Respi

pathology
SYLLABUS
Lesions of Upper Respiratory Tract: (P. 1097)
Tumours of larynx. (P. 1097)
Bronchial Asthma: (P. 1097)
Mechanism and pathogenesis (P. 1098)
Bronchiectasis: (P. 1099)
Pathogenesis, gross and microscopic features (P. 1100), complication (P. 1100)
Atelectasis: (P. 1101)
Definition, types, morphology, pathogenesis and complications.
Hyaline Membrane Disease (P. 1102) and Adult Respiratory Distress Syndrome (P. 1103):
Definition, pathogenesis
Chronic Obstructive Pulmonary Disease (P. 1105) and Cor-Pulmonale (P. 1109):
Chronic Bronchitis: (P. 1106)
Aetiology, gross and microscopic features.
Emphysema: (P. 1107)
Definition, types, pathogenesis
Pneumonia: (P. 1110)
IV
Types, aetiopathogenesis, stages (P. 1112), complication
Lung Abscess: (P. 1113)
Aetiopathogenesis, morphology
Tuberculosis: (P. 1114)
Aetiopathogenesis (P. 1114), primary complex- definition , Ghon’s focus-Morphology (P. 1115)
Secondary tuberculosis (P. 1116)- types of lesion
Fibrocaseous, cavitary and miliary tuberculosis
Gross and microscopic features , complications
Pneumoconiosis: (P. 1117)
Definition, pathogenesis.
Anthracosis (P. 1118), asbestosis (P. 1117), silicosis (P. 1118)
Bronchogenic Carcinoma: (P. 1119)
Aetiology, gross and microscopic features of:
Squamous cell carcinoma (P. 1119), adenocarcinoma (P. 1120), small and large cell carcinomas (P. 1121),
bronchioloalveolar carcinoma
Pleural Lesions: (P. 1121)
Mesothelioma (P. 1122), pleural effusion (P. 1121), pneumothorax (P. 1122)
Investigations (P. 1122): examination of sputum and pleural fluid

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IV

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PATHOLOGY

TUMORS OF LARYNX
BRONCHIAL ASTHMA
 Occurs as a spectrum or epithelial alterations in
Past Questions:
the larynx ranging from hyperplasia, atypical
hyperplasia, dysplasia, carcinoma in situ, to 1. Short notes on:
invasive carcinoma. a. Bronchial asthma
(5) [07 July, 04 June, 03 June]
Risk factors:
b. Pathogenesis of bronchial asthma (4) [010]
1. Tobacco smoke
 Asthma is a chronic inflammatory disorder of the
2. Alcohol airways that causes recurrent episodes of wheezing,
3. Nutritional factors breathlessness, chest tightness and cough ,
particularly at night and or in the early morning.
4. Exposure to asbestos
 These symptoms are usually associated with
5. Irradiation and
widespread but variable bronchoconstriction and
6. Infection with HPV airflow limitation that is, at least partly reversible,
Morphology: either spontaneously or with treatment.
- 95% of laryngeal carcinomas are typical  The hallmarks of the disease are:
squamous cell tumors. i. Increased airway responsiveness to a variety of
stimuli resulting in episodic
- Site: bronchoconstriction.
i. Vocal cord ii. Inflammation of the bronchial walls. IV
ii. Above or below the cord iii. Increased mucus secretion.
iii. On the epiglottis Note:
iv. Aryepiglottic folds or - COPD( chronic bronchitis and Emphysema) is a
v. In the pyriform sinuses. irreversible obstruction of airways but Asthma is a
reversible obstructive phenomenon.
- Intrinsic tumor: Those confined within the
larynx proper. Types:
1. Atopic 2. Non- Atopic
- Extrinsic tumor: Those that arise or extend
3. Drug induced 4. Occupational
outside the larynx.
Atopic:
Gross:
- Most common type of asthma
 Pearly gray, wrinkled plaques on the - A classical example of type I, IgE- mediated
mucosal surface, ultimately ulcerating and hypersensitivity reaction.
fungating. - Begins in childhood.
Microscopy: - Triggered by environment allergens, such as
 Growth pattern similar to squamous cell dust, pollens, animal dander and food.
carcinoma in other parts of the body. - A positive family history of asthma is common.
- A skin test with the offending antigen in these
 Bizzare tumors cells or giant cells may also
patients results in an immediate wheal and
be present. flare reaction.

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Non-atopic: Drug -induced asthma

- No evidence of allergen sensitization, - Aspirin- sensitive asthma
- Skin test results are usually negative. - They experience not only asthmatic attacks but
also urticaria.
- Positive family history of asthma is less
Occupational asthma:
common.
- Asthma induced by fumes(epoxy resins,
- Respiratory infections due to viruses (eg. Rhino plastics), organic and chemical dusts, wood,
virus, parainfluenza virus) are common trigger. cotton, platinum) gases (tolune) and other
- Inhaled air pollutants, such as SO2, O3 and NO2 chemicals(formaldehyde, penicllin products).
may also contribute to the chronic airway - Minute quantities of chemicals are required to
inflammation. induce the attack, which usually occurs after
repeated exposure.

Pathogenesis [010]
Most responsible factors are:
a. Genetic predisposition
b. Exposure to environmental triggers
Individuals with Respiratory infections
Exposure with genetically
environment susceptible genes Aspirin

Sensitization of the airways with

inhaled allergens

Stimulation of TH2 cells

IV
TH2produces cytokines like IL-4, IL-5, IL-13

IL-4 stimulates B cells IL- 5 IL- 13

Prodution of IgE antibodies Activates locally recruited eosinophils Stimulates mucus production

IgE coats submucosal mast cells

Repeated exposure to the allergen

Degranulation of mast cells cause release of granules content and release of cytokines

Induction of early phase reactions

i. Brochoconstriction
ii. Mucus production
iii. Vasodilation

Late phase reaction consists largely of inflammation with recruitment of

leukocytes, notably eosinophils, neutrophils and more T cells.

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 Bronchoconstriction is also caused by direct known spiral shaped mucus plugs called
subepithelial vagal (parasympathetics) receptors curshman spirals
stimulation. - Numerous, eosinophils and charcot leyden
Morphology: crystals (collection of crystalloid made by
Gross: esosinophilic protein called galectin-10)
- In patients dying of status asthmaticsThe - Overall thickening of airway wall.
lungs are over distended because of over - Sub- basement membrane fibrosis (type I
inflation, with small areas of atelectesis. and type II collagen).
- Occlusion of bronchi and bronchioles by - Increase in size of the submucosal glands
thick, tenacious mucus plugs. and mucous metaplasia of airway epithelial
Note: TH1 cells are stimulated in TB, TH2 in bronchial cells.
asthma. - Hypertrophy and /or hyperplasia of the
bronchial wall muscle.
Microscopy:
- Increased vascularity.
- The mucus plugs contain whorls of shed
epithelium, which give rise to the well-

IV

 Bronchiectasis is a disease characterized by

BRONCHIECTASIS
permanent dilation of bronchi and bronchiloes
Past Questions: caused by destruction of the muscle and elastic
1. Describe etiopathogenesis of Bronchiectasis. tissue, resulting from or associated with chronic
Describe the gross morphology & complications necrotizing infections.
of Bronchiectasis. (5+4+1=10) [09 July] Etiology [09]
2. Write short notes on: 1. Congenital or hereditary, condition
a. Bronchiectasis [08 July, 05 June] - Cystic fibrosis
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- Intralobar sequestration of the lung 2. Cystic fibrosis

- Immunodeficiency states, and 
Primary defect in ion transport leads to defective
- Primary ciliary dyskinesia and Kartagener's
mucocilliary action
syndromes.

