This document discusses bronchial asthma, including its pathophysiology, clinical presentation, types, diagnosis and treatment. Asthma is a chronic inflammatory disease of the airways characterized by reversible airflow obstruction. It involves bronchial smooth muscle spasm and excessive mucus secretion. Treatment includes short-acting bronchodilators for acute symptoms and long-term controllers like corticosteroids and leukotriene modifiers for inflammation.

1. BRONCHIAL
ASTHMA

2. Introducation
 Asthma derived from Greek word
- To stay awake in order to breath
OR
Difficulty in breathing

3.  Asthma is a chronic inflammatory
disease in which patient suffers with
reversible episodes of airway
obstruction due to bronchial hyper
responsiveness.

4.  Early phase
(Acute)
-Due to bronchial
smooth muscle
spasm.
- Excessive
secretion of
mucus.
 Chronic phase
Continuous
Inflammation,
fibrosis, oedma,
necrosis of
bronchial
epithelial cells.
It has 2phases

5. Clinical hallmarks
 Recurrent episodic coughing
 Shortness of breathing
 Chest tightness
 Wheezing
Symptoms are worsening at night

6. Asthma described as two type
 Extrinsic
(Atopic extrinsic asthma)
It is associated with
exposure of specific
allergen
Ex:- House dust, pollen
It is episodic and less
prone to develop to
status asthmaticus.
 Intrinsic
(Non atopic extrinsic asthma)
It is associated with
some non specific
stimulants
Ex:- chemical irritants
It is perenial and prone
to develop to status
asthmaticus.

7. Pathophysiology
Allergen enter (Foreign body)
Immunological reaction (AG:AB Complex formation)
Circulation in blood
Basophiles, Neutrophilis engulf
Cause neutralization
contd..,

8. Whenever same allergen re exposed
Activation of AG:AB complex
Reacts with lung mast cells
(Degranulation of mast cells)
Spasmogens release
(Like Histamine,5HT,PGs,LT4, Cytokines)

9. Bronchial Tone
IgE-Antigen Complex
Basophil
Activation
Eosinophil
Activation
Chemical mediators
Histamine, LTC4, LTD4, LTB4,
Cytokines, Adenosine, PGD2, PAF,
ECP and Neuropeptides
Cause inflammation, oedema,
bronchospasm, muscus secretion,
epithelial damage
Mast Cell
Degranulation
 In early phase these
mediators leads to
bronchoconstriction
 In late phase
inflammation,
pulmonary oedema,
mucous secretion
bronchial
hypersensivity and
epithelial damage

10.  It divided into two categories
1. Short term relievers.( Bronchodilators)
2. Long term controllers.
Asthma therapy

11. Bronchial Tone
Bronchoconstriction
Bronchodilitation
Bronchial Smooth Muscle
β2
SALBUTAMOL
β2 AGONISTS
5AMP
AC
ATP
THEOPHYLLINE
M3
GTP
GC
cGMP
Adenosine
cAMP
PDE

12. Bronchial Tone
Bronchoconstriction
Bronchodilitation
Bronchial Smooth Muscle
IgE-Antigen Complex
Basophil
Activation
Eosinophil
Activation
Chemical mediators
Histamine, LTC4, LTD4, LTB4,
Cytokines, Adenosine, PGD2, PAF,
ECP and Neuropeptides
Cause inflammation, oedema,
bronchospasm, muscus secretion,
epithelial damage
CARTICOSTEROIDS
LT-ANTAGONIST
Leukotrienes
SOD. CROMOGLYCATE
Stabilises Mast Cells
Mast Cell
Degranulation
INFECTION
NITRIC
OXIDE
DONORS

13. Drugs Used in Bronchial Asthma
1. Selective β2–
Agonists
Short acting
 Salbutamol,
 Terbutaline,
 Remiterol,
 Fenoterol,
 Bitolterol
Long-acting
 Salmeterol,
 Formoterol,
 Bambuterol
2. Non-Selective
Sympathomimetics
 Adrenaline,
 Ephedrine,
 Isoprenaline,
 Orciprenaline
(Metaproterenol),
 Isoetharine
BRONCHODILATORS

