BRONCHIAL ASTHMA

Felistus
LEARNING OUTCOMES
At the end of the lesson, the learner should be able to: -
1) Describe the causes of asthma
2) Describe the pathogenesis and pathophysiology of
asthma
3) Investigate a patient with asthma
4) Discuss complications of asthma
INTRODUCTION
 Bronchial asthma is a chronic relapsing inflammatory
disorder characterized by increased responsiveness of
the tracheobronchial tree to various stimuli
 This results in widespread paroxysmal contraction of
bronchial airways due to muscular spasms and
plugging by increased thick mucous secretions from the
mucosal glands.
 The respiratory tree is drawn longer with a reduced
diameter forming a physiological valve mechanism that
leads to easy or normal inspiration and difficult and
prolonged expiration.
 The short inspiration and long expiration produces the
characteristic wheeze/rhonchi in bronchial asthma.
 Asthmatic attacks cause shortness of
breath and wheezing respirations
 There is restricted movement of air
through tightly constricted air passages.
The bronchial spasms exert great effect on
expiration than inspiration because the
caliber of bronchioles varies with the phase
of respiration
AETIOLOGY
 The aetiology is unclear but associations exist with
genetic makeup, atopy or allergy and increased
responsiveness of the airways.
THE PRECIPITANTS
 occupational sensitizes,allergens,
infections and non-specific e.g. cold air,
exercise, diet, atmospheric
pollution/irritants, dust, vapours, fumes,
emotion, drugs e.g. NSAIDS
AETIOLOGICAL CLASSIFICATION
1. Extrinsic (atopic, allergic) asthma
2. Intrinsic (cryptogenic, non-atopic, idiosyncratic) asthma.
3. Exercise induced asthma
4. Drug induced
5. Occupational asthma
6. Asthma associated with COPD
1. EXTRINSIC (ATOPIC, ALLERGIC)
ASTHMA
 definite cause
It is commonest type of asthma and has a
associated with the disease as it runs in families
and individuals with history of allergy.
 The individuals may have a history of diseases
such as rhinitis, urticaria and infantile eczema.
 It begins in childhood and early adult life. Those
predispose have increased levels of IgE
representing type I hypersensitivity reaction
mechanisms and show characteristic whealing
skin reactions to common allergens in the
environment
PATHOGENESIS
 Exposure of pre-sensitized IgE coated mast cells to
allergens (antigens) results in release of chemical
mediators
 There is opening of the intercellular tight junctions
thereby enhancing penetration of the mast cells by
antigens to reach the numerous submusocal mast cells.
 Direct stimulation of the subepithelial vagal
(parasympathetic) receptors provokes
bronchoconstriction through both central and local
reflexes.
 This is an acute or immediate response, which consists
of bronchoconstriction, oedema, mucous secretion
and in severe cases hypotension
 Mast cells release cytokines, which result in influx of
leucocytes that mediate the late phase reaction together
with recruited chemotaxic factors. (neutrophils,
monocytes, lymphocytes, basophils and oesinophils)
Other sources of mediators of the late phase reaction
include the vascular endothelium and airway
epithelial cells (produce cytokines in response to
infection, drugs and gases
2. INTRINSIC ASTHMA (NON-ATOPIC)
 Intrinsic asthma develops in adult life
starting during the middle age and is
commonly associated with chronic
bronchitis.
 There is a negative family history of the
disease as well as personal history of
allergy
3. DRUG INDUCED
 Drugs such as aspirin trigger asthma by
inhibiting COX pathway of arachidonic
acid metabolism
 It does not affect the lipoxygenase route
thus resulting in increased production of
bronchoconstritive leukotrienes.
4. EXERCISE INDUCED
 Is a phenomenon that can occur in isolation
or in association with any type of asthma.
 Patients experience airway obstruction, 5 to
20 minutes after completing the exercise or
in the course of itby a mechanism that
seems to include the cooling, the relative
dryness of the airway secondary to
increased ventilation and loss heat the air.
5.OCCUPATIONAL ASTHMA
Occupational asthma is stimulated by
fumes (epoxy resin, plastics), organic and
chemical dusts (wood, cotton, platinum),
gases (toluene), chemicals (formaldehyde
and penicillin products).
PATHOGENESIS
 The pathogenesis of bronchial asthma
pivots around:-
airway hypersensitivity,
inflammation and
airway obstruction
A. AIRWAY HYPERSENSITIVITY
 There is increased responsiveness of the respiratory
airways of the lung to allergens in the environment
whose inhalation triggers an immediate acute response
initiated by IgE sensitised mast cells in the mucosal
surface of the respiratory tree.
 The mast cells degranulate releasing mediators of
inflammation such as histamine, leukotrienes,
prostaglandins and platelet aggregating factor (PAF) and
chemostatic factors for oesinophils and neutrophils.
 The respiratory tree is hypersensitive to normal
allergens, which can trigger off reactions. These
allergens include inhaled and non-inhaled ones.
 The inhaled allergens include - aeroallergens
(house dust mites, pollens, animal dander and
fungal spores) air pollution, extreme cold.
 The non-inhaled are exercise and ingested
substances
B. INFLAMMATION
 An inflammatory reaction ensues causing
oedema formation, bronchoconstriction and
hypersecretion of mucous and accumulation of
oesinophils and neutrophils.
 There is infiltration of the airways with
inflammatory cells, T-helper lymphocytes,
oesinophils and mast cells, which is a common
feature in asthma.
C. AIRWAY OBSTRUCTION
The pathologic basis of airway obstruction is: -
1. Constriction of the airway’s smooth muscles
due to release of bioactive mediators and
neurotransmitters.
2. Thickening of the airway epithelium due to
oedema formation
3. Presence of liquids and mucous secretions
within the confines of the bronchial lumen
CELLS INVOLVED
 During this reaction, the following inflammatory
cells are involved
Mast cells
Epithelial cells
Inflammatory cells
Macrophages, monocytes and oesinophils
PATHOPHYSIOLOGIC CHANGES IN
ASTHMA
1. Airway obstruction due to smooth muscle
constriction, thickening of the airway
epithelium or free liquid within the
airways.
2. Increased resistance to airflow due to
increased resistance within the airways
3. Reduced flow rate throughout the vital
capacity
PATHOLOGY
Macroscopy (at autopsy)
 Overinflated lungs that do not deflate
when the thorax is opened
 Widespread plugging of airways with
thick mucous
PATHOLOGY
Microscopy
 Desquamation of the epithelium
 Hypertrophy of smooth muscle