2. Postinfectious conditions, including necrotizing
Accumulation of thick viscid secretions
pneumonia caused by

- Bacteria Obstruct the airways
 mycobacterium tuberculosis 
 Staph. aureus Marked susceptibility to bacterial infections
 H. influenza, Pseudomonas 
- Viruses(adenovirus, influenza virus, HIV Further damage the airways
- Fungi (Aspergillus species) 
3. Bronchial obstruction due to tumor, foreign Repeated infections
bodies and occasionally mucus impaction, in 
which the bronchiectasis is localized to the Destruction of supporting smooth muscle and
obstructed lung segment. elastic tissue, fibrosis, and further dilation of
bronchi
4. Other conditions include:

- Rheumatoid Arthritis (RA)
Bronchiectasis
- Systemic lupus Erythematosus (SLE)
IV - Inflammatory Bowel Disease (IBD) 3. Primary ciliary dyskinesia
- Post- transplantation: 
Poorly functioning cilia
(Chronic lung rejection, chronic graft Vs
host disease after bone marrow 
transplantation). Retention of secretions and recurrent infections

Pathogenesis [09] 
Bronchiectasis
1. Bronchial obstruction
Morphology [09]

Gross
Clearing mechanisms are impaired
- Bilateral
 - Lower lobes
Pooling of secretions distal to the obstruction - More severe in vertical & distal bronchi and
 bronchioles
- Bronchi and bronchioles are sufficiently
Inflammation of the airway
dilated (sometimes upto 4 times)
 - Bronchi and bronchioles can be followed
Necrosis, fibrosis and eventually dilation of directly out to pleural surface (normally
airways bronchioles can't)

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Cut surface: - Desquamation of the lining epithelium and

- Honey- Comb appearance extensive areas of necrotizing ulceration
- The transected dilated bronchi appear as - Pseudostratification of the columnar cells or
cysts filled with mucopurulent secretions. squamous metaplasia of the remaining
epithelium.
Morphological types:
1. Cylindroid bronchiectasis  In chronic case:

2. Fusiform bronchiectasis - Lung abscess

3. Saccular bronchiectasis - Fibrosis of the bronchial and bronchiolar

walls
Microscopic findings:
- Peribronchiolar fibrosis
 In active case:
- Subtotal or total obliteration of bronchiolar
- An intense acute and chronic inflammatory
lumens
exudation within the walls of the bronchi
and bronchioles

IV

Complications [09]
ATELECTASIS
1. Lung abscess
 Atelectasis refers either to incomplete expansion
2. Cor-pulmonale of the lungs (neonatal atelectasis) or the collapse
3. Brain abscesses of previously collapsed lung, producing areas of
relatively airless pulmonary parenchyma
4. Amyloidosis
Type
5. Recurrent pneumonia
1. Resorption (or obstruction)
6. Pleurisy 2. Compression
3. Contraction

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Resorption atelectasis HYALINE MEMBRANE DISEASE

1. Aspiration of foreign body
 Hyaline Membrane disease is defined as the
2. COPD disease due to the deposition of a layer of hyaline
3. Postoperative proteinaceous material in the peripheral airspaces
4. Mucous plugs of infants.
5. Bronchiectasis, bronchial asthma, Chronic
 Most common cause Respiratory Distress
bronchitis
syndrome in newborns.
Complete obstruction of an airway
Pathogenesis of hyaline membrane disease

Which in time leads to resorption of the oxygen [KU 2012]
trapped in the dependent alveoli. - Predisposed by
  Immature lungs
Resorption atelectasis  Low gestational age
Mediastinal shift: Towards the ateletatic lung
 Deficiency in the pulmonary surfactant
Compression atelectasis:
 Maternal diabetes and
- Result when the pleural cavity is partially or
completely filled by fluid exudates, tumor,  Delivery by cesarean section
blood or air.
Causes
- Cardiac failure
- Neoplastic pleural effusions
IV - Abnormal elevation of diaphragm due to:
Peritonitis, sub- diaphragmatic abscesses
- Tension pneumothorax
Mediastinal shift: Away from the affected lung.
Contraction atelectasis:
- Occurs when local or generalized fibrotic changes
in the lung or pleura prevent full expansion.
Morphology of atelectasis:
Gross:
- The lungs are small, dark blue, fleshy and non-
crepitant.
Microscopy:
- The alveolar spaces in the affected area are
small with thick interaveolar septa.
- The alveolar spaces contain protenaceous fluid
with few epithelial squamous cells and meconium.
- Scattered aerated areas of the lung are
hyperinflated causing interstitial emphysema
and pneumothorax.

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- Surfactant is produced by type II alveolar cells ADULT RESPIRATORY DISTRESS

after 35 weeks of gestation in the fetus.
SYNDROME
- Before 35 weeks  deficiency of surfactant 
 It is a severe form of acute lung injury
increase in surface tension lung collapse
characterized by the abrupt onset significant
with each successive breath  progressive
hypoxemia and diffuse pulmonary infiltrates in the
atelectasis and reduced lung compliance.
absence of cardiac failure.
Note:
Etiology:
i. Labor is known to increase surfactant synthesis,
1. Infection
hence, cesarean section before the onset of labor
may increase the risk of RDS. - Sepsis
ii. Surfactant synthesis is increased by cortisol, - Diffuse pulmonary infections:
thyroxine, insulin, TGF-. So, intrauterine stress   Viral, mycoplasma and pneumocystis
increase in corticosteroid synthesisincrease in pneumonia, miliary tuberculosis
surfactant synthesis. - Gastric aspiration.
Morphology: 2. Physical injury
Grossly: - Mechanical trauma Eg. Head injuries
- Solid, airless, and reddish purple, similar to - Pulmonary contusions
the color of the liver. - Near-drowning
- Usually sink in water. - Fractures with fat embolism
Microscopy: - Burns
- Alveoli are poorly developed or are
IV
- Ionizing radiation
collapsed.
3. Inhaled irritants:
- The necrotic material becomes
- Oxygen toxicity
incorporated within eosinophilic hyaline
membrane lining the respiratory - Smoke
bronchioles, alveolar ducts and random - Irritant gases
alveoli. - Chemicals
- The membranes are largely made up of
4. Chemical injury
fibrin admixed with cell debris derived
- Heroin or methadone overdose
chiefly from necrotic type II pneumocytes.
- Acetylsalicylic acid
Prophylaxis:
- Administration of exogenous surfactant at - Barbiturate overdose
birth to extremely premature infants 5. Hematologic conditions
(gestational age of 26 to 28 weeks) and - Multiple transfusion
- Administration of surfactant to older - Disseminated intravascular coagulation
premature infants who are symptomatic.
6. Pancreatitis
7. Uremia

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8. Cardio pulmonary bypass regulated under normal conditions, has

- Organic solvents emerged as a likely candidate shifting the
balance in favour of pro- inflammatory state.
- Chemical
- Inflammatory damage to the alveoli
Pathogenesis:
i. By locally produced pro-inflammatory
- In ARDS, lung injury is caused by an imbalance mediators
of pro- inflammatory and anti- inflammatory ii. Remotely produced and arriving via
reaction  Pulmonary artery
- Nuclear factor KB (NF-KB) , a transcription  Through inhalation (eg. gastric contents)
factor whose activation itself is tightly

Acute insult to the lung by: infections, physical injury, inhaled irritants, chemical injury and other
various injuries.

