1. RESPIRATORY PATHOLOGY
Congenital abnormalities
Atelectasis
Acute Pulmonary Injury (eg:pulmonary oedema)
Pulmonary Infections
Obstructive Pulmonary Disease (COPD)
Restrictive (Infiltrative) Pulmonary Disease
Vascular Pulmonary Diseases
Tumors

2. Pathology of Common
Respiratory Conditions Part [3]
OBJECTIVES
TO DISCUSS CAUSES, PATHOGENESIS, TYPES,
MORPHOLOGY,CLINICAL COURSE OF
ATELETASIS
BRONCHIETASIS
PNEUMOCONIOSIS

3. LEARNING OUTCOMES
At the end of this lecture student will be able to
• Define actelectasis
• Compare resorption actelectasis, compression actelectasis and
contraction actelectasis in regards predisposing factors,etiology
and morphology
• Define bronchiectasis
• Discuss the predisposing conditions ,pathogenesis,gross
&microscopic morphology ,clinical course and prognosis of
bronchiectasis
• Discuss the etiology, pathogenesis, basic morphology and
pulmonary reaction and complications of occupational lungs
diseases (pneumoconiosis- anthracosis, silicosis, asbetosis)

4. BRONCHIECTASIS
permanent dilation of bronchi and bronchioles
and is secondary to cycles of obstruction and
infection
Irreversible Dilation of Bronchi and
bronchioles
Caused by Destruction of Bronchial Wall
Muscle and Elastic Elements

5. BRONCHIECTASIS

6. BRONCHIECTASIS
Associated with chronic necrotizing
infection
A characteristic symptom complex
dominated by
Cough
expectoration of copious amounts of
purulent sputum

7. ETIOLOGY & PATHOGENESIS
Predisposing conditions
Obstruction & infection are the major
influences
Obstruction is caused by
Tumors
Inhaled foreign bodies
Mucous plugs in asthma
lymph node enlargement
Under these conditions, the bronchiectasis is localized to the obstructed lung
segment

8. Post infectious conditions including
Necrotizing pneumonia
Caused by
Bacteria ( Mycobacterium tuberculosis,
Staphylococcus aureus, Haemophilus influenzae,
Pseudomonas )
viruses ( adenovirus, influenza virus, HIV )
fungi ( Aspergillus )

9. Congenital or hereditary conditions
Cystic fibrosis (genetic defect, abnormal viscid mucus
secretion → obstruction organ passages)
Intralobar pulmonary sequestrations presence
of a discrete mass of lung tissue without normal connection to the airway system
Immunodeficiency states
Primary ciliary dyskinesia
Kartagener syndrome (bronchiectasis, sinusitis, and
situs inversus or partial lateralizing abnormality )

10. Other conditions :
rheumatoid arthritis
SLE
inflammatory bowel disease
post transplantation ( chronic lung rejection &
chronic graft-versus-host disease after bone marrow
transplantation)

11. MORPHOLOGY
Gross
Site :
Obstructive bronchiectasis is localized to a single
segment of the lungs
Nonobstructive bronchiectasis may be localized
or generalized

13. Size :
Airways are dilated up to 4 times normal
size → sufficiently dilated that they can be
followed directly out to the pleural surfaces
Shape :
 cylindrical
 fusiform
 saccular
Bronchial lumens : filled with thick
mucopurulent secretion

16. Bronchiectasis
The resected upper lobe
shows widely dilated bronchi,
with thickening of the
bronchial walls and collapse
and fibrosis of the pulmonary
parenchyma

17. Bronchiectasis
Cross-section of lung demonstrating dilated bronchi extending almost to the pleur

18. Histology vary with activity & chronicity of the disease
In the full blown active case,
intense acute & chronic inflammatory exudates
desquamation of lining epithelium &
extensive areas of necrotizing ulceration
pseudostratification of columnar cells
squamous metaplasia of remaining epithelium
abscess formation
chronic case – fibrosis of bronchial and
bronchiolar walls → total or subtotal obliteration
of lumen

19. CLINICAL FEATURES
Due to accumulation of pus in dilated bronchi &
bronchioles
Chronic cough with production of copious
amount of purulent sputum
severe, persistent, worse in morning, induced by change in
posture, may be paroxysmal
Purulent sputum (foul-smelling) – copious amount
On standing → 3 layered sputum
1st – frothy layer
2nd – clear mucous layer
3rd – suppurated & necrotic debris, RBC

20. Chronic cough with
production of copious
amount of purulent sputum
severe, persistent, worse in morning,
induced by change in posture, may be
paroxysmal
Purulent sputum (foul-
smelling) – copious amount
On standing → 3 layered
sputum
1st – frothy layer
2nd – clear mucous layer
3rd – suppurated & necrotic
debris, RBC
CLINICAL FEATURES
Due to accumulation of pus in dilated bronchi &
bronchioles

21. CLINICAL FEATURES
due to inflammatory response of the lung
parenchyma & pleura
Fever → febrile episodes
Chest pain due to pleuritis
Haemoptysis or sometimes bloody sputum caused
by rupture of thin walled vessels situated in wall of
dilated bronchioles
Other respiratory symptoms
Dyspnoea, orthopnoea, cyanosis,
clubbing of fingers & toes.