 Thickening of the basement membrane

 Infiltration by oesinophils and inflammatory

cells
 Hyperplasia of mucosal glands
CONT…
 Goblet cell metaplasia
 Curschmann’s spirals – mucosal plugs containing normal
or desquamated epithelium forming twisted strips.
 Charcot Leyden crystals – sputum containing numerous
oesinophils and diamond shaped crystals derived from
eosinophils.
CLINICAL FEATURES
Depends with age, severity, duration of
disease, amount and nature of treatment
and presence of complications.
 Main Features include – cough, headache,
difficulty in breathing, hyperventilation,
wheezing and chest pain/tightness
Severe asthma
 Inability to complete a sentence in one
breath
 Respiratory rate > 25 breaths per minute
 Tachycardia > 110 (pulsus paradoxicus)
 PEFR< 50% of predicted normal best
 Lifethreatening asthma
Silent chest, cyanosis or feeble
respiratory effort
Exhaustion, confusion or coma
Bradycardia, hypotension
PEFR< 30%
DIFFERENTIAL DIAGNOSIS
1. Acute bronchiolitis (infections, chemical)
2. Aspiration (foreign body)
3. Bronchial stenosis
4. Cardiac failure
5. Chronic bronchitis
6. Cystic fibrosis
7. Eosinophilia pneumonia
INVESTIGATIONS
1. Lung Function tests – diagnosis of asthma is based on
demonstration of a > 15% improvement I FEV1 or PEFR
following inhalation of a bronchodilator.
 Peak flow charts – take PEFR on walking, middle of the
day and before bed.
 Reduced FEV1
2. Exercise tolerance
3. Analysis of arterial gases
Check for the partial pressures of oxygen and carbon
dioxide (normal - oxygen PaO2 is over 12 kPa (90
mmHg) and PaCO2 is less than 6.0 kPa (45 mmHg).
This is reversed in asthma due to carbon dioxide retention
resulting from the physiological valve.
4. Haemogram - increased haemoglobin, normal WBC
(only increase in the presence of an infection),
eosinophils> 0.4 x 109/L
5. Sputum Examination - Charcot Leyden spirals,
Curschmann’s crystals, White blood cells
6. Bronchial provocation test (is not done if the FEV1 is <
1.5 litres)
7. Chest X-ray - shows hyperinflation, depressed
diaphragm and excludes pneumothorax (a complication)
8. Skin test
9. Allergen provocation test
COMPLICATIONS
 1. Pneumothorax
 2. Pneumomediastinum

 3. Respiratory failure

 4. Heart failure/CCF/Cor Pulmonale

 5. COPD