Respiratory pathology Flashcards
Acute inflammation
Hallmark features are swelling, vasodilation, mediators like histamine, increased permeability, neutrophil migration (cells leaving). Triggers to this would be infection, trauma. Acute inflammation in lower lung causing fluid in space is pneumonia, self-resolving - macrophages come in and mop it up
Chronic inflammation
Tissue remodelling, fibroblast deposition. Key cell here is macrophages plus/minus lymphocytes. Key cell in acute inflamm is neutrophils. New vessel formation - these are often quite leaky because you actually want to get things leaked out to form new BVs etc.
Differences between acute and chronic inflammation
In acute inflamm you will either die from it or get better but chronic lasts because you can’t cough and spit it out. This can be due to narrowing of airway e.g. pea getting stuck - this would cause chronic inflammation.
If airway is dilated, chronic inflamm in lung, this is bronchiectasis, post-viral
Immunological
Immunological may be different - systemic. Hypersensitivty - I, II, III and IV. I will cause asthma - eosinophils, leukotriene production, bronchospasm, obstructuve reverisble airway reaction - spasm of muscles, IgE
II - antibodies and complement - life-threatening sometimes
Iv - delayed type - t-cell mediated - marcophages too. Takes a while for T-cells to activate so therefore it is delayed
TB
TB - granuloma - T-cell-driven response with particular features - effector cell that is used is macrophage
COPD
COPD - two pathologies - chronic bronchitis, emphysema - a couple of ways of getting - scarred tissue or narrowed airway. Emphysema is loss of tissue - gas exchange doesn’t happen. Bronchitis is hypertrophy (inflammation) of mucous-producing glands, progressive airway limitation
Pulmonary fibrosis and thrombosis
Pulmonary fibrosis - LE of 2 years, 10% get lung cancer - it is a type of pneumonia
Thrombosis - forms in vessel, clot forms outside.
