CHRONIC OBSTRUCTIVE PULMONARY DISEASE

CHRONIC BRONCHITIS EMPHYSEMA ASTHMA

Extrinsic: Allergic Intrinsic: Idiosynchratic

Irritants: Chronic Infection Smoking Genetic Infection
Smoking

Inhaled allergen: IInfection (viral), physical

Bronchial and Increase number Pollen, dander. exertion, aspirin, smoke
Bronchial of neutrophils in etc fumes, psychological
Irritation alveoli and stress
increase activity
of elastase but
decrease effect Sensitization of
Hypertrophy and of alpha1- bronchial
hypersecretion of Increase stimulus
antitrypsin mucosa by tissue
Goblet cells and level of the irritant
specific atibodies receptors in the
bronchial (immunoglobulin
mucous glands tracheobronchial
s of the Ige tree
goblet cells [type1] class)
extend distally Low alpha1-antitrypsin
into the terminal
bronchioles
Reflex
IgeE mediators stimulation of
Increase activity of elastase are affixed to the tracheobronchial
Small Airway congestion mast cells of the receptors
narrowing of bronchial tracheobronchial
lumen and increase tree
amount of sputum Breakdown elastic fibers
Colonization of Bronchial Enlargement and Reflex Vagal stimulation
Bacteria inflammation and destruction of alveoli stimulation of of bronchial
eventual tissue or bronchioles or both parasympathetic smooth muscle
destruction nervous system contraction
receptors in
bronchial
mucosa
AcH is
Abnormal small airway released in
and weakened walls SA node of
Bronchial wall the heart
diseased with
granulated and fibrotic
squamous epithelium Loss of elastic Lung overinflated
recoil with air Slowing the
heart ensues

Ribcage
Air trapping and expanded
decrease gas Activate the K
Scarring Altered function of channels in
alveolar exchange
supraventricular
macrophages cells of the heart
Barrel Chest

More susceptible
to respiratory Bradycardia
infections
Reflex
stimulation of
parasympathetic
nervous system
receptors in
bronchial
mucosa

Mast cell
stabilizer

Chemical
Mediators:
Histamines
Leukotrines
Prostaglandins
Bradykinins
SRS-A

Increase vascular
permeability, casing
leakage of proteins
and fluids into tissue
 Tissue changes Increase IgE in serum

Increase cellular
permeability Bronchial wall response

Fluid leaks to the

lungs Vasodilation with Smooth muscle Narrowed Increase mucous
mucosal edema contraction bronchiole secretions
s

Pulmonary
edema

Pulmonary Obstruction of airway of the lungs

hypertension
 Poor Gas Exchange

Decrease amount of oxygen to

the blood (hypoxemia)

As a compensatory Excessive immature Eventually

mechanism, overproduction of RBC RBC will die
oxygen- carrying RBC
(polycythemia)

Increase volume Spleenomegaly

of RBC
Eventually clogs small blood
vessels
Increase blood
viscosity
Blood vessels constrict

Sluggish blood
flow
 Decrease O2
Heart will work harder to circulation
force blood through fewer
constricted blood vessels

Decrease O2 to Increase CO2

Right ventricle the brain levels in blood
becomes enlarged (hypoxia)

Walls of the heart Respiratory

thickens -headache acidosis
-dizziness
-fatigue
-weakness
Body will
Chamber of the compensate
heart loses its ability
to contract efficiently

Increase venous pressure COMA and

will lead to edema of legs, DEATH
liver, abdominal organs, Kussmaul’s
distended neck vein and respiration (deep
cerebral edema Right ventricle weakens rapid breathing)
(right sided hear failure)