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DOO Brosterhood Inc.
SYSTEMIC PATHOLOGY
ASTHMA, EMPHYSEMA &

BRONCHIECTASIS
FRANK DARTEY
AMANKONAH
1
BRONCHIAL ASTHMA
Asthma is a
chronic relapsing
inflammatory
disorder
characterized by
hyperreactive
airways, leading to
episodic,
reversible
bronchoconstrictio
n, owing to
increased
responsiveness of
2
BRONCHIAL ASTHMA cont’d
Associated with atopy :-

increased susceptibility to
generate immunoglobulin E (IgE)
in response to external allergens
Those afflicted experience
unpredictable disabling attacks of
severe dyspnea, coughing, and
wheezing triggered by sudden
episodes of bronchospasm
Rarely a state of unremitting
3
4
PATHOGENESIS
The two major components of
asthma are chronic airway
inflammation and bronchial
hyperresponsivness
The inflammation involves many
cell types and numerous
inflammatory mediators
The precise relationship of specific
inflammatory cells and the
mediators to airway hyperreactivity
5
TYPES
ATOPIC ASTHMA
NONATOPIC ASTHMA
DRUG-INDUCED ASTHMA
OCCUPATIONAL ASTHMA
6
ATOPIC ASTHMA
Most common type of asthma
Usually begins in childhood
Triggered by environmental
antigens (e.g. Dusts, pollens, foods
e.t.c.)
Attacks are often preceded by
allergic rhinitis, eczema or
urticaria.
Positive family history of atopy is
7
NONATONIC/ NONREAGINIC
Frequently triggered by respiratory
tract infection
Viruses (e.g., rhinovirus,
parainfluenza virus) rather than
bacteria are the most common
provokers
A positive family history is
uncommon, serum IgE levels are
normal, and there are no other
associated allergies
It is thought that virus-induced
inflammation of the respiratory 8
DRUG-INDUCED ASTHMA
Asthma provoked by
pharmacological agents
E.g. Aspirin
(Aspirin-sensitive asthma is an
uncommon)
9
OCCUPATIONAL ASTHMA
This form of asthma is stimulated by
fumes (epoxy resins, plastics), organic
and chemical dusts (wood, cotton,
platinum), gases (toluene), and other
chemicals (formaldehyde, penicillin
products)
The underlying mechanisms vary
according to stimulus and include
type I IgG-mediated reactions, direct
liberation of bronchoconstrictor
substances, and hypersensitivity
10
BRONCHIECTASIS
11
Bronchiectasis
is a chronic
necrotizing
infection of the
bronchi and
bronchioles
leading to or
associated with
abnormal
dilation of these
12
13
manifested clinically by
Cough
fever, and
expectoration of copious amounts of

foul-smelling, purulent sputum
To be considered bronchiectasis, the
should be
dilation
permanent 14
Bronchiectasis ...
Usually develops in association with the following conditions:
Bronchial obstruction, owing to tumor, foreign

bodies, and occasionally mucous impaction, in which the
bronchiectasis is localized to the obstructed lung segment,
or owing to diffuse obstructive airway diseases, most
commonly atopic asthma and chronic bronchitis
Congenital or hereditary conditions,

including congenital bronchiectasis (caused by a defect in
the development of bronchi), cystic fibrosis , intralobar
sequestration of the lung , immunodeficiency states, and
immotile cilia and Kartagener syndromes
15
Etiology and Pathogenesis...

Obstruction and infection are the
major influences associated with
bronchiectasis
After, air is resorbed from the

airways distal to the obstruction,
with resultant atelectasis
Often accompanying atelectasis are

early bronchial wall inflammation
and the presence of intraluminal
secretions that result in dilation of
the walls of those airways that are
patent 16

The changes, however, become
irreversible
3. if the obstruction persists,

especially during periods of
growth, because the airways
will not be able to develop
normally
5. If there is added infection 17


Infection plays a role in the
pathogenesis of bronchiectasis in
two ways:
(1)It produces bronchial wall
inflammation, with weakening,
and further dilation, and
(2) the extensive bronchial and

bronchiolar damage causes
endobronchial obliteration, with
atelectasis distal to the 18
EMPHYSEMA
19
Emphysema...
a 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 20
TYPES
There are four major types:
(2)Centriacinar
(2) Panacinar
(3) Paraseptal
(4) irregular.
Of these, only the first two cause

clinically significant airflow
obstruction
21
Centriacinar(Centrilobular)
Emphysema
Centriacinar emphysema is far
more common than the panacinar
form, constituting greater than 95%
of cases
The distinctive feature of this type

of emphysema is the pattern of
involvement of the lobules; the
central or proximal parts of the
acini, formed by respiratory
bronchioles, are affected, whereas
22
Panacinar (Panlobular)
Emphysema
the acini are uniformly enlarged from
the level of the respiratory bronchiole
to the terminal blind alveoli
In contrast to centriacinar
emphysema, panacinar emphysema
tends to occur more commonly in
the lower zones and in the
anterior margins of the lung, and
it is usually most severe at the
base
is associated with alpha1 - 23
Paraseptal (Distal Acinar)

