ASTHMA

DEFINITION :
• Asthma is a chronic heterogeneous disease of the lower airways
characterized by chronic inflammation and airway hyper-
reactivity leading to cough, wheeze, difficulty in breathing, and
chest tightness.

• It is usually characterized by chronic airway inflammation,

bronchial reversible obstruction and hyperresponsiveness to
direct or indirect stimuli.
• CAUSES :

• Asthma triggers

• Exposure to various irritants and substances that trigger allergies (allergens)

can trigger signs and symptoms of asthma. Asthma triggers are different
from person to person and can include:

• Airborne allergens, such as pollen, dust mites, mold spores, pet dander
or particles of cockroach waste

• Respiratory infections, such as the common cold

• Physical activity

• Cold air

• Air pollutants and irritants, such as smoke

• Certain medications, including beta blockers, aspirin, and
nonsteroidal anti-inflammatory drugs, such as ibuprofen and
naproxen sodium

• Strong emotions and stress

• Preservatives added to some types of foods and beverages,

including, dried fruit, processed potatoes, beer and wine

• Gastroesophageal reflux disease (GERD), a condition in which

stomach acids back up into your throat
RISK FACTOR :
• Family history

• Viral respiratory
infections

• Allergies

• Occupational exposures

• Smoking

• Air Pollution

• Obesity
Types of Asthma:
a. Allergic Asthma (extrinic asthma)

b. Non-Allergic Asthma ( intrinsic asthma)

c. Mixed Asthma

d. Cough-Variant Asthma (very common in children)

e. Exercise Induced Asthma

f. Noctornal Asthma

g. Occupational Asthma
A. Allergic Asthma:

• When the symptoms are induced by a hyperimmune response to the inhalation

of specific allergens. Type –I (IMMEDIATE ) hypersensitivity reaction is the
basis of the IgE.

• When person come across an allergy trigger, our body makes molecules called
IgE antibodies. These trigger a series of reaction that cause swelling , runny nose
and sneezing.

• Extrinsic asthma symptoms occur in response to allergens, such as dust mites,

pollen, and mold. It is also called allergic asthma and is the most common form
of asthma.
 B. Non –Allergic Asthma:
• This type of asthma is triggered by the presence of irritants in the air that
are not related to allergies.
• This irritants stimulate parasympathetic nerve fibers in the airways
causing broncho-constriction and inflammation.

• Non-allergic asthma is triggered by factors other than allergens.

• These can include :
• Viral respiratory infections
• Exercise
• Irritants in the air
• Stress
• Drugs and certain food additives
• Weather conditions
C. Mixed Asthma:
• Mixed asthma is the combination of both allergic and non-
allergic asthma. This is the most common form of asthma.
D. COUGH –VARIANT ASTHMA:

• Cough variant asthma is a type of asthma that features a

dry, non productive cough.

• There may be no traditional asthma symptoms, such as

wheezing or shortness of breath.

• An ongoing cough is often the only symptom. Cough variant

asthma (CVA) is a common asthma variation in children.
E. EXERCISE INDUCE ASTHMA:

• Exercise-induced asthma is asthma that is triggered by vigorous or

prolonged exercise or physical exertion.

• Most people with chronic asthma experience symptoms of asthma during

exercise.
F. OCCUPATIONAL ASTHMA:

• People with this condition usually work around chemical fumes,

dust or other irritants in the air. If you’ve been diagnosed with
asthma that has another cause, it can be worsened by airborne
irritants at work.

• Triggers may include chemicals used in manufacturing; paints;

cleaning products; dusts from wood, grain and flour; latex
gloves; certain molds; animals; and insects.
Normal and Bronchial Asthma Tissues 
PATHOPHYSIOLOGY:
PATHOPHYSIOLOGY:
• Asthma is associated with T-helper cell type-2 (Th-2) immune responses.

• Its may include allergic and non-allergic stimuli.

• which produces a cascade of events leading to chronic-airway

inflammation.

• Elevated levels of Th-2 cells in airways releases specific cytokines including

IL-4,IL-5,IL-9 and IL-13 and promote eosinophilic inflammation and
immunoglobulin E (IgE) production.

