OBSTRUCTIVE LUNG DISEASES – Pathology.

OVER VIEW

Atelectasis (collapse)
It is a complication that is divided based on the underlying factor.

1. Absorptive atelectasis /Resorption

Occurs when an obstruction prevents air from reaching the distal airways. The
air that already existed was gradually absorbed and caused overlapping of
lungs on each other.

Depending on where the level of obstruction is, all parts of a lung, a whole
lobe, or one or more segments of the lungs may be affected.

The most common cause of absorptive atelectasis is the blockage of a

bronchus by a mucous ball or purulent mucus. This complication is often after
surgery but bronchial asthma, bronchiectasis or chronic bronchitis may also
cause this complication.

Sometimes obstruction due to aspiration of foreign bodies (in children's

especially) or blood clots occur during oral surgery or anaesthesia.

Airway obstruction may be caused by: -

1. Tumors (especially bronchogenic carcinoma originating from central)

2. Enlarged lymph nodes during inflammatory diseases or metastases (if
formed in tuberculosis)
3. Vascular aneurysms rarely occur

2. Pressure Atelectasis Compression passive relaxation

It is also called passive or expansive atelectasis, usually accompanied by

accumulation of fluid (hydrothorax), blood, lymph, or air inside the pleural
cavity which mechanically causes the adjacent lung to overlap.

This patient has one common event following pleural effusion of which the
most common cause is congestive heart failure (CHD).
Pneumothorax (air leakage into the side cavity) can also be one of its other
causes.

(((picture shows pressure-type atelectasis. This disease is caused by

Chylothorax. In this condition, the thoracic ducts are opened and the lymph is
poured into the pleural cavity, causing lung to collapse)))

3. Contraction-cicatrisation Atelectasis

It is caused by local or widespread fibrosis in the lungs or pleural space and

prevents lung expansion during inhalation.

Atelectasis (with the exception of contractile type) is potentially reversible and

should be treated with prompt treatment to avoid complications such as
Prevent hypoxemia and secondary infection of the collapsed lung.
 OBSTRUCTIVE LUNG DISEASES:

Obstructive lung diseases are as follows: -

A. Asthma
B. Emphysema
C. Chronic bronchitis
D. Bronchiectasis

Obstructive disease (airway disease) which is characterized by the restriction of air

flow and is usually caused by an increase in resistance due to relative or complete
obstruction at any level.

Obstructive disorders (with the exception of tumours or inhalation of foreign bodies)

include: asthma, emphysema, chronic bronchitis, cystic fibrosis and bronchiectasis.

Total lung capacity is normal or increased and forced vital capacity (FVC) is normal or
decreased.

The decrease in expiratory flow is considered their main symptom, which is usually
measured by the forced expiratory volume in the first second (FEV1).

Therefore, the ratio of FVC, FEV1 has obviously decreased

There is a possibility that expiratory obstruction may occur, whether it is the result of
anatomic narrowing of the airway, which is classically seen in asthma, or whether it is
due to the reduction of elastic recoil, which is characteristic of emphysema.

Spirometry: Normal and Patients with COPD

 A. Asthma
• Asthma is characterized by reversible and periodic bronchospasm of the bronchi,
which results in excessive contraction of the bronchi in response to various stimuli.
• The basis of bronchial overreaction has not been fully revealed, but many believe
that it is caused by continuous inflammation of the bronchi.
• Clinically, asthma appears periodically with shortness of breath, cough and
wheezing.
• It affects about 5% of adults and 7-10% of children
• Classify asthma into two main groups based on the presence or absence of an
underlying immune disorder.

1- Atopic-Asthma
• Asthmatic episodes usually begin with a type I hypersensitivity reaction that is
caused by contact with a foreign antigen.

• It is the most common type of asthma: its onset is usually in the first two decades of
life

• And it is commonly associated with other allergic manifestations in the patient as

well as other family members

• The serum lgE level is usually elevated, as is the blood eosinophil count

• Researchers believe that this type of asthma originates from the TH2 subset of TCD4+
cells.