Activation of pulmonary macrophages

Release of proinflammatory cytokines by macrophages: IL-8,IL-1,TNF-

Adherence of neutrophils to the pulmonary capillaries

Extravasation of neutrophils into the alveolar space
IV 
Activation of neutrophils

Activated neutrophils release leukotrienes, oxidants, proteases, platelet activating factor(PAF)

Injury to the alveolar epithelium Infiltration of inflammatory Damage to pulmonary

 cells and edema in vascular endothelium
Swelling, vacuolization, bleb interstitial space

formation and frank necrosis 
 Decrease in pulmonary gas Activation of endothelin and
Alveolar flooding, damage to type II exchange VWF
pneumocytes  
 Arterial hypoxemia & Dysregulation of coagulation
Decrease in surfactant synthesis cyanosis system

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IV

 There is considerable overlapping between those

CHRONIC OBSTRUCTIVE spectrums of diseases.
PULMONARY DISEASES
Past Question:
1. Short notes on COPD (5) [11 July]
 It is the spectrum of lung disease which consists of
chronic bronchitis and emphysema characterized
by inflammation of the terminal bronchioles and
alveoli.
 Though asthma is also an obstructive disease, it is
distinguished from chronic bronchitis and
emphysema by the presence of reversible
bronchospasm.
 In most patients, COPD is the result of long-term
heavy cigarette smoking; about 10% of patients
are nonsmokers.

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 Spectrum of COPD Chronic irritation by smoking

Predominant Predominant Proteases released
Bronchitis Emphysema from neutrophils
Hypersecretion of mucus in the large airways
Age (Yr) 40-45 50 -75
Dyspnea Mild; late Severe; early
Hypertrophy of the submucosal glands in the
Cough Early; copious Late; scanty
trachea and bronchi
sputum sputum
Bronchospasm
Infections Common Occasional Hypersecretion Infection
of mucus
Respiratory Repeated Terminal
insufficiency Further Bronchiolar and bronchial injury
Cor-pulmonale Common Rare; terminal Continued and Continued and
repeated repeated
Airway increased Normal or slightly injury(smoking) infection
resistance increased
Elastic recoil Normal Low Reversible obstruction in bronchioles and
small bronchi
Chest Prominent Heperinflation;
radiograph vessels; large small heart
heart Chronic bronchitis

appearance Blue bloater Pink puffer Morphology:

IV Goss:
Chronic Bronchitis
- Hyperemia, swelling and edema of the
 Chronic bronchitis is defined clinically as any
mucous membranes
patient who has persistent cough with Sputum
- Accompanied by excessive mucinous to
production for at least 3 months in at least 2
mucopurulent secretions layering the
consecutive years, in the absence of any other
epithelial surfaces.
identifiable cause.
Microscopy:
Etiology:
- Chronic inflammation (predominant
- Habitual smokers
lymphocytes)
- Inhabitants of smog-laden cities
- Hypertrophy and hyperplasia of bronchial
Pathogenesis: glands that secrete mucus (increase in
- Chronic irritation by inhaled substances such as Reid's index)
tobacco smoke (90% of patients are smokers) - Increase number of goblet cells
are grain, cotton, and silica dust.
- Cilia are destroyed
- Gender: M=F, more common in middle age
- Bronchial epithelium may exhibit
male.
squamous metaplasia & dysplasia
- Chronic bronchitis is 4-10 times more common
- Bronchiolitis obliterans (obliteration of
in heavy smokers, regardless of age, sex,
lumen due to fibrosis)
occupation and place of dwelling.
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- More common type

- More severe in the upper lobes, particularly in
the apical segments
- Common in heavy smokers
- Chronic bronchitis is pathologically regarded as
centriacinar emphysema.
Panacinar(Panlobular):
- The acini are uniformly enlarged from the level
of respiratory bronchioles to terminal blind
alveoli.
- Tends to occur more commonly in the lower
zones and in the anterior margins of the lungs
- Most severe at the bases
- Associated with 1- antitrypsin((1-AT)
deficiency.
Distal Acinar (paraseptal ) emphysema
Emphysema [10 Jan] - The proximal portion of the acinus is normal
Past Questions: but the distal part is predominantly involved.
- The upper half of the lungs.
1. Morphological types of emphysema
- Common sites: adjacent to the pleura, along
[06 June, 03 Dec]
a. Emphysema [10 Jan]
the lobular connective tissue septa, and at the IV
margins of the lobules, adjacent to areas of
 Emphysema is a condition of the lung fibrosis/ scarring or atelectasis.
characterized by abnormal permanent
- Multiple, continuous, enlarged airspace from
enlargement of the airspaces distal to the terminal
less than 0.5 cm to more than 2cm in diameter.
bronchiole, accompanied by destruction of their
walls and without obvious fibrosis. Irregular (Airspace enlargement with
fibrosis):
Types [06,03}
- The acinus is irregularly involved
1. Centriacinar
- Is associated with scarring
2. Panacinar
- Asymptomatic and significant clinically
3. Paraseptal
Other types:
4. Irregular
i. Compensatory hyperinflation (emphysema)
Centriacinar:
ii. Obstructive overinflation
- Central or proximal parts of the acini, (Formed
iii. Bullous emphysema
by respiratory bronchioles ) are affected.
iv. Interstitial emphysema
- Distal alveoli are spared (normal).

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Note: Protease- antiprotease:

IV - Centriacinar emphysema occurs predominantly in - An imbalance between proteases (mainly
heavy smokers, often in association with chronic elastase) and antiproteases in the lung.
bronchitis. - 1-AT is synthesized in the liver
- Emphysema clinically present as barrel shaped - It is also present in serum, tissue fluids, and
chest, pursed lip breathing, hyperinflation of lung, macrophages.
resonant on percusion, cachexia.
- It is a major inhibitor of proteases secreted
- Mismatch of ventilation-perfusion ratio.
by neutrophils during inflammation.
Etiology: - 1-AT deficiency, leads of emphysema in
- Heavy cigarette smoking early life and in a greater severity if the
- 1 antitrypsin deficiency individual smokes.
- Aging - Sometimes even if 1–AT is present it is
deactivated. This is called functional 1AT
Pathogenesis: [08]
deficiency.
Destruction of alveolar wall by:
- Major cause of 1AT deficiency is genetic.
1. Protease-antiprotease
2. Oxidant antioxidant imbalance

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Oxidant Antioxidant imbalance: - Large apical blebs or bullae are more

- Normally, the lung contains a healthy characteristic of irregular emphysema
secondary to scarring and distal acinar
complement of antioxidants (superoxide IV
dismutase, glutathione) that keeps emphysema.
oxidative damage to a minimum. Microscopy:
- Tobacco smoke contains abundant reactive - Abnormally large alveoli separated by thin
oxygen species (free radicals), which septa with only focal centriacinar fibrosis
deplete these antioxidant mechanisms, - Loss of attachments of the alveoli to the
thereby inciting tissue damage. outer wall of small airways.
- Activated neutrophils also add to the pool Cor-Pulmonale
of reactive oxygen species in the alveoli.  Isolated pulmonary hypertensive heart disease
characterized by right ventricular hypertrophy/
- A secondary consequence of oxidative
dilation and potentially failure secondary to
injury is inactivation of native antiprotease,
pulmonary hypertension.
resulting in "functional" 1-antitrypsin
 May or may not be associated with cardiac failure
deficiency even in patients without enzyme
 Pressure overload of the right ventricle
deficiency.
Types:
Morphology: - Acute: Follow massive pulmonary embolism
Gross: - Chronic: Results from right ventricular
- Voluminous lungs hypertrophy (and dilation) secondary to
prolonged pressure overload, such as can occur
- The upper two thirds of the lungs are more with chronic lung disease and a variety of other
severely affected conditions.

