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ASTHMABarte, Anne Bernadette B.

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What is Asthma?

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Asthma syndrome characterized by airfloobstruction that varies markedly, both

spontaneously & with treatment

Narrowing of airways is usually reversible;

contrast with chronic asthma w/c is irreverairflow obstruction

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EPIDEMIOLOGY

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Asthma is one of the most common chronicdiseases globally

Currently affects 300 million people

Present at any age w/ a peak age of 3

Childhood: males > females

Adulthood: sex ratio has equalized Asthmatic children became asymptomatic d

adolescence/until they reach age 40, howevreturns in some during adult life

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Death are uncommon & have been steadilydeclining in many affluent countries over th

decade

Widespread use ofinhaled corticosteroids(ICSs) in pxs w/ persistent asthma is respofor the decrease in mortality in recent year

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ETIOLOGY

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Heterogeneous disease w/ interplay begenetic & environmental factors; these

the ff:

Atopy

Intrinsic Asthma

InfectionsEnvironmental Factors: hygiene hypothesis, diet

air pollution, allergerns, occupational exposure

Other Factors

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PATHOGENESIS

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Pathology

Inflammation

Inflammatory Mediators: cytokines, chemokines, oxidative stressoxide, transcription factors

Effects of Inflammation: airway epithelium, fibrosis, airway smoomuscle, vascular responses, mucus hypersecretion, neural effects

Airway remodeling

Asthma triggers: allergens, virus infections, pharmacologic agentexercise, physical factors, food, air pollution, occupational factorshormonal factors, gastroesophageal reflux, stress

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Pathology

airway mucosa is infiltrated with activated eosinophils and Tlymphocytes, and there is activation of mucosal mast cells

inflammation is reduced by treatment with ICSs

these pathologic changes are found in all airways but do not extelung parenchyma; small airway inflammation is found particular

patients with severe asthma.

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Inflammation

there is inflammation in the respiratory mucosa from trachea to bronchioles, but with a predominance in the bronchi (cartilaginoairways).

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Inflammatory Mediators

Mediators such as histamine, prostaglandins, and cysteinyl-leukocontract airway smooth muscle, increase microvascular leakage, airway mucus secretion, and attract other inflammatory cells.

Because each mediator has many effects, the role of individual min the pathophysiology of asthma is not yet clear.

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Effects of Inflammation

Airway epithelium: damage may contribute to airwayhyperresponsiveness, including loss of its barrier function to allopenetration of allergens; loss of enzymes (such as neutral endoploss of a relaxant factor (so called epithelial-derived relaxant factexposure of sensory nerves, which may lead to reflex neural effecairway

Fibrosis: basement membrane is apparently thickened due tosubepithelial fibrosis with deposition of types III and V collagen btrue basement membrane, and it is associated with eosinophil in

Airway smooth muscle: still debate about the role of abnormalitibe secondary to the chronic inflammatory process

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Vascular responses: microvascular leakage from postcapillary veresponse to inflammatory mediators is observed in asthma, resuairway edema and plasma exudation into the airway lumen

Mucus hypersecretion: increased mucus secretion contributes to

viscid mucus plugs that occlude asthmatic airways, particularly iasthma

Neural effects: release of acetylcholine acting on muscarinic rececause bronchoconstriction and may be activated reflexly in asthm

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Airway remodeling

observation suggests that the accelerated decline in lung functionin a smaller proportion of asthmatics, and these are usually patiemore severe disease

may lead to irreversible narrowing of the airways

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Asthma triggers

Allergens

virus infections

pharmacologic agents

exercise, physical factors

Food

air pollution

occupational factor

hormonal factors

gastroesophageal re

stress

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PATHOPHYSIOLOGY

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Limitation of airflow is due mainly to bronchoconstriction, but aiedema, vascular congestion, and luminal occlusion with exudate contribute.

Early closure of peripheral airway results in lung hyperinflation (trapping), and increased residual volume, particularly during acuexacerbations.

