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COPD, WhatsApp Image 2020-12-06 at 16.48.37 - Coggle Diagram
COPD
changes in aged lung
Decline of strength and endurance of respiratory muscles
Enlargement of alveolar ducts
Decreased surface of gas exchange
Anatomic dead space increases
Loss of lung elastic tissue
decreases recoil
Diaphragm flattens and becomes weaker
Altered surfactant composition
Increased content of proinflammatory proteins and reduced anti-inflammatory
Cough is weaker
Because of age effects on respiratory muscle strength
Vital capacity decreases
Smaller airways
increase risk for collapse due to degeneration of collagen and elastin
Maximal O2 uptake declines
Caused by decreasing muscle mass and reduced cardiovascular/pulmonary function
Prevalence
3 million deaths annually
Mean global prevalence 13.1%
Africa (13.9%)
Europe (12.4%)
Americas (13.2%)
Asia (13.5%)
Oceania (11.6%)
Global increase since 1990 (~10.7%)
Treatments
Smoking cessation
Influenza and pneumococcal vaccination
Physical activity
Pulmonary rehabilitation
Pharmacotherapy
Oxygen and ventilatory support
Interventional treatments (surgery)
Steroids
Symptoms
chronic bronchitis
inflammation + excess mucus in bronchial tubes
emphysema
damaged air sacs
refractory asthma
coughing
lack of energy
weight loss
inflammmation linked to COPD
Increased number of innate cells
Neutrophils
LTB4, CXCL1, CXCL5 and CXCL8
Neutrophils secrete serine proteases, including neutrophil elastase, cathepsin G, and proteinase-3, as well as MMP-8 and MMP-9
Macrophages
TNF-α, CXCL1, CXCL8, CCL2, LTB4, and ROS
Attract neutrophils, monocytes and T- cells
Secrete elastolytic enzymes, including MMPs, cathepsins and neutrophil elastase
Eosinophils
IL-33
Th2: IL-5
ILC2: IL-13
Increased number of adaptive cells
T lymphocytes
More CD8+ cells than CD4+
B lymphocytes
Activation of structural cells
Epithelial cells
Produce inflammatory mediators inducing TNF-α, IL-1β, IL-6, GM-CSF, and CXCL8 (IL-8)
Mucus hyperplasia
EGFRs
Mediators
Lipids
Increased prostaglandin (PG) and LT levels
Free radicals (ROS)
Oxidative stress
NLRP3 inflammasome
Cytokines
TNF-α is a potent activator of NF-κB
Growth factors
Chemokines
Risk factors
Lifestyle factors
genetics
age
diet
exercise
Environmental factors
smoking
pollution
infections
Host factors
Atopy & asthma
Low lung function
Family history of COPD
Perinatal factors
Preterm birth
Mode of delivery
Maternal smoking
Maternal exposure to pollutants
Antibiotic use
genetics involved
hydrolytic-antihydrolystic systems
SeRPINA1
Mutation in gene induces loss of elastic tissue
SeRPINA2
ADAM33
MMPs
inflammation-related genes
VDBP
TGF-ß1
TNF-α
oxidative-antioxidative systems
GST
HO-1
SOD
Diagnosis
spirometry
FEV = volume of exhaled breath in 1 sec
FVC = forced vital capacity (total amount that can be exhaled)
When FEV/FVC < 0.7 = COPD
GOLD scale
