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Normal Lung
The major function of the lung is to excrete
PATHOLOGY carbon dioxide from blood and replenish oxygen.
OF Trachea
RESPIRATORY SYSTEM Bronchi
Bronchiole
Terminal bronchioles
Acinus
Azham Purwandhono
Alveoli

Normal Lung Normal Lung

Nasopharyngeal Carcinoma

Nasopharyngeal Carcinoma

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Nasopharyngeal Carcinoma Nasopharyngeal Carcinoma

Distinctive geographic distribution Nasopharyngeal examination
Close anatomic relationship to lymphoid Fossa of Rosenmuller most common location
tissue Variable appearance - exophytic, submucosal
Association with EBV infection NP may appear normal
Nitrosamines - salted fish
Male > female
Young people YSR>>

Nasopharyngeal Carcinoma Nasopharyngeal Carcinoma

Three patterns
Keratinizing squamous cell carcinoma
Nonkeratinizing squamous cell carcinoma
Undifferentiated carcinoma

Clinical Features Clinical Features

Symptoms: Ears:
1. Nasopharyngeal tinnitus,
pain
2. Ears inconvenience
3. Eyes Serous otitis media tympani membran
4. Neural perforation
Unilateral Conductive Deafness
5. Metastasis or Neck

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Clinical Features
Nose:
Bloody rhinorheae,
post nasal drip, PNEUMONIA
epistaxis
unilateral/bilateral obstruction

Symptoms of ear, nose, headache >3 weeks

NPC suggested

PNEUMONIA
Pneumonias are broadly defined as any infection of
the lung parenchyma
Classified by the specific etiologic agent or the clinical
setting
One type of pneumonia (e.g., viral) often predisposes
to another type (e.g., bacterial) due to compromise of
systemic or specific pulmonary defenses
Although most pneumonias begin via the respiratory
tract, hematogenous spread from other sites can occur
Many patients with chronic diseases develop terminal
infections when hospitalized (nosocomial infections)
PNEUMONIA
Pulmonary infections occur when lung or systemic defenses
are impaired
These can be compromised by:
Decreased cough reflex leading to aspiration (e.g., coma,
anesthesia, neuromuscular disorders)
Injury to mucociliary apparatus (e.g., cigarette smoking, viral
infection, genetic defects)
Secretion accumulation (e.g., cystic fibrosis, chronic bronchitis)
Decreased phagocytic or bactericidal function of alveolar
macrophages (e.g., tobacco smoke, oxygen toxicity)
Edema or congestion (e.g., congestive heart failure)

Community-Acquired Acute Pneumonias LOBAR PNEUMONIA

Streptococcus pneumoniae, or pneumococcus : the most
common cause of community-acquired pneumonia.
Haemophilus influenzae can cause life-threatening lower
respiratory tract infections and meningitis in children and is
a common cause of pneumonia in adults, especially COPD
Staphylococcus aureus pneumonia often complicates viral
illnesses and has a high risk of abscess formation and
empyema
Klebsiella pneumoniae is the most common cause of Gram
negative pneumonia
Pseudomonas aeruginosa is a common cause of
nosocomial infections with a propensity to invade blood
vessels and spread systemicall

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LOBAR PNEUMONIA LOBAR PNEUMONIA

Four stages of the inflammatory response
Congestion
Red hepatization
Gray hepatization
Resolution

Stage of Congestion Stage of Congestion

initial stage of lobar pneumonia The lung is heavy, boggy, and red.
early acute inflammatory response It is characterized by vascular engorgement,
1 to 2 days intra-alveolar fluid with few neutrophils, and
often the presence of numerous bacteria

Stage of Congestion Stage of Red Hepatization

2 to 4 days
Massive confluent exudation with red cells
(congestion), neutrophils, and fibrin filling the
alveolar spaces.
The lobe now appears distinctly red, firm, and
airless, with a liver-like consistency, hence the
term hepatization.

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Stage of Red Hepatization Stage of Gray Hepatization

Progressive disintegration of red cells
The persistence of a fibrinosuppurative
exudate.
The gross appearance
A grayish brown, dry surface

Stage of Gray Hepatization Stage of Resolution

The consolidated exudate within the alveolar
spaces undergoes progressive enzymatic
digestion to produce a granular, semifluid,
debris that is resorbed, ingested by
macrophages, coughed up, or organized by
fibroblasts growing into it.

