LUNG PATHOLOGY

OUTLINE
• Overview of the Anatomy of the Lungs
• Congenital Lung Diseases
• Lung Collape (Atelectasis)
• Obstructive Lung Diseases
• Restrictive Lung Diseases
CONGENITAL LUNG DISEASES
• Common types
• Pulmonary Hypoplasia
• Foregut cysts
• Pulmonary sequestration

• Less common
• Tracheal and Bronchial anomalies (atresia, stenosis, tracheoesophegeal fistula)
• Vascular anomalies
• Congenital pulmonary airway malformations
• Congenital lobar overinflation (emphysema)
 LUNG

• The lungs are the major organs of the

respiratory system, and are divided into
sections, or lobes. The right lung has three
lobes and is slightly larger than the left lung,
which has two lobes.
• The lungs are the organs of respiration.
• They are located in the thorax, either side of
the mediastinum.
• The function of the lungs is
to oxygenate blood. They achieve this by
bringing inspired air into close contact with
oxygen-poor blood in the pulmonary
capillaries.
LUNG CON’T
• The lungs are roughly cone shaped, with an apex, base, three surfaces and three borders.
• The left lung is slightly smaller than the right – this is due to the presence of the heart.
• Each lung consists of:
Apex – The blunt superior end of the lung. It projects upwards, above the level of the 1st
rib and into the floor of the neck.
Base – The inferior surface of the lung, which sits on the diaphragm.
Lobes (two or three) – These are separated by fissures within the lung.
Surfaces (three) – These correspond to the area of the thorax that they face. They are
named costal, mediastinal and diaphragmatic.
Borders (three) – The edges of the lungs, named the anterior, inferior and posterior
borders.
 BRONCHIAL TREE
• The bronchial tree is a series of passages that
supplies air to the alveoli of the lungs. It begins
with the trachea, which divides into a left and right
bronchus.
• The left and right bronchus divides into lobar
bronchi – one supplying each lobe.
• Each lobar bronchus then further divides into
several tertiary segmental bronchi.
• The segmental bronchi give rise to many
conducting bronchioles, which eventually lead
into terminal bronchioles.
•  Each terminal bronchiole gives off respiratory
bronchioles, which feature thin walled
outpocketings that extend from their lumens. These
are the alveoli – the site of gaseous exchange.
•.
•.

THE ALVEOLAR
• The alveoli are made up of two different types
of cells. Each type has different functions:
Type I pneumocytes. These are the cells
responsible for the exchange of oxygen and
CO2
Type II pneumocytes. These cells perform
two important functions. They
produce surfactant, which helps keep the
balloon shape from collapsing. They can also
turn into type I cells in order to repair damage
• They also contain immune cells called
alveolar macrophages. Macrophages are like
the garbage trucks of the immune system.
These cells phagocytize, or eat debris.
ATELECTASIS
• Also known as collapse, is loss of lung volume caused by inadequate
expansion of air spaces. It results in shunting of inadequately
oxygenated blood from pulmonary arteries into veins, thus giving rise
to a ventilation perfusion imbalance and hypoxia.
FORMS OF ATELECTASIS
• Resorption atelectasis- Resorption
atelectasis occurs when an obstruction
prevents air from reaching distal airways.
• Compression atelectasis- is usually
associated with accumulation of fluid,
blood, or air within the pleural cavity, which
mechanically collapses the adjacent lung.
• Contraction atelectasis- occurs when either
local or generalized fibrotic changes in the
lung or pleura hamper expansion and
increase elastic recoil during expiration.
ACUTE LUNG INJURY
• acute lung injury encompasses a spectrum of bilateral pulmonary
damage (endothelial and epithelial), which can be initiated by
numerous conditions
Clinically, acute lung injury manifests as
 acute onset of dyspnea
 decreased arterial oxygen pressure (hypoxemia)
 development of bilateral pulmonary infiltrates on the chest
radiograph, all in the absence of clinical evidence of primary left-sided
heart failure.
 CHEST X-RAY
NORMAL CHEST X- SHOWING BILATERAL
RAY LUNG INFILTRATES
Acute Respiratory Distress Syndrome

