in response to external
stimuli.
It’s characterized by activation of mast cell,
infiltration of eosinophil, T2 helper cells,
Innate type 2 lymphocytes.
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9. Bronchial asthma
• Bronchial asthma is characterized by
hyperresponsiveness of tracheobronchial smooth
muscle to a variety of stimuli, resulting in narrowing
of air tubes, often accompanied by increased
secretion, mucosal edema and mucus plugging.
• Symptoms include dyspnoea, wheezing, cough
and may be limitation of activity.
• Infection, irritants, pollution, exercise, exposure to
cold air, psychogenic.
• Extrinsic asthma: It is mostly episodic, less prone
to status asthmaticus.
• Intrinsic asthma: It tends to be perennial, status
asthmaticus is more common.
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10. Bronchial asthma
•Acute Asthma. It is characterized by episodes
of dyspnoea associated with expiratory
wheezing.
•Chronic Asthma. There is continuous wheeze
and breathlessness on exertion; cough and
mucoid sputum with recurrent respiratory
infection are common.
•Status Asthmaticus (Acute Severe Asthma).
When an attack of asthma is prolonged with
severe intractable wheezing, it is known as
acute severe asthma.
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11. Causes
 Exogenous chemicals or irritants
 Chest infections
 Stress
 Exercise (cold air)
 Pets
 Seasonal changes
 Emotional conditions
 Some drugs as aspirin, β-bockers

12. Pathophysiology
• Mast cells (present in lungs) and inflammatory cells
recruited as a result of the initial reaction produce a
multitude of mediators by the following processes
• Release of mediators stored in granules (immediate):
histamine, protease enzymes, TNF -a.
• Release of phospholipids from cell membrane followed
by mediator synthesis (within minutes): PGs, LTs, PAF.
• Activation of genes followed by protein synthesis (over
hours): Interleukins, TNFa.
• These mediators together constrict bronchial smooth
muscle, cause mucosal edema, hyperemia and
produce viscid secretions.
• All resulting in reversible airway obstruction.
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14. Airways of the asthmatic patients are characterized
by:
1. Inflammation
• Swelling
• Thick mucus production.
2. Bronchospasm
• constriction of the muscles around the airways,
causing the airways to become narrow.
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15. Airway hyper-reactivity: abnormal sensitivity of the airways to wide range of external
stimuli as pollen, cold air and tobacco smoke.
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16. Symptoms of asthma
Asthma produces recurrent episodic attack of
Acute bronchoconstriction (immediate)
 Shortness of breath
 Chest tightness
 Wheezing
 Rapid respiration
 Cough
Symptoms can happen each time the airways
are irritated.
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17. CLASSIFICATION OF ANTIASTHMATIC DRUGS
1. Bronchodilators
(a) Sympathomimetics
• Selective Beta 2-adrenergic agonists: Salbutamol and terbutaline
(short acting);
bambuterol, salmeterol and formoterol (long acting).
(b) Methylxanthines: Theophylline, aminophylline, etophylline,
doxophylline.
(c) Anticholinergics: Ipratropium bromide, tiotropium bromide.
2. Leukotriene receptor antagonists: Zafirlukast, montelukast,
zileuton.
3. Mast cell stabilizers: Sodium cromoglycate, ketotifen.
4. Glucocorticoids
(a) Inhaled glucocorticoids: Beclomethasone, budesonide,
fluticasone, ciclesonide.
(b) Systemic glucocorticoids: Hydrocortisone, prednisolone,
methylprednisolone.
5. Anti-IgE monoclonal antibody: Omalizumab.
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18. Anti asthmatic drugs:
1) Quick relief medications:
Bronchodilators used to relieve acute episodic
attacks of asthma.
2) Control therapy (prophylactic drugs):
anti-inflammatory drugs used to reduce the
frequency of attacks, and nocturnal awakenings.