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Disorders predisposing to cor-pulmonale: 3. Parenchymal or alveolar lung disorders

1. Disease of the pulmonary parenchyma: 
i. COPD Anatomic compromise of the pulmonary vascular
ii. Diffuse pulmonary interstitial fibrosis bed
iii. Pneumoconiosis 
iv. Cystic fibrosis Elevated pulmonary blood pressure
v. Bronchiectasis 
2. Disease of the pulmonary vessels: Cor-pumonale
i. Recurrent pulmonary thromboembolism.
4. Blood disorder (e.g polycythemia vera, sickle
ii. primary pulmonary hypertension. cell disease, macroglobulinemia)
iii. Extensive pulmonary arteritis (e.g. Wegener 
granulomatosis).
Increased blood viscosity
iv. Drug-Toxin, or radiation-induced vascular

obstruction.
Elevated pulmonary blood pressure
v. Extensive pulmonary tumor microembolism

3. Disorders affecting chest movement.
Cor-pulmonale
i. Kyphoscoliosis-( forward bending)
ii. Marked obesity (sleep apnea, pickwickian PNEUMONIA
syndrome)
Past Questions:
iii. Neuromuscular disease
1. Write short notes on:
4. Disorder inducing pulmonary arterial
hypertension a. Lobar pneumonia-stages, morphology and
IV complications. (5)[05 June]
i. Metabolic acidosis
b. Lobar pneumonia (5) [08 Jan, 04 Dec]
ii. Hypoxemia
c. Lobar pneumonia- Stages and complications
iii. Chronic attitude sickness
(5) [02 Dec]
iv. Obstruction of major airways
d. Gross and microscopic changes in lobar
v. Idiopathic alveolar hypoventilation
pneumonia (5) [03 June]
Pathogenesis:
e. Stages of lobar pneumonia
1. Massive pulmonary embolism (5) [08 July, 06 June]

 Pneumonia is defined as acute inflammation of
Sudden increase in pulmonary resistance
lung parenchyma with consolidation.

Acute Cor-pulmonale Types:
A. Anatomical
2. Alveolar hypoxia or blood acidemia 1. Lobar pneumonia
 2. Bronchopneumonia
Pulmonary vasoconstriction B. Etiological:
 1. Community -Acquired acute pneumonia
Pulmonary hypertension
i. Streptococcus pneumonia

ii. H. influenzae
Cor-pulmonale

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iii. Moraxella cararrhalis iv. Invasive aspergillosis

iv. Staph aureus v. Invasive candidiasis
v. Legionella pneumophila Pathogenesis:
vi. Enterobacteriaceae (klebsiella pneumoniae, - It occurs when systemic resistance of the host
Pseudomomas) is lowered and when local defense mechanism
2. Community Acquired Atypical pneumonia are impaired.
i. Mycoplasma pneumoniae 1. Impaired local defence mechanisms:
ii. Chlamydia species (C. Pneumoniae, C. i. loss or anaesthesia , neuromuscular
psittaci, C. Trachomatis) disorders, drugs
iii. Coxiella burnetti (Q fever) ii. chest pain, aspiration of gastric contents
iv. Viruses: Respiratory syncytial virus, para- 2. Injury to the mucociliary apparatus.
Influeza virus (Children), Infuenza A and i. Impairment of ciliary function or
B (adults), Adenovirus. ii. Destruction of ciliated epithelium due to
3. Hospital -Acquired Pneumonia cigarette smoke.
i. Gram negative rods. iii. Inhalation of hot or corrosive gases
ii. Enterobacteriaceae (klebsiella, Serratia, iv. Viral disease
marcescens, E.coli)
v. Genetic defects of ciliary function (immotile
iii. Pseudomonas cilia syndrome)
vi. Staph. aureus (penicillin resistant)
3. Accumulation of secretions:
4. Aspiration pneumonia
i. Cystic fibrosis
i. Anaerobic oral flora (bacteroids, prevotella,
ii. Bronchial obstruction
fusobacterium, peptostreptococcus admixed
with aerobic) 4. Interference with the phagocytic or bacterial IV
action of alveolar macrophage by:
ii. Bacteria: strep. Pneumoniae, staphylococcus
aureus, H. influenzae. i. Alcohol
5. Chronic Pneumonia: ii. Tobacco smoke
i. Nocardia, Actinomyces granulomatous iii. Anoxia or oxygen intoxication
ii. Mycobacterium tuberculosis and atypical 5. Pulmonary congestion and edema
mycobacteria. Bronchopneumonia
6. Necrotizing pneumonia and lung abscess:
Gross:
i. Anaerobic bacteria (Extremely common),
- Patchy consolidation of lung.
with or without mixed aerobic infection
staph. aureus - One lobe but is more often multilobar
ii. Klebsiella pneumoniae - Bilateral
iii. Streptococcus pyogens - Basal
iv. Type 3 pneumococci - Lesion
7. Pneumonia in the immunocompromised  3-4 cm in diameter
host:
 Slightly elevated, dry, granular, gray-red to
i. Cytomegalovirus
yellow, and poorly delinited at their
ii. Pneumocystis jirovecii
margins.
iii. Mycobacterium avium-intracellulare

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Microscopy: Stage of Red hepatization (early consolidation

- A suppurative, neutrophil-rich exudate that fills of lung)
the bronchi, bronchioles, and adjacent alveolar Gross:
spaces.
- The lobe appears distinctly red, firm, and
Lobar pneumonia [05,02,08,04] airless, with a liver- like consistency, hence
 Fibrinosuppurative consolidation of large portion the term hepatization
of a lobe or of an entire lobe of one or both lungs. Cut surface: dry, granular, airless, red
Stages: [05,02,08,06] Microscopy:
i. Congestion (1-2 days). - Fluid is replaced by fibrin
ii. Red Hepatization (2-4 days). - massive confluent exudation of neutrophils
iii. Gray Hepatization (4-8 days). and Red cells.
iv. Resolution (1-3 weeks)
- Bacteria phagocytosed by neutrophils
Stage of Congestion (1-2 days)
- Alveoler septa becomes less prominent
Gross:
- Lung is heavy, boggy, enlarged and
congested
- Vascular engorgement
Cut surface: blood -stained frothy fluid
Microscopy:
i. Intra-alveolar fluid with few neutrophils
ii. Presence of numerous bacteria
iii. Dilation and congestion of capillaries

IV

Stage of Gray hepatization (late

consolidation for 4-8 days)
Gross:
- A grayish brown, dry surface
Cut surface: dry, granular, grey.
Microscopy:
- Fibrin strands become more dense &
numerous

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 Respi

- Cellular exudate is primarily composed of

macrophage.
- Disintegration of red cells and neutrophils.
- Organisms are scanty.