2- Non-Atopic Asthma
Non-immune initiating mechanisms are involved in this type of stimuli that are
ineffective or less effective in normal people can be the initiators of
bronchoconstriction.

Such factors include: Aspirin, lung infections, especially those caused by viruses, cold,
stress, exercise, and inhalation irritants such as sulfur dioxide and occupational
asthma.

These patients usually have no personal or family history of allergic manifestations

and serum lgE level is normal
Pathogenesis
• What characterizes all types of asthma is an exaggerated bronchoconstrictor
response (also called airway hyperresponsiveness) to a variety of stimuli.

• Airway hyperresponsiveness can actually be shown as increased sensitivity to

bronchoconstrictor agents such as histamine or methacholine (a cholinergic agonist).

• Airway hyperresponsiveness has been proven, but the basis of the abnormal
bronchial response is not fully understood

• Most of the current evidence suggests that bronchial inflammation is a background

for increased responsiveness.

• Basic inflammation of the bronchi, which is manifested by the presence of

inflammatory cells (especially eosinophils, lymphocytes, and mast cells) and damage
to the bronchial epithelium.

• What starts the inflammation? In extrinsic hypersensitivity reactions, type 1, but in

intrinsic, the cause is less known.

Pathogenesis of Atopic Asthma

• Allergic asthma, like type I hypersensitivity reactions, is caused by the sensitization of
TH2 + CD4 cells

• TH2 cells release cytokines such as interleukin 4, 5, 13, IL-5, which support the
production of lgE, the growth of mast cells, and the growth and activation of
eosinophils.

• Induction of TH2 response plays an essential role in the pathogenesis of allergic

asthma, and lgE of mast cells and eosinophils are key players in its development.

• One of the susceptibility loci is on the long arm of chromosome 5 (5q), where several
genes involved in regulation of lgE synthesis and mast cell and eosinophil growth and
differentiation map

• Atopic asthma attacks often show two phases: an acute phase that begins 30 to 60
minutes after inhaling the antigen, then subsides, and a longer delayed phase occurs 4
to 8 hours later.

• As can be expected, the primary stimulation of mast cells occurs on the mucosal
surface. The release of the resulting mediator opens the mucosal intercellular
junctions and facilitates the penetration of the antigen into the mucosal mast cells.
 ➢ The intermediates of the early stage of asthma are:

• Histamine, which causes

bronchial contraction and
increases vascular permeability

• Mast cell tryptase, which

inactivates bronchodilator peptide

• F2, E2, D2 prostaglandins that

cause bronchial contraction and
vasodilation.

• Leukotrienes E4, D4, C4: These

are very strong mediators that
cause prolonged contraction of
the bronchi, increase permeability
and blood vessels, and increase
mucin secretion.

• Platelet activating factor (PAF)

which causes the accumulation of
platelets and the release of
histamine from their granules.

➢ Delayed (or cellular) phase:

• Which calls for more leukocytes

(basophils, neutrophils and
eosinophils). IL-5 mast cell
mediators are responsible for
calling inflammatory cells

• Leukotriene B4, which calls and

activates eosinophils and
neutrophils

• Platelet activating agent, which

is a strong chemotactic agent for
eosinophils in the presence of IL-5.

• Tumor necrosis factor that increases adhesion molecules located on vascular

endothelium and inflammatory cells.
• When the leukocytes reach the emptying place of the mast cell granules, two
phenomena occur:
1- These cells release another wave of mediators that activate mast cells and
intensify the initial response.
2- They cause damage to epithelial cells, which is characteristic of asthma attacks.
Epithelial cells themselves are sources of mediators such as nitric oxide (NO)
that can cause smooth muscle expansion. The loss of epithelial integrity, due to
the reduction of available NO, may contribute to increased airway
responsiveness.

• Eosinophils are of special importance in the delayed stage

• Accumulated eosinophils exert various effects

• In addition, they produce basic basic protein (MBP) and eosinophil cationic protein
(ECP), which are considered toxic for epithelial cells.

• Eosinophil peroxidase causes cell damage in oxidative stress

• Therefore, eosinophils can intensify and sustain the inflammatory response without
being exposed to initiating antigens in addition to what happened.