19. Anti asthmatic drugs
Bronchodilators
(Quick relief medications)
treat acute attack of asthma
• Short acting 2-agonists
• Antimuscarinics
• Xanthine preparations
Anti-inflammatory Agents
(Prophylactic therapy)
reduce the frequency of attacks
• Corticosteroids
• Mast cell stabilizers
• Leukotrienes antagonists
• Anti-IgE monoclonal antibody
• Long acting ß2-agonists

20. Bronchodilators:
A bronchodilator is a substance
that dilates the bronchi and bronchioles,decreasing
resistance in the respiratory airway and increasing
airflow to the lungs.
Medications administered for the treatment of
breathing difficulties.
They are most useful in obstructive lung diseases, of
which asthma and chronic obstructive pulmonary
disease are the most common conditions
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21. Bronchodilators
These drugs can produce rapid relief of
bronchoconstriction.
Bronchodilators:
 2 - adrenoreceptor agonists
 Antimuscarinics
 Xanthine preparations

22. Sympathomimetics
- adrenoceptor agonists
Classification of  agonists
Non selective  agonists:
epinephrine - isoprenaline
Selective 2 – agonists (Preferable).
Salbutamol (albuterol)
Terbutaline
Salmeterol
Formeterol

23. Mechanism of Action
direct 2 stimulation  stimulate adenyl
cyclase   cAMP  bronchodilation.
Increase mucus clearance by (increasing
ciliary activity).
Stabilization of mast cell membrane.

24. Non selective -agonists.
Epinephrine
• Potent bronchodilator
• Given subcutaneously, S.C.
• rapid action (maximum effect within 15 min).
• Has short duration of action (60-90 min)
• Drug of choice for acute anaphylaxis (hypersensitivity
reactions).

25. Disadvantages
Not effective orally.
Hyperglycemia
Skeletal muscle tremor
CVS side effects:
tachycardia, arrhythmia, hypertension
Not suitable for asthmatic patients with hypertension
or heart failure.
Contraindications:
CVS patients, diabetic patients

26. Selective 2 –agonists
 Are mainly given by inhalation by (metered
dose inhaler or nebulizer).
 Can be given orally, parenterally.
 Short acting ß2 agonists
e.g. salbutamol, terbutaline
 Long acting ß2 agonists
e.g. salmeterol, formoterol

27. Nebulizer Inhaler

28. Short acting ß2 agonists
Salbutamol, inhalation, orally, i.v.
Terbutaline, inhalation, orally, s.c.
 Have rapid onset of action (15-30 min).
 short duration of action (4-6 hr)
 used for acute attack of asthma (drugs of
choice).

29. Long acting selective ß2 agonists
Salmeterol & formoterol
are given by inhalation
Long acting bronchodilators (12 hours) due to
high lipid solubility (creates depot effect).
are not used to relieve acute episodes of asthma
used for nocturnal asthma.
combined with inhaled corticosteroids to control
asthma (decreases the number and severity of
asthma attacks).

30. Advantages of ß2 agonists
 Minimal CVS side effects
 suitable for asthmatic patients with
CV disorders as hypertension or heart failure.
Disadvantages of ß2 agonists
 Skeletal muscle tremors.
 Nervousness
 Tolerance (β-receptors down regulation).
 Overdose may produce tachycardia due to
β1stimulation.

31. Muscarinic antagonists
Ipratropium – Tiotropium
Act by blocking muscarinic receptors .
given by aerosol inhalation
Have delayed onset of action.
Quaternary derivatives of atropine (polar).
Does not diffuse into the blood
Does not enter CNS.
Have minimal systemic side effects
Ipratropium has short duration of action 3-5 hr
Tiotropium has longer duration of action (24 h).

32. Pharmacodynamics
 Inhibit bronchoconstriction and mucus secretion
 Less effective than β2-agonists.
 No anti-inflammatory action only bronchodilator
Uses
 Main choice in chronic obstructive pulmonary
diseases (COPD).
 In acute severe asthma combined with β2 agonists
& corticosteroids.
 Never use as a rescue medication.

