respirtory disease pathology Flashcards
2 features of loss of airway control
airway inflammation - different types in different conditions
airway remodelling - not fit for purpose
asthma definition
clinical syndrome characterised by increased responsiveness to variety of stimuli
antigen, laughter, emotional stress, cold weather, low weight molecules
causes airway obstruction - varies over time and is reversible
varying degrees
symptoms of asthma
dyspnoea
wheezing (airways are tube like)
cough
airways of an asthmatic
mucous plug in lumen
epithelial cells are fragile - may come off, because of goblet cell hypertrophy
sm hypertrophy
submucosal gland hypertrophy
vasodilation - congested vessels
inflammatory cell infiltration - eosinophils - aggressive
bronchoconstriction
describe bronchoconstriction
sm contract so epithelium folds
and then lumen is blocked by the mucous plug
theory of asthma pathophysiology
fragility of epithelium expose sensory nerve
cholinergic response
bronchoconstriction and mucous secretion, both from hypertrophy and hyperplasia
vasodilation - plasma leak, oedema
infiltration of inflammatory cells and mediators which cause sm hypertrophy
common lung problems
particulants from external insult cough COPD - tabacco asthma - allergic/temperature mechanical response cancer knock on effect to cardiology
COPD and emphysema
bronchitis
small airway disease
emphysema
effect of COPD
lung rots away = holes = loss of elasticity so no GE
increased goblet cell numbers - hyperplasia = increased mucous secretion in attempt to deal with particulates - bronchitis
secretions viscoelastic - not cleared properly - breeding ground for microbes - COPD
goblet cells can become cancerous
less cilia
cilia asynchronous
move down airways to bronchioles - block the smaller airways
unable to transport thicker mucus - because of asynchrony - bronchitis
broken attachment between alveoli and vessels - vessels collapse. and there are more secretions = blockage
fibrosis - attempt to repair, collect around collapsed tissue so it cant repair the damage
stenotic airways - no GE distal to stenosis
septi go first
caused of destruction of septi
can be from genetics of where live and work
emphysema histopathology
centrilobular - where the particles deposit
if have alpha 1 - antitrypsin deficiency and smoke - inhibit neutrophil elastase = emphysema - lung degrade more rapidly
alveolar fibrosis
increased type 2 cells - repair
in idiopathic fibrosis or interstitial fibrosis increased fibroblasts - prevent type 2 differentiation
type 2 release factor that help fibroblast make more connective tissue
stromal cells
epithelial cells divide and differentiate into T1, T1 die - GF help normal repair
abnormal path: t1 die - elevated GF, cells remain as t2 and fibroblast proliferate = more connective tissue.
when t2 cells damaged can be apoptosed or turn into myofibroblasts - more fibrosis
smoking and lungs
more T2 apoptosis
less repair
more holes in epithelium
increase inflammation because of macrophages and neutrophils
