BRONCHIAL ASTHMA

COPD
BRONCHITIS
BRONCHIECTASIS
EMPHYSEMA

DR. GIRISHMA SHRESTHA

MD, PATHOLOGY
LECTURER, PAHS
WEIGHT
LOBES
SEGMENTS
BRONCHI
ARTERIES,
pulmonary
ARTERIES,
bronchial
VEINS
PLEURA, visceral
PLEURA, parietal
NERVES
Bronchi
Bronchioles
Terminal
bronchioles
Alveolar ducts
Alveoli
Type 1
pneumocytes
Type 2
pneumocytes
Macrophages
Capillaries
N
O C
R X
M
A R
L
CHRONIC OBSTRUCTIVE LUNG
DISEASES
 CHRONIC OBSTRUCTIVE LUNG
DISEASES

Emphysema
Chronic bronchitis
Asthma
Bronchiectasis
Bronchial
Asthma
 ASTHMA

Asthma is a chronic inflammatory disorder of

the airways that causes recurrent episodes of
wheezing, breathlessness, chest tightness, and
cough, particularly at night and/or in the early
morning associated bronchoconstriction and
airflow limitation that is at least partly
reversible, either spontaneously or with
treatment.
 Asthma
• Chronic inflammatory disease of the airways.

• Under allergens’ influence.

• Increased airway responsiveness Episodic

reversible bronchial obstruction  dyspnea,
breathlessness, cough, wheezing, chest
tightness, rales.
 Some allergens which may cause
asthma
Spittle, excrements,
House-dust mites which live in hair and fur
carpets, mattresses and of domestic
upholstered furniture animals

Plant pollen

Dust of Food components

Pharmacological agents
book (stabilizers, genetically
(enzymes, antibiotics,
depo- modified products)
vaccines, serums)
sitories
• Patients may be virtually
asymptomatic in
between attacks.

• Rarely, status
asthmaticus, may be
fatal, a state of
unremitting attacks.
Normal Airway
Airway During Asthma Exacerbation
Atopic (evidence of allergen sensitization).
– Often in patients with a history of allergic rhinitis.

– Type I hypersensitivity : IgE-mediated.

– Positive family history.

– Skin test positive (wheal and flare reaction).

Non-atopic (without evidence of allergen sensitization).
• Viruses (e.g. rhinovirus, parainfluenza virus) rather than
bacteria are most common provokers.
• No positive family history.
• Normal serum Ig E levels.
• No other associated allergies.
• Skin test results for allergens are usually negative.
• Pathogenesis:
– Virus induced inflammation of the respiratory mucosa lowers the
threshold of the sub epithelial vagal receptors to irritants.
Drug-Induced Asthma :
– Aspirin sensitive asthma.

Occupational Asthma:
– Fumes, dusts, gases, formalin, penicillin.
 ASTHMA
PATHOGENESIS
• Exposure of presensitised IgE coated mast cells to
the airborne antigen stimulates cross linking of IgE
and the release of chemical mediators on the
mucosal surface.

• Direct stimulation of sub epithelial vagal receptors

provokes bronchoconstriction through both central
and local reflexes.

• This occurs within minutes after stimulation and is

called the acute or immediate response which
comprises of
– Bronchoconstriction
– Edema
– Mucus secretion
– Hypotension, in extreme circumstances
• Late phase reaction: mediated by the influx of
leucocytes including neutrophils, monocytes,
lymphocytes, basophils and eosinophils, recruited by
the chemotactic factors and cytokines derived from
the mast cells during the acute phase response.
MORPHOLOGY
• Gross:

– Lungs overdistended because of overinflation,

– Small areas of atelectasis may be present,

– Occlusion of bronchi and bronchioles by thick

tenacious mucous plugs.
Histopathology

– The mucus plugs contain whorls of

shed epithelium: Curschmann spirals.
– Numerous eosinophils and Charcot
leyden crystals (crystralloid made of
eosinophil membrane protein)
– Thickening of the basement
membrane of the bronchial
epithelium
– Edema and an inflammatoy infiltrate
in the bronchial walls with a
prominence of eosinophils and mast
cells.
– Increase in size of the submucosal
glands
– Hypertophy of the bronchial wall
muscle.
CLINICAL COURSE
• Acute asthmatic attack can last up to several
hours.
• Chest tightness, dyspnea, wheezing, cough.
• In severe forms, status asthmaticus, that persists
for days or even weeks may cause cyanosis and
even death.
• Difficulty in exhalation, elevated eosinophil
count,
• Charcot-Leyden crystals in the sputum.
• Appropriate therapy  productive life.
 BRONCHIECTASIS

Bronchiectasis is a disease characterized by

permanent dilation of bronchi and bronchioles
caused by destruction of the muscle and
elastic tissue, resulting from or associated
with chronic necrotizing infections.
• It may be either focal or diffuse

• Typically affects older individuals

• Approximately 2/3 of patients are women

Viruses : Adenovirus and Influenza virus (most common causing URTI
AND LRTI)

Infectious Causes
Bacterial infections, especially with potentially necrotizing organisms :
Staphylococcus aureus, Klebsiella, and Anaerobes

Bordetella pertussis : in childhood

HIV infection

Tuberculosis & nontuberculous

Impaired host defense mechanisms are often involved in the predisposition to recurrent
infections :

Localized impairment of host defenses is endobronchial

obstruction:-

Endobronchial neoplasms eg :carcinoid tumors .

