Pulmonary infections /certified fixed orthodontic courses by Indian dental academy

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Lung
Type I
pneumocyte

Type I
pneumocyte
Alveolar
space

Capillary
lumen
Type II
pneumocyte
Endothelium

Pneumonia
• Pathology:
– Alveolar

–

• Bronchopneumonia
(Streptococcus pneumoniae,
Haemophilus influenza,
Staphylococcus aureus)
• Lobar (Streptococcus
pneumoniae)
Interstitial (Influenza virus,
Mycoplasma pneumoniae)

• Pathogenesis
– Inhalation of air droplets
– Aspiration of infected
secretions or objects
– Hematogenous spread

Pulmonary infections
Predisposing factors
• Decreased cough reflex
• Injury to cilia
• Decreased function of
alveolar macrophages
• Edema or congestion
• Retention of secretions


Lung abscess
• Localized suppurative necrosis
• Organisms commonly cultured:
–
–
–
–
–

Staphylococci
Streptococci
Gram-negative
Anaerobes
Frequent mixed infections

• Pathogenesis:
–
–
–
–
–

Aspiration
Pneumonia
Septic emboli
Tumors
Direct infection


Pulmonary tuberculosis
• Caused by Mycobacterium
tuberculosis.
• Transmitted through inhalation
of infected droplets
• Primary
– Single granuloma within
parenchyma and hilar lymph
nodes (Ghon complex).
• Infection does not progress
(most common).
• Progressive primary
pneumonia
• Miliary dissemination (blood
stream).

Pulmonary tuberculosis
• Secondary

– Infection (mostly through
reactivation) in a previously
sensitized individual.
– Pathology
• Cavitary fibrocaseous
lesions
• Bronchopneumonia
• Miliary TB

Fibrocaseous


Miliary

Granuloma

Mycobacterium

Opportunistic pneumonias
• Infections that affect
immunosuppressed patients
• Associated disorders:
– AIDS
– Iatrogenic
• Cancer patients
• Transplant recipients
Aspergillus

Pneumocystis carinii


Cytomegalovirus

Chronic obstructive pulmonary disease (COPD)

Chronic bronchitis

• Definition
– Persistent cough with sputum
production for:
– at least 3 months,
– in at least 2 consecutive years.

• Pathology
– Inflammation of airways
– Hyperplasia of mucous producing
cells
– Squamous metaplasia
– Injury to cilia


Chronic obstructive pulmonary disease (COPD)

Emphysema

• Destructive enlargement of
airspaces distal to terminal
bronchioles
• Two main types

Normal acinar
unit
Centriacinar
emphysema

– Centriacinar
• Destruction of central portion
with sparing of distal airways
• Upper lobes > lower
• Cause: smoking
– Panacinar
• Unform injury
• Lower lobes > upper
• Cause: alpha-1-antitrypsin
deficiency

Panacinar
emphysema


Neutrophils

Alpha-1-AT

Bronchiectasis
• Dilatation of bronchi
and bronchioles
secondary to chronic
inflammation
• Associated conditions
–
–
–
–

Obstruction
Cystic fibrosis
Immotile cilia syndromes
Necrotizing pneumonia


Bronchial Asthma
• Chronic inflammatory disorder of the airways resulting
in contraction of bronchial muscle
• Types
– Extrinsic (atopic, allergic).
• Allergens: food, pollen, dust, etc.

– Intrinsic (non-atopic)
• Initiated by infections, drugs, pollutants, chemical irritants

ATOPIC ASTHMA
Allergen
IgE

Mucus
secretion

Mast cell

Epithelial cell injury

Muscle
contraction

Mucus
secretion

Muscle contraction
Release of inflammatory
mediators
Recruitment of leukocytes

Acute phase


Late-phase

Atelectasis
• Collapse or incomplete expansion
of part or all of the lung
• Types:
– Resorption (obstruction of airway).
– Compressive (pleural effusion or
pneumothorax)


Pulmonary edema
Oncotic pressure

Hydrostatic pressure
Normal

Oncotic pressure

Causes:
- Heart failure
- Mitral stenosis


Causes:
- Infections
- Aspiration
- Drugs
- Radiation

Oncotic pressure

Microvascular injury

Causes:
- Nephrotic
syndrome
- Liver diseases

Diffuse alveolar damage
• Acute respiratory distress syndrome
(respiratory failure and arterial
hypoxemia refractory to O2 therapy).
• Basic lesions: injury to pneumocytes
and endothelial cells by:
– Oxygen-derived free radicals
– Activated neutrophils and macrophages
– Loss of surfactant.

