these slides contain information about the introduction, classification etiopathogenesis of astha and the treatment too.

1. ASTHMA-
 MADE BY- MANASVI SRIVASTAVA

2. DEFINITION
 Asthma is a chronic disease involving the airways
(tubes) that carry air in and out of the lungs. These
airways are inflamed in people with asthma. The
inflammation makes the airways very sensitive, and
the tubes often react to allergens or irritations. There
is no cure for asthma. But with the proper diagnosis,
medication and an asthma management plan,
symptoms can be controlled.

3. Clinical manifestations
 Cough: can occur at night, during exercise, can be
chronic, dry, with phlegm, mild, or severe
 Respiratory: difficulty breathing, wheezing,
breathing through the mouth, fast breathing, frequent
respiratory infections, rapid breathing, or shortness
of breath at night
 Also common: chest pressure, flare, anxiety, early
awakening, fast heart rate, or throat irritation

5. classification
 Extrinsic asthma- starts at an early age ,occurs in
episodes;the patient has a family history of
allergens.
 Intrinsic asthma- starts in the middle age and
assumes chronic form .there’s no family history of
allergens.

6. pathophysiology
 During an asthma episode, inflamed airways react to environmental triggers such as
smoke, dust, or pollen. The airways narrow and produce excess mucus, making it
difficult to breathe. In essence, asthma is the result of an immune response in
the bronchial airways.[3]
 The airways of asthma patients are "hypersensitive" to certain triggers, also known
as stimuli (see below). (It is usually classified as type I hypersensitivity.)[4][5] In
response to exposure to these triggers, the bronchi (large airways) contract
into spasm (an "asthma attack"). Inflammation soon follows, leading to a further
narrowing of the airways and excessive mucus production, which leads to coughing
and other breathing difficulties. Bronchospasm may resolve spontaneously in 1–2
hours, or in about 50% of subjects, may become part of a 'late' response, where this
initial insult is followed 3–12 hours later with further bronchoconstriction and
inflammation.[6]
 The normal caliber of the bronchus is maintained by a balanced functioning of the
autonomic nervous system, which both operates reflexively.
The parasympathetic reflex loop consists of afferent nerve endings which originate
under the inner lining of the bronchus. Whenever these afferent nerve endings are
stimulated (for example, by dust, cold air or fumes) impulses travel to the brain-stem
vagal center, then down the vagal efferent pathway to again reach the bronchial small
airways. Acetylcholine is released from the efferent nerve endings. This acetylcholine
results in the excessive formation of inositol 1,4,5-trisphosphate (IP3) in bronchial
smooth muscle cells which leads to muscle shortening and this initiates
bronchoconstriction.

7. treatment
 1.bronchodialators
 A. sympathomimetics
 I.selective B2 agonists
Short acting- salbutamol,terbutaline
Longer acting- salmeterol,fenoterol
ii. Nonselective agents-adrenaline isoprenaline
B. methylxanthines-theophylline,amiophylline
c.anticholinergics-tiotropium,atropine

8.  2. anti-inflammatory agents
a.systemic- glucocorticoids
b.inhalational-baclomethasone,budesonide
3.Mast cell stabilizers-disodium cromoglycate
4.LT receptor antagonists-
monteleukast,zafirleukast
5.anti-igE antibody-omalizumab
6.PDE4 inhibitor-roflumilast