Pathology of lung
Atelectasis
 Loss of lung volume due to inadequate
expansion of air spaces
1. Resorption
2. Compression/passive/relaxation/flaccid
3. Contraction /Cicatriztion
4. Non obstructive/micro
Acute lung injury
Spectrum of endothelial and epithelial
pulmonary lesions
Acute onset of dyspnea
B/l pulmonary edema
Hypoxemia
No LHF
Pathology of vasculature- alveolar
capillary membrane damage
Non cardiogenic pulmonary edema
 Acute injury can be
1. Direct injury- Pneumonia,aspiration of
gastric contents
2. Indirect injury- sepsis,severe trauma with
shock
3. A/c injury----------- ARDS
ARDS
 Diffuse alveolar capillary and epitrhelial
damage
1. Respiratory insufficiency
2. Cyanosis
3. Severe arterial hypoxemia-not
responding to oxygen therapy
4. Progress to mutisystem organ failure
 Neutrophils hav a imp role in ARDS
Destructive forces are counter acted by
anti proeases, oxidents ,etc
Degree of tissue injury depends on
balance of two
Emphysema
1. Centri acinar/centri lobar- in smokers-
2. Pan acinar/pan lobar- ass. With alpha 1
anti trypsin deffi.
3. Distal acinar/para septal- adj. to scarring,
fibrosis,atelectasis
4. irregular- associated with scarring-
assymptomatic
C/C Bronchitis
 Persistent productive cough for 3 consecutive
months for 2 consecutive years
 Three types
1. Simple c/c bronchitis-productive cough—
mucoid sputum—air flow not obstructed
2. C/C asthmatic bronchitis-hyper responsive
airways—intermittent bronchospasm and
wheezing
3. C/C obstructive bronchitis-associated with
emphysema
Asthma
 Air way remodeling
 ADAM33
1. Thickening of basement membrane of
bronchial epithelium
2. Edema & inflammatory infiltrate in the
bronchial walls,with a prominnce of eosinophils
and mast cells
3. An increase in size of submucosal glands
4. Hypertrophy of bronchial smooth muscles
Bronchiectasis
Pneumonia
 Two types
1. Broncho
2. Lobar
 Mostly occurs by aspiration of
pharyngeal flora
 Lower lobes/ right middle lobes are
mostly affected
1. Community- acquired Acute pneumonia-
pyogenic org.
2. Community acquired atypical pneumonia-
virus, mycoplasma, candida
3. Nosocomial- pseudomanas,gram neg.
4. Aspiration – anerobic
5. Chronic – Mtb
6. Necrotizing pneumonia and lung abcess-
Anerobic + pyogenic
7. Pneumonia in the immunocompramised host
– chlamydia, aspergillosis, CMV
Complications of pneumonia
 Lung abscess
 Empyema- suppurative materials may
accumulate in the pleural cavity
 Bacterial dissemination leading to
meningitis,arthritis, infective endocarditis
 Complications are much more with
serotype 3 pneumococci
Atypical pneumonias
Acute febrile respiratory d/s characterized
by patchy consolidation of lungs, largely
confined to alveolar septa and pulmonary
interstitium
Atypical-moderate amounts of sputum,
absence of physical finings of
consolidation,only moderate inc in WBC
coun,lack of alveolar exudate
Mostly by Mycoplasma pneumoniae
Lung Abscess
Suppurative destruction of lung
parenchyma with central area of cavitation
Good Pasture’s syndrome
RPGN
Haemorrhagic interstitial pneumonitis
Lung tumours
1. Squamous cell carcinoma/epidermoid
carcinoma
2. Adinocarcinoma-bronchial derived,
acinar,papillary,broncioloalveolar,solid
3. Small cell carcinoma-oat cell, intermediate
4. Large cell carcinoma,undiff,giant cell, clear cell
5. Others- combined small cell
carcinoma,Adenosquamous carcinoma
Adenocarcinoma has replaced SCC as
the most common primary lung tumour
Most common in women,non
smokers,persons younger than 45yrs
Therapeutic classification
1. Small cell lung cancer (SCLC)
2. Non small cell lung cancer (NSCLC)
Pathology of lung

Pathology of lung

  • 1.