Pathogenesis Of Non-Atopic Asthma

• Inflammatory mechanism and bronchial hyperresponsiveness in patients with
intrinsic (non-atopic) asthma has become less evident.

• In such cases, viral infections of the respiratory system and air pollutants such as
sulphur dioxide, ozone and nitrogen dioxide are blamed

• These factors increase airway responsiveness in both normal and asthmatic

individuals

• However, in the latter case (asthmatics), the bronchial response, which appears as
contraction, is much more intense and stable.

• Recent experimental studies have shown that the cellular and humoral effects of non-
atopic asthma overlap a lot with atopic asthma.

• According to one hypothesis, RSV increases cytokine secretion from specific T cells
and therefore induces eosinophilic infiltration.

• Bronchial epithelium itself is a rich source of pro-inflammatory cytokines during viral

infections, and some of them play a role in the maturation and chemotaxis of
eosinophils.

• Therefore, eosinophil plays an essential role in both types of asthma

• Researchers believe that aspirin-induced asthma is largely caused by the effect of

leukotrienes (especially leukotriene C4), remember the role of leukotrienes in external
asthma.
Morphology
• The appearance of the lungs is excessively expanded, which occurs due to
overinflation, and there may be small areas of atelectasis. The most remarkable
macroscopic finding is the blockage of bronchi and bronchioles by thick and hard
mucous balls.

• Histologically, the mucous balls contain rings of shed epithelium (Kurschmann's

spirals).

• Numerous eosinophils and Charcoleiden crystals (clusters of crystalloids composed

of eosinophil proteins) are also present.

• Eosinophils make up 50-50% of cellular infiltration. Also, mast cells, basophils,

macrophages, lymphocytes, plasma cells and some neutrophils are present, many of
the CD4+ lymphocytes are of TH2 type, which secrete IL-5 and IL-4.

• Specular necrosis and shedding of epithelial cells

• An increase in the collagen that is immediately below the basement membrane leads
to the formation of an apparently thick basement membrane. It is believed that this
change is caused by the activation of myofibroblasts through cytokines that secrete
collagen. This change in the basement membrane is not seen in patients with chronic
bronchitis

• An increase in the size of submucous mucous glands (or an increase in the number
of goblet cells in bronchiolar epithelium.)

• Hypertrophy and hyperplasia of smooth muscle in the bronchial wall (Figure 3-13)
Unlike chronic bronchiolitis, smooth muscle hyperplasia in asthma occurs in the large
and medium airways.
Clinical course
• An asthma attack is characterized by severe shortness of breath with wheezing. The
main problem is exhalation

• In a normal case, the attacks last from 1 to several hours, and either spontaneously
or with the treatment of bronchodilators and corticosteroids, they subside.

Patients between attacks are clearly without respiratory problems, but minor and
permanent respiratory defects can be detected by spirometry methods.

• Sometimes a severe attack occurs that does not respond to treatment and remains
stable for days or even weeks (status asthmaticus), hypercapnia, acidosis.

• Associated severe hypoxia may be fatal

The Relationship Between Chronic Bronchitis and Emphysema:
• At the beginning, it should be emphasized that the definition of emphysema is a
definition at the morphological level, while chronic bronchitis is defined based on
clinical manifestations such as the presence of chronic and recurring cough with
excessive mucus secretion.

• Second, the anatomical pattern of distribution is different: chronic bronchitis involves

large and small airways (inflammation of small airways is called chronic bronchiolitis
to specify the level of involvement); on the other hand, emphysema is limited to the
acini. They are located after the terminal bronchioles

• - Although chronic bronchitis may exist without visible emphysema and almost pure
emphysema may also occur (especially in patients with a-1 antitrypsin deficiency), but
these two diseases especially coexist because the main mechanism of Pathogenicity is
smoking which is common in both. As can be expected, when both exist together, the
clinical and physiological manifestations will overlap.

B. Emphysema
• Emphysema is characterized by
permanent enlargement of the air spaces
in the distal region of acinus compared
to the terminal bronchioles along with
the destruction of their walls.