Emphysema
The proximal portion of the acinus
is normal, but the distal part is
dominantly involved
The emphysema is more striking
adjacent to the pleura, along the
lobular connective tissue septa, and
at the margins of the lobules.
It occurs adjacent to areas of
fibrosis, scarring, or atelectasis and
is usually more severe in the upper
half of the lungs
The characteristic findings are of
multiple, continuous, enlarged 24
airspaces from less than 0.5 mm to
Paraseptal (Distal Acinar)

Emphysema
probably underlies many of the
cases of spontaneous
pneumothorax in young adults.
25
Irregular Emphysema
so named because the acinus is
irregularly involved, is almost
invariably associated with scarring
In most instances, these foci of

irregular emphysema are
asymptomatic.
26
Emphysema lung
27
Pathogenesis
the most plausible hypothesis to
account for the destruction of
alveolar walls is the protease-
antiprotease mechanism
the most plausible hypothesis to

account for the destruction of
alveolar walls is the protease-
antiprotease mechanism
Thus, emphysema is seen to result

from the destructive effect of high 28
Pathogenesis
Smokers have greater numbers of neutrophils and
macrophages in their alveoli. The increased
recruitment of neutrophils into the lung is likely to
result, in part, from the release by activated alveolar
macrophages of neutrophil chemotactic factors ( e. g.,
IL-8), this release being stimulated by smoking
nicotine is chemotactic for neutrophils, and cigarette

smoke activates the alternative complement pathway.
Smoking stimulates release of elastase from

neutrophils.
Smoking enhances elastolytic protease( s) activity in

macrophages. Macrophage elastase is not inhibited by
alpha1 -AT and can proteolytically digest this enzyme.
Oxidants in cigarette smoke and oxygen free radicals

secreted by neutrophils inhibit alpha1 -AT and thus 29
30
OTHER TYPES
OF
EMPHYSEMA
31
1 .Compe nsa tor y Emph yse ma

(C ompen sa tor y Hy pe rin flatio n).
The term compensatory

emphysema is sometimes used
to designate dilation of alveoli
but not destruction of septal
walls in response to loss of lung
substance elsewhere. It is best
exemplified by the
hyperexpansion of the residual
lung parenchyma that follows
surgical removal of a diseased 32
2. Senil e Em ph ys em a
Senile emphysema refers to the
overdistended, sometimes
voluminous lungs found in the
aged. These changes result from
age-related alterations of the
internal geometry of the lung--
larger alveolar ducts and smaller
alveoli--that occur without loss of
elastic tissue or destruction of lung
substance
33
3.Ob stru ctiv e Ov er in flat ion .

Obstructive overinflation refers to
the condition in which the lung
expands because air is trapped
within it. A common cause is
subtotal obstruction by a tumor or
foreign object.
A classic example is congenital
lobar overinflation in infants,
probably resulting from hypoplasia
of bronchial cartilage and
sometimes associated with other
congenital cardiac and lung
abnormalities.
34
5.B ullous Em ph ysema.

Bullous emphysema refers merely
to any form of emphysema that
produces large subpleural blebs or
bullae (spaces >1 cm in diameter in
the distended state) .
They represent localized

accentuations of one of the four
forms of emphysema, are most
often subpleural, and occur near
the apex, sometimes in relation to
old tuberculous scarring.
On occasion, rupture of the bullae

may give rise to pneumothorax 35
5. In ter stitial Emph yse ma

The entrance of air into the connective tissue
stroma of the lung, mediastinum, or
subcutaneous tissue is designated
interstitial emphysema.
In most instances, alveolar tears in
pulmonary emphysema provide the avenue
of entrance of air into the stroma of the lung,
but rarely a wound of the chest that allows
air to be sucked in or a fractured rib that
punctures the lung substance may underlie
this disorder.
Alveolar tears usually occur when there is a
combination of coughing plus some
bronchiolar obstruction, producing sharply
increased pressures within the alveolar sacs.
E.g. Children with whooping cough and
bronchitis, patients with obstruction to the 36
airways (by blood clots, tissue, or foreign
Chronic bronchitis
37
introduction
Chronic bronchitis, so common among
habitual smokers and inhabitants of smog-
laden cities, is not nearly so trivial as was
once thought.
When persistent for years, it may
(1) be associated with chronic obstructive
airway disease, as discussed earlier;
(2) lead to cor pulmonale and heart failure;
(3) cause atypical metaplasia and dysplasia

