obstructive diseases 1 Flashcards
consolidation
fluid or cells in alveoli
lung is more solid
lungs are more white in X-ray
transmit sound and vibration easily
major respiratory tract causes of morbidity and mortality
respiratory tract infections
lung cancer
chronic airway diseases
asthma
smoking
1 in 5 deaths atherosclerotic cardiovascular disease COPD increases the risk of tuberculosis worsens asthma low birth weight babies lung cancer mesothelioma
lung cancer
the most common cancer
mortality decreasing
incidence increasing
if lung tissue becomes stiffer
loss of compliance
inflating and deflating becomes harder
If thorax is opened
pneumothorax - negative pressure space equalises with the atmosphere
if bronchial tree is narrowed/damaged
it is harder to get air in and out
hyperinflation
air that doesn’t get out
obstructive diseases
airway diseases
increase to resistance to airflow due to partial or complete obstruction
restrictive diseases
parenchymal diseases
reduced expansion of lung parenchyma, often loss of gas transfer surface area, decreased total lung capacity
obstructive analogy
pinch the neck of the balloon
restrictive analogy
grip the sides of the balloon
obstructive effects
v decreased FEV1 decreased/normal FVC decreased FEV1/FVC increased TLC increased residual volume
restrictive effects
increased FEV1 decreased FVC increased FEV1/FVC decreased TLC decreased residual volume
dyspnoea
difficult or laboured breathing
shortness of breath
symptom not a sign
wheeze
high pitched, polyphonic sound produced predominantly in expiration by airways of any size
stridor
single high pitch
upper airway, inspiratory, usually laryngeal
stertor
low pitch, upper airway, nasal back of throat
eg. snoring
chronic bronchitis
mucous gland hypertrophy and hyperplasia, hypersection
caused by tobacco smoke and air pollutants
causes cough and sputum production
bronchiectasis
airway dilation and scarring
caused by persistent and severe infections
causes cough, purulent sputum, fever
asthma
smooth muscle hypertrophy and hyperplasia, excessive mucous and inflammation
immunologic or undefined causes, often triggered by air pollutants
causes episodic wheezing, cough and dyspnoea
three clinical entities in the bronchus
asthma
chronic bronchitis
bronchiectasis
emphysema
in the acinus/alveoli
air space enlargement and wall destruction
caused by tobacco smoke
causes dyspnoea
bronchiolitis - small airway disease
in the bronchioles
inflammatory scarring, partial obliteration of bronchioles
caused by tobacco smoke, air pollutants
causes cough and dyspnoea
COPD
chronic obstructive pulmonary disease
spectrum between chronic bronchitis and emphysema
mixed features of both
isolated emphysema and pure chronic bronchitis are both relatively uncommon - most patients have a combination of both
2 groups of asthma
extrinsic and intrinsic
four subtypes of asthma
atopic
drug induced
occupational
non atopic
atopic asthma
type 1 IgE mediated hypersensitivity reaction
childhood, string family history, associated with allergic rhinitis
triggered by allergens
positive skin tests
drug induced asthma
aspirin and other drugs
occupational asthma
fumes - plastics, epoxy resins
organic and chemical dusts
gases and other chemicals
usually requires repeatd exposure
intrinsic asthma
non atopic
no evidence of allergen sensitisation
negative skin test
don’t always have family history
asthma clinical presentation
dyspnoea with wheezing
lasts for several hours or more
subsides naturally with response to bronchodilators
status asthmaticus
failure to subside for days to weeks
possibly caused respiratory failure or death
pathogenesis of asthma
atopic
excesive type 2 helper T cells
cytokine production of type 2 helper T cells
produce cytokines
- IL-5 activates eosinophils
- IL-13 stimulates mucus production
- IL-4 and IL-3 stimulate IgE production which causes mast cells to degranulate
asthma reaction
early phase - bronchoconstriction, histamine, prostaglandin D2 and leukotrienes, increased mucus, vasodilation
late phase reaction - inflammatory mediators stimulate epithelial cells to produce chemokine, recruit Th2 cells and eosinophils which amplifies the inflammatory response
repeated bouts of asthma lead to
airway remodelling
smooth muscle hypertrophy, mucus gland hypertrophy and increased collagen deposition
often occurs before the patient presents with symptoms
re exposure to pre sensitised antigen is the trigger
asthma histologically
mucus plugging of bronchi
focal necrosis of epithelium with eosinophilic inflammation and oedema of bronchial walls - triggered by excessive inflammation
thickening of epithelial basement membrane
hypertrophy of bronchial mucous glands
hypertrophy of smooth musclee of the bronchial wall
emphysema description
abnormal parmanent enlargement of the airspaces distal to terminal bronchiole
destruction of walls, without interstitial firbrosis
trapping of air in dilated airspaces and loss of elastic recoil due to damage of parenchyma