• There are several situations in which

the size of air spaces is not associated
with destruction; Therefore, it is more
correct to call them excessive inflation

• As an example, expansion of the air

spaces in the opposite lung after
unilateral pneumonectomy is over-
compensatory inflation rather than
emphysema.
Types Of Emphysema:
• Acinus is a part of the lung distal to the terminal
bronchiole and includes respiratory bronchioles,
alveolar ducts and alveoli.

• A cluster of three to five acini is called a lobule

1- the Centri-acinus,
2- the Pan-acinar,
3- the para-septal acinus.
4- Irregular or para-cicatricial Emphysema (due to
scarring/fibrosis, irregularly affects acini, MOST
COMMON)

• The first & second one is more important, but their

differentiation is often difficult in advanced disease

1- Centri-Acinar Emphysema (Lobular Centre):

• The central or proximal parts of the acini, which are composed of respiratory
bronchioles, are affected, while the distal alveoli are not affected.

• Therefore, both emphysema and normal air spaces exist within an acinus and lobule

• Lesions in the upper lobes, especially in the apical parts, are more common and
severe

• In severe emphysema of the centre of the acinus, the distal acinus is also involved,
so it is difficult to distinguish it from emphysema of the entire acinus.

• This type of emphysema is often a consequence of smoking in people who do not

have a congenital defect of antitrypsin-α1.

• Most common Clinically with symptoms. (At second after Irregular Emphysema but is
without visible symptoms).

2- Pan-Acinar Emphysema (all lobe):

• In this type of emphysema, the acini are uniformly enlarged from the surface of the
respiratory bronchiole to the terminal blind alveoli (Whole acinus = Respiratory
bronchioles + Alveolar Ducts + Alveolar Sacs).

Unlike emphysema of the centre of the acini, emphysema of the whole acini tends to
occur more in the lower regions of the lung.

• It occurs in α-1 antitrypsin deficiency.

3- ParaSeptal-Acinar Emphysema:
• In this type of emphysema, the proximal part of the acinus looks normal, but the
distal part is mainly affected (Alveolar ducts + Alveolar sacs).

• Emphysema is especially severe in the vicinity of the pleura along the septa of the
lobular connective tissue and in the margins of the lobules.

• Emphysema occurs in the vicinity of areas of fibrosis or atelectasis

• It is usually more intense in the upper half of the lungs

• The existence of large, contiguous and numerous air spaces, whose diameter
reaches from less than 0.5 mm to more than 2 cm, and sometimes they form cyst-like
structures with progressive size, which are called bullae. (fusion of whole acinus).

• Probably, this type of emphysema is the basis of many cases of spontaneous

pneumothorax in young adults.

Pathogenesis:
• Researchers believe that emphysema is the result of two imbalances

1- Protease-antiprotease imbalance
2- Oxidant-antioxidant imbalance

• These two exist in almost all cases and in fact they strengthen each other's effect in
causing tissue damage

1- Protease-Antiprotease Imbalance Hypothesis:

• Protease/ Elastase/α1-trypsin– causes destruction of Alveolar wall;

• Antiprotease/Anti-Elastase/ α1-Antitrypsin – prevents destruction of alveolar wall.

• According to this finding, it was suggested that patients with genetic deficiency of
antitrypsin-a1 (an antiprotease) are at risk of pulmonary emphysema (especially Pan-
Acinar), which is aggravated by smoking.

• About 1% of emphysema patients have this defect

• α1-Antitrypsin, which is naturally present in the serum of tissue fluids and

macrophages, is a major inhibitor of proteases (especially elastase) that is secreted by
neutrophils during inflammation.

• Protease inhibition gene (Pi) has been identified in chromosome 14, this enzyme is
stagnant. Pi locus is highly polymorphic and has very different alleles.

• The most common of them is the natural allele (M) and the corresponding phenotype
(PiMM).
• About 0.012% of the population of the United States are homozygous for Z allele
PiZZ, which is associated with a severe decrease in the serum level of α1-Antitrypsin.
Many of these patients progress to symptomatic emphysema.

