Download - MF3 - Asthma
-
7/30/2019 MF3 - Asthma
1/42
ASTHMABarte, Anne Bernadette B.
-
7/30/2019 MF3 - Asthma
2/42
What is Asthma?
-
7/30/2019 MF3 - Asthma
3/42
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
-
7/30/2019 MF3 - Asthma
4/42
EPIDEMIOLOGY
-
7/30/2019 MF3 - Asthma
5/42
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
-
7/30/2019 MF3 - Asthma
6/42
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
-
7/30/2019 MF3 - Asthma
7/42
ETIOLOGY
-
7/30/2019 MF3 - Asthma
8/42
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
-
7/30/2019 MF3 - Asthma
9/42
PATHOGENESIS
-
7/30/2019 MF3 - Asthma
10/42
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
-
7/30/2019 MF3 - Asthma
11/42
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.
-
7/30/2019 MF3 - Asthma
12/42
Inflammation
there is inflammation in the respiratory mucosa from trachea to bronchioles, but with a predominance in the bronchi (cartilaginoairways).
-
7/30/2019 MF3 - Asthma
13/42
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.
-
7/30/2019 MF3 - Asthma
14/42
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
-
7/30/2019 MF3 - Asthma
15/42
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
-
7/30/2019 MF3 - Asthma
16/42
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
-
7/30/2019 MF3 - Asthma
17/42
Asthma triggers
Allergens
virus infections
pharmacologic agents
exercise, physical factors
Food
air pollution
occupational factor
hormonal factors
gastroesophageal re
stress
-
7/30/2019 MF3 - Asthma
18/42
PATHOPHYSIOLOGY
-
7/30/2019 MF3 - Asthma
19/42
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.
-
7/30/2019 MF3 - Asthma
20/42
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
-
7/30/2019 MF3 - Asthma
21/42
Bronchodilators and Controllers
TREATMENT
-
7/30/2019 MF3 - Asthma
22/42
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
-
7/30/2019 MF3 - Asthma
23/42
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
-
7/30/2019 MF3 - Asthma
24/42
Bronchodilator Therapies
-
7/30/2019 MF3 - Asthma
25/42
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
-
7/30/2019 MF3 - Asthma
26/42
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
-
7/30/2019 MF3 - Asthma
27/42
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
-
7/30/2019 MF3 - Asthma
28/42
Controller Therapies
-
7/30/2019 MF3 - Asthma
29/42
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
-
7/30/2019 MF3 - Asthma
30/42
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
-
7/30/2019 MF3 - Asthma
31/42
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
-
7/30/2019 MF3 - Asthma
32/42
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).
-
7/30/2019 MF3 - Asthma
33/42
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
-
7/30/2019 MF3 - Asthma
34/42
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
-
7/30/2019 MF3 - Asthma
35/42
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
-
7/30/2019 MF3 - Asthma
36/42
-
7/30/2019 MF3 - Asthma
37/42
Acute Severe Asthma
-
7/30/2019 MF3 - Asthma
38/42
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
-
7/30/2019 MF3 - Asthma
39/42
OT Management
-
7/30/2019 MF3 - Asthma
40/42
Relaxation Techniques Energy Conservation Program
Education
Group therapy
-
7/30/2019 MF3 - Asthma
41/42
-
7/30/2019 MF3 - Asthma
42/42