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Bronchial asthmaDisease characterized by increasedresponsiveness of the tracheobronchialtree to various stimuli, potentiatingparoxysmal constriction of the bronchialtree.
Bronchial asthmaPatients with asthma experience:1. Attacks of severe dyspnea, coughing, and wheezing.2. Rarely, “status asthmaticus” - may prove fatal.3. Patients may be asymptomatic between the attacks.In some cases, the attacks are triggered by exercise and cold or by exposure to an allergen, but often no trigger can be identified.There has been a significant increase in the incidence of asthma in theWestern world in the past three decades.In Bangalore 50% of children suffer from asthma. Air pollution isthought to be the main culprit.
DefinitionChronic inflammatory disorder of airways that causes recurrent episodes of: – Wheezing – Breathlessness – Chest tightness & – Cough particularly at night and /or early morning
These symptoms are usually associated with wide spread but variable bronchoconstriction and air flow limitation that is at least partially reversible, either spontaneously or with treatmentIt is thought that inflammation causes increase in airway responsiveness (bronchospasm) to a variety of stimuli
Frequency and severity of symptoms 1. Mild, intermittent 2. Moderate 3. Severe, persistent
Figure 15-12Comparison of a normalbronchiole with that in apatient with asthma.
Atopic / Allergic asthma• Most common type• Environmental agent: dust, pollen, food, animal dander• Family history - present• Serum IgE levels - increased• Skin test with offending agent –wheal flare
Two reactionsClassic Ig E mediated hypersensitivity reaction has 2 responses1. Acute immediate response2. Late phase reaction
Figure 15-11 A modelfor allergic asthma.
Pathogenesis• Ag + presensitised IgE coated mast cells to same or cross reacting antigen• Chemical mediators• Mucosal surface• Submucosal mast cells• Direct stimulation of subepithelial vagal receptors• Minutes – Bronchoconstriction.
Primary mediators1.Th2 cells > IL 4,5 > IgE production+EØ & Mast cell recruitment2.Histamine - bronchconstriction by direct and cholinergic reflex actions3.ECF and NCF
Late phase reaction starts 4-8hrs later and persits for 12-24hrsCaused by recruitment of BØs, NØs, EØs• HRF – Histamine releasing factor• MBP – Major basic protein from EØs Direct epithelial damage• Neutrophils – inflammatory injury.
Non atopic asthma• Triggered by respiratory tract infection• Viruses - most common culprits• Family history uncommon• IgE level normal• No associated allergy• Skin tests NEGATIVE• Cause- hyperirritability of bronchial tree.
Drug induced asthma• Several pharmcologic agents• Aspirin sensitive asthma occurs in recurrent rhinitis nasal polyposis.• Increased bronchoconstrictor leukotrienes. Exqusitively sensitive to small doses of aspirin.• Inhibits COX pathway, without affecting LPO pathway
Allergic Bronchopulmonary Aspergillosis• Caused by spores of aspergillus fumigatus• Antigen challenge• Type I IgE induced reaction• 4 to 6 hr later Type III mediated response.
Occupational asthma• Fumes (epoxy resins, plastics)• Organic / chemical (dust, wood, cotton)• Gases (toluene)• Other chemicals (formaldehyde, penicillin)• Mechanism of injury: type I IgG mediated reactions liberation of bronchoconstrictors directly unknown hypersensitivity.
Morphology - gross• Lungs, over distended due to over inflation• Small areas of atelectasis• Occlusion of bronchi and bronchioles by thick tenacious mucous plugs.
These lungs appear essentially normal, but are the hyperinflated lungs ofa patient who died with status asthmaticus.
This cast of the bronchial tree is formed of inspissated mucus and was coughed up by apatient during an asthmatic attack. The outpouring of mucus from hypertrophiedbronchial submucosal glands, the bronchoconstriction, and dehydration all contribute tothe formation of mucus plugs that can block airways in asthmatic patients.
Morphology - Micro• Mucous plugs-whorls of shed epithelium CURSHMANN’S SPIRALS• Numerous Eøs and CHARCOT-LEYDEN CRYSTALS• Crystalloids made of MBP.
Microscopy (Airway remodeling)• Thickening of BM of bronchial epithelium• Edema and infammatory infiltrate in bronchial walls with EØ (5 to 50 % )• Increased in size of submucosal mucous glands• Hypertrophy of bronchial wall muscle.
Walk thru wheeze ?Walk thru angina ?
Contact:Dr.CSBR.Prasad, M.D.,Associate Professor,Deptt. of Pathology,Sri Devaraj Urs Medical College,Kolar-563101,Karnataka,INDIA.CSBRPRASAD@REDIFFMAIL.COM