22. COMPLICATIONS
Lung abscess- the necrosis destroys the bronchial or
bronchiolar walls
Pneumonia – infection spread to whole lung parenchyma
Bacteremia, septicemia with metastatic
abscess formation e.g. brain abscess, meningitis
Emphysema – secondary to obstruction
Secondary amyloidosis
peribronchiolar fibrosis in chronic widespread
disease → increase pressure in pulmonary circulation → Cor
pulmonale and cardiac failure

23. COMPLICATIONS

24. COMPLICATIONS

25. COMPLICATIONS

26. Chronic Diffuse Interstitial
(Restrictive) Diseases
Chronic interstitial diseases are
heterogeneous group of disorders
characterized predominantly by
inflammation and fibrosis of the
pulmonary connective tissue, principally
the most peripheral and delicate interstitium in
the alveolar walls

27. PNEUMOCONIOSIS
Pneumoconioses are
pulmonary diseases caused by mineral
dust inhalation in workplace
The specific types of pneumoconioses are
named by the substance inhaled
(e.g., silicosis, asbestosis, anthracosis)

29. PNEUMOCONIOSIS
Mineral Dust-Induced Lung Disease
Coal dust Simple coal workers' pneumoconiosis:
macules and nodules
Complicated coal workers' pneumoconiosis:
PMF
Coal mining
Silica Silicosis Sandblasting,
quarrying, mining,
stone cutting,
foundry work,
ceramics
Asbestos Asbestosis pleural effusions, pleural plaques, or
diffuse fibrosis; mesothelioma; carcinoma of the
lung and larynx
Mining, milling,
and fabrication of
ores and
materials;
installation and
removal of
insulation

31. Pathogenesis
The reaction of the lung to mineral dusts
depends on
size, shape, solubility, and reactivity of the
particles
PNEUMOCONIOSIS

32. Pathogenesis
The development of a pneumoconiosis depends on
(1) the amount of dust retained in the lung and
airways
(2) the size, shape, and buoyancy of the particles
(3) solubility and physiochemical reactivity
(4) the possible additional effects of other irritants
(e.g., concomitant tobacco smoking)
PNEUMOCONIOSIS

33. Pathogenesis
(1)The amount of dust retained in the lungs
is determined by
dust concentration in surrounding air
duration of exposure
effectiveness of clearance mechanisms
PNEUMOCONIOSIS

34. Pathogenesis
(2) the size, shape, and buoyancy of the
particles
The most dangerous particles range from
1 to 5 μm in diameter because they may reach the
terminal small airways and air sacs and settle in
their linings
PNEUMOCONIOSIS

35. (3)The solubility and cytotoxicity of particles
modify the nature of the pulmonary response
Smaller particles tend to cause acute lung injury
Larger particles resist dissolution and so may
persist within the lung parenchyma for years -
tend to evoke fibrosing collagenous pneumoconioses
PNEUMOCONIOSIS

36. Pathogenesis
The key factor in the gene-sis of
symptomatic pneumoconioses is the
capacity of inhaled dusts to stimulate
fibrosis
The pulmonary alveolar macrophage is a
key cellular element in the initiation and
perpetuation of lung injury and fibrosis
PNEUMOCONIOSIS

37. The more reactive particles trigger the
macrophages
to release a number of products that
mediate an inflammatory response and
initiate fibroblast proliferation and
collagen deposition
PNEUMOCONIOSIS

38. Pathogenesis
(4) the possible additional effects of other
irritants (e.g., concomitant tobacco
smoking)
tobacco smoking worsens the effects of
all inhaled mineral dusts
PNEUMOCONIOSIS

39. In simple coal workers’
pneumoco-niosis
massive amounts of dust are
inhaled and engulfed by macrophages
macrophages pass into the interstitium of
the lung and aggregate around the
respiratory bronchioles
Pathogenesis

40. Pathogenesis
In silicosis
the silica particles are toxic to
macrophages,
which die and release a fibrogenic factor
In turn,
the released silica is again phagocytosed
by other macrophages
The result is a dense fibrotic nodule
the sili-cotic nodule

41. Pathogenesis
Asbestosis
is characterized by
little dust and much interstitial fibrosis
Asbestos bodies are the classic features

