EMPHYSEMA

Nagie M. Ilayat
Chronic Bronchitis and Emphysema
They are often found in combination in patient with COPD
COPD is the 5th leading cause of death for person aged to 45-
64 and 4th leading cause beyond 65 years (Price and Wilson).
COPD affects men twice as often as women, presumably bec
men have been heavier smokers; however, the incidence is
increasing in women and leveling off in men (Price and Wilson).
the prime etiologic factors seems to be cigarette smoking and the
forms of air pollution.
EMPHYSEMA

condition of the lung characterized by abnormal

permanent enlargement of the airspaces distal to the
terminal bronchiole, accompanied by destruction of
their walls, and without obvious fibrosis.

Overinflation- the enlargement of airspaces

unaccompanied by destruction.
Pathogenesis
EMPHYSEMA-Classified according to the pattern of involvement of the acini.

ANATOMY small glandular sac: a rounded sac containing secretory

cells, found at the ends of the ducts in an exocrine gland. Same as alveolus

Two types
1. Centrilobular emphysema (CLE) selectively affects the respiratory
bronchioles .
is more prevalent in men than in women. It is usually associated with
chronic bronchitis and is seldom found in the non-smokers.
2. Panlobular Emphysema (PLE), or panacinar emphysema, is less common
morphologic pattern in which there is nearly uniform enlargement and
destruction of the alveoli distal to the terminal bronchiole .
 As the disease progress ,there is gradual loss of all
components of the acinus until only a few strands of tissue
remain, which are usually blood vessels.
PLE-is characteristically uniform in distribution throughout
the lung, although the basal sections tends to be more
severely affected.
PLE, but not CLE is associated with a small group of patients
with primary emphysema.
This form of emphysema is characterized by the insidious
development of increased airway resistance without evidence
of chronic bronchitis.
 Patient with COPD have Primary emphysema w/c affects women
as often as men is of unknown cause ,but a familial kind associated
with deficiency of the enzyme alpha1-antitrypsin has been
described.
alpha1-antitrypsin is a protease.
It has been hypothesized that alpha1-antitrypsin is essential in
protection against naturally accruing proteases(Cherniack )
Proteases are found by bacteria ,polymorphonuclear leukocytes,
monocytes, and macrophages during the phagocytic process and
have the ability to breakdown the elastin and other
macromolecule in lung tissue.
 In healthy person ,lung tissue damage is prevented by the action of
antiproteases, which inhibit protease activity.
Certain persons may inherit alpha1-antitrypsin as an autosomal
recessive trait (Guenter and Buchan).
Homozygotes (type ZZ)with two abnormal genes have less than
10% of the normal amount of alpha1-antitrypsin and have 70%-
80% chance of the developing emphysema of the primary type
(panlobular, or emphysematous).
Heterozygote's (type MZ) with one abnormal gene have 60% of
the normal amount of alpha1-antitrypsin and are believed to have
an increased predisposition to develop emphysema, usually of the
bronchitic type (centrilobular).
 Smoking can produce an inflammatory response with the
consequent release of proteolytic enzymes (proteases),while
at the same time the oxidants in smoke inhibit alpha1-
antitrypsin (Cherniack).
 Panlobular emphysema associated with chronic bronchitis is
thought to be an end of the centrilobular emphysema bec both
morphologic patterns may exist in the same lung.
During inspiration, the bronchiolar lumen widens so that the air is
able to pass by the obstruction caused by thickening of the
mucosa and excess mucus .
During expiration, however, when the bronchiolar lumen becomes
narrowed ,the obstruction may prevent the aggress of air.
A loss of elasticity of the bronchiolar walls in emphysema may
cause premature collapse.
Air is thus trapped in the affected pulmonary segment ,leading to
over distension and coalescence of several alveoli.
 This effect is caused by fragmentation of the interaloveolar elastic
tissue and subsequent rupture of the attenuated interalveolar
septa, resulting in a bulla.
Bulla-is a thin- walled-air filled space in the lung
Emphysema have single or many bulla, which may or may not
communicate with each other.
Blebs ,which are formed by ruptured alveoli ,may rupture into
the pleural cavity and cause a spontaneous pneumothorax
(collapse the lung).
Other changes commonly seen in the COPD lung are a reduction
in the capillary bed and histologic evidence of chronic
bronchiolitis (involvement of the minute bronchioles ).
CLINICAL COURSE OF PATIENT WITH
COPD
Ranges from what is known as the pink puffers to the blue
bloaters
