Lung pathology 1

Global institute of medical sciences
1.www.gims-org.com
2.www.usmletutor.org

Dr.G.Bhanu prakash

1. Respiratory SystemRespiratory System

2. Anatomy of Respiratory Tract

3. Trachea
↓
Principal Bronchi
↓
Bronchi
↓
Bronchiole
↓
Terminal Bronchiole
↓
Respiratory Bronchiole
↓
Alveoli

4. •Acinus is the functional unit of lung whereas alveoli are
the chief sites of gaseous exchange.
•Lobule is composed of 3-5 terminal bronchioles with
their acini.
•Alveoli are lined by type I pneumocytes (forming 95%
of alveolar surface) and type II pneumocytes
(responsible for secretion of surfactant and repair of
alveoli after type I pneumocyte destruction). The
alveoli wall has the presemce of pores of KohnQ for
allowing the passage of bacteria and exudate between
adjacent alveoli.

5. •The entire respiratory tract is lined by
pseudostratified, tall, columnar ciliated epithelial
cells except vocal cords (these have stratified
squamous epithelium.
Bronchioles do not have cartilage and submucosal
glands in wall like bronchi.
Terminal bronchiole contain maximum smooth
muscle relative to the wall thickness.
Broadly, the disease of lung may be divided into
obstructive, restrictive, vascular and neoplastic
etiologies.

6. INFECTIVE LUNG DISEASES

7. 1. PNEUMONIA
Infection of the lung parenchyma is called
pneumonia. It can be of two types.
Pneumonia
Typical Pneumonia
Atypical Pneumonia

8. Typical Pneumonia Atypical Pneumonia
Infection caused by bacteria
most common cause of
community acquired
pneumonia is streptococcus
pneumoniae
And the most common cause
of Nosocomial pneumonia is
staphylococcus aureus
Infection caused by
Mycoplasma, Chlamydia
pnemoniae and viruses like
RSV Influenza virus, rhinovirus
(most common cause is
Mycoplasma pneumoniae.

Characterized by neutrophilic
infiltration and presence of
intra-alveolar exudates
(leading to consolidation).
Characterized by lymphocytic
infiltration and presence of
alveolar septal and interstitial
inflammation with absence of
alveolar exudates
Clinical features include onset
high grade fever and
mucopurulent cough which
may also be associated with
pleuritic pain.
Clinical features include fever,
headache and myalgia. Cough
and pleural involvement is
uncommon.

9. •Viral pneumonia result in interstitial infiltrates
(therefore called interstitial pneumonia) and may
result inn variety of cytopathic effects. E.g. RSV
shows bronchiolitis and multinucleate giant cells
and CMV and herpes show inclusion bodies.

10. Furthermore , typical pneumonia can be of
two types.
Typical Pneumonia
BronchopneumoniaLobar Pneumonia

11. LOBAR PNEUMONIA
Consolidation of entire lobe usually caused
by streptococcus pneumonia
Following 4 stages of inflammation
Congestion: it is due to vasodilation. There
is bacteria rich intra-alveolar fluid.
Red hepatization: exudate is rich in RBC,
neutrophils and fibrin .

12. 3. Gary hepatization: Degradation of RBC
and fibrinosuppurative exudates.
4. Resolution: enzymatic degradation of
exudate and healing.
Chest X-ray shows opacification of the
entire lobe.

13. Bronchopneumonia
Patch consolidation in the lobe of lung
Usually bilateral basal In location due to gravitation of
secretions.
Affects extremes of age (Infants or old)
Chest X-rays shows patchy opacification of the lobe.

14. 2. Lung Abscess
•Local suppurative process within the lung
associated with necrosis of the lung tissue is called
lung abscess.
• it is most commonly caused by aspiration of
infective material.
•Commonest etiological agent is Staphylococcus
aureus.