Foreign-body aspiration.
Bronchostenosis : from impacted secretions or extrinsic
compression by enlarged lymph nodes
Generalized impairment of pulmonary defense mechanisms
occurs with:-

immunoglobulin deficiency
primary ciliary disorders
cystic fibrosis (CF)
 Etiology and Pathogenesis
Microorganisms such as Pseudomonas aeruginosa and Haemophilus influenzae
produce pigments, proteases, and other toxins that injure the respiratory
epithelium and impair mucociliary clearance

The dilated airways become more susceptible to colonization and growth of

bacteria

A reinforcing cycle can result, with inflammation producing airway damage,

impaired clearance of microorganisms, and further infection, which then
completes the cycle by inciting more inflammation.
 Clinical Manifestations

Persistent or recurrent cough and purulent sputum

Hemoptysis 50–70% of cases

Systemic symptoms  fatigue, weight loss, myalgias

Chronic cough and sputum production(if pneumonia )

May be insidious onset of symptoms

Some cases are either asymptomatic or have a nonproductive

cough  dry bronchiectasis in an upper lobe

Dyspnea or wheezing widespread bronchiectasis

With exacerbations of infection, the amount of sputum

increases, becomes more purulent and often more bloody;
systemic symptoms, including fever, may also be prominent.
Bronchiectasia of
the right middle
lobe
Bronchiectasia:
destruction of
pulmonary
parenchyma
Bronchopneumonia*
* *
and
lung abscesses**
with bronchiectasia

*
BRONCHIECTASIS
 COMPLICATIONS :

• Coughing up blood(massive hemoptysis)

• Low oxygen levels (in severe cases)arterial spasmpulmonary

hypertensionthickening of left heartCor pulmonale

• Recurrent pneumonia and other infections.

• Lung abscess
• Empiema of pleura
• Septicemia
• Meningitis
• Metastatic abscesses eg:in brain
 Major
Signs/Sympto
Clinical Term Anatomic Site Pathologic Etiology
ms
Changes
Mucous gland Tobacco
Chronic Cough, sputum
Bronchus hyperplasia, smoke, air
bronchitis production
hypersecretion pollutants
Persistent or Cough,
Airway dilation
Bronchiectasis Bronchus severe purulent
and scarring
infections sputum, fever
Smooth muscle
Immunologic or Episodic
hyperplasia,
Asthma Bronchus undefined wheezing,
excess mucus,
causes cough, dyspnea
inflammation
Airspace
Emphysema Acinus enlargement; Tobacco smoke Dyspnea
wall destruction
Tobacco
Small airway Inflammatory
smoke, air Cough,
disease, * Bronchiole scarring/obliter
pollutants, dyspnea
bronchiolitis ation
miscellaneous
 Pulmonary emphysema

• Definition
– Abnormal irreversible increase in airspace distal of
the terminal bronchioli, due to destruction of the
alveolar wall but without significant fibrosis
• Main types
– Centroacinar (centrolobular)
– Panacinar (panlobular)
Bullous emphysema
Pulmonary emphysema:
enlarged alveolar spaces
 Pulmonary emphysema

Pathogenesis

Disequilibrium between proteolytic activity of

elastase (released by neutrophils and
macrophages) and antiproteolytic activity of
a1-antitrypsin, leading to destruction of the
alveolar wall.
 antiprotease a1-antitrypsin
deficiency
a1-antitrypsin

smoking

Loss of elastic
recoil

elastase

macrophage neutrophil
Emphysema
Normal
condition

Bronchioles
and
lobules
Centroacinar
emphysema
Centroacinar emphysema
Panacinar
emphysema
Panacinar
emphysema
Bullous panacinar
emphysema
 Pulmonary emphysema

Other forms

- compensatory emphysema
- senile emphysema
- obstructve emphysema
- bullous emphysema
- interstitial emphysema
 Complications

• Pulmonary hypertension

• Right ventricular failure

 Natural defense mechanisms of the
respiratory system

• Warming and moistening of the air by the upper

airways
• Ciliated respiratory epithelium moves the mucus
layer upwards
• Bactericidal properties of the mucus
• Phagocytic activity of alveolar macrophages
 Chronic bronchitis

• Pathogenesis
- Chronic irritation by inhalation of different
substances (tobacco smoke, dust, etc...)
- repetitive infections
• Forms
- simple, without signs of obstruction
- obstructive type
 Chronic bronchitis
Morphological changes
– hyperplasia of mucin producing cells
– hyperplasia of smooth muscle cells
– squamous metaplasia of the respiratory
mucosa
– thickening of the epithelial basement
membrane
Chronic
bronchitis

Hyperplasia of
mucinous cells
and reserve cells et
Chronic
bronchitis

Thickened
basement
membrane

Bronchial biopsy
 Chronic
bronchitis

Squamous
metaplasia

Hyperplasia of
mucous glands
CHRONIC OBSTRUCTIVE PULMONARY
DISEASE (COPD)
• Emphysema
+
• Chronic Bronchitis
THANK YOU