• ARDS is a clinical syndrome of progressive respiratory insufficiency

caused by diffuse alveolar damage in the setting of sepsis, severe
trauma, or diffuse pulmonary infection.
• Neutrophils and their products have a crucial role in the pathogenesis
of ARDS by causing endothelial and epithelial injury.
• The characteristic histologic picture is that of alveolar edema,
epithelial necrosis, accumulation of neutrophils, and presence of
hyaline membranes lining the alveolar ducts.
OBSTRUCTIVE VRS RESTRICTIVE LUNG
DISEASES
CHRONIC OBSTRUCTIVE PULMONARY
DISEASE
• Obstructive (airway) disease, characterized by limitation of airflow,
usually resulting from an increase in resistance caused by partial or
complete obstruction at any level.
COPD consist of;
 Emphysema
Chronic bronchitis
Bronchiectasis
Asthma.
CAUSES OF BRONCHIAL NARROWING
• Increase mucous secretion
• Metaplasia of the goblet cells
• Inflammation with exudation
• Accumulated pigmented alveolar macrophages
• Fibrosis of the wall of the bronchioles
• Obliteration of bronchi and bronchioles obliterans
 EMPHYSEMA
• Emphysema is characterized by abnormal permanent enlargement of the
air spaces distal to the terminal bronchioles, accompanied by destruction
of their walls without significant fibrosis.
RISK FACTORS OF EMPHYSEMA
• SMOKING
• EXPOSURE TO SECOND HAND SMOKING
• OCCUPATIONAL EXPOSURE TO FUMES
• EXPOSURE TO INDOOR AND OUTDOOR POLLUTION
• ALPHA 1 ANTITRYPSIN DEFICIENCY
PATHOGENESIS
PATHOGENESIS
TYPES OF EMPHYSEMA
• Classified according to its anatomic distribution within the lobule.
 Centriacinar
Panacinar
Distal acinar
Irregular.
CENTRIACINAR
• The central or proximal parts of the acini, formed by respiratory
bronchioles, are affected, while distal alveoli are spared.
• The lesions are more common and severe in the upper lobes,
particularly in the apical segments.
• It is most commonly seen as a consequence of cigarette smoking in
people who do not have congenital deficiency of α1-antitrypsin.
PANACINAR/PANLOBULAR
• The acini are uniformly enlarged, from the level of the respiratory
bronchiole to the terminal blind alveoli.
• Occurs more commonly in the lower lung zones and is the type of
emphysema that occurs in α1-antitrypsin deficiency.
DISTAL ACINAR (Paraseptal)
EMPHYSEMA
• In distal acinar (paraseptal) emphysema, the proximal portion of the
acinus is normal but the distal part is primarily involved.
• The emphysema is more striking adjacent to the pleura, along the
lobular connective tissue septa, and at the margins lobules.
• It occurs adjacent to areas of fibrosis, scarring, or atelectasis and is
usually more severe in the upper half of the lungs.
IRREGULAR ACINAR EMPHYSEMA
• Irregular emphysema, so named because the acinus is irregularly
involved, is almost invariably associated with scarring, such as that
resulting from healed inflammatory diseases.
MORPHOLOGY OF EMPHYSEMA
• Panacinar emphysema, when the pathologic process is well developed, produces pale,
voluminous lungs that often obscure the heart when the anterior chest wall is removed at
autopsy
• In centriacinar emphysema the upper two thirds of the lungs are more severely affected than
the lower lungs. The lungs are a deeper pink than in panacinar emphysema and less
voluminous, unless the disease is well advanced.
• Histologic examination reveals destruction of alveolar walls without fibrosis, leading to enlarged
air spaces In addition to alveolar loss, the number of alveolar capillaries is diminished.
• Terminal and respiratory bronchioles may be deformed because of the loss of septa that help
tether these structures in the parenchyma.
• With the loss of elastic tissue in the surrounding alveolar septa, radial traction on the small
airways is reduced. As a result, they tend to collapse during expiration—an important cause of
chronic airflow obstruction in severe emphysema.
CLINICAL FEATURES
• DYSPNEA
• WEIGHT LOSS
• HYPERVENTILATION
• BARREL CHEST
CHRONIC BRONCHITIS
• Defined on clinical basis as; the presence of a persistent productive
cough for at least 3 consecutive months in at least 2 consecutive
years.
RISK FACTORS OF CHRONIC
BRONCHITIS
• SMOKING
• EXPOSURE TO SECOND HAND SMOKING