  • 4.
    Atelectasis  Loss oflung volume due to inadequate expansion of air spaces 1. Resorption 2. Compression/passive/relaxation/flaccid 3. Contraction /Cicatriztion 4. Non obstructive/micro
  • 5.
    Acute lung injury Spectrumof endothelial and epithelial pulmonary lesions Acute onset of dyspnea B/l pulmonary edema Hypoxemia No LHF Pathology of vasculature- alveolar capillary membrane damage Non cardiogenic pulmonary edema
  • 6.
     Acute injurycan be 1. Direct injury- Pneumonia,aspiration of gastric contents 2. Indirect injury- sepsis,severe trauma with shock 3. A/c injury----------- ARDS
  • 7.
    ARDS  Diffuse alveolarcapillary and epitrhelial damage 1. Respiratory insufficiency 2. Cyanosis 3. Severe arterial hypoxemia-not responding to oxygen therapy 4. Progress to mutisystem organ failure  Neutrophils hav a imp role in ARDS
  • 9.
    Destructive forces arecounter acted by anti proeases, oxidents ,etc Degree of tissue injury depends on balance of two
  • 11.
    Emphysema 1. Centri acinar/centrilobar- in smokers- 2. Pan acinar/pan lobar- ass. With alpha 1 anti trypsin deffi. 3. Distal acinar/para septal- adj. to scarring, fibrosis,atelectasis 4. irregular- associated with scarring- assymptomatic
  • 15.
    C/C Bronchitis  Persistentproductive cough for 3 consecutive months for 2 consecutive years  Three types 1. Simple c/c bronchitis-productive cough— mucoid sputum—air flow not obstructed 2. C/C asthmatic bronchitis-hyper responsive airways—intermittent bronchospasm and wheezing 3. C/C obstructive bronchitis-associated with emphysema
  • 17.
    Asthma  Air wayremodeling  ADAM33 1. Thickening of basement membrane of bronchial epithelium 2. Edema & inflammatory infiltrate in the bronchial walls,with a prominnce of eosinophils and mast cells 3. An increase in size of submucosal glands 4. Hypertrophy of bronchial smooth muscles
  • 19.
  • 20.
  • 21.
     Two types 1.Broncho 2. Lobar  Mostly occurs by aspiration of pharyngeal flora  Lower lobes/ right middle lobes are mostly affected
  • 22.
    1. Community- acquiredAcute pneumonia- pyogenic org. 2. Community acquired atypical pneumonia- virus, mycoplasma, candida 3. Nosocomial- pseudomanas,gram neg. 4. Aspiration – anerobic 5. Chronic – Mtb 6. Necrotizing pneumonia and lung abcess- Anerobic + pyogenic 7. Pneumonia in the immunocompramised host – chlamydia, aspergillosis, CMV
  • 24.
    Complications of pneumonia Lung abscess  Empyema- suppurative materials may accumulate in the pleural cavity  Bacterial dissemination leading to meningitis,arthritis, infective endocarditis  Complications are much more with serotype 3 pneumococci
  • 25.
    Atypical pneumonias Acute febrilerespiratory d/s characterized by patchy consolidation of lungs, largely confined to alveolar septa and pulmonary interstitium Atypical-moderate amounts of sputum, absence of physical finings of consolidation,only moderate inc in WBC coun,lack of alveolar exudate Mostly by Mycoplasma pneumoniae
  • 27.
    Lung Abscess Suppurative destructionof lung parenchyma with central area of cavitation
  • 29.
  • 30.
    Lung tumours 1. Squamouscell carcinoma/epidermoid carcinoma 2. Adinocarcinoma-bronchial derived, acinar,papillary,broncioloalveolar,solid 3. Small cell carcinoma-oat cell, intermediate 4. Large cell carcinoma,undiff,giant cell, clear cell 5. Others- combined small cell carcinoma,Adenosquamous carcinoma
  • 31.
    Adenocarcinoma has replacedSCC as the most common primary lung tumour Most common in women,non smokers,persons younger than 45yrs
  • 32.
    Therapeutic classification 1. Smallcell lung cancer (SCLC) 2. Non small cell lung cancer (NSCLC)