33. Methylxanthines
 Theophylline - aminophylline
Mechanism of Action
 are phosphodiestrase inhibitors
  cAMP  bronchodilation
 Adenosine receptors antagonists (A1)
 Increase diaphragmatic contraction
 Stabilization of mast cell membrane

34. Bronchodilation
Adenyl cyclase
Phosphodiesterase
ATP
cAMP
3,5,AMP
+ B-agonists
Theophylline

35. Pharmacological effects :
Bronchial muscle relaxation
contraction of diaphragm improve ventilation
CVS: ↑ heart rate, ↑ force of contraction
GIT: ↑ gastric acid secretions
Kidney: ↑renal blood flow, weak diuretic action
CNS stimulation
* stimulant effect on respiratory center.
* decrease fatigue & elevate mood.
* overdose (tremors, nervousness, insomnia,
convulsion)

36. Pharmacokinetics
Theophylline is given orally
Aminophylline, is given as slow infusion
 metabolized by Cyt P450 enzymes in liver
T ½= 8 hours
has many drug interactions
Enzyme inducers:
as phenobarbitone & rifampicin
 ↑ metabolism of theophylline → ↓ T ½.
Enzyme inhibitors:
as erythromycin
↓ metabolism of theophylline → ↑ T ½.

37. Uses
 Second line drug in asthma (theophylline).
 For status asthmatics (aminophylline, is given
as slow infusion).
Side Effects
 Low therapeutic index (narrow safety margin)
monitoring of theophylline blood level is
necessary.
 GIT effects: nausea & vomiting
 CVS effects: hypotension, arrhythmia.
 CNS side effects: tremors, nervousness,
insomnia, convulsion

38. Prophylactic therapy
Anti - inflammatory drugs include:
Glucocorticoids
Leukotrienes antagonists
Mast cell stabilizers
Anti-IgE monoclonal antibody
e.g. omalizumab

39. Anti - inflammatory drugs:
(control medications / prophylactic
therapy)
↓ bronchial hyper-reactivity.
↓ reduce inflammation of
airways
↓ reduce the spasm of airways

40. Glucocorticoids
Mechanism of action
 Anti-inflammatory action due to:
 Inhibition of phospholipase A2
 ↓ prostaglandin and leukotrienes
 ↓ Number of inflammatory cells in airways.
 Mast cell stabilization →↓ histamine release.
 ↓ capillary permeability and mucosal edema.
 Inhibition of antigen-antibody reaction.
 Upregulate β2 receptors (have additive effect to B2
agonists).

42. Pharmacological actions of glucocorticoids
 Anti-inflammatory actions
 Immunosuppressant effects
 Metabolic effects
– Hyperglycemia
– ↑ protein catabolism, ↓ protein anabolism
– Stimulation of lipolysis - fat redistribution
 Mineralocorticoid effects:
–sodium/fluid retention
–Increase potassium excretion (hypokalemia).
–Increase blood volume (hypertension).

43.  Behavioral changes: depression
 Bone loss (osteoporosis) due to
• Inhibit bone formation
• ↓ calcium absorption from GIT.

44. Routes of administration
 Inhalation:
e.g. Budesonide & Fluticasone, beclometasone
•Given by inhalation (metered-dose
inhaler).
• Have first pass metabolism
•Best choice in asthma, less side effects
 Orally: Prednisone, methyl prednisolone
 Injection: Hydrocortisone, dexamethasone

45. Glucocorticoids in asthma
Are not bronchodilators
Reduce bronchial inflammation
Reduce bronchial hyper-reactivity to stimuli
Have delayed onset of action (effect usually attained after
2-4 weeks).
Maximum action at 9-12 months.
Given as prophylactic medications, used alone or
combined with β2 agonists.
Effective in allergic, exercise, antigen and irritant-induced
asthma,

46. Systemic corticosteroids are reserved for:
• Status asthmaticus (i.v.).
Inhaled steroids should be considered for
adults,
children with any of the following features
•using inhaled β2 agonists three times/week
•symptomatic three times/ week or more;
•or waking one night/week.

47. Clinical Uses of glucocorticoids
1. Treatment of inflammatory disorders (asthma,
rheumatoid arthritis).
2. Treatment of autoimmune disorders (ulcerative
colitis, psoriasis) and after organ or bone marrow
transplantation as immunosuppressants.
3. Antiemetics in cancer chemotherapy.

48. Side effects due to systemic corticosteroids
• Adrenal suppression
• Growth retardation in children
• Susceptibility to infections
• Osteoporosis
• Fluid retention, weight gain, hypertension
• Hyperglycemia
• Fat distribution
• Cataract
• Psychosis

49. Inhalation has very less side effects:
• Oropharyngeal candidiasis (thrush).
• Dysphonia (voice hoarseness).
Withdrawal of systemic corticosteroids
• Abrupt stop of corticosteroids should be
avoided and dose should be tapered (adrenal
insufficiency syndrome).

