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Asthma and COPDAsthma:
Asthma in Greek=Panting
Characterized by:
Chronic inflammation leading to an increase in responsiveness of tracheo-bronchial tree to a variety of stimuli causing smooth muscle contraction and narrowing of airway.-Expiration is more difficult that inspiration-3% of population have Asthma-Males have it more than females-It is common in those who are younger than 30 yrsAsthma: It is a chronic-episodic in nature with exacerbation it develops at any age
Pathogenesis:
-Exposure to Allergen
synthesis of IgE these bind with the mast cells in the airway of themucosa and triggers the release of mediators of anaphylaxis-Antihistamines are not used in treatment because there are other substances that are releasedother than histamines.-Leukotrien Antagonists are used because Leukotriens cause bronchospasm and they are moreeffective.-There is cytokine release and IL4, IL5 which are inflammatory mediators. That’s why we useanti-inflammatory drugs
Mediators of anaphylaxis cause:
-Contraction of airway smooth muscle cells-Infiltration of inflammatory cells-Edema, Mucus hyper secretion
For the treatment:
-Contraction
we use B agonists-Inflammation
we use anti-inflammatory mediators (steroids)
Etiology and types:
1-Extrinisic Asthma:-Immune mechanism plays a role-There is increase in IgE level-Positive Family history
 
2- intrinsic Asthma:-No immune response-No IgE-No family history
Asthma management:
Intrinsic asthma:A-Management of patient with education of the patientb-Assess and monitor the severity of the diseasesFEV1
VERY Important investigationAPDF
Anti-platelet derived factorABG
Increase in arterial blood gasesIn acute stage: PO2 decrease and PCO2 decrease
-NOTE:
Low PO2, LOW CO2
Not in resp. failureOnce there is an increase in PCO2 then this is an indication that there is a risk of respiratoryfailurec-Establish management plan for managing the exacerbationd- Regular follow upFor each patient management must be individualized
Anti-Asthma Agents
1-B2 Agonist
Salbutamol, (Long acting), Formetrol (long acting)2-Corticosteroid
Hydrocortisone-Methylprednisolone3-Leukotrien anatagonist
Montelaukast4-Anticholenergic drug
Ipratropium,butamol5-Methylxanthine
Theophylline, aminophylline
Management:Acute Asthma:
Initial assessment which includes, history, physical examination, PEF, FEV1
 
Most important is FEV1
this is an indicator of the severity of the diseaseInitial ttt is bronchodilator. There are 2 ways of giving a drug to a lung:a-Inhalation (you should train the patient on how to use it)b-NebulizerNebulizer
vaporized drug which is dissolved in O2
Advantages of Nebulizer:
1- Hydration: It helps to liquefy the mucous lugs2- No need to train the patient3-Drug reaches the site where it is required4-Systemic effects of the drug are low
So in severe cases it is best to use a nebulizer rather than inhaler.
If the response is good, observe the patient for one hour and if he is stable discharge and sendhim home. If the response is not good, this indicates respiratory failure and admit to ICU
Diagnosis of severe Asthma is based on:
Severe asthmatic attack will not respond to B2 agonist
B2 receptor becomes insensitive to B2agonist There will be wheezing for a day and patient will go into respiratory failure
Chronic asthma:Treatments used: Beta 2 agonists, Cortiosteroids, Leukotrien antagonistsPatients will have:
reduced FEV1 and inflammation so they will have a certain degree of constriction at all timesBeclomethasone and Bedasonide are the inhaled steroids which are used. They are NOT givenalone, they are given along with B2 agonists. The steroids are give because of chronic inflammation.If the patient still doesn’t improve, Leukotrien Antagonist are added
Montelaukast cannot beused alone. It is added to B2 agonist or inhaled corticosteroids-if patient has difficulty in breathing we give him systemic steroids but this has more systemicSide effects-Long term therapy is with B2 agonists.
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