Complication of pneumonia: [05,02]

i. Organisation
ii. Abscess
iii. Bronchiectasis
iv. Empyema IV
v. Bacteremic dissemination to the heart valves,
Stage of resolution (1-3 weeks): pericardium, brain, kidney, spleen or joints
Gross: causing, metastatic abscesses, endocarditis,
meningitis or suppurative arthritis.
- Normal aeration in the affected lobe is
restored by enzymatic digestion of solid LUNG ABSCESS
fibrinous constituent Past Question:
- Softening occurs first in Centre and then to 1. Write short notes on lung abscess. [10]
periphery  Is defined as a local suppurative process within
Cut surface: Grey-red/ dirty brown and frothy, the lung, characterized by necrosis of lung tissue.
yellow creamy fluid Etiopathogenesis:
Microscopy: 1. Aspiration of infective material
- Macrophage predominant - Acute alcoholism, coma, anesthesia,
- Neutrophils and debris engulfed by sinusitis, gingivodental sepsis and
macrophages. debilitation in which cough reflexes are
- Granular and fragmented fibrin strands. depressed.
- Progressive removal of fluid content and 2. Antecedent primary lung infection
cellular exudate from air spaces - S. aureus, K. pneumonia and the type 3
pneumococcus

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 Pathology

3. Septic embolism TUBERCULOSIS

- Thrombophlebitis from the vegetation of Past Questions:
infective bacterial endocarditis.
4. Neoplasia 1. Short notes on:
- When bronchopulmonary segment obstructed a. Ghon’s Focus [10 Jan]
by a primary and secondary malignancy. b. Pulmonary tuberculosis [03 Dec]
5. Miscellaneous
c. Primary pulmonary tuberculosis [09 Jan, 06 Dec]
- Direct traumatic penetration of the lungs
- Spread of infections from a neighboring  It is a chronic inflammatory granulomatous
organ, such as suppuration in the disease caused by mycobacterium tuberculosis.
esophagus, spine, sub-phrenic space or Etiology:
pleural cavity, and.
1. Mycobacterium tuberculosis
- Hematogenous seeding of the lung by
pyogenic organisms 2. Mycobacterium bovis
6. Primary cryptogenic lung abscesses Mode of transmission:
- When all those causes are excluded, there 1. Inhalation of aerosol: M. tuberculosis
are still cases in which no reasonable basis
2. Oropharyngeal: M. bovis
for the abscess formation.
Morphology: Pathogenesis: [03,09,10]
Gross: - Pathogenesis of TB depends on the
- few membrane to large cavities of 5-6cm development of cell mediated immunity which
- Single or multiple confers resistance to the bacteria and also
- More common on the right and are most results in the development of type IV
often single hypersensitivity reaction.
- Abscess due to pneumonia or
IV bronchiectasis are usually multiple, basal
- This hypersensitivity reaction results in the
positive tuberculin test, tissue destruction and
and diffusely scattered.
formation of cavitary lesion.
Microscopy:
A. Primary TB(0-3 weeks)
- Abscess cavity might be filled with
suppurative debris. Mycobacterium TB inhaled into the lung
- Continued infection leads to large, fetid, 
green-black, multilocular cavities with poor
Taken up by the alveolar macrophages via
demarcation of their margins, designated
receptor mediated binding.
gangrene of lung.
- The cardinal histological change in all ↓
abscesses is suppurative destruction of the TB bacilli manipulates endosome/ lysosome by:
lung parenchyma within the central area of maturation arrest/ lack of acid PH
cavitation. Ineffective phaglogysosome formation in
Complications of lung abscess: macrophage
i. Brain abscess

ii. Empyema
Unchecked replication of the TB bacilli in the
iii. Coughing of blood
macrophage
iv. Meningitis
v. Pneumothorax 
vi. Respiratory failure Bacteria and seeding to the multiple sites

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B. Primary TB(3 weeks after infection) ii. Some lesions change to progressive TB causing
Antigen presenting cell (alveolar macrophage) further damage
presents MTB antigen to the T helper cells in iii. Some spread by lymphatic and hematogenous
the lymph node and APC also release IL-I2 route
 iv. Some remain dormant.
IL-12 differentiated T helper cells to TH1 cells
Primary tuberculosis: [03, 06, 09]
positive tuberculin test.
 Morphology
TH1 cell releases varieties of cytokines, TNF Gross:
including IFN -  - Site: lower part of the upper lobe or the
IV
upper part of the lower lobe, usually close
Stimulates formation of
to the pleura.
phagolysosome
- Ghon Focus: [10]
Increase expression of
inducible NO synthase  A 1 to 1.5cm area of gray-white
inflammation with consolidation.
- Recruitment and activation of
macrophages  It is a characteristic features of
- Macrophage differentiate into pulmonary TB that occurs due to
epithelioid cells
- Fuse to form giant cells
development of sensitization to
implantation of inhaled bacilli in the
Ongoing hypersensitivity distal airspaces of the lower part of the
results in tissue destruction upper lobe or upper part of the lower

Caseation and cavitation lobe, usually close to the pleura.
 The center of this focus undergoes
caseous necrosis.
Granuloma formation
 Tubercle bacilli, either free or within
phagocytes, drain to the regional nodes,
Note: Fate of primary TB: which also often caseate.
i. Some lesions heal by scarring and calcification

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 Pathology

 This combination of parenchymal lung - Can progress to spread by airways and /or
lesion and nodal involvement is referred bloodstream.
to as the Ghon complex (Ghon complex: Types of lesions:
Ghon’s focus + lymphadenitis +
Fibrocaseous:
lympangitis).
- Sharply circumscribed, firm, gray-white to
 Ghon complex undergoes progressive
yellow areas that have a variable amount of
fibrosis, often followed by radiologically
central caseation and peripheral fibrosis.
detectable calcification (Ranke Complex)
Cavitory tuberculosis
in 95% of cases due to development of
cell-mediated immunity. - In elderly and immunosuppressed

Microscopy: - Progressive pulmonary tuberculosis

- Granulomatous inflammatory reaction that - Apical lesion expands into adjacent lung and
forms both caseating and noncaseating eventually erodes into bronchi and vessels.
tubercles. - Evacuation of caseous center, creating a
- The granulomas are usually enclosed within ragged, irregular cavity that is poorly walled
a fibroblastic rim punctuated by off by fibrous tissue.
lymphocytes Miliary tuberculosis:
- Macrophages are activated to form - Organisms draining through lymphatics
epithelioid cells. enter to the venous blood and circulate
- These fuse to form multinucleated giant cells. back to the lung.