• OCCUPATIONAL EXPOSURE TO FUMES
• EXPOSURE TO INDOOR AND OUTDOOR POLLUTION
• ALPHA 1 ANTITRYPSIN DEFICIENCY
PATHOGENESIS
The distinctive feature of chronic bronchitis is
hypersecretion of mucus, beginning in the large airways.
The most important cause is cigarette smoking, other air
pollutants, such as sulfur dioxide and nitrogen dioxide,
may contribute.
 These environmental irritants induce hypertrophy of
mucous glands in the trachea and main bronchi, leading to
a marked increase in mucin-secreting goblet cells in the
surface epithelium of smaller bronchi and bronchioles.
 In addition, these irritants cause inflammation with
infiltration of CD8+ lymphocytes, macrophages, and
neutrophils. In contrast with asthma, there are no
eosinophils in chronic bronchitis.
CLINICAL FEATURES OF CHRONIC
BRONCHITIS
• A prominent cough
• Chronic production of sputum
• Hypercapnia
• Hypoxemia
• Wheezing on expiration
• Dyspnea on exertion
• Cyanosis (hence the term “blue bloaters”).*In severe cases*
MORPHOLOGY OF CHRONIC
BRONCHITIS
• The mucosal lining of the larger airways usually is hyperemic and
swollen by edema fluid.
• Covered by a layer of mucinous or mucopurulent secretions.
• On histologic examination, the diagnostic feature of chronic bronchitis
in the trachea and larger bronchi is enlargement of the mucus-
secreting glands.
• Chronic bronchiolitis (small airway disease), characterized by goblet
cell metaplasia, mucous plugging, inflammation, and fibrosis, is also
present.
BRONCHIECTASIS
• Bronchiectasis is the permanent dilation of bronchi and bronchioles
caused by destruction of the muscle and the supporting elastic tissue,
resulting from or associated with chronic necrotizing infections.
PATHOGENESIS
• Two processes are crucial and intertwined in the pathogenesis of bronchiectasis:
obstruction and chronic persistent infection.
• Normal clearance mechanisms are hampered by obstruction, so secondary infection
soon follows; conversely, chronic infection over time causes damage to bronchial walls,
leading to weakening and dilation
• . For example, obstruction caused by a primary lung cancer or a foreign body impairs
clearance of secretions, providing a favorable substrate for superimposed infection.
• The resultant inflammatory damage to the bronchial wall and the accumulating
exudate further distend the airways, leading to irreversible dilation.
• Conversely, a persistent necrotizing inflammation in the bronchi or bronchioles may
cause obstructive secretions, inflammation throughout the wall (with peribronchial
fibrosis and traction on the walls), and eventually the train of events already described.
CONDITIONS THAT PREDISPOSE TO
BRONCHIECTASIS
1. Bronchial obstruction: Common causes are tumors, foreign bodies, and occasionally impaction of mucus.
2. Bronchiectasis can also complicate atopic asthma and chronic bronchitis. Congenital or hereditary
conditions—
In cystic fibrosis, widespread severe bronchiectasis results from obstruction caused by the secretion of
abnormally viscid mucus thus predisposing to infections of the bronchial tree. This is an important and
serious complication.
 In immunodeficiency states, particularly immunoglobulin deficiencies, localized or diffuse bronchiectasis is
likely to develop because of an increased susceptibility to repeated bacterial infections.
 Kartagener syndrome is a rare autosomal recessive disorder that is frequently associated with bronchiectasis
and with sterility in males. In this condition, structural abnormalities of the cilia impair mucociliary clearance
in the airways, leading to persistent infections, and reduce the mobility of spermatozoa.
• Necrotizing, or suppurative, pneumonia, particularly with virulent organisms such as Staphylococcus aureus
or Klebsiella spp., may predispose affected patients to development of bronchiectasis. Post tuberculosis
bronchiectasis continues to be a significant cause of morbidity in endemic areas.
MORPHOLOGY OF BRONCHIECTASIS
• Bronchiectasis usually affects the lower lobes bilaterally.
• The airways may be dilated to as much as four times their usual
diameter and on gross examination of the lung can be followed
