RESPIRATORY TRACT

PATHOLOGY
BY DR. Mersha M.(MD.ASS.PROFF. OF PATHOLOGY)

04/27/2023 PATHOLOGY FOR PC II RT 1

Disease of upper airway
The upper airway includes nose, pharynx, & larynx
Nose
 Inflammations
Rhinitis
Infectious Rhinitis
 Commonly called common cold
 Common offenders are adenovirus, rhinoviruses,
echinovirus
 Evoke profuse catarrhal discharge
 Secondary bacterial infection…

2
04/27/2023 PATHOLOGY FOR PC II RT 2
Ctd…
Allergic rhinitis
It is an IGE mediated immune reaction i.e initiated by
sensitivity reactions to allergens
is usually complicated by Nasal polyps , it is focal
protrusion of mucosa which can ulcerate, infected or
can impair sinus discharge

3
04/27/2023 PATHOLOGY FOR PC II RT 3
Sinusitis
Commonly preceded by rhinitis
Impairment of drainage of the sinus by inflammatory
edema of mucosa
Etiologies are the normal flora of oral cavity
Complications include osteomyelitis & septic
thrombophlebitis

4
04/27/2023 PATHOLOGY FOR PC II RT 4
Nasopharynx
Inflammations
Pharyngitis & tonsillitis(tosilopharyngitis)
Frequent concomitants of viral infections
Commonest bacterial offender is beta hemolytic
streptococcus sometimes s.aureus
Pseudomembrane – exudative
May have a late sequale

5
04/27/2023 PATHOLOGY FOR PC II RT 5
Tumors
Tumors in these locations are infrequent, arise from the
mesenchym or epithelium
- Nasopharyngeal angiofibroma
- Sinonasal papillomas
- Isolated plasmacytoma
- Olifactory neuroblastomas
Nasopharyngeal carcinoma – may take one of the three
paterns
- Keratinizing scc
- Non-Keratinizing scc
- Undifferentiated carcinoma

6
04/27/2023 PATHOLOGY FOR PC II RT 6
Nasopharyngeal ca
Three factors affect its origin
- Heredty
- Age
- Infection with EBV
Common in Africa
Grow silently until they spread to LNs
Unlike keratinized,the undifferentiated ca is the most
radiosensitive

7
04/27/2023 PATHOLOGY FOR PC II RT 7
Nasopharynx
 Pharyngitis and tonsillitis are frequently viral .
 Etiology : rhinoviruses, echoviruses, and adenoviruses, and, less frequently, respiratory syncytial
viruses and influenza virus.
 Bacteria: β-­hemolytic streptococci, staphylococcus aureus.
 Late sequelae, such as
 Rheumatic fever
 Glomerulonephritis

04/27/2023 PATHOLOGY FOR PC II RT 8

 Pulmonary pathology

04/27/2023 PATHOLOGY FOR PC II RT 9

 Acquired diseases of the lung can be classified into four general categories:
(1) obstructive lung disease
(2) restrictive lung disease
(3) infectious disease
(4) neoplastic disease
The key clinical difference between obstructive and restrictive lung disease is the
forced expiratory volume at one second (FEV1) and the forced vital capacity (FVC)
ratio, which is decreased in obstructive lung disease and normal in restrictive lung
disease.

04/27/2023 PATHOLOGY FOR PC II RT 10

OBSTRUCTIVE , COPD
 Air is trapped within the parenchyma
 Emphysema, asthma, bronchiectasis, and
chronic bronchitis
RESTRICTIVE
 Airway filling is impaired due to fibrosis of
alveolar septae.
 Acute and chronic forms,
 chronic forms can be subdivided by
etiology (i.E., Work related, drug induced,
autoimmune, and idiopathic).

04/27/2023 PATHOLOGY FOR PC II RT 11

ATELECTASIS
 Atelectasis is collapse of the pulmonary parenchyma. (collapse or incomplete expansion of lung)
 Because of atelectasis, airways and alveoli are unable to fill, and blood is shunted from the arteries to
the veins without adequate oxygenation.
 Types :-
1.COMPRESSIVE ATELECTASIS
 A condition or lesion external to the lungs (i.e., in the pleural cavity) compresses the lung and
impairs filling of the alveoli upon respiration.
 Causes
 Hemothorax
 Pneumothorax
 Pulmonary edema
 Mediastinal shift away from the source of the atelectasis.