- Immunocompromised people do not form - Lesions are either microscopic or small

IV visible (2-mm) foci of yellow-white
the characteristic granulomas.
consolidation scattered through the lung
Progressive Pulmonary TB:
parenchyma.
- Due to lymphatic spread or haematogeneous
Complications of TB:
dissemination.
1. Local spread to pleura, lung:
- Lung: consolidation of large region or whole
lung too, pleural effusion, tuberculous - Pleural effusion
empyema or obliterative fibrous pleuritis. - Pleural empyema
- It progresses causing endobronchial, - Obliterative fibrous pleuritis
endotracheal and laryngeal TB - Collapse of lung
- Systemic military TB: liver, bone marrow, 2. Blood Spread:
spleen, adrenals, kidney, meninges, fallopian - TB meningitis
tubes and epididymis - Renal TB
Secondary Tuberculosis: - Addison disease
- Reinfection or reactivation of disease in a - Pott disease(When vertebrae affected)
person with some immunity. 3. Swallowed- Intestinal TB:
- Disease tends initially to remain localized, 4. Endobronchial , endotracheal, laryngeal TB
often in apices of lung. 5. Cervical lymphadenitis (scrofula)
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PNEUMOCONIOSIS v. Mesotheliomas
vi. Laryngeal and perhaps other extra pulmonary
Past Questions:
neoplasms, including colon carcinomas
1. Short notes on:
Pathogenesis
a. Pneumoconiosis
[11July,10 July, 07 July, 04 June, 02 Dec] Asbestos
b. Asbestosis [06 Dec]
c. Coal worker's pneumoconiosis- pathogenesis
Serpentine Amphibole
and morphology [04 Dec]
 
 The non-neoplastic lung reaction to inhalation of
Chrysotile Straight stiff
mineral dusts encountered in the workplace.
 amphiboles may
Pathogenesis: Flexible, curled structure align themselves in
Development of pneumoconiosis depends on:  the airstream
i. The amount of dust retained in the lung and Become impacted in the 
airways: upper respire passages
Delivered deeper into
- It is determined by:  the lungs
Removed by the mucociliary
a. The dust concentration in ambient air, 
elevator
b. The duration of exposure, Penetrate epithelial

c. The effectiveness of clearance cells and reach the
Once trapped in lungs
mechanisms, interstitium

ii. The size, shape and therefore buoyancy of the Gradually leached from the
particles: tissues
IV
- Size ranging from 1 to 5 micrometer is most
dangerous.
Morphology:
- Small size particles acute lung injury
Gross
- Large size  resist dissolution and evoke
- Diffuse pulmonary interstitial fibrosis.
fibrosing collagenous reaction.
- Fibrosis around respiratory bronchioles and
iii. Particle solubility and physiochemical reactivity
alveolar ducts and extends to involve
iv. The possible additional effects of other irritants adjacent alveolar sacs and alveoli.
(Eg. Concomitant tobacco smoking). - Fibrous tissue distorts the architecture
Asbestosis [06] creating enlarged airspaces enclosed within
 Lung disease caused by occupational exposure to thick fibrous walls, eventually the affected
asbestos. regions become honeycombed.
 Asbestos related disease are: - Affects lower lobes and subpleurally.
Microscopy:
i. Localized fibrous plaques, or rarely diffuse
pleural fibrosis. - The presence of multiple asbestos bodies
ii. Pleural effusions. - Golden brown, fusiform or beaded rods
with a translucent center.
iii. Parenchymal interstitial fibrosis (asbestosis)
- Asbestos fibers coated with an iron-
iv. Lung carcinoma
containing proteinaceous material.

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 Pathology

Pleural plaques: Gross:

- Are well- circumscribed plaques of dense - Black scar ranging from 2cm-10cm.
collagen often containing calcium. - Multiple
- Site: Anterior and posterolateral aspects of Microscopy:
the parietal pleura and over the domes of - Lesion consist of dense collagen and
diaphragm. pigment
- Later diffuse involvement - Central of lesion is often necrotic, most
- Both lung carcinomas and mesotheliomas likely, due to local ischemia.
(pleura and peritoneal ) develop in workers
Silicosis
exposed to asbestos
 Caused by inhalation of crystalline silicon dioxide
- The risk of lung carcinoma > 5 fold for
(silica).
asbestos workers
 The most prevalent chronic occupation disease in
- The relative risk of mesothelioma >1000-
the world
fold greater.
 Usually presents after decades to exposure as a
Anthracosis (Coal workers
slowly progressing, nodular, fibrosing
pneumoconiosis) [04]
pneumoconiosis.
 Caused by carbon dust/coal dust in people
Pathogenesis:
working in coal mines
- Occurs in both crystalline and amorphous forms,
 The spectrum of lung findings ranges from:
- Crystalline form(including quartz, crystobalite,
i. Asymptomatic anthracosis
and tridymite) are much more fibrogenic.
ii. Simple CWP
Inhalation of silica particles
iii. Complicated CWP
IV 
Morphology:
Simple CWP The particles interact with epithelial cells and
macrophages
Gross:

- Coal macules of size (1-2mm)
- Upper lobes and upper zone of lower Within the macrophage silica causes activation and
lobes are heavily involved release of mediators:
Micro: IL-1, TNF, fibronectin, lipid mediators, oxygen derived
free radicals, and fibrogenic cytokines.
- Macule consists of (carbon-laden
macrophages) 
- Also consists of small amounts of Formation of fibrotic nodules
delicate network or collagen fibers Morphology:
- Located primarily adjacent to respiratory Gross:
bronchioles. - Upper zones of the lungs
- Centribobular emphysema may occur - Tiny, barely palpable, discrete pale to
due to dilation of adjacent alveoli blackened (if coal dust is also present)
Complicated CWP (progressive massive fibrosis) nodules
- Occurs on the back ground of CWP and - As the disease progresses these nodules
generally requires many years to develop may coalesce into hard, collagenous scars.

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- Some nodules may undergo central Etiopatogenesis [05]

softening and cavitations (superimposed TB 1. Tobacco smoking
or ischemia) i. Amount of daily smoking
- Fibrotic lesions may also occur in the hilar ii. Tendency to inhale
lymph nodes and pleura
iii. Duration of smoking
- thin sheets of calcification occur in the
- 10 times increased risk in average smoker
lymph nodes and are seen radiographically
as eggshell calcification. - 60 times increased risk in heavy smoker
- These may progressively expand and - Strongest association with squamous cell
coalese to form progressive massive fibrosis carcinoma and small cell carcinoma
Microscopy: - Act both as initiators (polycyclic aromatic
- Concentric layers of hyalinized collagen hydrocarbons) and promoters (phenol
surrounded by a dense capsule of more derivatives)
condensed collagen. 2. Industrial hazards:
- Nodular examination by polarized microscopy - High dose of ionizing radiation
reveals the birefringent silica particles. - Asbestos, uranium
- Arsenic

BRONCHOGENIC CARCINOMA - Beryllium

3. Air pollution
Past Questions:
4. Dietary factors:
1. Describe the histological classification of
Vitamin A deficiency
bronchogenic carcinoma. Explain the etiology
5. Genetic factors
and morphology of squamous cell carcinoma of IV
lung. (4+4+2=10) [05 Dec] - Increased expression of oncogenes
2. Bronchogenic carcinoma [08 Jan, 09 Jan] - C-myc: small cell carcinoma

Classification [05] - KRAS: Adenocarcinoma

Squamous cell carcinoma - Loss or inactivation of tumor suppressor
Small cell carcinoma gene: P53, Rb gene

combined small cell carcinoma 6. Scarring

Adenocarcinoma - Adenocarcinoma associated with scarring,
also called as scar cancers
acinar, papillary, bronchioalveolar, solid, mixed
subtypes. Squamous cell carcinoma
Large cell carcinoma:  Associated with smoking
large cell neuroendocrine carcinoma. Morphology: [05,12]
Adenosqumous carcinoma, Gross:
carcinomas with pleomorphic, sarcomatiod or - Central in origin (hilar)
sarcomatous elements,
- Obstruct the lumen or major bronchus
Carcinoid tumor
producing distal ateletasis
Typical, atypical
- It can also rapidly penetrate the wall of the
Carcinomas of salivary gland type bronchus to infiltrate along the peribronchial
Unclassified carcinoma tissue.
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 Pathology