almost to the pleural surfaces.
• An intense acute and chronic inflammatory exudate within the walls
of the bronchi and bronchioles and the desquamation of lining
epithelium cause extensive areas of ulceration.
• Fibrosis of the bronchial and bronchiolar walls and peribronchiolar
fibrosis develop in more chronic cases
ASTHMA
• Is a chronic inflammatory disorder characterized by intermittent and
reversible airway obstruction, chronic bronchial inflammation with
eosinophils, bronchial smooth muscle cell hypertrophy and
hyperreactivity, and increased mucus secretion.
• It causes recurrent episodes of wheezing, breathlessness, chest
tightness, and cough, particularly at night and/or early in the
morning.
PATHOGENESIS
CATEGORIES OF ASTHMA
• Atopic Asthma
 This is the most common type of asthma, usually beginning in childhood, and is a classic example
of type I IgE–mediated hypersensitivity reaction. A positive family history of atopy and/or asthma
is common, and asthmatic attacks are often preceded by allergic rhinitis, urticaria, or eczema. The
disease is triggered by environmental antigens, such as dusts, pollen, animal dander, and foods.
Infections can also trigger atopic asthma.
 A skin test with the offending antigen results in an immediate wheal-and flare reaction. Atopic
asthma also can be diagnosed based on serum radio-allergosorbent tests (RASTs) that identify the
presence of IgE specific for a panel of allergens.
• Non-Atopic Asthma
 Patients with nonatopic forms of asthma do not have evidence of allergen sensitization, and skin
test results usually are negative. A positive family history of asthma is less common. Respiratory
infections due to viruses (e.g., rhinovirus, parainfluenza virus) and inhaled air pollutants (e.g.,
sulfur dioxide, ozone, nitrogen dioxide) are common trigger.
CLASSIFIACTION OF ASTHMA
• Drug-Induced Asthma
 Patients with aspirin sensitivity present with recurrent rhinitis and nasal polyps,
urticaria, and bronchospasm. The precise mechanism remains unknown, but it is
presumed that aspirin inhibits the cyclooxygenase pathway of arachidonic acid
metabolism without affecting the lipoxygenase route, thereby shifting the
balance of production toward leukotrienes that cause bronchial spasm.
• Occupational Asthma
 This form of asthma is stimulated by fumes (epoxy resins, plastics), organic and
chemical dusts (wood, cotton, platinum), gases (toluene), and other chemicals.
Asthma attacks usually develop after repeated exposure to the inciting antigen(s)
MORPHOLOGY OF ASTHMA
• In gross specimens obtained in fatal cases, the lungs are overdistended because of overinflation,
and there may be small areas of atelectasis.
• . The most striking macroscopic finding is occlusion of bronchi and bronchioles by thick,
tenacious mucous plugs.
• Histologically, the mucous plugs contain whorls of shed epithelium (Curschmann spirals).
Numerous eosinophils and CharcotLeyden crystals (collections of crystalloids made up of
eosinophil proteins) also are present.
• Thickening of airway wall
• Sub-basement membrane fibrosis
• Increased vascularity in submucosa
• An increase in size of the submucosal glands and goblet cell metaplasia of the airway epithelium
• Hypertrophy and/or hyperplasia of the bronchial muscle.
CLINICAL FEATURES OF ASTHMA
• Wheezing
• Dyspnea
• Chest tightness
• Cough
RESTRICTIVE LUNG
DISEASES
PULMONARY INFECTIONS
MICROORGANISMS ENTER THE LUNGS THROUGH THE FOLLOWING
ROUTES:
 Inhalation
 Aspiration of organism from nasopharynx or oropharynx
 Hematogenous spread form a distant focus of infection
 Direct spread from an adjoining site of infection
Defense mechanism of the lungs
• Nasopharyngeal filtering action
• Mucocilliary action of the upper respiratory airways
• Cough reflex
• Phagocytosing alveolar macrophages
• Phagocytosis and killing by neutrophils
• Opsonization by complement (C3b) in the alternative pathway for
enhanced phagocytosis
• IgA blocks attachment microbial attachment to URT epithelium
• Serum IgG&IgM activate C3b more effeciently in the classical pathway
• T cell involvement in intracellular pathogens
Pneumonia can be very broadly defined as any infection in the lung.

