Medicine Lecture Note: Asthma

Asthma →chronic inflammatory disorders of the branched tree in which breathing is periodically rendered diskull by en dispend hermaning of the breonchi →clinically charecterised by recurent episodes of wheezing, breathlewnew, Highres of chest & laugh. 7 episodes of bronchoconstrictor mucus sevation. - perlly reversible. y inflamator of the bronchid wells. I hereand Classification According to dype of Antigen! 4 Atopic - Non-atopic Acordy do agents / cunts that trigger deosonal Exercice induced dung induced. Occupational astthue. Asthriche breenchidis in Amaker. Adopic asthm common type (begins in childhood) → Somly hishay of asthan /allergic discer Comhiên. eig dyre I IgE Ludeled Lypasensitivity. -> Allergens can be recognised. Ahin test results in immediode wheed & here reaction. Nem atopic asthme → no causebiue exogenous factor, no allergen sensitscher. Skin dels negative. family history lus connues. Triggerity events respiratory infutors der to wruses →inhold air pollutants → du do hyper vartably of the bronchid tree. Deug indured asthma → many dongs trigger arttime. eg Aspirin inhibits cyclo argenese puthurry of AA hutebolism ↓ produes leuko ferioress (broncho constricta) Causes aithne. Occupation Asthma Triggerine agents →Sunes → Organic & chemical dusts →gans → other chemials. Ehology Endogenous risk fahrs. + genele pusdisposition →pendispositon do typu I hypersensitivity reacher & exparn to environment frigger. Susceptibility locus is cha 5 Conderal several genes involved. in (gt synthuss & mast cell, csinophil growth & differentiated Y Airway hyperxsponsivenes abnormality where there is excesive tenderney for enters to Contruct. 4 Genele bure Common in boys then girls after pubely wonen slightly with then wen. Environ hund Risk factors Inhaled allergens 4 URT Vil infechens Air pollutes Passwe sheoking daugs. Pathogenesis & Atopic ethmo Major chilogical factos Y gantic perdisposition to type I hypersensitivity State & chesnic aireny inflements. hyperresponse branch: do Various environment antigas Inflamator invalues way cell types & inflemintory medictors →genetic prodiposita with susceptible genes peros to develop Strong Tits compose rechers. TH₂ cells sevek cytokines Stimulet B cells to prodire gf & other antibodies. 12--> Stimulate pasducton of IgE 12-5 Alivetes eosinophils. 11-13 Aimable huvessel secutor & promote lyf secchon by Bella Steps in pathogenesis → allergen is token up APCs Chocerophage Idendrite cells) E cliol Tits dominated response (promotes producten of lat by B celles). →19 E coxproduced during sensitisolon cools bronchial submucosd host cells e-exposure Allergan binds de 196 bound to bronchid sub hacest mast cells Activates hast cells. dubeese bronchoconstsada mudrotors from mast cell granules → Mast cell sulcem preformed mulichs ( resposite for Carly phase eechers produs cytokines lake phos rechts. y Early reaction. charadand by briancho constrichen • increased mucous productos. Vasodilaton with incrend vasculos. Permuability 4 Lote phese res don > by recruitment of leukocytes → by Suech nedictors endeaved Ar Last cells, eosinophils LL eg i) cotain puudured by airway epithelial cells, Activator of cosinophils. iⅱ) chematinereummitunt of more Tits cells. ii) basic puolen of eosinophil denage to epithelial cells, more constrider. Morphology guess Airway occluded by plugs of thick, tenacious on patients who die of cuttin mucus. lungs an grily distended atelectass (callopse) E Show shall microscopy → hoja puren which wanthithule do narrowing of airways 1. Irurend amant of hucus hucus plligs seen in bromhules mumus plug conteas desquereld epithelial cells & cosine phils →form spiral shaped cast of airwerp ↓ Called Carchmann spieds. 2. Ilemelas sammas eosinophils found in the walls of bronh Chorest- heyden crystals found. Jeden & congestion of airways. 3. Airuky remodelling group of structural changes in bronchiel will die to repered bouts of information. in size & number. of submucod glands hyperteply / Hyperplasia of broncbvel wall death mache 4 infreand varcubrity - deplastion of supepithelial collagen