04/27/2023 PATHOLOGY FOR PC II RT 12

Atelectasis cont ‘
2. OBSTRUCTIVE ATELECTASIS (RESORPTIVE ATELECTASIS)
An obstruction in the airway impairs filling of alveoli.
All air in the alveoli is eventually resorbed and the alveoli collapse.
Causes
Aspirated foreign body, tumor, and mucus (e.g., in chronic bronchitis, brochiectasis, foreign body and cystic fibrosis).
Mediastinal shift toward the source of the atelectasis.
3. MICROATELECTASIS
Loss of surfactant.
Causes:
Prematurity,
interstitial inflammation,
postsurgical.
4. CONTRACTION ATELECTASIS
Due to localized or generalized fibrosis impairing the ability of the alveoli to expand and contract.
Cause:
Pulmonary fibrosis and scarring.
04/27/2023 PATHOLOGY FOR PC II RT 13
OBSTRUCTIVE LUNG DISEASE
Disease of the lungs that impairs the ability of air to leave the alveoli during
expiration trapping it.
It is clinically defined by the decreased FEV1/FVC ratio.
The residual volume and functional residual capacity (FRC) are increased, but the
total lung capacity may remain normal.
The condition eventually leads to hypercapnic respiratory failure, with pCO2 of>45
mm Hg.

04/27/2023 PATHOLOGY FOR PC II RT 14

EMPHYSEMA
 Permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by
destruction of their walls without significant fibrosis
 Types
Centriacinar (centrilobular) emphysema
 Affects central or proximal part of acini and spares the distal part except sever
 common in upper lobes
 Predominantly in heavy smokers in association with chronic bronchitis
 May coexist with coal worker’s pneumoconiosis
 Peribronchial and bronchiolar spaces commonly show inflammation

Panacinar (panlobular) emphysema

 Acini are uniformly enlarged from the level of respiratory bronchiole to terminal
blind alveolar sac
common in lower zones and anterior margin of lungs.
 Most severe at the bases
04/27/2023
Associated with a-1 antitrypsin (a-1 AT) deficiency
PATHOLOGY FOR PC II RT 15
 Paraseptal (distal acinar)
 Distal part of acinus is involved; proximal part is normal
 Localized along pleura and perilobular septae
 Usually seen in upper part of lungs; adjacent to areas of fibrosis and atelectasis
 Spontaneous pneumothorax is a common complication
 Characteristic finding is presence of multiple, continuous and enlarged airspaces
 0.5–2 cm, forming cyst-like structures.
Irregular (paracicatricial) emphysema
 Irregular involvement of acinus
 Usually asymptomatic and clinically insignificant

04/27/2023 PATHOLOGY FOR PC II RT 16

 Causes of emphysema

Alpha 1 anti trypsin deficiency

Imbalance in protease-antiprotease and oxidant-antioxidant.

cigarette smoking.

nicotine plays several roles.
Causes inactivation of antiproteases.
Production of ros
Complications of emphysema
■Pulmonary hypertension as a result of hypoxia-induced
vasospasm and loss of vascular surface area (i.e., losing alveolar septae causes loss of alveolar
capillaries).
■Cor pulmonale
■Mismatched ventilation-perfusion,with shunting of blood to areas of poor ventilation.
Morphology of emphysema: Dilation of airspaces; bullae formation at the pleural surface


04/27/2023 PATHOLOGY FOR PC II RT 17

 Clinical presentation of emphysema
Dyspnea, hypoxemia, hypercapnia, hyperventilation (patients are referred to as “pink
puffers”).
Weight loss (pulmonary cachexia)
digital clubbing
X- ray : Flattened diaphragm and expanded hyperlucent lung fields