Acute bacterial pneumonias can manifest as one of two anatomic

and radiographic patterns, referred to as;
 bronchopneumonia and
 lobar pneumonia.
 BRONCHOPNEUMONIA/ LOBAR
PNEUMONIA
• Bronchopneumonia implies a patchy distribution of
inflammation that generally involves more than one
lobe . This pattern results from an initial infection of
the bronchi and bronchioles with extension into the
adjacent alveoli.
• Lobar pneumonia the contiguous air spaces of part or
all of a lobe are homogeneously filled with an exudate
that can be visualized on radiographs as a lobar or
segmental consolidation.
Differences between broncho and lobar
pneumonia
BRONCHOPNEUMONIA LOBAR PNEUMONIA
PATCHY CONSOLIDATION (distributed in patches DIFFUSE CONSOLIDATION
throughout one or several lobes, most frequently
bilateral and basal).
Mostly found in children and the aged Mainly found in adults
Main causative organisms - Staphylococci, Main causative organisms - Pneumococci, Klebsiella
streptococci, Pseudomonas, pneumoniae, staphylococci, streptococci
Haemophilus influenzae
Preexisting diseases e.g. chronic debility, terminal More often affects healthy individuals
illness, flu, measles
Response to treatment variable, organisation may Better response to treatment, resolution common,
occur, prognosis poor prognosis good
CLASSIFICATION OF PNEUMONIA
• Community-Acquired Acute Pneumonia( Streptococcus pneumoniae
Haemophilus influenzae Moraxella catarrhalis Staphylococcus aureus Legionella
pneumophila Enterobacteriaceae (Klebsiella pneumoniae) and Pseudomonas
spp).
• Community-Acquired Atypical Pneumonia –(Mycoplasma pneumoniae Chlamydia
spp.—Chlamydia pneumoniae, Chlamydia psittaci, Chlamydia trachomatis Coxiella
burnetii (Q fever) Viruses: respiratory syncytial virus, human metapneumovirus,
parainfluenza virus (children); influenza A and B (adults); adenovirus (military
recruits)}
• Nosocomial Pneumonia Gram-negative rods belonging to Enterobacteriaceae
(Klebsiella spp., Serratia marcescens, Escherichia coli) and Pseudomonas spp. S.
aureus (usually methicillin-resistant)
CLASSIFICATION OF PNEUMONIA
• Aspiration Pneumonia Anaerobic oral flora (Bacteroides, Prevotella,
Fusobacterium, Peptostreptococcus), admixed with aerobic bacteria (S.
pneumoniae, S. aureus, H. influenzae, and Pseudomonas aeruginosa)
• Chronic Pneumonia Nocardia Actinomyces Granulomatous: Mycobacterium
tuberculosis and atypical mycobacteria, Histoplasma capsulatum, Coccidioides
immitis, Blastomyces dermatitidis
• Necrotizing Pneumonia and Lung Abscess Anaerobic bacteria (extremely
common), with or without mixed aerobic infection S. aureus, K. pneumoniae,
Streptococcus pyogenes, and type 3 pneumococcus (uncommon)
• Pneumonia in the Immunocompromised Host Cytomegalovirus Pneumocystis
jiroveci Mycobacterium avium complex (MAC) Invasive aspergillosis Invasive
candidiasis “Usual” bacterial, viral, and fungal organisms
STAGES/CLINICAL COURSE OF
PNEUMONIA
• CONGESTION – 1st stage (1-2 days). Affected lobes are red, heavy and boggy. Vascular
congestion with proteinaceous fluid, scattered neutrophils and bacteria in aveoli

