Mansoura UniversityMansoura-Manchester Medical

ProgramFaculty of Medicine

2 nd year

Semester III

Abstract

Bronchial asthma is a common disease that develop over time. It occur mainly in developing country that usually have a chronic air pollution. There are two type of bronchial asthma:

Atopic (extrinsic) Implying as definite external cause

Non-atopic (intrinsic) When no causative agent can be identified

This is important for parent to be fully understand deeply about this disease. This is because, bronchial asthma usually present on children at age 3-5 year old, but it also important for an adult to take note because the bronchial asthma that present during their childhood might get worsen or improve when they aged.

This essay i will explain more about bronchial asthma and its clinical factor in order to make rational diagnosis and its management. Here also included its pharmacology at glance for the treatment of bronchial asthma. There also information, data, flow chart and table that presented in this essay were base on my research and further study of the topic. Hope this essay will make easier for other to understand.

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Acknowledgment

“In the Name of Allah, Most Gracious, Most Merciful”

Alhamdullilah, thank to Allah swt that gave permission, strength, health and time for me to complete this essay within time. Also warmly thanks to my PBL doctor Dr Mohamed Abdul Monaem, whom not only guide me on this topic but also help me to fully understand during classes.

Not forgetting my parent, especially Dr Abdullah Zawawi that guide me each time I face hard time on writing this topic. Also thank to Dr. El-Said Abdel-Hady, the coordinator of Mansoura-Manchester Programme, for his beneficial guidance during first step on writing essay through his lecture on how to write an essay.

I would like to show my gratitude to my roommate Siti Nur Batrisyia binti Muhammad Roslan that help me on this essay. Lastly thank to other that also

contribute on this essay.

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Content

Title Page number

ABSTRACT

ACKNOLEDGMENT

TABLE OF CONTENT

INTRODUCTION

o Anatomy of the lung

o Histology of the bronchus

LITERATURE REVIEW

o Epidemiology of Bronchial Asthma

o Pathophysiology

o Classification of Bronchial Asthma

Aetiology

Severity

o Pathology

Aetiology

Pathogenesis

Morphology

o Clinical Aspect

Sign & Symptoms

Investigation

Diagnosis

Management

Treatment

SUMMARY AND CONCLUSION

REFERENCES

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Introduction

Asthma is a common chronic inflammation disorder of the airway that cause recurrent episode of wheezing, breathlessness, chest tightness or cough, particularly night and/or early in the morning. These symptom usually associated with widespread but variable bronchoconstriction and airflow limitation that is at least partly reversible.

It is important to research and explore this topic because Asthma because number of asthma patient is increasing around the world, mainly in the urban country and in the poor environment country.

As the asthma listed in the one of the main chronic disease worldwide, it is important to understand deeply it manifestation and pathogenesis, in term of cost for health resource as well as risk for loss of productivity due to the disease.

After you read this essay you may answer, how high are the risk? What kind of manifestations appear due to asthma? Is the health-related quality of life effected by this disease? Pathogenesis of asthma and it manifestation will be discussed in here.

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Anatomy

A pair of respiratory organs for exchanged of CO2 and O2 between alveolar and blood capillary. The lung situated in the pleura cavities separated from each other by mediastinum. The lung is conical in shape and has dark gray colour, spongy texture and weight about 600 gm. It has an apex (above), base (below) and surface (costal and medial) and 3 borders (anterior, posterior and inferior)

Apex of the lung projects up through thoracic inlet into root of neck. It reach about 1 inch above medial 1/3 of clavicle, and covered by cervical pleura and suprapleural membrane. Grooved anteriorly by subclavian artery. The base of lung concave and rests on convex surface of diaphragm. The right lung is separated from right lobe of liver and left lung from the left lobe of liver, and separated fundus of stomach and spleen. Right lung is deeper than the left lung.