04/27/2023 PATHOLOGY FOR PC II RT 18

ASTHMA
 Disease process characterized by episodic reversible bronchoconstriction of hyperreactive airways in
response to various exogenous and endogenous stimuli.
 Associated with chronic inflammation and mucus secretions.
Types of asthma
Atopic asthma
 Occurs more frequently in children.
 Patients may have hay fever or eczema.
 Mechanism : Type I hypersensitivity reaction.
 Causes:Pollens, dust, drugs.
■Non atopic asthma
 Occurs more frequently in adults.
 Mechanism : Not type I hypersensitivity reaction; IgE levels are normal.
 Causes:Exercise, cold air, drugs, gastroesophageal reflux, viral infections
 Drug-induced asthma.
 Occupational asthma.
04/27/2023 PATHOLOGY FOR PC II RT 19
Pathogenesis
Genetic predisposition to Type I hypersensitivity (atopy) and exposure to certain
environmental triggers (inhaled allergens
 TH2 cells induce bronchial inflammation and secrete cytokines

04/27/2023 PATHOLOGY FOR PC II RT 20

 Morphology of asthma
Hyperinflated lungs; mucous plugging of airways.
Hypertrophy of smooth muscle, increased collagen under basement membrane,
hyperplasia of mucous glands, and eosinophilic infiltrate;
Charcot-Leyden crystals (composed of major basic protein); and Curschmann
spirals (i.e., sloughed epithelial cells in mucous cast in the shape of airways).

04/27/2023 PATHOLOGY FOR PC II RT 21

Clinical presentation of asthma
Classic triad is persistent wheezing, chronic episodic dyspnea, and chronic
nonproductive cough.
Symptoms may be worse, or only present at night, due to the physiologic drop in
cortisol secretion.
Night-time cough, which may be the only symptom, is a classic symptom of asthma.
Dark rings under the eyes (“allergic shiners”) and a dark transverse crease on the
nose (“allergic salute”) are often seen, especially in children.
Status asthmaticusis a prolonged asthmatic attack, which can be fatal.

04/27/2023 PATHOLOGY FOR PC II RT 22

CHRONIC BRONCHITIS
Productive cough for at least 3 months in 2 consecutive years.
Pathogenesis related to cigarette smoking.
Complications of chronic bronchitis
Obstruction of the airway by mucus, leading to bronchiectasis or atelectasis.
Pulmonary hypertension.
Morphology of chronic bronchitis
■Gross:Mucous plugging.
■Microscopic:Submucosal gland hypertrophy

04/27/2023 PATHOLOGY FOR PC II RT 23

Clinical presentation of chronic bronchitis
Chronic productive cough;
Hypercapnia (patients are referred to as “blue bloaters”).
Can have asthmatic component (“asthmatic bronchitis

04/27/2023 PATHOLOGY FOR PC II RT 24

BRONCHIECTASIS

Bronchiectasis is the permanent dilation of bronchi and bronchioles caused by destruction of
smooth muscle and the supporting elastic tissue; it typically results from or is associated with
chronic necrotizing infections

Pathogenesis: Requires two components, infection and obstruction, each one of which can occur
first and start the disease process.

The infection results in destruction of the smooth muscle and elastic fibers in the wall of the
airway.

Causes
Allergic bronchopulmonary aspergillosis,
Cystic fibrosis,
kartagener syndrome
Necrotizing pulmonary infections leading to obstruction (e.G., Staphylococcus, klebsiella)
Tumors, foreign bodies,and mucus in the airways (e.G., From asthma, chronic bronchitis, cystic
fibrosis).

04/27/2023 PATHOLOGY FOR PC II RT 25

 
Complications of bronchiectasis
Hemoptysis, with potentially life-threatening hemorrhage.

Rarely, pulmonary hypertension,

Abscess formation,

Amyloidosis.


Morphology of bronchiectasis
Dilation of airways, usually involving lower lobes,

right side more often than left,

with airways almost extending to the pleural surface


Microscopic:Appearance depends upon stage, inflammatory infiltrate, and tissue
destruction
04/27/2023 PATHOLOGY FOR PC II RT 26
Clinical presentation of bronchiectasis
Dyspnea, chronic cough (dry, or with large amounts of purulent sputum production).
Hemoptysis is common.
Clubbing of the fingers (i.E.,Pulmonary osteoarthropathy)
Hypoxemia, and hypercapnia

04/27/2023 PATHOLOGY FOR PC II RT 27

RESTRICTIVE LUNG DISEASE( interstitial diseases)