• Neutrophils (which are the main source of cellular proteases) are naturally arrested in
peripheral capillaries, including lung capillaries, and some of them manage to reach
the alveolar spaces.

• Any stimulus that increases the number of leukocytes (neutrophils and

macrophages) in the lung or the release of granules containing their protease,
increases proteolytic activity.

• With low levels of serum α1-Antitrypsin, the destruction of elastic tissue is not
inhibited and results in Emphysema.

• Also, it has helped the researchers in explaining the effect of smoking in causing
emphysema, especially the type of centri-acinar in people with normal levels of
antitrypsin.

• Smokers have accumulations of neutrophils and macrophages in their alveoli. The

inflammation mechanism is not completely clear, but it probably includes the
chemotactic effect of nicotine and the effects of oxygen free radicals in cigarette
smoke. These activate transcription of the nuclear factor (NF-KB) KB, which activates
the genes related to IL-8 and TNF. These factors in turn attract neutrophils.

• Accumulated neutrophils are activated and release granules that are rich in cellular
proteases (neutrophil elastase, proteinase 3 and cathepsin G) and cause tissue
damage.

2- Oxidant-Antioxidant Imbalance:
• Cigarette smoking plays an important role in oxidant-antioxidant imbalance. Under
normal conditions, the lung has several antioxidants (such as superoxide dismutase,
glutathione) that minimize oxidative damage. Cigarette smoke has a large amount of
oxygen free radicals, which start tissue damage with the use of antioxidants.

• Active neutrophils are also added to this pool of oxygen free radicals in the alveoli.
The secondary effects of oxidative damage led to the practical deficiency of
antioxidants.

Morphology:
• Pan-acini emphysema, when fully advanced, produces pale, bulky lungs that often
obscure the heart at autopsy, when the anterior chest wall is removed.

• Macroscopic views of emphysema of the centr-acinar leave less impression. The

lungs are bright pink and have a smaller volume

• In emphysema of the upper 3.2 acinous centre, the lungs are more severely affected
than the lower part, and in severe cases emphysema bullae may be clearly visible.
Cognitive Histology:
• Thinning and destruction of alveolar walls is observed

• In advanced disease, adjacent alveoli merge and create large air spaces.

• Terminal and respiratory bronchioles may be deformed and this is due to the
destruction of the septa that help to maintain these structures inside the parenchyma.

• With the destruction of the elastic tissue in the

surrounding alveolar septa, the radial stretch of the
small airways decreases. As a result, they tend to
overlap during exhalation, which is an important
cause of chronic airflow obstruction in severe
emphysema.

• In addition to the loss of alveoli, the number of

alveolar capillaries has also decreased

• There is fibrosis of the respiratory bronchioles

and there may also be evidence of associated
bronchitis and bronchiolitis.
Clinical course:
• Shortness of breath is usually the first symptom; This symptom starts slowly but
progresses steadily

• In patients with chronic bronchitis or chronic asthmatic bronchitis, cough and

wheezing are the primary complaints.

• Weight loss is common and may be severe enough to suggest an occult malignancy

• Pulmonary function tests show reduced FEV1 with normal or close to normal FVC.
Therefore, the ratio of FEV1 to FVC is reduced.

Classic Manifestation in People Without "Bronchitis" Component:

• The chest is barrel-shaped and there is shortness of breath with obvious

prolongation of exhalation; The patient, sitting in a hunched position, tries to force the
air out of the lungs with each exhalation effort.

• In these patients, the size of the air space is severe and the diffusion capacity is
reduced.

• Shortness of breath and increased ventilation (hyperventilation) are evident, so that

gas exchange is sufficient until the very end stages of the disease and blood gas levels
are relatively normal.

• Congestive right heart failure IS seen but with small heart (cor pulmonale).

• These patients are sometimes called "pink puffers".

Patients With Overt Chronic Bronchitis:

• They usually suffer from shortness of breath and respiratory pressure (effort) less, so
they get carbon dioxide retention, become hypoxic and often have cyanosis.