of the respiratory epithelium, providing a
possible soil for cancerous transformation 38
definition
Chronic bronchitis per se is defined clinically: It is present
in any patient who has persistent cough with sputum
production for at least 3 months in at least 2 consecutive
years.
In simple chronic bronchitis, patients have a productive

cough but no physiologic evidence of airflow obstruction.
Some individuals may demonstrate hyperreactive airways

with intermittent bronchospasm and wheezing. This
condition is called chronic asthmatic bronchitis.
Finally, some patients, especially heavy smokers, develop

chronic airflow obstruction, usually with evidence of
associated emphysema, and are classified as showing
obstructive chronic bronchitis.
39
Pathogenesis
(1) chronic irritation by inhaled
substances
(2) microbiologic infections. Both sexes

and all ages may be affected, but
chronic bronchitis is most frequent in
middle-aged men
Cigarette smoking remains the
paramount influence. Chronic bronchitis
is 4 to 10 times more common in heavy
40
PATHOGENESIS...
The hallmark and earliest feature of
chronic bronchitis is hypersecretion of
mucus in the large airways, and it is
associated with hypertrophy of the
submucosal glands in the trachea and
bronchi.
As chronic bronchitis persists, there is also

a marked increase in goblet cells of small
airways-- small bronchi and bronchioles--
leading to excessive mucus production that
contributes to airway obstruction. It is
thought that both the submucosal gland
hypertrophy and the increase in goblet
cells are caused by tobacco smoke or other 41
PATHOGENESIS...
Histologic studies of the small airways in
young smokers disclose
(2)goblet cell metaplasia with mucous
plugging of the lumen,
(3)clustering of pigmented alveolar
macrophages,
(4)inflammatory infiltration, and
(5)fibrosis of the bronchiolar wall (in a
somewhat older group of patients).
42
Clinical Features.
The clinical sine qua non of chronic

bronchitis is a persistent cough productive
of copious sputum
For many years, no other respiratory

functional impairment is present, but
eventually dyspnea on exertion develops
With the passage of time, and usually with

continued smoking, other elements of
COPD may appear, including hypercapnia,
hypoxemia, and mild cyanosis 43
Long-standing severe chronic bronchitis

commonly leads to cor pulmonale with
cardiac failure
Death may also result from further

impairment of respiratory function
incident to acute intercurrent bacterial
infections.
44
TH ANK Y OU!
45

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DOO Brosterhood Inc.

ASTHMA, EMPHYSEMA &

BRONCHIAL ASTHMA cont’d

Associated with atopy :-

expectoration of copious amounts of

Bronchial obstruction, owing to tumor, foreign

Congenital or hereditary conditions,

Etiology and Pathogenesis...

After, air is resorbed from the

Often accompanying atelectasis are

Etiology and Pathogenesis...

3. if the obstruction persists,

5. If there is added infection 17

Etiology and Pathogenesis...

(2) the extensive bronchial and

Of these, only the first two cause

The distinctive feature of this type

Paraseptal (Distal Acinar)

Paraseptal (Distal Acinar)

In most instances, these foci of

the most plausible hypothesis to

Thus, emphysema is seen to result

nicotine is chemotactic for neutrophils, and cigarette

Smoking stimulates release of elastase from

Smoking enhances elastolytic protease( s) activity in

Oxidants in cigarette smoke and oxygen free radicals

1 .Compe nsa tor y Emph yse ma

The term compensatory

3.Ob stru ctiv e Ov er in flat ion .

5.B ullous Em ph ysema.

They represent localized

On occasion, rupture of the bullae

5. In ter stitial Emph yse ma

(2) lead to cor pulmonale and heart failure;

(3) cause atypical metaplasia and dysplasia

In simple chronic bronchitis, patients have a productive

Some individuals may demonstrate hyperreactive airways

Finally, some patients, especially heavy smokers, develop

(2) microbiologic infections. Both sexes

As chronic bronchitis persists, there is also

The clinical sine qua non of chronic

For many years, no other respiratory

With the passage of time, and usually with

Long-standing severe chronic bronchitis

Death may also result from further

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