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Airway Hyperresponsiveness

AHR is the characteristic physiologic abnormality of asthma, anddescribes the excessive bronchoconstrictor response to multiple triggers that would have no effect on normal airways.

important aim of therapy is to reduce AHR

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Bronchodilators and Controllers

TREATMENT

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Bronchodilator Therapies: B2-agonists (5), Anti-cholinergics,Theophylline (2),

Controller Therapies: Inhaled corticosteroids (3), Systemiccorticosteroids, Antileukotrienes, Cromones, Steroid-sparing TheAnti-IgE, Immunotherapy, Alternative therapies, Future therapie

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The main drugs for asthma can be divided in

Bronchodilator Therapies: Controller Therapies:

B2-agonists

Anti-cholinergics

Theophylline

Inhaled corticosteroids

Systemic corticosteroids

Antileukotrienes

Cromones

Steroid-sparing TherapiesAnti-IgE

Immunotherapy

Alternative therapies

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Bronchodilator Therapies

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B2-agonists

relax airway smooth-muscle cells of all airways, where they act afunctional antagonists, reversing and preventing contraction of asmooth-muscle cells by all known bronchoconstrictors

given by inhalation

rapid onset of bronchodilation and are therefore used as needed symptom relief

short-acting 2-agonists (SABAs), such as albuterol and terbutalinduration of action of 36 hours

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Anti-cholinergics

used as an additional bronchodilator in patients with asthma thacontrolled on other inhaled medications

most common side effect is dry mouth; in elderly patients, urinarretention and glaucoma may also be observed

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Theophylline

Inexpensive

lower doses has anti-inflammatory effects, and these are likely tomediated through different molecular mechanisms

most common side effectsnausea, vomiting, and headachesaphosphodiesterase inhibition

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Controller Therapies

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Inhaled corticosteroids

ICSs are the most effective anti-inflammatory agents used in asththerapy, reducing the number of inflammatory cells and their actthe airways

reduce eosinophils in the airways and sputum, and numbers of alymphocytes and surface mast cells in the airway mucosa

local side effects include hoarseness (dysphonia) and oral candid

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Systemic corticosteroids

used intravenously (hydrocortisone or methylprednisolone) for ttreatment of acute severe asthma, although several studies now soral corticosteroids are as effective and easier to administer

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Antileukotrienes

Cysteinyl-leukotrienes are potent bronchoconstrictors, causemicrovascular leakage, and increase eosinophilic inflammation ththe activation of cys-LT1-receptors

given orally once or twice daily and are well tolerated

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Cromones

Cromolyn sodium and nedocromil sodium are asthma controllerthat appear to inhibit mast cell and sensory nerve activation

relatively little benefit in the long-term control of asthma due to tshort duration of action (at least 4 times daily by inhalation).

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Steroid-sparing Therapies

Methotrexate, cyclosporine, azathioprine, gold, and intravenous gglobulin have all been used as steroid-sparing therapies, but nontreatments has any long-term benefit and each is associated withrelatively high risk of side effects

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Anti-IgE

Omalizumab is a blocking antibody that neutralizes circulating Igwithout binding to cell-bound IgE; it thus inhibits IgE-mediated r

reduce the number of exacerbations in patients with severe asthmay improve asthma control

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Immunotherapy

injected extracts of pollens or house dust mite has not been very in controlling asthma and may cause anaphylaxis

not recommended in most asthma treatment guidelines becauseevidence of clinical efficacy

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Acute Severe Asthma

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Clinical Features & Treatment

Patients are aware of increasing chest tightness, wheezing, and dthat are often not or poorly relieved by their usual reliever inhale

Treatment: The mainstay of treatment is high doses of short-actiinhaled 2-agonists that are given either by nebulizer or via a meteinhaler with a spacer; patients may benefit from an anesthetic, suhalothane, if they have not responded to conventional bronchodi

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OT Management

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Relaxation Techniques Energy Conservation Program

Education

Group therapy

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