15. Causes of Lung abscess
Miscellaneous
Septic
emboli
Post
Obstructive
Post pneumonic
infection
Aspiration
Most
common
Cause
Right lower
Lobe is the
Most frequently
Affected
Infection caused
By Staph.aureus,
Klebsiella or type 3
pneumococcus
Usually basal,
Multiple and
Diffusely scattered
Due to primary
Or Secondary

Direct
Hematogenous
Spread to lung
From infection
In esophagus or
Pleural cavity

16. •Clinical feature: fever, productive cough with large
amount of sputum, chest pain, weight loss and
presence of clubbing of the fingers and toes.
•Characteristic histologic feature:
Suppurative destruction of lung parenchyma within the
central area of cavitation. Complication include
empyema, brain abscess or meningitis, pulmonary
hemorrhage and secondary amyloidosis .

17. Pulmonary diseases
Obstructive Lung disease Restrictive lung disease
Characterized by increased
resistance to airflow due to
airway obstruction.
Spirometry reveals
FEV1
FVC
Ratio is decreased.
Characterized by decreased
Expansion of the lung
Spirometry reveals
reduced total lung capacity
and vital Capacity Q
Example
2.Chest wall disorder- Polio,
Obesity; kyphoscoliosis
2. Interstitial /infiltrative disease:
Pneumoconiosis, ARDS, Pulmonary fibrosis

18. 3. TUBERCULOSIS
(KOCH’S DISEASE)
•Pulmonary tuberculosis is caused by droplet
infection (coughing, sneezing etc) due to
Mycobacterium tuberculosis.
•It is a strict aerobic bacteria having mycolic acid in
its cell wall making it acid fast which means it
resists decolourisation by a treatment with a mixture
of acid and alcohol.

19. •The reservoir of infection is a human being with
active tuberculosis.
•However, certain clinical condition can increase the
risk of tuberculosis like diabetes mellitus, Hodgkin’s
lymphoma, chronic lung disease (particularly
siliocosis), chronic renal failure, Malnutrition,
alcoholism and immunosuppression.

20. •Infection with M.tuberculosis is different from disease.
Infection is the presence of organisms, which may or
may not cause clinically significant disease.
•In most of the people, primary tuberculosis is
asymptomatic thought it may be associated with fever
and pleural effusion.
•Infection with M. tuberculosis typically leads to the
development of delayed hypersensitivity to M.
tuberculosis antigens, which can be detected by the
tuberculin (Mantoux) test.

21. •A positive tuberculin test result signifies
cell-mediated hypersensitivity to tubercular
antigens but does not differentiate
between infection and diseased.

22. False- negative Mantoux
test
False-positive Mantoux
test
Sarcoidosis
Malnutrition
Hodgkin disease
Immunosuppression
Fulminant tuberculosis
infection by atypical
mycobacteria
Previous vaccination with
BCG

23. Pathogenesis
Macrophages are the primary cells infected by
M.tuberculosis. The bacteria enter macrophages by
endocytosis.
The bacterial cell wall glycolipid lipoarabinomannan
blocks the fusion of the phagosome and lysosome.
This is followed by bacterial multiplication inside the
macrophages.

24. •Thus, the initial stages of primary tuberculosis (<3
weeks) in a nonsensitized individual is characterized
by bacterial multiplication in the pulmonary alveolar
macrophages and airspaces, with resulting
bacteremia and spread to multiple sites in the body.
•After about 3 weeks of infection, the TH1 cells are
stimulated by mycobacterial antigens and these cells
differentiate into mature TH1 cells by the action of
IL-12.

25. •The mature TH1 cells in the lymph nodes and lungs
produce IFN-g which stimulates formation of
phagolysosome in infected macrophages and causes
nitric oxide induced oxidative damage to the cell wall
and DNA of the mycobacteria.
•Activated macrophages, stimulated by IFN- g, produce
TNF and recruit monocytes which then differentiate
into the “epithelioid histiocytes”, a characteristic feature
of granulomatous inflammation.