14. 3. Anticholinergics
Ipatropium, Tiotropium, Oxitropium
4. Methyl Xanthines
Theophylline, Aminophylline, Diprophylline,
Choline theophyllinate
Anti inflammatory Drugs (Controllers)
Corticosteroids
1. Oral : Prednisolone, Methylprednisolone
2. Parenteral : Methyl prednisolone,
Hydrocortisone
3. Inhalational : Beclomethasome, Fluticasone,
Triamcinolone, Budesonide, Flunisolide

15.  Mast Cell Stabilisers
Sodium Cromoglycate, Nedocromil, Ketotifen
 Leukotriene Modulators:
1. 5-Lipoxygenase Inhibitor : Zileuton
2. LT – Receptor Antagonists : Zafirlukast,
Montelukast, Iralukast, Pranlukast
 Monoclonal Anti-IgE Antibody
Omalizumab
 Miscellaneous:
NO, Calcium channel blockers

16. Sympathomimetic agents
 ß2 receptors are present in the airway
smooth muscle. cause Bronchodilatation
 These are only provide relief
 M.O.A:
 cAMP
 Bronchodilatation
 Release of broncho constricting mediators
from mast cells
Inhibit macrovascular leakage
 Mucociliary clearance

17.  Epinephrine:
 Rapid bronchodilator when SC/inhaled(320µg/puff)
 Onset of action 15min after inhalation
 Duration of action:60-90min.
ADR:- Acts on β1 receptor cause
 Tachycardia
 Arrhythmias
 Worsening angi
 So rarely prescribed.

18.  Ephedrine: α,β1, β2
 Ephedrine has a longer action
 Oral activity
 Lower potency
 Pronounced central effects.

19. β2 Selective
 Short acting : Terbutaline, Salnutamol
 On inhalation they have rapid onset(1-5Min)
 Short duration of action preferred for acute attack
 Route: Inhalation 100-200µg/6hourly
 Other MDI, Oral, IM, IV
 Terbutaline is the only one drug safely used during
the pregnancy.

20. Long acting: Salmeterol, bambutarol
 Long acting but slow onset of action
 Preferred for maintenance therapy
 Not useful in acute attack due to slow onset of
action
Route: Inhalation 50µg twice daily.
Formoterol:
 Long acting
 Rapid onset
 Preferred for prophylaxis due to long acting
Route: Inhalation 12-24µg twice daily

21. ADR of Sympathomimetics
 By oral route stimulate β2 receptors in skeletal
muscle cause tremors, Orthostatic hypotension.
 Tachycardia (High dos also stimulate β1
receptors in heart)
 Restlessness
 Tolarance occurs.

22. Antimuscurnic agent
 Less effective then β agonists
 MOA: By blocking M3 receptors on air way smooth
muscle and prevents Ach action.
-They acts by cGMP levels in bronchial smooth
muscle.
Ipatropium:-
-Poor absorption from bronchi into systemic
circulation
-Do not cross BBB.
-Also mucus secretion
Ipatropium + β2 (Salbutamol) work better in serve
asthma and long duration of action

23. Methyl Xanthenes
 MOA:
i) Inhibition of PDE 3,4. These enzyme are responsible
for metabolism of cAMP.
ii) Blockade of Adenosine receptors.
 Actions:
 Theophyline exhibits bronchodilatory action
 Anti Inflammatory
 Immunomodulator
 Respiratory stimulation
 Diaphragmatic contractility
 Mucociliary clearance

24.  Pharmaco Kinetics:
 Oral/Parental
Food delay the rate of absorption
Well distributed
Cross placental & BBB
Metabolized in Liver
Excreted in urine