• Etiology:
–
–
–
–

Exudative stage

Infections (viral)
Gas inhalation or liquid aspiration
Drugs, chemical, radiation
Hypotension, sepsis, trauma

• Pathology:
– Acute (exudative) stage
– Proliferative or organizing stage

Proliferative stage


Pulmonary embolism
• Most emboli arise in veins from the
legs
• Large emboli (10%) are a cause of
sudden death
• Small emboli (70%) may be:
– Clinically silent
– Cause infarctions (in patients with heart
failure).
– Cause hemoptysis

• Medium sized emboli (20%)
generally cause infarctions.


Infarct

Pulmonary hypertension
• Secondary (most common):
– Chronic obstructive pulmonary
disease
– Chronic interstitial pulmonary
disorders
– Chronic heart failure
– Recurrent pulmonary emboli

Expected luminal opening
in normal individual

Plexiform changes

• Primary (idiopathic)


Hypersensitivity pneumonitis
• Immunologically mediated disorder affecting
airways and interstitium.

Farmer’s lung
Thermophilic actinomycetes in hay

Pigeon Air-condition lung
breeder’s Thermophilic bacteria


Usual interstitial pneumonia /
idiopathic pulmonary fibrosis
• Progressive fibrosing disorder of of unknown cause
• Adults 30 to 50 y/o
• Respiratory and heart failure (cor pulmonale) ~ 5 y


Pneumoconioses
• Disorders caused by inhalation
of inorganic elements,
primarily metals.
• Injury is determined by:
– Length of exposure
– Physicochemical characteristics
– Host factors

• Carbon dust - Coal worker’s
pneumoconiosis:
– Anthracosis
– Simple coal worker’s
pneumoconiosis
– Progressive massive fibrosis

• Silicosis

– Silicotic nodules

• Asbestos

– Asbestosis (pulmonary fibrosis)
– Pleural disease (fibrous plaques,
mesothelioma).


Carcinoma of the Lung
• 6.5 % of all deaths
• #1 cause of cancer deaths in males & females
– 31% of male cancer deaths in 2001
• 90,367 deaths

– 25% of female cancer deaths
• 65,506 deaths


Lung cancer

Lung cancer in
males


Lung cancer in
females

Cancer Deaths estimated for 2004
Sites

New Cases

Deaths

ALL

1,368,300

563,700

Lung

173,770

160,440

Colon-Rectum

146,940

56,808

Breast

217,440

40,580

Prostate

230,110

29,900


Smoking-related diseases


Annual death rate for lung cancer


Causes of Lung Cancer
• 85-95% smoking
• 1%asbestos + smoking (estimate)
• Rare arsenic, chromium, mustard gas, nickel,
vinyl chloride, bis (chloromethyl) ether
• Speculation
– 0.3-3% passive smoking
– 3-14% radon

Classification of Lung Carcinoma
(Major Types)
• Squamous cell carcinoma
35%
• Adenocarcinoma
30%
• Small cell carcinoma
25%


Squamous cell carcinoma

•
•
•
•
•
•
•

Frequency: 35%
Smoking: X 25 (increased risk)
Males > females
Survival (5 years): 15 - 20%
Arises in bronchial squamous metaplasia
Centrally located
May cavitate

Adenocarcinoma

•
•
•
•
•

Frequency: 30%
Smoking: X 3 (increased risk)
Males < females
Survival (5 years): 15 - 20%
Peripheral

Bronchioloalveolar carcinoma

•
•
•
•
•

Frequency: 2 %
Smoking: yes
Males = females
Survival (5 years): 25 a 40 %.
Presentation:
– Single or multiple tumor nodules
– Miliary tumor
– “Pneumonic form”

Small cell carcinoma

•
•
•
•

Frequency: 25 %
Smoking: 95% of patients
Males >> females
Survival (5 years): 1 - 5 %.

Large Cell Carcinoma
• Frequency: 10 %
• Gross
– Peripheral lesion

• Microscopic
– Wastebasket group of tumors that do not fit the
criteria of a squamous cell carcinoma,
adenocarcinoma, or small cell carcinoma

• Prognosis
– Similar to adenocarcinoma

100
pa tie nts

35
ope ra ble

25-30
re se cte d for cure
8-12
survive for 5 ye a rs
( 3 0 % of those re se cte d for cure )

Mesothelioma
• Mesothelioma:
– Malignant tumor of
mesothelial cells
– Highly malignant
neoplasm with short
survival
– Most patients (70%)
have an asbestos
exposure history

• Asbestos exposure
also increases the risk
of pulmonary cancer
• Smoking is not related
to mesothelioma

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