- Bulky tumors consists of focal area of Bronchioloalveolar carcinoma

hemorrhage or necrosis Gross:
- May extend to pleural surface, pleural cavity or - Arise from the peripheral portion of lung
upto pericardium
- Arise either as single nodule or more often,
- Spread to tracheal, bronchial and mediastinal as a multiple nodules that sometimes
lymph node coalesce to produce a pneumonia-like
Microscopy [12 KU] consolidation .
1. Well differentiated form: - These nodules have a mucinous, gray
- Presence of keratinization and translucence when secretion is present but
intercellular bridges otherwise appear as solid, gray-white areas
- Keratin pearls formed by marked that can be confused with pneumonia on
eosinophilic dense cytoplasm gross inspection.
2. Moderately differentiated forms: Microscopy:
- Individual cell Keratinization, - Pure bronchioloalveolar growth pattern
intercellular bridges and keratin pearls with no evidence of stromal, vascular, or
are easily seen but not as extensive as
pleural invasion
well differentiated forms.
- Grow along preexisting structures without
3. Poorly differentiated:
destruction of alveolar architecture (lepidic
- Keratin pearl and keratinization are focal
growth pattern)
& not well developed.
- Two subtypes:
- High mitotic activity
 Nonmucinous: columnar, ped shaped,
cuboidal cells
IV
 Mucinous: distinctive tall, columnar cell
with cytoplsamic and intra-alveolar
mucin.

Adenocarcinoma
 Malignant epithelial tumor with glandular
differentiation or much production by tumor cells.
 Grow in various patterns: Acinar, papillary,
bronchioloalveolar, and solid with mucin
formation.

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Small cell carcinoma Paraneoplastic syndromes of lung tumors:

Morphology: 1. SIADH causing hyponatremia
- Highly malignant tumor, most aggressive 2. ACTH producing cushing syndromes
- Cells are relatively small, with scant cytoplasm, 3. Parathyroid, prostaglandins E, and some
ill – defined cell borders, finely granular cytokines causing hypercalcaemia
nuclear chromatin (salt and pepper pattern), 4. Cacitonin causing hypocalcaemia
absent or inconspicuous nuclei. 5. Gonadotropins causing gynecomastia
- Cells are round oval, or spindle shaped. 6. Serotonin and bradykinin associated with the
- Nuclear molding is prominent. carcinoid syndrome

- Mitotic count is high. The cells grow in dusters PLEURAL LESIONS

that exhibit neither glandular nor squamous
organization.
Pleural Effusion
 Refers to the collection of fluid in the pleural
- Necrosis is common and often extensive
cavity that occurs in primary and secondary
- Azzopardi effect (Basophilic staining of
pleural disease which may be inflammatory or
vascular wall) is present
non- inflammatory.
 Accumulation of pleural fluid occurs in following
settings:
i. Increased hydrostatic pressure as in CHF
ii. Increased vascular permeability, as in
pneumonia
iii. Decreased osmotic pressure as in nephrotic
syndrome IV
iv. Increased intrapleural negative pressure, as in
atelectasis
v. Decreased lymphatic drainage, as in
mediastinal carcinomatosis.
 Inflammatory pleural effusions.
i. Are caused by serous, serofibrinous or
fibrinous pleuritis
Large cell carcinoma ii. Pleuritis are commonly caused by
inflammatory disease within the lung.
Morphology:
Causes:
- Undifferentiated malignant epithelial tumor
lacks the cytologic feature of small-cell i. Tuberculosis
carcinoma and glandular or squamous ii. Pneumonia
differentiation iii. Lung infarcts
- The cells typically have large nuclei, prominent iv. Lung abscess
nucleoli and a moderate amount of cytoplasm. v. Bronchiectasis
- Neuroendocrine variant is characterized by: Other:
organoid nesting, trabecular, rosette-like and i. Rheumatoid arthritis
palisading patterns.
ii. Systemic lupus erythematosus

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 Pathology

iii. Uremia Malignant mesothelioma

iv. Diffuse systemic infections  In the thorax arise from either the visceral or the
v. Metastatic involvement of the pleura parietal pleura.
vi. Radiation used in therapy for tumors in the Etiology:
lung or mediastinum. - Heavy exposure to asbestos
Pneumothorax - No relation with asbestos workers who smoke
- Genetic→60% to 80% cases show dele ons in
 Refers to presence of air or gas in the pleural
chromosomes 1p,3p, 6q, 9p or 22q→31% have
cavities.
p16 mutations
Types:
- Viral: simian virus 40→demonstra on of SV 40
1. Spontaneous
Morphology:
2. Traumatic
Gross:
3. Therapeutic - Diffuse lesion spread widely in the pleural
4. Tension space
Spotaneous pneumothorax: - Usually associated with extensive pleural
- Due to any complicantions in pulmonary effusion & direct invasion of thoracic structures
disease that leads to rupture of an alveolus. - Affected lung becomes ensheathed by a
thick, layer of soft, gelatinous, grayish pink
- Causes: tumor tissues.
i. Abscess cavity Microscopy:
ii. Emphysema 1. Epitheliod type: Cuboidal , columnar or
iii. Tuberculosis flattened cells forming tubular or papillary
structure resembling adenocarcinoma.
Traumatic pneumothorax:
2. Mesenchymal type (sarcomatoid type):
IV - Caused by some perforating injury to the chest appears as a spindle cell sarcoma
wall.
3. mixed type: contains both epithelioid and
- If original communication seals itself, there is sarcomatoid patterns
resorption of the pleural space air slowly in
Investigation of pleural effusions
spontaneous and traumatic pnemothorax.
1. X ray
Spontaneous idiopathic pneumothorax: - Obliteration of costophrenic angle
- Due to rupture of small, peripheral, usually - At least 200 ml is required
apical subpleural blebs.
2. USG thorax
- Subside spontaneously as the air is resorbed - Can detect less amount of fluid of about 20 ml
- Recurrent attacks are common 3. Pleural fluid examination
- Can be disabling. A. Naked eye appearance
Tension pneumothorax: - Colour of the fluid
- Air in the pleural cavity which may be sufficient B. Biochemical
to compress the vital mediastinal structures - Protein , LDH , sugar , ADA , amylase
and the contralateral lung. C. Microscopic examination
- The defect acts as one way valve  inspiration D. Gram staining
 permits the entrance of air in pleural cavity E. Culture
 expiration  fails to permit its escape  F. PCR or ELISA
progressively increasing pressures  Tension 4. Pleural biopsy
pneumothorax 5. Thoracoscopy
6. HRCT
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SPECIAL POINTS FOR MCQs