On the costal surface or lateral surface of the lung, which is smooth and grooved by overlaying ribs and related also to intercostals spaces; which contain intercostals muscles, vessels and nerves. On medial surface, its divided into medialstinal surface that anteriorly and contain helium of the lung and related to pericardium.

Anterior border of the lung is sharp and thin, it separate costal and medial surface anteriorly. It also has a cardiac notch in the left lung and thin projection below called lingula. Posterior border of the lung is thick and rounded, it separate costal and medial surface posteriorly. It extends from spine of C7 till spine of T10 and related to heads of ribs and sympathetic trunk. Inferior border of the lung is thin and sharp, it separate base from costal and medial surface. It extends down into costodiaphragmatic recesses during deep inspiration.

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Histology

Bronchus is divide into 2 part, conducting and respiratory passage. The conducting passage include bronchi and bronchioles, and the respiratory passage contain respiratory bronchioles.

Bronchi (A)o The trachea bifurcates into two primary bronchi, which enter the lung

and then branch several times to give rise to smaller secondary and tertiary bronchi. Bronchi differ from the trachea in having plates rather than rings of cartilage, and in having a layer of smooth muscle between the lamina propria and submucosa. In smaller branches, the amount of cartilage decreases, whereas the amount of smooth muscle increases. Also, the number of glands and goblet cells decreases.

Bronchioles (B)o Bronchioles are smaller branches of the bronchi, and are

distinguished from them by the absence of cartilage and glands. In larger bronchioles, the epithelium is still ciliated, but is now usually simple columnar, whereas in the smallest bronchioles, the epithelium will be simple cuboidal (mostly Clara cells) and lack cilia altogether. The smooth muscle layer is generally quite prominent in these structures as demonstrated in where the bronchiole was cut in a grazing longitudinal section allowing you to see the circularly arranged bundles of smooth muscle in the bronchiolar wall. As mentioned above, the smallest conducting bronchioles consist of a simple cuboidal (or perhaps “low columnar”) epithelium of mostly Clara cells, a few ciliated cells, and NO goblet cells, and are called terminal bronchioles.

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Respiratory Bronchioleso Branch of the terminal bronchioles. On the transitional regions, the

bronchioles have alveoli in their walls. These bronchioles with alveoli in their walls are called respiratory bronchioles. The alveolar ducts, rise by branching of respiratory bronchioles; walls made up of alveolar sacs and alveoli. The alveolar sacs: Cluster of alveoli that open into the lumen of the alveolar ducts. Composed of squamous epithelial cells, basement membrane, and capillaries. Site of respiratory exchange.

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Literature Review

Epidemiology

It is estimated that 300 million people in the world currently have asthma. Asthma appears to be most common in English-speaking countries, e.g the UK, USA, Canada, New Zealand, and Australia, where there is also evidence of high prevalence of sensitization to common allergens. Increased urbanization and industrialization in some countries also affecting asthma prevalence.

The World Health Organization (WHO), 20.3 million people currently had asthma of which 6.3 million were children under age 18 years. Over recent years, the number of people suffering from asthma has increased at an alarming rate. Since the 1980's the incidence of asthma has more than doubled and the American Lung Association believes it will double again by the year 2020. Also estimated that 15 million disability-adjusted life years (DALYs) are lost each year due to asthma, i.e. 1% of total global disease burden.

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Through this graft the incidence of diagnose of asthma in children is high at age 4 year old. In childhood males have higher incidence than female, a ratio that reverses in adolescence. Between the ages of 15 and 50 year women have higher incidence than men, and in later life the prevalence seems to reverse again.

