@2024 by Evans Mwansa Chama

1
ANATOMY of The LUNGS and TRACHEOBRONCHIAL TREE

a. The tracheobronchial tree:

Is composed of tubular structures of varying sizes that
conduct air and respiratory secretions. It runs from the
trachea to the alveolar sacs.

● Trachea;
➔ It's a cartilaginous "trunk" of the tree.
➔ Contains 15 – 20 C-shaped cartilaginous rings.
The cartilagenous rings are stacked vertically and
connected via anular rings. They also contain
submucosal glands.
➔ The posterior wall of the trachea moves to
accommodate foods passing through the esophagus.

@2024 by Evans Mwansa Chama

2
● Bronchi;
➔ They also have cartilage and submucosal glands.
➔ Primary bronchi enter the lungs.
➔ Secondary bronchi serve lobes of lung
("lobar" bronchi).
➔ Tertiary bronchi serve bronchopulmonary
segments ("segmental" bronchi); 10 on the right,
8-10 on the left.
● Bronchioles;
➔ They are numerous, and narrow as they branch.
➔ They Have more smooth muscles in their walls.
➔ They differ from bronchi by the lack of cartilage
and submucosal glands within their walls.
● Terminal bronchioles;
➔ Terminal bronchioles are the final passageway of
the conducting portion of the respiratory system.
● The pulmonary acinus;
➔ The acinus is the part of the lung distal to the
terminal bronchiole. It is composed of the;
■ respiratory bronchioles;
◆ Emanates from the terminal bronchioles
and proceeds into the alveolar ducts.
◆ They have thin walls that allows for some
gaseous exchange.

@2024 by Evans Mwansa Chama

3
■ alveolar ducts;
◆ Emanates from respiratory bronchiole and
immediately branches into the alveolar sacs.
■ alveolar sacs;
◆ They are blind ends of the respiratory
passages. Each alveolar sac is comprised of a
group of alveolus.
■ alveoli (“singular = alveolus");
◆ They are thin-walled out-pocketings of the
alveolar sacs.
◆ They are surrounded by pulmonary
capillaries.
◆ They facilitate gaseous exchange between
the respiratory and cardiovascular systems.
◆ The thin wall that separates the alveoli
from one another (or in simpler terms the
thin wall that separates an alveolus from
another alveolus) is known as the alveolar
septa (plural: septum). Each alveolar septa
in between adjacent alveoli consists of the
following components, proceeding from blood
to air:
○ The capillary endothelium and basement
membrane.

@2024 by Evans Mwansa Chama

4
○ The pulmonary interstitium, composed of
elastic fibers, collagen, fibroblast-like
cells, smooth muscle cells, mast cells, and
mononuclear cells.
○ The alveolar epithelium, consisting of a
continuous layer of two principal cell
types:
➢ type I pneumocytes; flattened
cells covering the alveolar surface.
➢ type II pneumocytes; rounded
cells that produce pulmonary
surfactant.

○ Note that the The alveolar pores function

primarily as conduits for interalveolar
movement of alveolar liquid, surfactant
components, and macrophages.

@2024 by Evans Mwansa Chama

5
 ◆ The alveoli also contain alveolar macrophages
which usually lie free within the alveolar space.
➔ Note that a cluster of 3 to 5 acini is called a
lobule.
b. The lungs:
● Left lung = contains two lobes. Namely superior and
inferior lobes; heart nestles into medial left lobe in the
cardiac notch.
● Right lung = contains three lobes. superior, middle, and
inferior lobes.
● The lungs are covered by a serous membrane known as
pleura.
c. The pleura and pleura cavity:
● The pleura consists of a parietal and a visceral part.
● The parietal pleura; it lines the walls of the thorax,
diaphragm, and mediastinum, is continuous with the
visceral pleura.
● The visceral pleura; it covers the surface of the lung.
@2024 by Evans Mwansa Chama
6
 ● The pleura cavity or pleura space; lies in between the
parietal and visceral pleura. It contains a lubricanting
fluid called pleara fluid.

PULMONARY DISEASES

1. ATELECTASIS (Collapsed lung);

★ Definition: is the loss of lung volume caused by inadequate
expansion (air filling) of the alveoli air spaces.