• They tend to be obese for reasons that are not completely clear

• They often go to the doctor after the onset of congestive right heart failure (cor
pulmonale) (big heart) and the accompanying fever.

• Sometimes patients with this clinical picture are called "blue bloaters".
• In all patients, secondary pulmonary hypertension occurs gradually. Its causes are

(1) Spasm of pulmonary vessels due to hypoxia and

(2) Reduction of the cross-sectional area of pulmonary capillaries due to the
destruction of alveoli

• Death caused by emphysema is related to:

1- pulmonary failure with respiratory acidosis, hypoxic coma; or

2- right heart failure (cardiopulmonary).
C. Chronic Bronchitis
• This disease is a constant phlegm cough that continues for at least 3 consecutive
months and for at least 2 consecutive years.

• Chronic bronchitis is common among smokers and residents of smog cities; Some
studies show that 20-25% of men aged 40 to 65 have this disease.

• Disease of Trachea & Principal Bronchi.

Types Of Chronic Bronchitis:

• Most of the patients have simple chronic bronchitis: secretory cough produces
mucoid sputum, but the airway is not blocked.

• If the sputum contains pus, it is probably due to secondary infections and it is said
that the patient has chronic purulent mucous bronchitis.

• Some patients with chronic bronchitis may have excessive airway response and
intermittent episodes of asthma. It is often difficult to distinguish this condition, which
is called chronic asthmatic bronchitis, from atopic asthma.

• A group of bronchitis patients progress towards chronic obstruction of the outflow

tract, which is measured by pulmonary function tests. They are called by people with
chronic obstructive bronchitis (evidence of emphysema).

Although the characteristic manifestation of chronic bronchitis (excessive secretion of

mucus) is primarily a reflection of large bronchial involvement, the morphological
basis of airway obstruction in chronic bronchitis is more peripheral and occurs as a
result of the following factors.

• Inflammation, fibrosis and resulting narrowing in the bronchioles ("small airway

disease)

• Associated emphysema

It is generally believed that while small airway disease (chronic bronchiolitis) is

involved in airflow obstruction, chronic bronchitis with obvious airflow obstruction is
complicated by emphysema in almost all cases.
Pathogenesis:
• The distinguishing feature of chronic
bronchitis is increased mucus secretion
that starts in the large airways.

• Although the most important causative

factor is smoking alone, other air
pollutants such as sulphur dioxide and
nitrogen dioxide may be involved.

• These irritating substances increase the

secretion of bronchial mucous glands, hypertrophy and hyperplasia of mucous glands
and the formation of metaplasia of mucin-secreting goblet cells on the surface of the
bronchial epithelium.

• In addition, they cause inflammation and infiltration of T cells, macrophages and

neutrophils

• Unlike asthma, eosinophils are not seen in chronic bronchitis, unless asthmatic
bronchitis is present.

• Microbial infection is often present, which mainly plays a secondary role by

maintaining inflammation and aggravating symptoms.

Morphology:
• In the larger trachea and bronchi there is increased size & number of the mucus
secreting glands. The increase in size is measured by the ratio of the thickness of the
submucous gland layer to the thickness of the bronchial wall (R e i d index).

• Often, an increase in the number of goblet cells is seen in ciliated epithelium

• Squamous metaplasia often occurs. After that, there are changes in the form of
dysplasia in the cells of the lining epithelium, which is a sequence of events and may
lead to a change in shape towards bronchogenic carcinoma.

• A variable number of inflammatory cells, mostly mononuclear, but sometimes mixed

with neutrophils, is often seen in the bronchial mucosa.
Morphology
• Unlike asthma, eosinophils are not a major component of the inflammatory infiltrate,
except in patients with asthmatic bronchitis.

• Chronic bronchiolitis (a disease of the small airways) is also associated with goblet
cell metaplasia (whose number is small in the peripheral airways), inflammation and
fibrosis in the walls and smooth muscle hyperplasia.
Clinical Course:
• In patients with chronic bronchitis, severe cough and phlegm production may exist
indefinitely and without disturbing the ventilatory function.