Heterogeneous group of disorders characterized by bilateral, often patchy, pulmonary

fibrosis mainly affecting the walls of the alveoli
There are two categories of restrictive lung disease,
Extrapulmonary
Intrapulmonary.
Extrapulmonary sources include
Obesity and
Kyphoscoliosis, and externally impairing filling of the lung.
Intrapulmonary restrictive lung disease, two subcategories
Acute and chronic.
Acute restrictive lung disease is primarily confined to the diagnosis of acute respiratory
distress syndrome (ARDS).
Chronic restrictive lung disease is a broad group, which includes many distinct entities.
04/27/2023 PATHOLOGY FOR PC II RT 28
ACUTE RESTRICTIVE LUNG DISEASE

Develop over a short time period

 Usually secondary to a major systemic insult (e.G., Sepsis, shock),
 causes an acute restrictive lung disease,
Hypoxemic respiratory failure (po2 is 60 mm hg)
Diffuse pulmonary infiltrates, and
Not attributable to left sided heart failure.
The clinical term is acute respiratory distress syndrome (ARDS)
The pathologic term is diffuse alveolar damage

04/27/2023 PATHOLOGY FOR PC II RT 29

Pathogenesis of ARDS
Damage to the epithelium or endothelium causes the alveolar septae to become leaky
Allowing protein to enter the alveoli.
The epithelial cells undergo necrosis and slough into the alveoli.

04/27/2023 PATHOLOGY FOR PC II RT 30

  Main causes:
Severe pulmonary infection, aspiration, sepsis, and severe trauma with shock.
Other causes: Acute pancreatitis, fat emboli, viral infection (e.g., Hantavirus,
severe acute respiratory syndrome [SARS]).
Acute interstitial pneumonitis is diffuse alveolar damage of undetermined etiology.

04/27/2023 PATHOLOGY FOR PC II RT 31

CHRONIC RESTRICTIVE LUNG DISEASE
Chronic restrictive lung disease, also referred to as interstitial lung
disease, is characterized by
Chronic diffuse lung injury with inflammation and fibrosis
Impaired gas exchange (low diffusing capacity of lung for carbon monoxide
[DLCO]),
Decreased FEV1 and FVC, and
Normal FEV1 /FVC ratio.
Etiology:There are four general categories of causes of interstitial lung
disease,

04/27/2023 PATHOLOGY FOR PC II RT 32

 General Category Specific Causes
Autoimmune

Systemic lupus erythematosus
Wegener granulomatosis

Rheumatoid arthritis

Idiopathic

Idiopathic pneumonias (e.g., UIP, DIP)

Sarcoidosis

Work related

Asbestosis

Silica-induced lung disease

Coal-induced lung disease

Drug related

Bleomycin

Busulfan

Amiodarone

Methotrexate

04/27/2023 PATHOLOGY FOR PC II RT 33

Complications
Fibrosis
Pulmonary hypertension.
Morphology
Firm lungs.
Hyaline membranes in the exudative stage
type II pneumocyte hyperplasia in the proliferative stage; and fibrosis.
Clinical presentation of diffuse alveolar damage
Severe dyspnea and pink frothy sputum within 72 hours of exposure to an inciting
agent.
Diffuse crackles, hypoxemia, and diffuse alveolar infiltrates

04/27/2023 PATHOLOGY FOR PC II RT 34

 Clinical presentation of interstitial lung disease
Insidious onset of dyspnea on exertion and dry nonproductive cough;
Tachypnea.
Clubbing of fingers.
Signs and symptoms of right-sided heart failure may be present.

04/27/2023 PATHOLOGY FOR PC II RT 35

DIFFUSE PULMONARY HEMORRHAGE
Pulmonary hemorrhage is hemorrhage throughout the lung that may be secondary to
many cause:-
Coagulopathies,
Vasculitis,
Infections),
It may represent a primary disorder.
Two specific causes of primary diffuse pulmonary hemorrhage are
Goodpasture syndrome
Idiopathic pulmonary hemosiderosis

04/27/2023 PATHOLOGY FOR PC II RT 36

 GOODPASTURE SYNDROME

Pathogenesis:Type II hypersensitivity reaction with antibody versus alveolar and glomerular
basement membranes; specifically, the -3 chain of type IV collagen.

Male predominance.