50. Mast cell stabilizers
e.g. Cromoglycate - Nedocromil
 act by stabilization of mast cell membrane.
 given by inhalation (aerosol, nebulizer).
Have poor oral absorption (10%)

51. Pharmacodynamics
 are Not bronchodilators
 Not effective in acute attack of asthma.
 Prophylactic anti-inflammatory drug
 Reduce bronchial hyper-reactivity.
 Effective in exercise, antigen and irritant-
induced
asthma.
 Children respond better than adults

52. Uses
 Prophylactic therapy in asthma especially in
children.
 Allergic rhinitis.
 Conjunctivitis.
Side effects
 Bitter taste
 minor upper respiratory tract irritation
(burning sensation, nasal congestion)

53. Leukotrienes antagonists
Leukotrienes
synthesized by inflammatory cells found in
the airways (eosinophils, macrophages, mast
cells).
 produced by the action of 5-lipoxygenase on
arachidonic acid.
Leukotriene B4: chemotaxis of neutrophils
Cysteinyl leukotrienes C4, D4 & E4:
• bronchoconstriction
• increase bronchial hyper-reactivity
•↑ mucosal edema, ↑ mucus secretion

55. Leukotriene receptor antagonists
e.g. zafirlukast, montelukast, pranlukast
 are selective, reversible antagonists of cysteinyl
leukotriene receptors (CysLT1receptors).
 Taken orally.
 Are bronchodilators
 Have anti-inflammatory action
 Less effective than inhaled corticosteroids
 Have glucocorticoids sparing effect (potentiate
corticosteroid actions).

56. Uses of leukotriene receptor antagonists
 Not effective in acute attack of asthma.
 Prophylaxis of mild to moderate asthma.
 Aspirin-induced asthma
 Antigen and exercise-induced asthma
 Can be combined with glucocorticoids (additive
effects, low dose of glucocorticoids can be
used).
Side effects:
Elevation of liver enzymes, headache, dyspepsia

57. Anti-IgE monoclonal antibody
e.g. Omalizumab
is a monoclonal antibody directed against human
IgE – given by injection (s.c.)
prevents IgE binding with its receptors on mast
cells & basophiles.
↓ release of allergic mediators.
Expensive-not first line therapy.
used for treatment of moderate to severe allergic
asthma which does not respond to high doses
of corticosteroids.

60. Drugs used in chronic obstructive pulmonary
disease (COPD)
•COPD is a chronic irreversible airflow
obstruction, lung damage and inflammation
of the air sacs (alveoli).
•Smoking is a high risk factor but air
pollution and genetic factors can contribute.

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63. Treatment:
•Inhaled bronchodilators
•Inhaled glucocorticoids
•Oxygen therapy
•Antibiotics specifically macrolides such
as azithromycin to reduce the number of
exacerbations.
•Lung transplantation

64. Inhaled bronchodilators in COPD
Inhaled antimuscarinics
Ipratropium & tiotropium.
are superior to β2 agonists in COPD
β2 agonists
these drugs can be used either alone or combined
• salbutamol + ipratropium
• salmeterol + Tiotropium (long acting-less dose
frequency).

65. Summary

66. Drugs
Adenyl
cyclase
 cAMP
– Short acting
– main choice in acute
attack of asthma
– Inhalation
B2 agonists
Salbutamol, terbutaline
Long acting, Prophylaxis
Nocturnal asthma
Salmeterol, formoterol
Blocks M
receprtors
Main drugs For COPD
Inhalation
Inhalation
Antimuscarinics
Ipratropium (Short)
Tiotropium (long)
Inhibits
phosphodi
esterase
 cAMP
(orally)
(parenterally)
Xanthine derivatives
Theophylline
Aminophylline
Bronchodilators (relievers for bronchospasm)

67. Inhalation
Corticosteroids
(Inhibits phospholipase A2)
Dexamethasone, Fluticasone, budesonide
Orally
prednisolone
parenterally
Hydrocortisone
Inhalation,
prophylaxis in
children
Mast stabilizers
Cromoglycate (Cromolyn), Nedocromil
orally
Cysteinyl antagonists (CyLT1 antagoist)
Zafirlukast, montelukast
Injection, SC
Omalizumab (Anti IgE antibody)
Anti-inflammatory drugs (prophylactic)