• However, as mentioned before, some patients progress to marked COPD with

outflow tract obstruction. This condition is associated with hypercapnia, hypoxemia,
and (in severe cases) with cyanosis. (Blue bloaters).

• Advanced chronic bronchitis is complicated by increased pulmonary blood pressure

and right heart failure. Recurrent infections and respiratory failure are constant threats

D. Bronchiectasis
•: Bronchiectasis is the permanent dilation of the bronchi and bronchioles due to the
destruction of the supporting muscle and elastic tissue, which is caused by or
accompanied by chronic necrotizing infections.

• It is not a primary disease, but often secondary to persistent infection or obstruction

caused by various conditions.

• Diagnosis depends on a proper history, along with showing bronchial dilatation on

radiographs
Conditions Predisposing a Person to Bronchiectasis:
• Bronchiectasis. Common causes include tumours, foreign bodies, bronchiectasis can
also complicate atopic asthma and chronic bronchitis.

• Congenital or hereditary conditions

• In cystic fibrosis, as a result of obstruction and infection due to the abnormal

secretion of sticky mucus, severe and widespread bronchiectasis is created.

• In situations of immune deficiency, especially the deficiency of immunoglobulins, the

susceptibility to bronchiectasis increases due to the increased susceptibility to
frequent bacterial infections;

• Kartagener's syndrome, an autosomal recessive disorder, often causes

bronchiectasis and sterility in men. Structural abnormalities of cilia lead to
permanent infections and reduced sperm motility.
• Necrotizing or purulent pneumonia: Necrotizing or purulent pneumonia
(especially with virulent organisms such as Staphylococcus aureus or
Klebsiella) may make a person susceptible to bronchiectasis. Bronchiectasis
following tuberculosis is still considered as an important complication in
indigenous areas.

Pathogenesis:
• Two vital and related processes are considered vital in the pathogenesis of
bronchiectasis: 1-obstruction and 2-permanent chronic infection.

• Each of these two trends may appear at first

• The natural cleansing mechanisms are stopped by the blockage. Therefore,

secondary infection is created soon after it; Chronic infection in the long-term causes
damage to the bronchial wall and the accumulation of exudate causes further
expansion of the airways and leads to irreversible dilatation.

• On the contrary, a persistent necrotizing inflammation in the bronchi or bronchioles

may lead to obstructive secretions, inflammation of the entire wall (with peri-bronchial
fibrosis and boil formation) and finally the sequence of events described earlier.

Morphology:
• Involvement of the lungs in bronchiectasis usually involves the lower lobes
bilaterally, especially those where the air passes, which are often located vertically
• When tumours or aspiration of foreign bodies lead to bronchiectasis. The
involvement may be localized and affect exactly a single part of the lungs

• Usually, the most severe involvement is found in the more distal bronchi and
bronchioles

• Airways may expand up to four times their normal diameter, and in the physical
examination of the lung, they can be traced almost to the lateral levels.

• Contrary to this, in normal lungs, the bronchioles cannot be followed in the normal
physical examination up to 2-3 cm from the lateral surfaces.

• In the case of active and full-scale disease, a severe acute and chronic inflammatory
exudate inside the walls of the bronchi and bronchioles and peeling of the lining
epithelium cause areas of severe scarring.

• Fibrosis of bronchial and bronchiolar walls and around bronchioles occurs in more
chronic cases

• In some cases, necrosis destroys bronchial and bronchiolar walls and a lung abscess
is formed.

Clinical course:
• Clinical manifestations include a persistent and severe cough along with purulent
and sometimes foul-smelling mucus discharge.

• It is possible that the sputum has streaks of blood; overt Haemoptysis can occur.

• Symptoms are often periodic and are facilitated by upper respiratory tract infections
or exposure to new pathogens.

• Clubbing of the fingers may occur

• In severe and extensive cases of bronchiectasis, obvious ventilation defects occur in

the form of obstruction along with hypoxia, hypercapnia, increased pulmonary blood
pressure and (rarely) pulmonary heart disease.

• Abscesses of brain metastasis and reactive amyloidosis are other complications of

bronchiectasis that are less common.
TABLE…