• IgE production in turns triggers releate of inflammatory mediators,

• such as histamine and cysteinyl leukotrienes,

• that cause bronchospasm (contraction of the smooth muscle in the airways),

edema, and increased mucous secretion,

• which lead to the characteristic symptoms of asthma.

IL-4 drives Th2 IL-13 mediates goblet IL-4 and IL-13 play
cell differentiation cell hyperplasia and an important role in
and mediates the increased mucus class switching of B
production of secretion , and cells to produce IgE.
downstream Type promotes airway
2 cytokines obstruction , bronchial
hyperactivity, smooth
muscle hypertrophy ,
and airway
remodelling.

IL-5 mediates the differentiation of eosinophils in bone marrow;

IL-4 and IL-13 drive the tracking of eosinophils to sites of inflammation.
ALLERGIC-
ASTHMA

IL-4 drives Th2 cell differentiation

IL-4 and IL-13 promote class switching of B cells to produce IgE.
DIAGNOSIS:

• Patient history
• Physical Examination
• Chest X-ray
• Pulmonary Function Test
• Blood and Sputum Test
• Allergy Prick skin Test
• Spirometry Test
• FEV ( Force Expiratory Volume)
• FVC ( Force Vital Capacity)
Asthma diagnosis algorithm
DRUGS FOR ASTHMA:
 BRONCHODILATORS: Beta-2 agonists:
• Beta-2 agonists are bronchodilators that play an important role in asthma
control and treatment of acute exacerbations.

• They bind to the beta-2 adrenergic receptors on the bronchial smooth

muscle cells, causing smooth muscle relaxation and bronchodilation.

• Increased levels of energy –producing cAMP.

• This is done by competitively inhibiting phosphodiesterase(PDE) ,the

enzyme, that breaks the cAMP.

• Its result into decreased cAMP levels, cause SM relaxation,bronchodialation

and increased air flow.
 LEUKOTRIENE ANTAGONISTS:
• Leukotrienes are lipid mediators involved in bronchoconstriction and airway
inflammation.

• Leukotriene-modifying drugs, including zafirlukast, montelukast, and zileuton, work by

inhibiting leukotriene synthesis or as competitive antagonists of the leukotriene receptors.

• Cysteinyl leukotrienes are released from mast cells and eosinophils and are involved in bronchial
smooth muscle contraction and increased mucus secretion.

• By working as receptor antagonists and inhibiting leukotriene synthesis, these drugs

downregulate airway inflammation; they have also been shown to improve asthma
symptoms and lung function and serve as an add-on therapy to ICS.

• Current guidelines recommend the use of leukotriene receptor antagonists only as an

alternative treatment to ICS in those with moderate persistent asthma who cannot tolerate
ICS and as an add-on therapy to those receiving combined LABA/ICS.
MAST CELL STABILIZERS:
• Its inhibits degranulation of mast cells.

• Release of mediators like histamines,LT,IL is inhibited.

• Chemotaxis of inflammatory cells is inhibited.

• Bronchial hyperactivity of histamine is reduced.

• Bronchospam due to various stimuli is prevented.

• It can’t be used to prevent attack of asthma because it does not affect the
constrictor action.
 COTICOSTEROIDS:

• Corticosteroids are not bronchodialators.

• It is given as prophylactic medications,use alone or combined with

beta- agonists.

• Inhibition of phospholipase A2 , decreased prostaglandin and

leukotrienes.

• Mast cell stabilization ,decreased histamine release.

• Upregulation of beta2 receptors.

ANTI-IgE ANTIBODY:
• The drug omalizumab is actually a humanized monoclonal
antibody.

• It is administered I.M or S.C.

• It neutralizes free IgE in circulation without activating mast

cellls and other inflammatory cells.

• So IgE level in plasma is down and so,mast cell-IgE

mediated histamine release is inhibited.