68. Understanding the Common Cold
 Most caused by viral infection
(rhinovirus or influenza virus—the “flu”)
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69. Understanding the Common Cold
 Virus invades tissues (mucosa) of upper
respiratory tract, causing upper respiratory
infection (URI).
 Excessive mucus production results from the
inflammatory response to this invasion.
 Fluid drips down the pharynx into the
esophagus and lower respiratory tract,
causing cold symptoms: sore throat,
coughing, upset stomach.
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70. Understanding the Common Cold
 Irritation of nasal mucosa often triggers the
sneeze reflex.
 Mucosal irritation also causes release of
several inflammatory and vasoactive
substances, dilating small blood vessels in
the nasal sinuses and causing nasal
congestion.
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71. Treatment of the Common Cold
 Involves combined use of antihistamines,
nasal decongestants, antitussives, and
expectorants.
 Treatment is SYMPTOMATIC only, not
curative.
 Symptomatic treatment does not eliminate
the causative pathogen.
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72. Cough: protective reflex which helps
to expel irritant matter from the
respiratory tract
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73. 4/24/2024
Dr. Nitin Mirgane Drugs for respiratory system
Antitussive Agents
 Depress the area in CNS which controls the
cough refles
 Stimulate the flow of respiratory secretions

74. Expectorants
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75. Expectorants
“Drugs that help in removing sputum from the respiratory tract.
-either by increasing the fluidity (or reducing the viscosity) of
sputum or
-increasing the volume of fluids that have to be expelled from
the respiratory tract by coughing.”
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76. Expectorants: Mechanisms of
Action
 Direct stimulation
or
 Reflex stimulation
Final result: thinner mucus that is easier to remove
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77. Expectorants: Mechanism of
Action
Direct stimulation:
 The secretory glands are stimulated directly
to increase their production of respiratory
tract fluids.
Examples: terpin hydrate, iodine-containing
products such as iodinated glycerol and
potassium iodide (direct and indirect
stimulation)
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78. Expectorants: Mechanism of
Action
Reflex stimulation:
 Agent causes irritation of the GI tract.
 Loosening and thinning of respiratory tract
secretions occur in response to this irritation.
Examples: guaifenesin, syrup of ipecac
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79. Expectorants: Drug Effects
 By loosening and thinning sputum and
bronchial secretions, the tendency to cough
is indirectly diminished.
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80. Both the action and mechanism of expectorants have been questioned
and remain controversial. However, these may serve a placebo role
and help the patient
• Ammonium chloride
• Potassium iodide
• Sodium iodide
placebo is a simulated or otherwise medically ineffectual treatment for a disease
.
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81. Dose related side-effects
• If the patient is sensitive, dose of expectorant is high enough, this
may induce vomiting (emetic action).
• Hence, it is advisable to give the doses of expectorants that could be
tolerated (by the patient) along with other pharmaceutical aids
(flavours, sweetners, etc.) and cough suppressants.
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82. Classification of Expectorants
• According the their mechanism of action…
(1) Sedative type
(2) Stimulant type
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83. Sedative expectorants
• These are stomach irritant expectorants which are able to produce
their effect through stimulation of gastric reflexes.
• e.g.
Bitter drugs – Ipecac, Senega, Indian Squill
Compounds – Antimony potassium tartrate,
Ammonium chloride, Sodium citrate,
Potassium iodide, etc.
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84. Stimulant type
• These are the expectorants which bring about a stimulation of the
secretory cells of the respiratory tract directly or indirectly.
• Since these drugs stimulate secretion, more fluid in respiratory tract
and sputum is diluted.
• e.g. - Eucalyptus, lemon, anise
- Active constituents of oil like terpine hydrate,
anethole
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85. Ammonium chloride
• Assay: It was previously assayed by precipitation titration by
using the Volhard’s method.
Now, it is assayed by acid-base titration method.
• Uses:
(1) It acts as mild expectorant and diaphoretic when
administered in small doses.
It does so due to local irritation which produces increasing
secretion of respiratory tract, and makes the mucus less
viscous. NH4Cl and NH4HCO3 are therefore used in cough
preparations.
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86. Mucolytes
 Mucolytics are medicines that make the mucus
(sputum) less thick and sticky and easier to
cough up.
 They are usually prescribed for people who have
a chronic (long-term) cough.
 They work best if they are taken regularly.
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87.  An expectorant increases bronchial
secretions and mucolytics help loosen thick
bronchial secretions.
 Expectorants reduce the thickness or viscosity
of bronchial secretions thus increasing mucus
flow that can be removed more easily through
coughing.
 Mucolytics break down the chemical structure
of mucus molecules.
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88. Bronchitis is inflammation or swelling of the
bronchial tubes (bronchi), the air passages between
the nose and the lungs.
More specifically, bronchitis is when the lining of the
bronchial tubes becomes inflamed or infected.
Bronchitis is caused by viruses, bacteria, and other
particles that irritate the bronchial tubes.
Bronchitis
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89. Acute bronchitis
Acute bronchitis is a shorter illness that commonly follows a
cold or viral infection, such as the flu
Acute bronchitis usually lasts a few days or weeks
Chronic bronchitis
Chronic bronchitis is characterized by a persistent, mucus-
producing cough on most days of the month, three months of
a year for two successive years in absence of a secondary
cause of the cough.
TYPES OF BRONCHITIS
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90. Bronchial asthma
 Types of Asthma based on clinical condition:
 Mild episodic asthma:
 Seasonal asthma:
 Mild chronic asthma:
 Moderate asthma with frequent exacerbations:
 Severe asthma:
 Status asthmaticus/Refractory asthma
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91.  Inflammation or swelling of the bronchi
 Coughing
 Production of clear, white, yellow, grey, or green mucus
(sputum)
 Shortness of breath
 Wheezing
 Fatigue
 Fever and chills
 Chest pain or discomfort
 Blocked or runny nose
Signs & symptoms of bronchitis
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92. Antiasthmatic drugs are medicines that
treat or prevent asthma attacks.
 BRONCHODILATORS:
 CORTICOSTEROIDS
 1ST choice in patients with any degree of persistent asthma
 ANTI Ig-E ANTIBODY: In moderate to severe asthma patients who are poorly
controlled with conventional therapy.
 ◦Reduces steriod requirements
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Dr. Nitin Mirgane
Drugs for respiratory system 92

