Respiratory Pathogenesis from ALL of module Flashcards
outline the early/immediate reaction in asthma
- Eliciting agent (allergen or non-specific stimulus) stimulates mast cells leading to 2 outcomes:
- production of different mediators like spasmogens,
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- promoting bronchospasm and bronconstriction
production of chemotaxins, which initiate the late phase
outline what happens in the late reaction of asthma
- inflammation causes recruitment of eosinophils to maintain the inflammatoin + activates and other leukocytes
2.mucosal oedema and muscle hypertrophy occurs, narrowing the lumen
- epithelial cells produce chemokines to attract more Th2 cells and eosinophils
- repeated inflammation leads to airway remodelling
outline 5 steps of the pathogenesis in ARDS
- damaging stimulus to lung
- this leads to damage to cells lining the alveoli and damage to the alveolar capillary endothelium, leading to increased permeablility
- this leads to interstitial oedema and high protein exudation into the alveoli, which impairs oxygen gas exchange
- this can lead to either a good outcome with regenerate of type II alveolar lining cells, OR a bad outcome with inflammation of the interstitium.
- this leads to organisation of scar tissue, leading to interstitial fibrosis, which then becomes marked intersititial fibrosis (honeycomb lung), and can then cause death
what are the 4 steps in IPF morphology in the disease IPF
- stimulated fibroblasts deposit collagen and ECM excessively for an extended time
- patchy interstitial fibrosis worses over time
- fibroblastic foci - become more collagenous and less cellular
- causes collapse of alveolar wall and formation of cystic spaces (honeycomb lung)
outline the 5 steps involving how low surfactant levels leads to lung tissue changing into fibrin hyaline membrane
- low surfactant
- lung collapse
- leads to hypoxia
- causes pulmonary vasoconstriction and alveolar epithelial damage
- produces fibrous exudate that causes free radicals to change structure of lung tissue into fibrin hyaline membrane
outline the 4 steps that happen in the first 3 weeks to someone that acquires TB
- inhaled mycobateria engulfed by macrophages
- the mycobacteria maipulate endosomes in macrophages to be able to HIDE in macrophages
- this causes defective phagolysosome formation
- mycobacteria will then proliferate in the endosomes in macrophages, usually leading to mild flu symptoms
outline 6 steps of what happens towards the end of the first 3 weeks of TB infection, regarding steps before granuloma inflammation and the formation of epithelioid macrophages.
- Macrophages that have phagocytosed mycobacteria drain to lymph nodes and prime lymphocytes, causing T cells to be recruited to the lung
2.antigens from mycobacteria displayed on macrophage surface and presented to T cells.
- T cells are converted to Th1 cells
- Th1 cells activate more macrophages for phagocytosis by secreting interferon-𝛄
- Monocytes are also recruited to release free radicals and Reactive Oxygen species, causing necrosis
- this causes granuloma inflammation and the formation of epithelioid macrophages
Dissemination can occur in TB when caseating TB granuloma erodes into lung vasculature
If pulmonary vein involved:
- systemic dissemination to organs like liver, kidney and spleen
If pulmonary artery involved:
- lymph drainage to right side of heart, leading to miliary TB of lung