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Pathophysiology

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A, sensitization to allergen. Inhaled allergens (antigens) elicit a TH2-dominated response favouring IgE production and eosinophil recruitment (priming or sensitization). B, allergen-triggered asthma. On re-exposure to antigen (Ag) the immediate reaction is triggered by Ag-induced cross-linking of IgE bound to IgE receptors on mast cell in the airways. These cell release preformed mediators that open tight junction between epithelial cell. Antigen can enter the mucosa to activate mucosal mast cells and eosinophils, which in turn release additional mediators. Collectively, either direct or through neuronal reflexes the mediator induce bronchospasm, increase vascular permeability, and mucus production, beside recruiting additional mediator-releasing cells from the blood. C, late phase (hours). The arrival recruited leukocyte (neutrophils, eosinophils, basophils and TH2 cells) signals the initiation of the late phase of asthma and a fresh round of mediator release from leukocytes, endothelium, and epithelial cells. Factors, particularly from eosinophils (e.g., major basic protein, eosinophil cationic protein), also cause damage to the epithelium.[1]

Classification

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There are two different way to classified asthma, it is etiologic and severity of disease.

Classification of asthma by aetiology

o Extrinsic asthma: Occur most frequently in atopic individuals who show positive skin-prick

reactions to common inhalant allergens, positive ski-prick tests to inhalant allergens are shown in 90% of children and 70% of adults with persistent asthma. Childhood asthma is often accompanied by eczema (atopic dermatitis). A frequently overlooked cause of late-onset asthma in adults is sensitization to chemicals or biological products in the workplace.[4]

o Intrinsic asthma: Often start in middle age(‘late onset’). Positive allergen skin tests and on close

questioning give a history of respiratory symptoms compatible with childhood asthma.[4]

o Exercise induce asthma Symptoms occurs 5 to 10 min after exercise.[4]

o Occupational asthma Symptoms attributed to a particular occupation.[4]

o Drug-induced asthma Asthma provoked by drugs e.g:

Aspirin induced asthma (and other none steroidal anti inflammatory drugs)

Beta blockers Angiotensin converting enzyme inhibitors (ACEI)

o Cough variant asthma

o Acute severe asthma

o Near-fatal asthma

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Classification of Asthma by Severity

o Patient with severe asthma have daily symptoms and require urgent or emergency treatment several times per year. They have poor exercise tolerance. They may have a poor bronchodilator response due to chronic inflammation. Patient with moderate asthma are intermediate between the mild and severe asthma.[4]

STEP 1: IntermittentSymptoms less than once a week (≤ 1/week)Brief exacerbationsNocturnal symptoms not more than twice a month (≤ 2/month)FEV1 ≥ 80% predicted or PEF ≥ 80% of personal bestPEF or FEV1 variability 20-30%

STEP 2: Mild PersistentSymptoms more than once a week (≤ 1/week) but less than once a dayExacerbations may affect activity and sleepNocturnal symptoms more than twice a month (> 2/month)FEV1 ≥ 80% predicted or PEF ≥ 80% of personal bestPEF or FEV1 variability 20-30%

STEP 3: Moderate PersistentSymptoms dailyExacerbation may affect activity and sleep Nocturnal symptoms more than once a week (> 1/week)Daily use of inhaled short-acting β2-agonistFEV1 60-80% predicted or PEF 60-80% of personal bestPEF or FEV1 variability >30%

STEP 4: Severe PersistentSymptoms dailyFrequent exacerbationsFrequent nocturnal asthma symptomsLimitation of physical activitiesFEV1 ≤60% predicted or PEF ≤60% of personal bestPEF or FEV1 variability >30%

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Pathology

Aetiology

Development of asthma can be cause by these triggered:

Environmental exposure to allergen Viral infection Cold air Emotional Irritant dusts, vapour and fumes Occupational sensitizers Atmospheric pollution Drugs Genetic factors

Pathogenesis

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The major etiologic factors of asthma are genetic predisposition to type I hypersensitivity (“atopy”)., acute chronic airway inflammation, and bronchial hyper-responsiveness to a variety of stimuli. The inflammation involve many cell types and numerous inflammatory mediator, but the role of type 2 helper T (TH2) cell may be critical to the pathogenesis of asthma.[1]

The classic “atopic” form of asthma is associated with an excessive TH2 reaction against environmental antigens and cause inflammatory reaction to the airway. The inflammatory response mediated by TH2 type cell, asthma characterised by structural change in bronchial wall, referred to as “airway remodeling.” These change also include hypertrophy of bronchial smooth muscle and deposition of subepithelial collagen. These condition was considerate a late, secondary change of asthma that occur over severe year.