• cause bronchoconstriction
Asthma comorbidities and stroke:
• Asthma is not an exception and there list of commonly encountered
comorbidities includes chronic rhinitis, chronic sinusitis/rhino-sinusitis,
gastro-esophageal reflux disease, obstructive sleep apnea/sleep-disordered
breathing, psychological disturbances (particularly depression and anxiety
disorders), chronic/recurrent respiratory infections, hyperventilation
syndrome, hormonal disturbances and other .
• There are also possible emerging comorbid conditions such as cardiovascular,
obesity, metabolic syndrome, diabetes mellitus, degenerative joint
disease/arthritis and psychiatric diseases.
• Some of these comorbidities lead to an increased risk of stroke and are highly
prevalent in asthma patient. This raises the question that the increased risk
of stroke in asthma patients may be due to confounding effect. Nevertheless,
the important point is that proper screening and diagnosis of comorbidities
in asthmatics is essential for preventing serious complications including
stroke.
 Bronchial Thermoplasty:
• Bronchial thermoplasty (BT) offers a nonpharmacologic therapy for
those with asthma unresponsive to standard treatment with ICS
and bronchodilators.
• Bronchial thermoplasty is a treatment for severe asthma approved by
the FDA in 2010 involving the delivery of controlled, therapeutic
radiofrequency energy to the airway wall, thus heating the tissue and
reducing the amount of smooth muscle present in the airway wall.

• BT uses thermal energy to bronchoscopically ablate airway smooth

muscles to decrease bronchoconstriction and airway hyperplasia.

• The effectiveness of this treatment was initially seen in the AIR

(ASTHMA INTERVENTION RESEARCH) trial in 2007, which
randomised patients with moderate or severe asthma to BT or a control
group.
• COPD is also known as chronic obstructive
lung disease (COLD), chronic obstructive
airway disease (COAD), chronic airflow
limitation (CAL) and chronic obstructive
respiratory disease (CORD)

• Chronic obstructive pulmonary disease (COPD)

refers to chronic bronchitis and emphysema, a
pair of two commonly co-existing diseases of
the lungs in which the airways become
narrowed. This leads to a limitation of the flow
of air to and from the lungs causing shortness
of breath.
• In COPD, less air flows in and out of the airways because of one or more of
the following:
• The airways and air sacs lose their elastic quality.
• The walls between many of the air sacs are destroyed.
• The walls of the airways become thick and inflamed.
• The airways make more mucus than usual, which tends to clog them.
1)Smoking
2) Occupational exposures- exposure to workplace dusts found in coal mining, gold mining,
and the cotton textile industry and chemicals such as cadmium, isocyanates, and fumes
from welding have been implicated in the development of airflow obstruction.
3) Air pollution
4) sudden airway constriction in response to inhaled irritants
5) Bronchial hyperresponsiveness is a characteristic of asthma.
6) Genetics-Alpha 1-antitrypsin deficiency is a genetic condition that is responsible
for about 2% of cases of COPD.
In this condition, the body does not make enough of a protein, alpha 1-
antitrypsin.
Alpha 1- antitrypsin protects the lungs from damage caused by protease enzymes,
such as elastase and trypsin that can be released as a result of an inflammatory
response to tobacco smoke.
 NUTRITION

INFECTIONS

SOCIO ECONOMIC STATUS

AGING POPULATION
Abnormal inflammatory response of the lungs due to toxic gases.

Response occurs in the airways parenchyma & pulmonary vasculature.

Narrowing of the airway takes place

Destruction of parenchyma leads to emphysema.

 Destruction of lung parenchyma leads to an imbalance of proteinases/anti
proteinases. (this proteinases inhibitors prevents the destructive process)

• Pulmonary vascularchanges
 Thickening of vessels
 Collagen deposit
 Destruction of capillary beds.

Mucus hypersecretion (cilia dysfunction, airflow limitation, corpulmonale(RVF))

Chronic cough and sputum production

• Chronic cough
• Sputum production
• Wheezing
• Chest tightness
• Dyspnoea on exertion
• Wt.loss
• Respiratory insufficiency
• Respiratory infections
• Barrel chest- chronic hyperinflation leads to loss of lung elasticity.
1) Bronchitis
2) Emphysema
Bronchitis :- Bronchitis (bron-KI-tis) is a condition in which the bronchial tubes
become inflamed.
• Acute (short term) and chronic (ongoing).
• Infections or lung irritants cause acute bronchitis.
• Chronic bronchitis is an ongoing serious condition. It occurs if the lining of the
bronchial tubes is constantly irritated and inflamed causing a long-term cough
with mucus.
• Chronic bronchitis: It is defined as the presence of cough and sputum
production for at least 3 months.
 Irritants irrritate the airway

Excess mucus production

Inflammation

Cause the mucus secreting glands and goblet cells to increase in number.
Ciliary function is reduced.