43. PNEUMOCONIOSIS
Coal Workers’ Pneumoconiosis Is Due to
Inhalation of Carbon Particles
The spectrum of lung findings in coal workers is wide,
varying from
(1)asymptomatic anthracosis
(2)simple CWP with little to no pulmonary
dysfunction
(3)complicated CWP
(4)progressive massive fibrosis (PMF),

44. PNEUMOCONIOSIS
Morphology
Anthracosis
Accumulation of carbon particles in the
lungs (in the connective tissue along the lymphatics,
including the pleural lymphatics, or in organized lymphoid
tissue along the bronchi or in the lung hilus)

45. Coal Workers’ Pneumoconiosis
Morphology
Simple CWP is characterized by
coal macules (1 to 2 mm in diameter, consists of
carbon-laden macrophages)
larger coal nodules (contains small amounts of a
delicate network of collagen
located primarily adjacent to respiratory
bronchioles

46. Complicated CWP (progressive massive fibrosis)
is characterized by multiple
intensely blackened scars larger than 2 cm,
sometimes up to 10 cm in greatest diameter
Occur on background of simple CWP by
coalescence of coal nodules and generally
requires many years to develop
Coal Workers’ Pneumoconiosis

47. Microscopically
The lesions consist of dense collagen and
pigment
The center of the lesion is often necrotic,
most likely due to local ischemia
Coal Workers’ Pneumoconiosis

48. Clinical Course
Simple CWP
-minor impairment of lung function
Complicated CWP
-cause significant respiratory impairment
Caplan syndrome was first described as rheumatoid nod-
ules (Caplan nodules) in the lungs of coal miners
with rheumatoid arthritis
Coal Workers’ Pneumoconiosis

49. Silicosis Is Caused by Inhalation
of Silicon Dioxide (crystalline Silica)
Silica occurs in both
crystalline and amorphous forms
crystalline forms (including quartz,
crystobalite, and tridymite) are much more
fibrogenic

50. After inhalation, the particles interact with
epithelial cells and macrophages
Causing
activation and release of mediators
IL-1, TNF, fibronectin, lipid mediators, oxygen-
derived free radicals, and fibrogenic cytokines
Pathogenesis

51. Silicosis
SIMPLE NODULAR SILICOSIS
most common form of silicosis
occur in any worker with long-term
exposure to silica
silicotic nodules less than 1 cm in
diameter (usually 2 to 4 mm)

52. Morphology
slowly progressing, nodular, fibrosing
pneumoconiosis
Silicotic nodules are characterized grossly in their
early stages by
tiny, barely palpable, discrete, pale-to-blackened
(if coal dust is also present) nodules in the
upper zones of the lungs

53. Silicotic nodules
characteristic whorled appearance, with
concentrically arranged hyalinized collagen.At the
periphery are aggregates of mononuclear
cells,mostly lymphocytes and fibroblasts.

54. As the disease progresses, the individual
nodules may coalesce into
hard, collagenous scars, with eventual
progression to PMF
The intervening lung parenchyma may be
compressed or overexpanded, and a
honeycomb pattern may develop
Silicosis

55. Fibrotic lesions may also occur in the hilar
lymph nodes and pleura
Thin sheets of calcification occur in the
lymph nodes and are seen radiographically
as eggshell calcification

56. Advanced silicosis
(transected lung).
Scarring has contracted
the upper lobe into a
small dark mass (arrow).
Note the dense pleural
thickening

57. Clinical Course
Simple silico-sis
does not usually lead to significant
respiratory dysfunction
Pro-gressive massive fibrosis
dyspnea on exertion and later at rest
Silicosis is associated with an increased
susceptibility to tuberculosis

58. Asbestos-Related Diseases
Asbestos
(Greek, “unquenchable”)
includes a group of fibrous silicate
minerals that occur as thin fibers
Asbestos is a family of crystalline hydrated
silicates that form fibers

60. 2 forms of asbestos2 forms of asbestos
a)serpentine (i.e., curly and flexible)
b) amphibole (i.e., straight, stiff and
brittle)
Asbestosis

61. Asbestosis
Asbestos
Causing fibrosis by interacting with lung
macrophages
also functions as both a tumor initiator
and a promoter

62. Morphology
Asbestosis is marked by diffuse pulmonary
interstitial fibrosis
Characterized by
the presence of asbestos bodies
which are seen as golden brown, fusiform or
beaded rods with a translucent center
coated with an iron-containing proteinaceous
material
Asbestosis

63. Asbestos body

64. Asbestos bodies
These ferruginous bodies are golden brown and beaded,
with a central, colorless, nonbirefringent core fiber

65. Pleural plaque. The dome of the
diaphragm is covered
by a smooth, pearly white, nodular plaque
Asbestos-related pleural plaques
Large, discrete fibrocalcific plaques are seen
on the pleural surface of the diaphragm

66. Which of the following inhaled pollutants is most likely to
produce extensive pulmonary fibrosis?
(A) Silica
(B) Tobacco smoke
(C) Ozone
(D) Wood dust
(E) Carbon monoxide
(A) Silica crystals incite a fibrogenic response after
ingestion by macrophages. The greater the exposure and
the longer the time of exposure, the greater is the lung
injury.