• RED HEPATIZATION – 2nd Stage (2-4 days) Lung lobe has a liver-liver consistency.
Aveolar spaces packed with neutrophils, red cells and fibrin

• GREY HEPATIZATION – 3rd stage (4-8days)Lung is dry, grey and firm due to haemolysis
with persistent fibrinosuppurative exudates in aveoli

• RESOLUTION – 4th Stage (8-21 days)enzymatic digestion of exudates to produce

granular, semifluid debris that is resorbed, ingested by macrophages, coughed up, or
organized by fibroblasts growing into it
•
PATHOGENESIS OF PNEUMONIA
COMPLICATIONS OF PNEUMONIA
• Organization - There is ingrowth of fibroblasts from the alveolar septa resulting in fibrosed,
tough, airless leathery lung tissue. This type of post-pneumonic fibrosis is called carnification

• Pleural Effusion

• Empyma

• Lung Abscess

• Metastic Infection

• * Complications are more likely with serotype 3 pneumococci

MORPHOLOGY
• In pneumococcal pneumonia, the morphology conforms with that of
the 4 stages outlined and may present as lobar or broncho
• Additionally, Broncho shows patchy foci of inflammatory consolidation
throughout one or several lobes; most frequently bilateral and basal.
• Grey-red to yellow lesions of about 3-4cm in diameter
• Lung substance immediately surrounding areas of consolidation is
usually hyperemic and edematous
• Histologically, the reaction consists of focal suppurative exudate that
fills the bronchi, bronchioles, and adjacent alveolar spaces.
TUBERCLOSIS
• Tuberculosis is a communicable chronic granulomatous disease
caused by Mycobacterium tuberculosis.
• Can occur in any part of the body but mostly occurs in the lungs
• Main causative organism is M. tuberculosis hominis
• In the severly immunocompromised, it is possible to find M. kansasi and M.
avium intracellulare
• Main mode of transmission is inhalation of respiratory droplets
containing these strains of Mycobacterium.
• Typically, the centers of tubercular granulomas undergo caseous
necrosis.
PATHOGENESIS (PRIMARY TB)
• In the unexposed immunocompetent person, MTB undergoes a 3-wk
period of incubation.
• MTB has a lot of glycolipids on its surface such as lipoarabinomannom
• In the lungs, Alveolar macrophages have receptors known as
Mannose Binding Receptors
• Binding of the receptors with the glycolipids leads to endocytosis
• Leading to the formation of a phagosome
• MTB has defense mechanism which inhibit lysosomal action of the
macrophages
• Inhibition of Calcium channels
• Prevent recruitment and assembly of certain proteins needed for fusion
PATHOGENESIS (PRIMARY TB)
• MTB begins to proliferate within the macrophage
• In the process, burst into the blood stream and lead to bacteremia and
seed into other organs of the body.
• No clinical symptoms may be observed; occasionally mild flu
• Natural Resistance-Associated Macrophage Protein 1 (NRAMP 1) gene
polymorphism in individuals determine disease progression.
• NRAMP 1 produces a transmembrane protein on endosome and
lysosome to pump out bivalent ions from the lysosome
• This limits the availability of certain bivalent ions that the bacteria will
use.
PATHOGENESIS (PRIMARY TB)
AFTER 3 WEEKS
• Infected Alveolar Macrophages presents MTB antigen via MHC II to T-
cell (CD4+)
• T Cell Differentiates into TH1 cell results from production of IL-12 by
macrophages
• Mature TH1 cell secretes INF-γ which activates macrophage and
makes it bactericidal