★ It can result either from:

○ Incomplete expansion of lungs (as in neonatal
atelectasis).
○ Or collapse of previously inflated lung (as in adult
atelectasis).
@2024 by Evans Mwansa Chama
7
★ Etiology:
○ The cause of atelectasis depends on the underlying
mechanism that is leading to collapsed lung.
○ H ence, atelectasis is classified into three forms. Namely;
■ Resorption (obstructive ) atelectasis: is due to
complete obstruction of an airway by
● mucus plugs or mucopurulent exudates blocking
the bronchi (as seen in bronchial asthma and
bronchiectasis).
● neoplasms (or intrabronchial tumors).
● foreign body aspirations that blocks the bronchi
(especially in children).
■ Compression atelectasis: is due to external pressure
exerted on the lung tissue, causing the air sacs
(alveoli) to lose air and collapse. The common
external pressure is an expanded pleura cavity
resulting from either
● excessive pleura fluid accumulation (pleura
effusions occuring in the setting of congestive heart
failure ).
● hemothorax (leakage of blood into pleural space
commonly due to injury or trauma).
● Pneumothorax (leakage of air into the pleural
space commonly due to blunt or penetrating injury
to the chest ).

@2024 by Evans Mwansa Chama

8
 ■ Contraction (cicatrization) atelectasis: is due to
fibrous scarring of the lungs or pleura, that makes it
hard for the lungs to expand.

★ Pathogenesis:
○ Note; under physiological conditions, adequate filling of
the alveoli air spaces generates adequate alveolar stretch
that triggers type II alveolar cells (type II
pneumocytes) to synthesize and release surfactant.
○ Now Under pathological conditions;
The etiology depending on the type of atelectasis causes
inadequate filling of the alveolar air spaces ➞ leads to
inadequate alveolar stretching ➞ resulting in poor
synthesis and poor secretion of surfactant ➞ the poor
secretion of surfactant leads to alveoli collapse and
consequent loss of alveoli volume ➞ which grossly
manifests as either partial or complete collapse of the
whole or part or section of the lung.
★ Diagnosis: chest x-ray imaging.

@2024 by Evans Mwansa Chama

9
 ★ Clinical features:
If atelectasis affects large areas of the lungs, the oxygen
level in your blood may go down (hypoxemia). This can
lead to symptoms like:
■ Trouble breathing/shortness of breath (dyspnea).
■ Coughing.
■ Chest pain.
■ Rapid breathing (tachypnea).
■ Skin and lips turning blue (cyanosis).

2. ACUTE RESPIRATORY DISTRESS SYNDROME;

★ It was formerly considered to be the severe end of a
spectrum of acute lung injury.
★ Definition:
○ It refers to; rapid onset (acute ) of widespread (diffuse )
inflammatory form of lung injury, which leads to
respiratory failure.
○ It is characterized by; respiratory failure occurring within
1 week of a known clinical insult”, with bilateral opacities
(white areas) on chest imaging, which can not be fully
explained by
● effusions,
● atelectasis,
● cardiac failure,
● or fluid overload.

@2024 by Evans Mwansa Chama

10
★ Etiology:
The common triggers of the inflammatory form of lung
injury can include;
■ sepsis and pneumonia (diffuse pulmonary infections).
■ aspirations (inhaled irritants such as smoke, gasses,
chemicals, gastric aspirations etc ).
■ trauma (i.e brain 🧠 injury, abdominal injury and
multiple fractures).
■ Pancreatitis.
■ Transfusion reactions.
★ Pathogenesis:
○ The etiology causes alveolar damage ➞ which triggers the
damaged alveolar pneumocytes to secrete inflammatory
cytokines (like TNF-ALPHA, IL-8 and IL-1) ➞ these
cytokines subsequently leads to the recruitment of
neutrophils into the vascular space, interstitium and the
alveoli ➞ the neutrophils then releases toxic mediators
(such as reactive oxygen species, leukotrienes and
proteases) which will further exercabate the alveolar
damage.
○ The major site of injury is the alveolar capillary
membrane ➞ which results in pulmonary edema
(extravasation of fluid from the capillaries into the
alveoli air space ) ➞ this impairs gaseous exchange
causing hypoxemia.