67. • A 63-year-old male worked for 20 years in the sand-
blasting business, and he used no respiratory precautions
during that time. He now has increasing dyspnea without
fever, cough, or chest pain. Which of the following
inflammatory cell types is most crucial to the development
of his underlying disease?
•(A) Plasma cell
•(B) Mast cell
•(C) Eosinophil
•(D) Macrophage
•(E) Natural killer (NK) cell

68. The correct answer is (D)
Silica is a major component of sand, which contains the
mineral quartz. The small silica crystals are inhaled, and
their buoyancy allows them to be carried to alveoli. There
they are ingested by macrophages, which then secrete
cytokines that recruit other inflammatory cells and
promote fibrogenesis.
Plasma cells secrete immunoglobulins, which are not a major
component of this process.
Mast cells and eosinophils are prominent in type I hypersensitivity
response.
NK lymphocytes are more likely to be a prominent component of
inflammatory processes directed against infectious agents.

69. A 75-year-old male experienced increasing dyspnoea. The
microscopic appearance of the lung is shown here. This is
most characteristic for
(A) Anthracosis
(B) Berylliosis
(C) Silicosis
(D) Calcinosis
(E) Asbestosis

70. The answer is (E)
The ferruginous bodies shown here are long, thin crystals of asbestos
that have become encrusted with iron and calcium. The inflammatory
reaction incited by these crystals promotes fibrogenesis and resultant
pneumoconiosis.
Berylliosis is marked by noncaseating granulomas.
Anthracosis is a benign process seen in all city dwellers as a consequence of
inhaled carbonaceous dust.
Silica crystals are not covered by iron and tend to result in formation of
fibrous nodules (i.e., silicotic nodules).
Calcium deposition may occur along alveolar walls with a high serum calcium
(i.e., metastatic calcification).

71. Which of the following morphologic changes can be
seen in advanced cases of both obstructive and restrictive
lung disease?
(A) Marked medial thickening of pulmonary arterioles
(B) Destruction of elastic tissue in the alveolar walls
(C) Fibrosis of the alveolar walls
(D) Hemorrhage in the alveolar lumen
(E) Hyaline membranes lining the airspaces
The correct answer is (A)
Changes of pulmonary hypertension are characteristic for restrictive and
obstructive lung diseases. This explains, for example, the occurrence of cor
pulmonale and right-sided CHF in persons with chronic obstructive pulmonary
disease or with pneumoconiosis

72. Atelectasis (Collapse)
Atelectasis
Neonatal atelectasis
incomplete expansion of the lungs
Acquired atelectasis
collapse of previously inflated lung
producing areas of relatively airless
pulmonary parenchyma

74. Acquired atelectasis may be divided
into
 Resorption (or obstruction)
 Compression
 Contraction atelectasis
ATELETASIS (Collapse)

75. Resorption atelectasis
is the consequence of
complete obstruction of an airway leads to
resorption of the oxygen trapped in the
dependent alveoli
without impairment of blood flow through the
affected alveolar walls
lung volume is diminished
the mediastinum shifts toward the atelectatic lung
ATELETASIS (Collapse)

76. Airway obstruction is caused by
 excessive secretions (e.g., mucus plugs) or
exudates within smaller bronchi (bronchial
asthma, chronic bronchitis, bronchiectasis)
 postoperative states
 aspiration of foreign bodies
 bronchial neoplasms (rarely)
ATELETASIS (Collapse)

77. Compression atelectasis
results whenever
pleural cavity is partially or completely filled by
fluid exudate, tumor, blood, or air (pneumothorax)
or with tension pneumothorax, when air pressure
impinges on and threatens the function of the
lung and mediastinum, especially the major
vessels
mediastinum shifts away from the affected lung
ATELETASIS (Collapse)

78. Compression atelectasis

79. Contraction atelectasis
occurs when
local or generalized fibrotic changes in the
lung or pleura prevent full expansion
ATELETASIS (Collapse)

80. reduces oxygenation
predisposes to infection
collapsed lung parenchyma can be re-
expanded (reversible disorder)
except that caused by contraction
ATELETASIS (Collapse)

81. ANY QUESTIONS?