There also may be an inherited predisposition associated with polymorphisms in genes that result n accelerated proliferation of bronchial smooth muscle cells and fibroblast. One candidate genes that has emerged in recent years is ADAM33, which is expressed by the cell types implication in airway remodelling (smooth muscle cell and fibroblasts), although there are undoubtedly other genetic factors involve. [1]

Mast cell, part of the inflammatory infiltrate in asthma, are also thought to contribute to airway remodeling by secreting growth factor that stimulate smooth muscle proliferation.[1]

Actopic asthma Usually occur during childhood and have positive family history and preceded by allergic rhinitis, urticaria, or eczema. Actopic asthma are usually triggered by environmental factor such as dust, pollen, animal dander, and food. A skin test with the offending antigen will result an immediate wheal-and-flare reaction, a classic example of the type I IgE-mediated hypersensitivity reaction. There is an initial sensation in the airway that will stimulate induction of TH2 type cell and release interleukins IL-4 and IL-5, that will synthesis of IgE. The IgE will bind to the mucosal mast cell. Subsequent IgE-mediated reaction to inhale allergens elicits an immediate response and a late-phase reaction. IgE-coated mast will cross linked with the same type of antigen, this will release chemical mediator that activate the mast cell on the respiratory mucosal surface, this result open of the mucosal intercellular junction. When it open, it will allow more antigen to penetrate and will activate more mucosal mast cell and eosinophils, cause release of additional mediator. Actopic asthma is a direct stimuli of subepithelial vugal (parasympathetic) receptor that provoke reflex of bronchoconstriction in central and local reflex.

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This occur minute after stimulation and called acute or mediate response, which consist of bronchoconstriction, oedema and mucus secretion. There are a variety of inflammatory mediator involve example:

o Leukotrienes C4, D4 and E4: prolong bronchoconstriction, increase vascular permeability and increase mucus secretion

o Acetylcholine: release from intrapulmonary motor that constrict smooth muscle at airway by direct stimulation of muscarinic receptor.

o Histamine: bronchospasm and increase vascular permeability.o Prostaglandin D2: elicits bronchoconstriction and vasodilatation.o Platelet-activating factor: aggregation of platelet and release of

histamine.

Mast cell release addition cytokines that cause influx of the leukocyte, this is at the late-phase reaction.

During late-phase reaction, eosinophils accumulate at allergic inflammation that favored by severe mast cell-derived chemotactic factor and chemokines(produced by bronchial epithelial cell). Eosinophil release major basic protein and eosinophil cationic, that directly toxic to the airway epithelial cell. Eosinophil perioxides will cause tissue damage by oxidative stress. Activated eosinophils are rich in leukotrienes, especially C4 that cause bronchoconstriction. Thus eosinophil can amplify and sustain the inflammatory response without additional exposure to the triggering factor.[1]

Non-Actopic asthma: The mechanism of bronchial inflammation and hyper-responsiveness is much less clear in individuals with non-actopic asthma. Incriminated in such case are viral infections of the respiratory tract and inhale air pollution such as sulfer dioxide, ozone, and nitrogen dioxide. These agent increase airway hyper-reactivity in both normal and asthmatic subjects. In the latter, however, the bronchial response, manifested as spasm, is much more severe and sustained. A positive family history is uncommon, serum IgE levels are normal, and there are no associated allergies. It is thought that virus-induce inflammation of the respiratory mucosa lower the threshold of the subephithelial vagal receptors to irritants. Although the connection are not well understood, the ultimate humoral and cellular mediators of airway obstruction (e.g., eosinophils) are common to both atopic and non-atopic variants of asthma, and hence they are treated in a similar way.[1]