Clinical hallmark of pink puffers (associated with panlobular
emphysema)is the development of dyspnea without
significant cough and sputum production.
Usually the dyspnea begins between the ages 30 and 40 yrs
and becomes increasingly severe.
In advanced disease the patient may be too breathless to eat
and characteristically has a thin, wasted appearance .
Later in the course of disease ,the pink chest of the patient is
burrel-shaped ;the diaphragm is low and moves poorly.
 Polycythemia and cyanosis are rare (hence the term
pink),and the cor pulmunale(heart disease resulting from
pulmonary hypertension and lung disease)rarely develops
until the terminal stage.
There is minimal ventilation perfusion imbalance, so that
by hyperventilating ,the pink puffer is usually able to keep
blood gas within the normal range until late in the course of
the disease.
Lung are usually greatly enlarge ,so that there is large
increase in total lung capacity and residual volume.
 At the other extreme of the COPD range are the blue
bloaters (Bronchitis with little evidence of obstructive
emphysema).Patient usually have productive cough and
frequent respiratory infections that continue for years before
there is noticeable functional impairment.
However, they develop dyspnea in exertion. Patient show a
diminished respiratory drive; they hypoventilate and they
become hypoxic and hypercapnic.
Dyspnea-labored or difficult breathing
Hypoxia-difficulty of oxygen in the tissue
hypercapnia-presence in the blood of an abnormally high conc. of CO2.
 There is also a markedly distorted ventilation/perfusion
ratio.
Chronic hypoxia stimulates the kidney to produce
erythropoietin, which in turn stimulates increased
production of red cells ,resulting to secondary polycythemia
Hemoglobin level maybe 20g/100 ml or more, and cyanosis
is more readily apparent because there may easily be
5g/100ml reduced hemoglobin when only a small
proportion of the circulating blood hemoglobin is in the
reduced form(hence the name blue bloater).
 As these patients are not dyspneic at rest, they appear to be
comfortable.
There is gen.not great wt.loss,and body build is normal.
Total lung capacity may be normal, and the diaphragm is in
normal position.
Death is usually results from cor pulmonale(w/c develop
early)or from respiratory failure.
At autopsy, emphysema is often, although not always seen.
Emphysema tends to be of the centrilobular type, although
panlobular type may also be present.
Contrast of pure bronchitic(blue bloater)and
emphysematous(pink puffer)types of COPD
 Most pt w/COPD lie somewhere between the two.
The typical course of COPD is long, beg. in pts twenties and
thirties with a cigarette cough or morning cough and the
production of a small amount of mucoid sputum.
Minor resp.infection tend to persist longer than usual to the
patient.
In pt with predominantly emphysematous type, the coarse
appear to be less protracted, with no previous history of a
productive cough; severe dyspnea may be develop within a
few years.
 Hypercapnia, hypoxemia, and cor pulmonale develop,the
prognosis is poor; and death usually comes within a few years
after the onset.
Combination of respiratory and heart failure presipited by
pneumonia is the usual cause of death.
 Therapy for the patient with chronic bronchitis and obstructive
emphysema requires measure to relieve obstruction of the small
airways.
*airway collapse secondary to emphysema is irreversible, many pt
have some degree of bronchospasm, retention of secretions, and
mucosal edema w/c may be relieve by appropriate therapy.
Cessation of smoking and avoidance of other forms of air pollution
or allergens that may aggravate symptoms.
Infection should be treated promptly, and pts who are particularly
susceptible to respiratory infection may be directed to use
Prophylactic antibiotics.
 *pt is instructed to seek this medication whenever dyspnea
or amt of sputum production increases.
Tetracycline
Amphicillin-
penicillin -usually drugs of choice

All pts should receive influenza vaccine.

Additional measures to relieve airway obstruction include
Provision of adequate hydration to thin bronchial secretion
Use of expectorants
Use of bronchodilator drugs-to relieve small muscle spasm
 Sympathomimetic drugs
Albuterol
Terbuteline

Xanthines (such as aminophylline) commonly administered.

Pt with copious secretions, percussion and postural drainage
are used.
Breathing exercises(helpful)
Slow,relaxed expiration against purse lips
To prevent collapse of small bronchioles and reduces the amt of trapped
air.
 Administration of low conc. Oxygen may be helpful in
improving pts sense of well being. Administration of oxygen
with caution when there is hypercapnea and hypoxemia

Pathopysiology by: Sylvia A. Price and Lorreine M.

Wilson