Hemoptysis;

later, crescentic glomerulonephritis and renal failure, progressing to uremia and death.

Idiopathic pulmonary hemosiderosis
■No known cause.
■More common in children than in adults.

Microscopic morphology of the lung in Goodpasture syndrome and idiopathic pulmonary
hemosiderosis
Alveolar hemorrhage.
Hemosiderin-laden macrophages;
Fibrosis and type ii pneumocyte hyperplasia

04/27/2023 PATHOLOGY FOR PC II RT 37

PULMONARY HYPERTENSION
 An increase in blood pressure within the pulmonary circulation (25 mm Hg),
 Can be primary, but is most often secondary to another condition.
 Secondary causes of pulmonary hypertension:
 Cardiac,
 Inflammatory,
 Pulmonary, and
 Vascular.
 Primary pulmonary hypertension
 Age 20–40 years; female predominance.
 Pathogenesis : Possibly chronic vasoconstriction from vascular hyperreactivity;
 May be due to a mutation in the bone morphogenetic protein receptor 2 (BMPR2) gene, whose
protein product causes inhibition of proliferation of vascular smooth muscle and favors apoptosis of
the vascular smooth muscle.

04/27/2023 PATHOLOGY FOR PC II RT 38

PULMONARY INFECTIONS
The categories of pulmonary infections are:-
Community-acquired typical pneumonia
Community acquired atypical pneumonia
Nosocomial pneumonia
Aspiration pneumonia
Necrotizing pneumonia
Chronic pneumonia
Pneumonia in the immunocompromised patient
04/27/2023 PATHOLOGY FOR PC II RT 39
COMMUNITY-ACQUIRED TYPICAL PNEUMONIA


Acquired outside the hospital setting and often follows a viral upper respiratory tract
infection.
Bacteria (e.g.,Streptococcus pneumoniae,Staphylococcus aureus, Haemophilus influenzae,
and Klebsiella pneumoniae,which occurs in chronic alcoholics).
Two types of community-acquired typical pneumonia:
Bronchopneumonia

Lobar pneumonia

Bronchopneumonia
Patchy distribution of neutrophilic infiltrate and bacterial organisms in one or many lobes
Causative organisms:
Streptococcus pneumoniae
Klebsiella pneumoniae.

04/27/2023 PATHOLOGY FOR PC II RT 40

Mechanism
 Loss of the cough reflex,
 Injury to the mucociliary escalator
 Dysfunction of alveolar macrophages
 Pulmonary edema and congestion
 Accumulation of secretions.
 Specific risk factors for development of bronchopneumonia
 chronic medical condition (e.g., malignancy, cirrhosis, ischemic heart disease, neurodegenerative
disease).
 The extremes age
 Immunoglobin deficiency (e.g., leukemia, lymphoma).
 Absent spleen:encapsulated organisms.
 Patients may be postsplenectomy status due to trauma, or they may have had an autosplenectomy
as a result of sickle cell anemia

04/27/2023 PATHOLOGY FOR PC II RT 41

Lobar pneumonia
Pneumonia confined to one lobe of the lung
Causative organisms:Almost all cases are due to Streptococcus pneumoniae.
Risk factors: lobar pneumonia can arise in an otherwise healthy individual.
Morphologic stages of lobar pneumonia in order of development
■ Edema and congestion.
■ Red hepatization:Lobe is red and firm, and alveoli are filled with neutrophils,
fibrin, and red blood cells.
■ Grey hepatization:Red blood cells have lysed; fibrin and macrophages remain.
■ Resolution.

04/27/2023 PATHOLOGY FOR PC II RT 42

04/27/2023 PATHOLOGY FOR PC II RT 43
 Clinical presentation of CAP
Acute onset of fever, chills, rigors, productive cough, and pleuritic chest pain.
Rales, dullness to percussion may indicate consolidation or a pleural effusion.
Blood-tinged “currant jelly” sputum is classically associated with Klebsiella
pneumoniae.
X-ray:Infiltrates; consolidation, pleural effusion

04/27/2023 PATHOLOGY FOR PC II RT 44

 Complications of CAP:
■Abscess
■Empyema
■Fibrosis and scarring.
■Hematogenous dissemination resulting in meningitis, arthritis, and endocarditis.