25. ADR: Low therapeutic window, CNS stimulant drugs
Plasma levels 10-20µg/ml, Narrow safety
Restlessness, insomnia, headache, tremors
Nausea,
Vomiting
Peptic ulcer
Tachycardia, palpitation, hypotension, arrythimias
Theophyline: potent vasodilator, reflex tachcardia, oral route
Aminophyline: Slow IV infusion
XanthenesGIT Diuresis
Heart
CNS
20µg/ml
40µg/ml
20µg/ml

26. Corticosteroids (Controllers)
 Glucocorticosteriods induce synthesis of lipocotrin
which inhibits pholipaseA2 there by preventing
formation of mediators such as PGs,TAX2, LTand
other mediators.
 Actions: Anti allergic, anti inflammatory,
immunosuppressant ( AG:AB reactions ), Mucosal
oedema, bronchial hyperactivity, Enhance β
adrenergic action by up regulation of β2 receptors in
lung.

27.  Inhalator glucocorticosteriods such as
beclomethasone, budesonide and fluticasone are
used as prophylactic agents in asthma.
 PK:
 Well tolerated
 less systemic side effects.
Common side effects:
 Dryness of mouth
 Voice change
 Oropharangeal candidiats.
Systemic are used in acute severe and chronic severe
asthma.

28. Mast cell stabilizers
 Non bronchodilating, Non steroid drugs, used for prophylactic
treat.
MOA:
 Prevent degranulation and release of chemical mediators from
the mast cells.
 They stabilize the mast cells by preventing transmembarane
influx of Ca ions.
PK:
 Highly ionized
 Least systemic absorption
 well tolerated.
Uses: Allergic asthma, allergic conjunctivitis, allergic rhinitis,
allergic dermatitis.
Ketotifen (Mast stab.+ Antihistamincs)

29. LT Modulators
 LT are powerful bronchoconstrictors.
 Action by preventing their synthesis or blocking
effect on cys LT receptors
 Synthesis inhibitors (Lipooxygenase)
Zafirlukast,Montelukast
 PK:
 Well absorbed after oral administration
 Highly bound to plasma protein
 Metabolized by liver
 Effective for prophylactic treat of mild asthma.

30. ADR:
 Head ache
 skin rashes
 rarely eosinophilia
 Zileuton cause hepatic toxicity.

31. Monoclonal anti IgE antibody
 MOA:- AG:Ab complex formation by AB action
 Omalizumab: Recombinant humanized
monoclonal antibody.
 Inhibit the binding site of IgE to mast cells and
basophils
 PK: administered parentarally
 Uses: Moderate to severe asthma and allergic
disorders.
 Indicated for asthmatic patients who are not
adequately controlled by inhalational
corticosteroids.
 ADR: Inj site redness, itching, stinging.

32. Miscellaneous
 NO: It dilate pulmonary blood vessels and
relax airway smooth muscle.
 Uses: For acute severe asthma and
management of pulmonary hypertension.
 Ca channel blockers:
 Broncho constriction ultimately involves
some degree of ca into cells Nefedpine /
Verapamil should provide relief in asthma.

33. RX Status asthmatics (Acute severe asthma)
 Status asthmatics a severe acute
asthma, which is a life threatening
condition involving exhaustion,
cyanosis, bradicardia,hypotension,
dehydration and metabolic
acidosis.

34.  Humidified O2 inhalation
 Neubulized β2 adrenergic agonist + anti
cholinergic agent
 Systemic glucocorticosteroids IV
(Hydrocortisone 200mgIV)
 IV fluids to correct dehydration.
 K supplements: To correct hypokalemia
produced by repeated administration of
salbutamol.
 NaHCo3 (Sodium bicarbonate) to treat
acidosis.
 Antibiotics to treat infection

35. DRUGS TO BE AVOIDED IN ASTHMA
 β adrenergic blockers
 Cholinergic agents
 NSAIDS ( cause hyperapoenia) except
paraceatamol.