Drug-Induced Asthma

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Several pharmacologic agents provoke asthma, aspirin being the most striking example. Individual with aspirin sensitivity present with recurrent rhinitis and nasal polyps, urticaria, and bronhospasm. The precise mechanism reains unknown, but it is presumed that aspirin inhibits the cyclooxygenase pathway of arachidonic acid metabolism without affecting the lipoxygenase route, thereby shifting the balance toward bronchoconstrictor leukotrienes.[1]

Occupational Asthma this form of asthma is stimulated by fumes (epoxy resins, plastics), organic and chemical dust (wood, cotton, platinum), gases (toluene), and other chemical. Asthma attacks usually develop after repeated exposure to the inciting antigen(s). [1]

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Morphology

It is described in person who are die with prolonged severe attack (status asthmaticus) and in mucosal biopsy specimens of persons challenge with allergens. In fatal cases grossly, the lung are overdistended because of overinflation, and there may be small areas of atelectasis. The most striking macroscopic finding is occlusion of bronchioles by thick, tenacious mucus plugs. Histologically, the mucus plugs contain whorls of shed epithelium (Curschmann spirals). Numerous eosinophils and Charcot-Leyden crystal (collection of crystalloids made up of eosinophil proteins) are also present. The other characteristic finding of asthma, collectively called “airway remodeling” include:

Thickening of the basement membrane of the bronchial epithelium. Edema anf an inflammatory infiltrate in the bronchial walls, with a prominence of

eosinophils and mast cells. An increase in the size of the submucosal glands. Hypertrophy of the bronchial muscle walls.

There are accumulation of mucus in the bronchial lumen resulting from an increase in the number of mucus-secreting goblet cells in the mucosa and hypertrophy of submucosal mucous gland. There also an intense chronic inflammation cause by recruitment of eosinophils, macrophage, TH2 cells and other inflammatory cells. Basement membrane

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under laying the mucosal epithelium is thickened, and there is hypertrophy and hyperplasia of smooth muscle cell.[1]

Gross:

Mucous plugging Bronchospasm Over inflation

Microscopic

Patchy necrosis epithelium Sub-mucosal glandular hyperplasia Hypertrophy of bronchial smooth muscle Eosinophil, mast cell: lympho (TH2, CD4) Mucous plugs, whorled mucous plugs (Curschmann’s sprals) Debris of eosinophils (Charcot-Leyden crystals)

Clinical Aspect

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Symptoms

Chronic cough, worsening during night Recurrent wheezing Recurrent difficulty in breathing and chest tightness Symptoms occur or worsen after exercise, upper respiratory tract infections, or

allergen exposure Symptoms occur or worsen at night, disturbing the patient sleep. Family history of asthma or actopic diseases[5]

Sign

In between attacks no signs are detected or minimal signs During attacks:

o Harsh vesicular breath sound with prolonged expirationo Audible wheezing and rhonchi on auscultationo There may be silent chest in severe cases.[5]

Investigation

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1) Pulmonary function test[5].a) May be normal between the attackb) Obstructive ventilator defect (decrease in FEV1 and FEV1/FVC%)c) PEFR variability: during variation in peak expiratory flow rate (>20%

difference between the highest and lowest PEFR) with morning dipping.d) Test of reversibility: significant reversibility which is indicated by an

increasing of > 12% or 200 l in FEV1 after inhaling a short acting β2

agonists.e) Non specific bronchoprovocation test: airway hyperresponsivness by

bronchoprovocation test with methacholic, histamine or exercise challenge indication when spirometer is normal.

f) Blood gases: in an acute severe attack there is decrease in arterial oxygen tension, and normal PaCO2. Increase in PaCO2 is an indication of mechanical ventilation.

2) Radiology.[5]Normal chest x-ray is the most common finding in patient with asthma. Chest x-ray is not diagnose for asthma but it is essential to detect complication or associated disease e.g:

a. Pneumothoraxb. Collapsec. Pneumoniad. Fracture rib.