04/27/2023 PATHOLOGY FOR PC II RT 45

COMMUNITY-ACQUIRED ATYPICAL PNEUMONIA
 Nonbacterial organism (excluding fungi)
 Acquired outside the hospital setting.
 So called cuz patients have only
 Moderate sputum production,
 No physical findings of consolidation,
 Lack of alveolar exudates,
 Only a moderate increase in the white blood cell count (unlike typical bacterial pneumonia).
 Causative organisms:
 Viruses (e.g., influenza A and B, respiratory syncytial virus, and adenovirus),Haemophilus parainfluenzae,
 Mycoplasma,andChlamydia pneumoniae.

 Complications :
 Bacterial superinfection.
 Most deaths due to influenza are caused by a secondary staph. Aureus

04/27/2023 PATHOLOGY FOR PC II RT 46

 NOSOCOMIAL PNEUMONIA
Pulmonary infection acquired while hospitalized; usually bacterial, but sometimes
fungal.
Causative organisms:gram-negative bacilli,pseudomonas,and, less
commonly,staphylococcus aureus.
Often multidrug-resistant to antibiotics.

04/27/2023 PATHOLOGY FOR PC II RT 47

 CHRONIC PNEUMONIA
Tuberculosis
Defn: TB is airborn a serious chronic pulmonary and systemic disease
caused most often by M. tuberculosis.
Risk factors
 poverty
Crowding
 chronic diseases

04/27/2023 PATHOLOGY FOR PC II RT 48

Pathogenesis
Entry into macrophages. By receptors expressed on the phagocyte, including mannose binding lectin and
CR3.
 Replication in macrophages. TB inhibits maturation of the phagosome and blocks formation of the
phagolysosome,
The TH1 response.
TH1-mediated macrophage activation and killing of bacteria by producing IFN-γ.
 IFN-γ
 Stimulates maturation of the phagolysosome
 Stimulates expression of inducible NO synthase
 mobilizes antimicrobial peptides (defensins) against the bacteria.
 stimulates autophagy, a process that sequesters and then destroys damaged organelles and intracellular
bacteria such as M. tuberculosis.

04/27/2023 PATHOLOGY FOR PC II RT 49

04/27/2023 PATHOLOGY FOR PC II RT 50
Clinical features
Primary TB:-

Previously unexposed and therefore unsensitized, person.

Resembles an acute bacterial pneumonia with consolidation of the lobe, hilar adenopathy, and
pleural effusion(ghon complex)

Lower part of the upper lobe/upper part of lower lobe

Lymphohematogenous dissemination:-TB meningitis and miliary TB

Secondary TB:
Previously sensitized host.
Follow shortly after primary tb /re infection/re activation
Apex of upper lobe lung
Cavitation
Regional LN less likely involved

04/27/2023 PATHOLOGY FOR PC II RT 51

04/27/2023 PATHOLOGY FOR PC II RT 52
 PULMONARY ABSCESS
Complication of pulmonary infections,
Other causes of a pulmonary abscess include
Bronchial obstruction,
Neoplasms
Septic emboli due to hematogenous dissemination from another source (e.G.,
Endocarditis).
Usually lower lobes (right side more frequently than left side).
Complications of lung abscess
 Pneumothorax, due to rupture into pleural cavity.

 Empyema

04/27/2023 PATHOLOGY FOR PC II RT 53

PULMONARY NEOPLASMS

Small cell and non–small cell carcinoma.

The importance of the small cell versus non–small cell designation is that small cell lung carcinoma is
considered to have already metastasized at the time of diagnosis; therefore, it is treated with radiation
and chemotherapy, and no further surgery.
About 85–90% of lung tumors arise in active smokers or those who have recently stopped smoking,
The favored sites of metastases for pulmonary neoplasms are, in descending order,
Liver
Brain
Bone
The three types of non–small cell carcinoma
Squamous cell carcinoma,
Adenocarcinoma,
Large cell carcinoma

04/27/2023 PATHOLOGY FOR PC II RT 54

 SQUAMOUS CELL CARCINOMA
Age 55–60 years or older; more common in males.
Location:Central or at or near the hilum of the lung
 Risk factors
 Cigarette smoking l---- squamous metaplasia---squamous dysplasia,--- carcinoma.
 Mutations: has the highest rate of p53 mutations among lung tumors
 can produce parathormone-like protein, which can result in hypercalcemia.
Morphology of squamous cell carcinoma
■Gross:Lung mass, which often cavitates due to necrosis.
■Microscopic:Keratin pearls and intercellular bridge