@2024 by Evans Mwansa Chama

11
 ○ The edema can also wash away alveoli surfactant ➞
leading to alveoli collapse and overtime a protein rich fluid
may form in the alveoli air space, which subsequently may
undergo fibrosis to form a waxy hyaline membrane (which
looks like a layer of glassy material )

★ Morphology:
○ acute phase;
■ Grossly: lungs are dark-red, firm, airless & heavy.
■ Microscopy: diffuse alveolar damage (DAD), hyaline
membranes and pulmonary edema.

@2024 by Evans Mwansa Chama

12
 ○ H ealing stage or resolution stage;
■ Proliferation of type II pneumocytes with formation
of granulation tissue.
■ Resorption of the hyaline membrane (breakdown and
absorption of the hyaline membrane constituents).
■ Fibrotic thickening of the alveolar wall or septa (due
to inflammatory cells, fibroblasts and collagen).
★ Diagnosis:
○ Cracking sounds called rales or crackles are heard during
lung auscultation (crackles are characterized by short,
discontinuous, popping or cracking sound heard due to
sudden opening of collapsed alveoli during inspiration).
○ Chest x-ray imaging showing opacities (white areas),
which are not due to pulmonary edema. (Note that lungs
appear black on X-rays due to air-filled spaces. Anything
that blocks X-rays will appear white ).

★ Clinical features:
○ Dyspnea (shortness of breath).
○ Tachypnea (rapid, shallow breaths)
○ Hypoxemia and cyanosis.
○ Diffuse interstitial disease(leading to chronic pulmonary disease).

@2024 by Evans Mwansa Chama

13
3. OBSTRUCTIVE 🆚 RESTRICTIVE PULMONARY DISEASES;
★ Diffuse pulmonary diseases are classified into two. Namely:
■ Obstructive (airway) lung disease.
■ Restrictive (interstitial, infiltrative ) lung disease.
★ Differences between the two:

Obstructive lung disease Restrictive lung disease

Characterized an increase in resistance to reduced expansion of the lung

by airflow caused by partial parenchyma (alveoli and
or complete obstruction at pulmonary interstitium) and
any level of the conducting decreased total lung capacity
zone causing air trapping.

Forced
expiratory
volume at 1 significantly reduced normal or reduced
second proportionately
(FEV1)
is

Forced vital
capacity either normal or slightly reduced
(FVC ) reduced
is

FEV1/FVC
ratio Characteristically near normal
is decreased

Examples ● Emphysema ● Pneumoconiosis

● Chronic bronchitis ● Interstitial fibrosis
● asthma of unknown etiology
● Bronchiectasis ● Sarcoidosis

@2024 by Evans Mwansa Chama

14
 ★ Note that:

○ FVC (Forced Vital Capacity): This is the total amount

of air you can exhale forcefully after taking the deepest
breath possible.
○ FEV1 (Forced Expiratory Volume in 1 second): This
measures the volume of air you can forcefully exhale in the
first second of a breath.

4. OBSTRUCTIVE (AIRWAY) LUNG DISEASES;

★ The four major obstructive disorders include:
○ Emphysema.
○ Chronic bronchitis.
○ asthma.
○ Bronchiectasis.
★ Note that:
○ Emphysema and Chronic bronchitis are grouped together
under the rubric of chronic obstructive pulmonary disease
(COPD).
○ This is because disorders of COPD tend to have
irreversible airway obstruction and also share the most
common cause “cigarette 🚬 smoking".
★ Summary table for the types of obstructive lung disease:

@2024 by Evans Mwansa Chama

15
A. Emphysema;
❖ Characterized by:
➢ Permanent enlargement of the air spaces distal
to the terminal bronchioles (meaning the
permanent enlargement affects the pulmonary
acinus).
➢ The permanent enlargement of the acinus is
accompanied by destruction of their walls without
significant fibrosis.
❖ Based on the anatomical distribution of the lesion,
Emphysema is classified into four major types:
➢ Centriacinar (centrilobular) emphysema;
■ It's the most common type of emphysema.
■ It affects the central or proximal parts of the
acini, specifically the respiratory bronchioles.
■ It doesn't affect the distal alveoli.
■ The lesions are generally localized to the upper
lobes, especially the apical segments.
■ Mostly common in heavy cigarette smokers.