3) Detection of allergen[5]:Skin prick test. Detection of total and specific IgE.Specific bronchoprovocation test using inhaled antigens.

4) Blood picture[5]:Leukocytosis due to infectionEosinosphilia ay be present in allergic cases.

5) Sputum[5]:a. Eosinophil are detected in the sputumb. Curshman’s spirals which are yellow white wavy long threads

composed of sheded epithelium, spiral aggregates of eosinophil, mucus in a fibril network.

c. Creola bodies which are clusters of columnar bronchial epithelium.d. Charcot – leyden crystal which are crystalloid derivatives of

eosinophils.

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6) ECG[5]: to exclude cardiac cause of dyspnea.

Diagnosis

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The are differences diagnosis of asthma in different age, these Additional studies as necessary to exclude alternate diagnoses.

INFANT AND CHILDREN[8]:

Upper airway diseases

Allergic rhinitis and sinusitis

Obstructions involving large airways

Foreign body in trachea or bronchus. Vocal cord dysfunction. Vascular rings or laryngeal webs. Laryngotracheomalacia, tracheal stenosis, or bronchostenosis. Enlarged lymph nodes or tumor.

Obstructions involving small airways

Viral bronchiolitis or obliterative bronchiolitis. Cystic fibrosis. Bronchopulmonary dysplasia. Heart disease.

Other causes

Recurrent cough not due to asthma. Aspiration from swallowing mechanism dysfunction or gastroesophageal

reflux.

ADULT[8]:

COPD (e.g., chronic bronchitis or emphysema). Congestive heart failure (left side heart failure). Pulmonary embolism. Mechanical obstruction of the airways (benign and malignant tumors). Pulmonary infiltration with eosinophilia. Cough secondary to drugs (e.g., angiotensin-converting enzyme (ACE)

inhibitors). Vocal cord dysfunction.

Management

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The aim of treatment are[2]: Abolish symptoms Restore normal or best possible lung function Reduce risk of several attacks Enable normal growth to occur in children Minimize absence from school or employment

This management also involve[2]: Patient and family education about asthma Patient and family participation in treatment Avoidance of identified causes where possible Use of the lowest effective doses of convenient medications to minimize

short-term and long-term side effects.

Also the asthmatic patient have to control the extrinsic factor, this emphasized that: The rapid identification of extrinsic cause of asthma and their removal is

necessary wherever possible (e.g. occupational agents, family pets) Once extrinsic asthma is initiated, it may become self-perpetuating, possibly

by non-immune mechanism.[2]

Treatment

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Aim: Minimal chronic symptoms, including nocturnal symptoms. Minimal (infrequent) exacerbations. No emergency visit . Minimal use of (as-needed) β2-agonist. No limitations on activities, including exercise. PEF circadian variation of less than 20%. (Near) normal PEF. Minimal (or no) adverse effects from medicine.

Guideline:1) Patient education to develop a partnership in asthma management.2) Assess and monitor asthma severity.3) Avoid asthma triggers. 4) Establish individual medications plans for long-term management.5) Establish individual plans for managing exacerbations.6) Provide regular follow-up care.

There are two main groups of drug in treatment of asthma.

A. Controller medicationUsually long-term drugs, that getting and keeping persistent asthma under control (also called prophylactic or preventive drugs).

Inhale and systemic corticosteroid Leukotrienes modifiers Sodium cromoglycate Nedocromide sodium Methylxanthines Long acting β2-agonists

B. Reliever (rescue) medications:Including rapid acting bronchodilators are used on need basis to get rapid bronchodilation:

Short acting β2-agonists Inhaled ipratropium broide

Bronchodilator:

i. β2-adrenergic agents:

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Stimulation of β2-receptors result in bronchial smooth muscle relaxation

Present in inhaled, oral and injection forms Aerosol deliver of these drug provide more rapid onset of acton and

less side effects than the oral delivery Side effects: muscle tremors, cramp, glaucoma, hypertension,

retention of urine in patient with senile prostate.