93. Decongestants
4/24/2024
Dr. Nitin Mirgane
Drugs for respiratory system 93

94. Nasal Congestion
 Excessive nasal secretions
 Inflamed and swollen nasal mucosa
 Primary causes:
– Allergies
– Upper respiratory infections (common cold)
4/24/2024
Dr. Nitin Mirgane
Drugs for respiratory system 94

95. Decongestants
Two main types are used:
 Adrenergics (largest group)
 Corticosteroids
4/24/2024
Dr. Nitin Mirgane
Drugs for respiratory system 95

96. Decongestants
Two dosage forms:
 Oral
 Inhaled/topically applied to the nasal membranes
4/24/2024
Dr. Nitin Mirgane
Drugs for respiratory system 96

97. Oral Decongestants
 Prolonged decongestant effects,
but delayed onset
 Effect less potent than topical
 No rebound congestion
 Exclusively adrenergics
 Examples: phenylephrine
pseudoephedrine (Sudafed)
4/24/2024
Dr. Nitin Mirgane
Drugs for respiratory system 97

98. Topical Nasal Decongestants
 Both adrenergics and steroids
 Prompt onset
 Potent
 Sustained use over several days causes
rebound congestion, making the condition
worse
4/24/2024
Dr. Nitin Mirgane
Drugs for respiratory system 98

99. Nasal Decongestants:
Mechanism of Action
Site of action: blood vessels surrounding
nasal sinuses
 Adrenergics
– Constrict small blood vessels that supply
URI structures
– As a result, these tissues shrink and nasal
secretions in the swollen mucous membranes
are better able to drain
– Nasal stuffiness is relieved
4/24/2024
Dr. Nitin Mirgane
Drugs for respiratory system 99

100. Nasal Decongestants: Drug
Effects
 Shrink engorged nasal mucous membranes
 Relieve nasal stuffiness
4/24/2024
Dr. Nitin Mirgane
Drugs for respiratory system 100