• Macrophages are now able to kill MTB with their lysosome
• Macrophages now produce NO and ROS which are bactericidal as well
PATHOGENESIS (PRIMARY TB)
AFTER 3 WEEKS (CONT’D)
• Activated macrophages will turn themselves into epithelioid cells
which sometimes fuse to form giant cells (Langhans giant cells)
• Macrophage activity leads to caseous necrosis
• Finally ends on granuloma formation
• The entire protective effect of this cell-mediated immunity can lead to
cavitation and caseating granulomas
CLINICAL FEATURES OF TUBERCLOSIS
• Persistent Cough (dry or mucopurulent sputum with haemoptysis)
• Dyspnea
• Chest pain
• Night sweats
• Anorexia
• Low grade Fever
• Weight loss
• Fatigue
MORPHOLOGY
• As sensitization develops, a 1- to 1.5-cm area of gray-white
inflammatory the Ghon focus .
• This combination of parenchymal lesion and nodal involvement is
referred to as the Ghon complex consolidation emerges.
• Hence, the Ghon complex undergoes progressive fibrosis, often
followed by radiologically detectable calcification (Ranke complex).
• On histologic examination, sites of active involvement are marked by
a characteristic granulomatous inflammatory reaction that forms both
caseating and noncaseating granulomas which consist of epithelioid
histiocytes and multinucleate giant cells.
CONSEQUENCES OF TUBERCLOSIS
• it induces hypersensitivity and increased resistance;
• the foci of scarring may harbor viable bacilli for years, perhaps for
life, and thus be the nidus for reactivation at a later time when host
defenses are compromised.
• it may lead to progressive primary tuberculosis.
• Hyalar lymphadenopathy
• Sometimes, pleural effusion
SECONDARY TUBERCLOSIS
• Also known as (Reactivation Tuberculosis) Secondary tuberculosis is the
pattern of disease that arises in a previously sensitized host. It may
follow shortly after primary tuberculosis, but more commonly it arises
from reactivation of dormant primary lesions many decades after initial
infection, particularly when host resistance is weakened.
• Secondary pulmonary tuberculosis is classically localized to the apex of
one or both upper lobes due to high oxygen tension in the apices.
• Cavitation occurs readily in the secondary form, leading to erosion into
and dissemination along airways becoming an important source of
infectivity, because the patient now produces sputum containing bacilli.
SECONDARY TUBERCULOSIS
LUNG TUMOR
• The four major histologic types of carcinomas of the lung are
• adenocarcinoma
• squamous cell carcinoma
• small cell carcinoma
• large cell carcinoma
• • Until recently, carcinomas of the lung were classified into two broad groups:
small cell lung cancer (SCLC) and non–small cell lung cancer (NSCLC), with the
latter including adenocarcinomas and squamous and large cell carcinomas.
• The key reason for this historical distinction was that virtually all SCLCs have
metastasized by the time of diagnosis and hence are not curable by surgery.
• Therefore, they are best treated by chemotherapy, with or without radiation
therapy. By contrast, NSCLCs were more likely to be resectable and usually
responded poorly to chemotherapy; however, now therapies are available that
target specific mutated gene products present in the various subtypes of
NSCLC, mainly in adenocarcinomas. Thus, NSCLC must be subclassified into
histologic and molecular subtypes.