Short-acting β2-agonists Salbutamol Orciprenaline Terbutaline Ephedrine

Long acting β2-agonists: Salmetrol Formotrol Bambuterol

ii. Methylxanthine (theophylline) Has a bronchodilator effect, that improves the diaphragmatic function

and has immunomodulatory effect in asthmatic patients. Present in injection, oral and suppository forms Dose of oral theophylline: 6mg/ kg/ day in 2 divided doses The oral form is used as a long acting drug, and intravenous route is

used in cases of acute severe asthma Side effect: hyperacidity, tremors, headache, cardiac arrhythmia and

convulsions.

iii. Anticholinergic drugs: Inhaled antcholinergic agent: ipratropium bromide (short acting) in

management of acute asthma, tiotropium bromide (long acting) in chronic asthma.

Ipratropium bromide is used in combination with β2 agonists in treatment of chronic asthma.

Anti-inflammatory drugs:

Corticosteroids

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o The anti-inflammatory effect of corticosteroids decrease airways inflammation, mucus and relieve airway obstruction, in addition it decrease airway hyperreactivity.

o It is the principle drug in treatment bronchial asthma.

i. Injected steroids: Methyl prednisilone Dexamethazone Hydrocortisone

ii. Oral steroids: Prednisone and prednisilone Dexamethasone Triamcinolone Betemethasone

iii. Inhaled steroids: Beclomethasone Fluticasone Butdesonide

Other anti-inflammatory agents(non-steroid):o Cromolyn sodiumo Nedocromil sodium

These drug are mainly in childhood asthma and in exercise-induce asthma, administered only by inhalation.[5]

Immunotherapy:

Allergen immunotherapy indicated when:a. There is clear evidence of relationship between symptoms and

exposure to allergenb. Symptoms occur in major portion of the yearc. There is difficulty in controlling symptoms with pharmacological

management.[5]

Conclusion and Summary

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Asthma can be classified into 2 major groups, which are etiology and severity. In etiology asthma can be divided into extrinsic, intrinsic, exercise induce, occupational, drug-induce , cough variant, near-fatal asthma. In the severity asthma is divide into intermittent, mild, moderate and severe. This classification is healpful during assess clinical condition prior to therapy

Pathology of asthma consist of aetiology, pathogenesis and morphology. the etiology of asthma are such as allergic, exercise, stress and other. Pathogenesis atopic, non-actopic, occupational and drug-induce asthma.

Here also include the clinical aspect of asthma include sign, symptoms, investigation, diagnosis and treatment. The sign and symptoms of sthma are wheezing, chest tightness and breathlessness. There also include a few type of investigation to diagnose asthma, like pulmonary function test, radiology, detection of allergen, blood picture, sputum and ECG. The main treatment of bronchial asthma is to abolish symptom, restore normal or best possible lung function and reduce risk of severe attacks.

Asthma is differently distributed in the world. Recently the population-dased data show that the asthma prevalence increase observed worldwide in the past 30 years has now stopped in industrialised countries.

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References

KUMAR, ABBAS, FAUSTO & MITCHELL. Robbins Basic Pathology. 8th ed. ELSEVIER SAUNDERS. p489-492

KUMAR & CLARK (2009). Clinical Medicine. 7th ed. Philadelphia: ELISEVIER SAUNDERS. p846-856

GRAHAM & KURTIS S ELWARD (2011). Clinician’s Desk Reference Asthma. MANSON PUBLISHING.

OMAR BARAKA. Anatomy of Thorax. p28 THE BOOK OF THORACIC MEDICINE DEPARTMENT MANSOURA

UNIVERITY (2005). Basic of Respiratory Medicine. 2nd ed. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001196/ http://www.webmd.com/asthma/guide/asthma-overview-facts http://www.asthmahelpline.com/asthma-diagnosis.htm http://www.who.int/genomics/public/geneticdiseases/en/index3.html

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