04/27/2023 PATHOLOGY FOR PC II RT 55

 ADENOCARCINOMA

Age younger than 45 years; female predominance. Non smokers

Location:Peripheral or at or near the pleural surface

Pathogenesis of adenocarcinoma
■Atypical adenomatous hyperplasia can lead to bronchioalveolar carcinoma, which
can lead to invasive adenocarcinoma.
Grows along the alveolar septae (referred to as lepidic growth)

No invasive component.


Can present in patchy distribution similar to pneumonia.
Classic symptom is bronchorrhea.


Microscopic :Infiltrative glandular formations; architecture includes papillary and
solid forms.
04/27/2023 PATHOLOGY FOR PC II RT 56
 LARGE CELL CARCINOMA
Most likely a poorly differentiated squamous cell carcinoma or adenocarcinoma.
Anaplasia inhibits determination of epithelial-type origin of tumor

04/27/2023 PATHOLOGY FOR PC II RT 57

 Small cell carcinoma
Older males.
Location:Central, along bronchi.
Risk factors : Smoking (99%)
Mutations:c-MYC,RB.
Associated paraneoplastic syndromes
■ can produce adrenocorticotropic hormone (ACTH), antidiuretic hormone (ADH), and
calcitonin-like substances.
■Clubbing of fingers.
■Lambert-Eaton syndrome,due to autoantibodies to neuronal calcium channels.
Microscopic : Small cells with little cytoplasm that have nuclear molding. Cells are
fragile and crush easily upon biopsy
04/27/2023 PATHOLOGY FOR PC II RT 58
 Complications of pulmonary neoplasms
■Partial obstruction of airway, predisposing to pneumonia.
■Complete obstruction of airway, leading to atelectasis.
■Suppurative bronchitis, can lead to bronchiectasis.
■Abscesses.
■Local extension can cause hoarseness (with involvement of recurrent laryngeal
nerve); local extension can also cause pleuritis and pericarditis

04/27/2023 PATHOLOGY FOR PC II RT 59

 ■Virchow node: Enlarged supraclavicular node; its presence is worrisome for
lung carcinoma.
■Superior vena cava syndrome:External compression of superior vena cava by
the tumor obstructs blood return to the heart from the upper body, resulting in
congestion and edema of the face and upper extremities.
■Pancoast tumor:Erosion of tumor through the apex of the lung can cause Horner
syndrome,with involvement of the cervical and brachial sympathetic ganglia.
The features of Horner syndrome are
 Ipsilateral enophthalmos (i.E., Recession of the eyeball within the orbit),
 Ptosis(i.E., Drooping of the eyelid),

 Meiosis(i.E., Pupil constriction), and

 Anhidrosis (i.E., Absence of sweating).

04/27/2023 PATHOLOGY FOR PC II RT 60

Clinical presentation
Depends upon location, size, metastases, and paraneoplastic syndromes.
Cough, hemoptysis, dyspnea, obstructive pneumonia, wheezing and stridor due to
airway obstruction, chest wall pain due to infiltration of chest wall and nerves, and
hoarseness due to involvement of recurrent laryngeal nerve.

04/27/2023 PATHOLOGY FOR PC II RT 61

PLEURAL EFFUSIONS
Transudate:Serous fluid; often due to left-sided heart failure.

Exudate:Most commonly due to pulmonary infections, carcinoma, infarction,
or viral pleuritis; occasionally due to connective tissue disorders and uremia.

Testing to determine source of exudate

If elevated red blood cell count, consider traumatic or malignant origin.
■If elevated white blood cell count, consider empyema
■If elevated eosinophil count, consider collagen vascular disease, pleural
air, or blood.
■If pH is 7.2, consider malignancy, rheumatoid arthritis, or infection.
■If amylase is elevated, consider esophageal rupture or acute pancreatitis.
04/27/2023 PATHOLOGY FOR PC II RT 62
04/27/2023 PATHOLOGY FOR PC II RT 63