1. Mediastinal shift in atelectesis:
i. Resorption: Towards the atelectic lung
ii. Compression: Away from the atelectic lung
iii. Contraction: Towards the atelectic lung
2. Patchy atelectesis occurs in
i. Deficiency in surfactant synthesis
ii. Hyaline membrane disease
iii. ARDS
3. Lobar pneumonia causes segmental opacifiacation or lobar opacification of lung whereas
bronchopneumonia causes patchy opacification of lung.
4. Bronchopneumonia tends to be bilateral, basal and multilobar in young, old and terminally ill
people.
5. Aspiration is the most common cause of lung abscess, right lower lobe is involved in this case. It is
caused by mixed aerobic and anaerobic organism.
6. Most common organisms involved in the lung abscess after pneumonia are staph aureus and
klebsiella.
IV
7. In secondary TB granuloma is formed at the lung apex called simons focus.
8. Chronic bronchitis is associated with
i. Hypoxia
ii. Weight gain
iii. Cyanosis
9. Emphysema is not associated with cyanosis. In emphysema there is weight loss.
10. Reid index is increased in chronic bronchitis. Reid index= ratio of thickness of the epithelial gland
layer to the thickness of the wall between epithelium and cartilage
11. Chronic bronchitis leads to pulmonary HTN and ultimately cor-pulmonale. This causes right
ventricular enlargement and in X-ray, cardiac enlargement is seen.
12. α1-antitrypsin protects lung from development of emphysema. It is synthesized in liver and
transported in lung. Defect in production or transport of α1 AT causes emphysema.
13. In bronchiectesis, there is production of sputum, which is aggravated by change of position.
14. In ARDS, there is diffuse damage of alveolar epithelium, endothelium of capillaries resulting in
progressive respiratory failure that is unresponsive to oxygen treatment .
15. “White out “X-ray is seen in ARDS. This is diffuse bilateral opacification of lung.
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16. Hyaline membrane disease is due to the deficiency of surfactant. It is associated with :
i. Prematurity
ii. Maternal diabetes
iii. Cesarean section delivery
17. Hyaline membrane disease shows:
i. X-ray :“ground glass “reticulonodular opacities.
ii. Lecithin/sphingomyelin < 2
18. 90 to 95 % of the pulmonary embolism arises from the DVT. Only 10% of those embolism causes
pulmonary infarction.
19. All the lung tumors are central in origin except Adenocarcinoma. Adenocarcinoma appears in
previous scar of the lung.
20. Incidence of lung tumors:
i. Adenocarcinoma( males 37% , females 47%)
ii. Squamous cell carcinoma ( males 32% , females 25% )
iii. Small cell carcinoma ( males 14%, females 18%)
iv. Large cell carcinoma (males 18% , females 10%)
21. Adenocarcinoma: Mostly in women, non smokers and asian origin.
22. Small cell carcinoma mostly implicated for paraneoplastic syndromes
IV
23. Treatment approach for tumors:

i. Non small cell carcinomas (squamous and Adenocarcinoma) surgery

ii. Small cell carcinoma(oat cell carcinoma) radiotherapy and chemotherapy

24. Small cell carcinoma are rapidly growing tumors and have worst prognosis than slow growing
tumors like Adenocarcinoma and squamous cell carcinoma. Squamous cell carcinoma has the best
prognosis.
25. Mutation in tumors:
i. Squamous cell carcinoma: p53 mutation ,RB1
ii. Adenocarcinoma: KRAS , p53
26. Cause for emphysema:

i. Centriacinar Smoking

ii. Panacinar 1 antitrypsin deficiency

iii. Paraseptal  Adjacent to the areas of fibrosis, scarring, or atelectasis

27. Bronchitis is called blue bloater and emphysema is called pink puffer.

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28. Types of lesions in pneumoconiosis:

i. Macular: Anthracosis
ii. Nodular: Silicosis
iii. Diffuse fibrosis: Asbestosis
29. Asbestosis is highly associated with development of lung carcinoma.
30. There is high chance of TB reactivation in silicosis. Caplan syndrome = rheumatoid arthritis+
anthracosis/silicosis/asbestosis
31. Development of pleural plaques do not correlate with level of exposure. Pleural plaques are most
often in anterior and posterolateral aspect of parietal pleura.
32. Anthracosis and silicosis occurs most often in upper lobes whereas asbestosis most often occurs
in lower lobes.
33. Egg shell calcification of hilar lymph nodes occurs in silicosis.
34. Supplemental O2 therapy in new born may lead to:
i. Retinoathy
ii. Bronchopulmonary dysplasia
35. In pneumonia, neutrophil and bacteria are more abundant in stage of congesation, macrophages in
stage of red hepatization, and fibrin in gray hepatization.
36. Curshman spirals and charcot leyden crystals are features of bronchial asthma.
37. Adenocarcinoma is more common in non smoker and arises from scar in lung. Most common
carcinoma in smoker is squamous cell carcinoma. [KU 2012]
38. Lung abscess is common in staph pneumonia.
39. Commonest age of presentation of TB in children is 1 to 4 yrs. Most children with TB are not
infectious, commonest type of TB in children is smear negative primary pulmonary progressive IV
TB.
40. The commonest termination of lobar pneumonia is resolution.
41. Pneumonia alba is caused by mycobacterium
43. The minimum amount of air required to produce symptoms of air embolism is 50 ml
44. The most common cavitating secondaries in lungs is seen in seminoma testis
45. Macrophage derived fibrogenic cytokine is TGF 
46. Crocidolite form of asbestosis is implicated in malignant tumor of pleura.
47. Particles of size less than 5 m are involved in development of pneumoconiosis.
48. Bronchioles involved:
i. Emphysema distal to terminal bronchioles
ii. Chronic bronchitis proximal to terminal bronchioles
iii. Bronchiectesismiddle sized airways (>2 mm)
49. Most fibrogenic dust is silica
50. Lung abscess secondary to aspiration pneumonia develops more often in lower lobe of right
lung.
51. Most common cause for lobar pneumonia is streptococcus pneumonia.
52. Pulmonary HTN develops when systolic BP in pulmonary artery is greater than 30 mmHg.

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53. Atypical pneumonia does not show characteristic features of typical pneumonia such as lung
opacity in x-ray. It is caused by
i. Mycoplasma
ii. Chlamydia
iii. Coxiella
54. Lung-physical abnormality
Tracheal
Pleural effusion Breath sound Percussion Fremitus
deviation
Pleural effusion  Dull  –
Atelectasis,  Dull  Toward side of
bronchial lesion
obstruction
Tension  Hyperresonant  Away
pneumothorax
Consolidation Bronchial Dull  –
(Pneumonial Breath sound
edema)
55. Lung tumors
Type Location Characters Histology
1. Adeno- Peripheral - Most common in non smoker - Apparent 'thickening'
carcinoma - Females > male of alveolar walls.
- Associated with clubbing
IV - CXR  hazy infiltrates similar to
pneumonia
2. Squamous cell Central - Hilar mass, slow growing - Keratin pearls and
carcinoma - Cavitation intercellular bridges
- Cigarettes (linked to smoking)
- HyperCalcemia
[@CCC]
Small cell Central - Produced ACTH, ADH - Kulchitsky cells 
carcinoma (oat) - Antibodies against presynaptic small dark blue cells.
calcium channels (Lambert eaton
syndrome), Inoperable, chemotherapy.
- Implication of my oncogenes
common.
Large cell Peripheral - Anaplastic Pleomorphic grant cells
Carcinoma - Poor prognosis

-1126- FAST TRACK BASIC SCIENCE MBBS