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BRONCHOPNEUMONIA

BRONCHOPNEUMONIA BRONCHOPNEUMONIA

BRONCHOPNEUMONIA
patchy areas of
pulmonary
consolidation
LUNG CANCER
confluent in the left
lower lobe on the
bottom left

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Lung cancer
Etiology and Pathogenesis
Cigarette smoking
Passive smoking increases the risk of developing
lung cancer to approximately twice that of
nonsmokers.
Industrial & environmental hazards
exposure to radioactive material, asbestos, nickel,
chromium, iron oxides and coal gas plants, radon
Molecular Genetics

Lung cancer Lung cancer

Molecular Genetics Lung cancer is currently the most frequently
K-ras oncogene mutations diagnosed major cancer in the world and the
25% of adenoca, 20% of large cell ca, and 5% of scc, rare in small cell ca most common cause of cancer mortality
Myc oncogene overexpression worldwide.
10% to 40% of small cell ca, rare in other types
Cancer of the lung occurs most often between
P53 suppresor gene mutations ages 40 and 70 years, with a peak incidence in
80% of small cell carcinomas and 50% of non-small cell carcinoma
the fifties or sixties.
Rb suppresor gene mutations
80% of small cell carcinomas and 25% of non-small cell carcinoma
The 5-year rate for all stages combined is only
Bcl-2 protooncogene expression 15%.
25% of squamous cell carcinomas and 5% of adenocarcinomas

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Lung cancer
Classification
Squamous cell carcinoma (25% to 40%)
Adenocarcinoma (25% to 40%)
Small cell carcinoma (20% to 25%)
Large cell carcinoma (10% to 15%)

Lung cancer Lung cancer

PATHOGENESIS

NORMAL BRONCHIAL MUCOSA

METAPLASTIC/DYSPLASTIC MUCOSA
CARCINOMA-IN-SITU (squamous, adeno)
INFILTRATING (i.e., INVASIVE) cancer

Lung cancer Lung cancer

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Squamous cell carcinoma of the lung Small cell carcinoma of the lung

Pancoast & Horner

CLINICAL FEATURE Syndrome
Clinical feature Pathologic basis
Cough, haemoptysis, dyspnoea, and Pulmonary symptoms
chest pain
Pneumonia, abscess, lobar collapse Tumor obstruction of airway
Pleural effusion Tumor spread into pleura
Hoarseness Recurrent laryngeal nerve invasion
Dysphagia Esophageal invasion
Diaphragm paralysis Phrenic nerve invasion
Rib destruction Chest wall invasion
SVC syndrome SVC compression by tumor
Horner syndrome Sympathetic ganglia invasion
Pericarditis, tamponade Pericardial involvement

PARANEOPLASTIC
SPREADING
SYNDROME
Local
invade locally either through the bronchial wall into the
surrounding lung or along the outside of the bronchi
Lymphatic spread
spread to the ipsilateral and contralateral peribronchial
and hilar lymph nodes.
Transcoelomic spread
Seed within the pleural cavity, causing a malignant pleural
effusion.
Haematogenous spread
to the brain, bone, liver, adrenal glands and skin

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LUNG CANCER STAGING LUNG CANCER STAGING

LUNG CANCER STAGING LUNG CANCER STAGING

SURVIVAL RATE TREATMENT

Surgical
Radiotherapy
chemotherapy

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METASTATIC TUMORS
LUNG is the MOST COMMON site for all
metastatic tumors, regardless of site of origin
most often from Ca breast, kidney, uterus, ovary,
testes and thyroid
Spread is usually via the blood
Bilateral deposits

CASE
A 48-year-old steelworker presented with a history of weight loss,
persistent cough, and occasional flecks of blood in his sputum. His
elder brother died 3 years ago from lung cancer.
On examination,
loss of the nailbed angle and increased fluctuation at the nailbed, a
feature known as finger clubbing.
dullness to percussion at the right lung base.
The liver was palpable three finger-breadths below the costal margin.
A chest radiograph showed shadowing in the right base of the lung
ultrasound showed multiple echogenic areas within the liver.
CASE
Blood biochemistry revealed deranged liver function tests,
ALP, indicating obstruction of biliary drainage.
Sputum was sent for cytological only inflammatory cells.
Microbiological culture grew Haemophilus influenzae
bronchoscopy showed obstruction of the right lower lobe
bronchus with bleeding.
Brushings for cytology showed only inflammatory cells but
a biopsy showed squamous cell carcinoma undermining the
bronchial mucosa.
Further imaging showed widespread metastases in hilar
and mediastinal lymph nodes.
The patients condition deteriorated rapidly and he died
within 3 weeks of presentation.

CASE CONCLUSION
Smoking is its main cause.
It has often metastasized by the time of
clinical presentation lymph nodes and liver. THANK YOU
Negative cytology (or biopsy) does not exclude
carcinoma.

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