More mucus production

Bronchial walls become thickened and lumen narrows and mucus plug the airway
Alveoli adjacent to the bronchioles may become damaged and fibrosed.

Alter function of alveolar macrophages

infection
• sore throat,
• fatigue (tiredness),
• fever, body aches,
• stuffy or runny nose,
• vomiting, and
• Diarrhea
• persistent cough
• cough may produce clear mucus
• shortness of breath
• coughing,
• wheezing, and
• chest discomfort.
• The coughing may produce large amounts of mucus. This type of
cough often is called a smoker's cough.
• History - medical history
• Mucus -to see whether you have a bacterial infection
• chest x ray,
• lung function tests,
• CBC
• ABG ( arterial blood gas) analysis
• IMPROVE VENTILLATION
1. BRONCHO DILATORS LIKE BETA2 AGONISTS(ALBUTEROL),
2. ANTICHOLINERGIC S(IPRATROPIUM BROMIDE-ATROVENT).
3. METHYLXANTHINES(THEOPHYLLINE,AMIN OPHYLLINE)
4. CORTICOSTEROIDS
5. OXYGEN ADMINISTRATION
⦿ BULLECTOMY
BULLAE ARE ENLARGED AIRSPACES THAT DO NOT CONTRIBUTE TO
VENTILLATION BUT OCCUPY SPACE IN THE THORAX,THESE AREAS MAY
BE SURGICALLY EXCISED
⦿ LUNG VOLUME REDUCTION SURGERY
IT INVOLVES THE REMOVAL OF A PORTION OF THE DISEASED LUNG
PARENCHYMA.THIS ALLOWS THE FUNCTIONAL TISSUE TO EXPAND.
⦿ LUNG TRANSPLANTATION
⦿ Definition:-Emphysema is defined as enlargement of the air
spaces distal to the terminal bronchioles, with destruction of
their walls of the alveoli.
⦿ Pathology :
⦿ As the alveoli are destroyed the alveolar surface area in contact
with the capillaries decreases.
⦿ Causing dead spaces (no gas exchange takes place)
 Leads to hypoxia in later stages:

CO2 elimination is disturbed and increase in CO2 tension in arterial

blood causing

Respiratory acidosis

(Decrease pulmonary blood flow is increased forcing the RV to maintain high

B.P. in PA.)
• Centrilobular-The respiratory bronchiole (proximal and central part
of the acinus) is expanded.
• The distal acinus or alveoli are unchanged. Occurs more commonly
in the upper lobes.
• Panlobular -The entire respiratory acinus, from respiratory bronchiole to
alveoli, is expanded.
• Occurs more commonly in the lower lobes, especially basal segments, and
anterior margins of the lungs.
a. History
b. PFT
c. Spirometry-to find out airflow obstruction.
d. ABG analysis
e. CT scan of the lung.
f. Screening of alpha antitrypsin deficiency
g. X-ray radiography may aid in the diagnosis.
• IMPROVE VENTILLATION
1. BRONCHO DILATORS LIKE BETA2 AGONISTS(ALBUTEROL)
2. ANTICHOLINERGIC S(IPRATROPIUM BROMIDE-ATROVENT).
3. METHYLXANTHINES(THEOPHYLLINE,AMIN OPHYLLINE)
4. CORTICOSTEROIDS
5. OXYGEN ADMINISTRATION
• TAKE YOUR MEDICATIONS REGULARLY AS PRESCRIBED,IF
YOU HAVE ANY DOUBT RING YOUR HOSPITAL.
• EXERCISE REGULARLY EVERYDAY OR ELSE ATLEAST 4 OUT
OF 7 DAYS.
THANK
YOU!