26. •So, immunity to M. tuberculosis is primarily mediated
by TH1cells, which stimulate macrophage to kill the
bacteria. The immune response is usually
accompanied by hypersensitivity and tissue
destruction.
•Reactivation of the infection or re-exposure to the
bacilli in a previously sensitized host therefore causes
activation of defense mechanism and increased tissue
necrosis.

27. Clinical Features
Primary tuberculosis
Develops in a previously unexposed and unsensitized
individual. The source of the organism is usually
exogenous. The majority of the patient with primary
tuberculosis develop latent disease while a minority
develops progressive infection.

28. Primary tuberculosis almost always begins in the
lungs. Typically, the inhaled bacilli implant in the
distal airspaces of the lower part of the upper lobe
or the upper part of the lower lobe due to most of
the inspired air being distributed here and form a
subpleural lesion.

29. This subpleural lesion along with the draining
lymphatics and the lymph nodes is called as Ghon’s
complex. During the first few weeks, there is also
lymphatic and hematogenous dissemination to other
part of the body.
 In majority of the people , development of cell-
mediated immunity control the infection. The Gohn’s
complex undergoes progressive fibrosis and
calcification
 (detected radiologically and called as Ranke complex)

30. •Hisologically, the sites of active disease show a
characterized granulomatous inflammatory reaction
having the presence of both caseating and non-
caseating tubercles.
• There is also presence of Langhans giant cells and
lymphocytes immunocompromised people do not
form the characterized granulomas.

31. Secondary tuberculosis :
Secondary tuberculosis is the pattern of disease that
arises in a previously sensitized host. It usually result
from a reactivation of latent primary lesion after many
yrs of an initial infection, particularly when host
immunity is decreased or uncommonly may follow
primary tuberculosis.
Secondary pulmonary tuberculosis is classically
localized to the apex of the upper lobes of the lung
(right lung affected more commonly as compared to
left) because of high oxygen tension in the apices.

32. The preexistence of hypersensitivity contributes to
an immediate and marked tissue response leading
to localization of the infection (the regional lymph
nodes are less prominently involved in secondary
tuberculosis) and cavitation followed by erosion
into an airway (leading to spread of bacilli during
coughing).

33. •Histologically, the active lesion show characteristic
tubercles composed of epithelioid cells and
Langhans cells with central caseation. The lesion of
secondary pulmonary tuberculosis may heal with
fibrosis either by itself or after therapy, or it my
progress along the following several different
pathways.

34. •Progressive pulmonary tuberculosis is seen in the
elderly and the immunosuppressed individuals.
•The apical lesion enlarges with increase in the area
of caseation. The erosion of blood vessels
(particularly bronchial artery) results in hemoptysis.
• The pleural cavity is associated with pleural
effusion or empyema.
• If the treatment is adequate, the disease may be
controlled but if it is inadequate, the infection may
disseminate through airways, lymphatics or the
vascular system.

35. •Miliary disease occurs when organism drain
through lymphatics and blood vessels to the
different organs of the body resulting in small
yellow- white consolidated lesion. Miliary
tuberculosis is most prominent in the liver, bone
marrow spleen, adrenal, meninges, kidneys,
fallopian, and epididymis.

36. Note: the most frequent form of extra- pulmonary
tuberculosis is lymphadenitis usually in the carvical
region and is knows as “ scrofula”. When the
vertebrae are affected it is known as pott’s disease.

37. •The patient present with insidious onset of symptoms
like low grade remittent fever usually associated with
night sweats, productive cough, weight loss,
hemoptysis, dyspnea and pleural effusion.
• The investigations usually reveal lymphocytosis and
increased ESR (on hemogram), hilar lymphadenopathy
and pleural effusion (on chest X-ray), presence of acid
fast bacilli with Ziehl Nielson stainig. The treatment is
provided with multiple drugs