@2024 by Evans Mwansa Chama

16
➢ Panacinar (panlobular) emphysema;
■ It's the second common type of emphysema.
■ Pan”means all", thus it affects the entire acini
(from the respiratory bronchiole to the
terminal blind end of the alveoli).
■ The lesions are generally localized in the lower
lung zones.
■ Mostly common in persons with
α1-anti-trypsin deficiency.

➢ Paraseptal (distal acini) emphysema;

■ Septum “refers to the alveoli wall”. Thus it
affects the distal acinus (the alveoli ducts and
alveoli).
■ The lesions are generally localized near the
pleura and interlobar septae (the area in
between different lobes of the lung), where
they form bullae (blebs). Thus rupture of
these blebs leads to spontaneous
pneumothorax.

@2024 by Evans Mwansa Chama

17
 ➢ Irregular emphysema;
■ It affects the acinus irregularly.
■ Its almost always associated with scarring.

❖ Etiology:
■ Cigarette 🚬 smoke.
■ Other air pollutants.
■ Congenital deficiency of α1-anti-trypsin. Note
that α1-anti-trypsin (antielastase ), under
physiological conditions inhibits the enzyme
elastase, which is the enzyme capable of
digesting the human lung.

@2024 by Evans Mwansa Chama

18
❖ Pathogenesis:
➢ Exposure of the acinus to irritants such as
cigarette 🚬 smoke and other inhaled air
pollutants ➞ this elicits an inflammatory reaction
by the irritated acini epithelial cells which releases
chemotactic mediators (such a as IL-1, IL-8,
Leukotriene-B4 and TNF-α) ➞ resulting in
recruitment of inflammatory cells such as
neutrophils, macrophages, and T cells.
➢ Then these immune cells releases several
amounts of proteases (such as elastase and
collagenase) ➞ leading to protease-antitrypsin
imbalance (there is more elastase and collagenase
compared to the amount of protective
antielastase ) ➞ The abundant inflammatory
proteases (elastase and collagenase ) then breaks
down structural proteins (such a as elastin and
collagen found in the pulmonary interstitium of
acini walls and are responsible for providing
elasticity and preventing the collapse of the acini
airway during low partial pressure ) ➞ hence
breakdown of collagen and elastin causes inward
pulling of the walls ➞ collapse of the acini wall
under low partial pressure ➞ air trapping in the
compartments distal to the point of collapse.

@2024 by Evans Mwansa Chama

19
➢ The break down of interstitial elastin and
collagen subsequently leads to septal breakdown
➞ resulting in the joining of neighboring alveoli
forming single large air spaces ➞ hence reducing
the surface area available for gaseous exchange due
to the expanded volume ➞ poor gaseous exchange
➞ hence hypoxemia.

➢ The loss of elastin also makes the acini walls

more compliant yet less elastic (more air will be
easily going in & but less air will be coming out ).

@2024 by Evans Mwansa Chama

20
 ➢ The poor gaseous exchange and hypoxemia can
stimulate the blood vessels supplying the damaged
alveoli to undergo vasoconstriction in an attempt to
shut blood to areas with better gas exchange ➞
but due to the many blood vessels shutting blood,
this might lead to blood overload (congestion) in
these blood vessels supplying the alveoli with
better gas exchange ➞ leading to pulmonary
hypertension in these blood vessels ➞ this
increases the workload needed to pump blood to the
lungs by the right ventricle ➞ enlargement of the
right ventricular wall ➞ right sided heart failure
(a process known as COR PULMONALE).

❖ Morphology:
➢ Grossly;
■ Voluminous lungs that overlap the heart
reducing cardiac tone during auscultation.
■ Large apical bullae (blebs).

@2024 by Evans Mwansa Chama

21
 ➢ Microscopically;
■ Alveolar wall destruction without fibrosis.
■ Enlarged air spaces.
❖ Clinical features:
● Dyspnea and hyperventilation.
● Exhaling slowly through pursed lips, but with
normal oxygenation of blood (thus such person's
are also called pink puffers).
● Weight loss due to energy loss spent on labored
exhalation.
● Barely chest due to air trapping.
● Hypoxemia and cyanosis.
● Pulmonary hypertension due to blood shutting.
● Right sided heart failure.

@2024 by Evans Mwansa Chama

22
B. Chronic bronchitis;
❖ Characterized by: its clinical definition as the
presence of a productive persistent cough with sputum
production for at least 3 consecutive months in at
least 2 years.
❖ In simpler terms:
■ It's called chronic because it produces a
persistent productive cough for at least 3
consecutive months each year, in at least 2
consecutive years.
■ It's called bronchitis because it causes
inflammation in the bronchial tubes.
■ Thus, chronic bronchitis is defined by its
clinical features.

❖ Etiology:
■ H eavy cigarette 🚬 smokers.
■ Urban dwellers in smog-ridden cities (with
SO2 and nitrogen dioxide air pollution).

@2024 by Evans Mwansa Chama

23
❖ Pathogenesis:
➢ Exposure of the airway to irritants such a as
cigarette 🚬 smoke, SO2 and nitrogen dioxide ➞
triggers local release of IL-13 from T cells and
lymphoid cells which stimulates hypertrophy of the
mucous glands (in the submucosa of the trachea
and main bronchi) and hyperplasia of the mucin
secreting goblet cells (in the epithelial surface of
smaller bronchi and bronchioles) ➞ this increases
mucus production and it's hypersecretion into the
trachea, bronchi and bronchioles ➞ leading to
obstruction, especially in the smaller airways (the
bronchioles) by the mucus plugs ➞This results in
the majority of air trapping in the airway
compartments distal to the mucus plugs.
➢ Cigarette 🚬 smoke stimulates the cilia shorten
and lose their beating function (they become non
mobile ) ➞ hence making it harder to sweep the
mucus up and out of the bronchioles ➞ thus due to
having too much mucus and non functioning cilia,
people with chronic bronchitis resort to coughing in
order to get rid of the mucus plugs.

@2024 by Evans Mwansa Chama

24
➢ In progressive disease, the air trapping can lead
to increased partial pressure of carbon dioxide in
the alveoli air space resulting in impaired CO2 and
O2 gas exchange ➞ leading to increased blood
CO2 (hypercapnia) and reduced blood O2
(Hypoxemia) ➞ This induces hypoxic
vasoconstriction of the blood vessels supplying the
alveoli with poor gaseous exchange, so as to shunt
blood to blood vessels supplying alveoli with good
gas exchange ➞ but due to the many blood vessels
shutting blood, this might lead to blood overload
(congestion) in these blood vessels supplying the
alveoli with better gas exchange ➞ leading to
pulmonary hypertension in these blood vessels ➞
this increases the workload needed to pump blood
to the lungs by the right ventricle ➞ enlargement
of the right ventricular wall ➞ right sided heart
failure (a process known as COR
PULMONALE).
➢ The mucus plugs can also predispose to lung
infections which can worsen other symptoms.

@2024 by Evans Mwansa Chama

25
❖ Morphology: (microscopy)
■ Enlargement of the mucous secreting glands.
■ Goblet cells metaplasia.
■ Bronchiolar wall fibrosis.
❖ Clinical features:
■ Persistent cough with sputum production.
■ Hypercapnia (increase in CO2 in blood ).
■ Hypoxemia (reduced O2 in blood ).
■ Cyanosis (blue discoloration of the lips, hence
people with chronic bronchitis are also referred
to as “blue bloaters").
■ Wheezing due to narrowing of the airways.
■ Crackers or rales, due to the pop and open of
small airways.
■ Progressive disease leads to pulmonary
hypertension, right sided heart failure (COR
PULMONALE ) and lung infections.

@2024 by Evans Mwansa Chama

26
➢ Diagnosis:
■ Clinical diagnosis is based on the definition
(a productive cough with sputum production,
for at least 3 consecutive months in at least 2
consecutive years).
■ Post mortem diagnosis uses the “Reid index";
● Is the ratio of the thickness of the mucous
gland layer to the thickness of the wall
between the basement membrane of the
epithelium and the cartilage.
● The normal Reid index is equal to or less
than 0.4 or 40%.
● Reid index is increased in chronic
bronchitis, due to the hypertrophy and
hyperplasia of the glands.

@2024 by Evans Mwansa Chama

27