Bronchial Athma Yoon Jung Oh, M.D. The Departments of Pulmonary and Critical care Medicine Ajou...

transcript

Bronchial AthmaBronchial AthmaBronchial AthmaBronchial Athma

Yoon Jung Oh, M.D.

The Departments of Pulmonary and Critical care Medicine

Ajou University School of Medicine

Definition

1. Variable and reversible airway obstruction

2. Airway inflammation

3. Bronchial hyperresponsiveness

Characteristics of asthma in 10 points

1. Episodic paroxysms of wheezy dyspnea2. Symptom-free periods3. Bronchial hyperresponsiveness4. Significant reversibility with beta2 agonists (≥ 20%)5. Significant reversibility with steroids (≥ 20%)6. Eosinophil inflammation7. Airway obstruction or narrowing: Increased resistance to airflow Reduced ventilatory capacity of obstructive type8. Rapid and considerable changes in lung function (peak flow variation ≥ 20%)9. Frequent nocturnal episodes and low morning peak flow values10.Frequent occurrence of allergy

Prevalence and Classification

• 4~5% of the population • Before age 10 (50%), Before age 30 (30%)• Childhood M : F = 2:1, Age 30 M : F = 1:1

AgePersonal or family history of allergic diseasesSkin testIgE level

Allergic asthma

Age 3 ~ 35Present

Positiveincreased

Idiosyncratic asthma

< age 3 or > age 35absent

Negativenormal

Pathogenesis of Asthma (1)

• Inflammatory changes in the bronchi

• The bronchial wall, its basement membrane and muscle layer are

thickened.

• There is accumulation and activation of eosinophils.

• There is shedding of ciliated epithelium.

clusters of epithelial cells(Creola bodies).

• The mucociliary clearance is grossly impaired.

• Extensive mucus plugging occludes the lumen.

• The lungs are hyperinflated with small atelectatic areas.

Smooth muscle

Mucous membrane

Normal adult

Muscular spasm

Mucosaledema

Stickymucus

Expiratory pressure

Airway inflammation : bronchoconstriction, vascular congestion, edema formation• Macrophages(antigen presenting cell)• Mast cells Primary mediator : histamine, serotonine, ECF-A Secondary mediator : LT(B,C,D,E), PGs(E2,F2,D2),bradykinin, PAF• Eosinophils (major basic protein, eosinophilic cationic protein)• Lymphocytes TH1 : IL-2 & IFN- growth and differentiation of B cell, activation of macrophages TH2 : IL-4 & IL-5 stimulate immunoglobulin secretion, eosinophil proliferation, differentiation, activation • Neutrophils

Chemotactic factor : LTB4, ECF-A, NCF-A

Pathogenesis of asthma (2)

Initial allergen exposure : allergic sensitization

Allergen

Hyperresponsiveness

Late response

Early response

Subsequent allergen exposure : allergic symptoms

Allergen

Cell membrane phospholipid

Arachidonic acid

Leukotriene A4

Leukotriene C4

Leukotriene D4

Leukotriene E4

Leukotriene B4 Prostaglandin G2

Prostaglandin H2

Thromboxane A2Prostacycline

Prostaglandin D2,E,F2

1. Allergens : dependent on IgE response House dust mite(most common) Pollen(tree, grass, weed)2. Pharmacologic stimuli aspirin, tartrazine beta-adrenergic antagonists sulfiting agents3. Environment and air pollution ozone, nitrogen dioxide, sulfur dioxide4. Occupational factors toluene diisocyanate(TDI), nickel 5. Infections : most common stimuli of acute exacerbation6. Exercise running, inhalation of cold air !! Swimming is good for asthma 7. Emotional stress

Etiology

Aspirin sensitive asthma

• Primarily affects adults• Preferential generation of leukotrienes• Begins with perennial vasomotor rhinitis hyperplastic rhinosinusitis with nasal polyps • Cross reactivity between aspirin and other NSAIDs Indomethacin, fenoprofen, naproxen, zomepirac sodium, ibuprofen, mefenamic acid, phenylbutazone!! Well tolerated drugs acetaminophen, sodium salicylate, choine salicylate, salicylamide, propoxyphene• Desensitized by daily administration of the drug Cross tolerance also develops to other NSAIDs

Pathology

• Hypertrophy of the bronchial smooth muscle• Hyperplasia of mucosal and submocosal vessels• Mucosal edema• Denudation of the surface epithelium• Pronounced thickening of the basement membrane• Eosinophilic infiltrates in the bronchial wall

Normal alveoli Hyperinflated alveoli Collapsed alveoli

Normal Lungs Asthmatic Lungs

Pathophysiology (1)

Contraction of smooth muscle,Vascular congestion Edema of the bronchial wall

Reduction of airway diameter

Increase in airway resistanceDecrease in forced expiratory volumes and flow ratesAlterations in respiratory muscle functionChanges in elastic recoilAbnormal distrubution of both ventilation and pulmonary blood flow with mismatched ratiosAltered arterial blood gas concentrations

Elastic recoil of lung Expiratory muscles

Ordinary and accessory inspiratory muscles

Asthmatic expiration with airway closure

Pathophysiology (2)

RVH, pulmonary hypertension

FVC ≤ 50% of normal

FEV1 ≤ 30% of predicted

Maximum/minimum midexpiratory flow rates ≤ 20%

Residual volume(RV) ≈ 400% of normal

Hypoxia is a universal finding but

frank ventilatory failure is relatively uncommon(10-15%)

Hypocapnia and respiratory alkalosis

Normal PaCO2 tends to be associated with quite severe levels of obstruction(impe

nding respiratory failure)

Normal Acute asthma

Pathophysiology (2)

RVH, pulmonary hypertension

FVC ≤ 50% of normal

FEV1 ≤ 30% of predicted

Maximum/minimum midexpiratory flow rates ≤ 20%

Residual volume(RV) ≈ 400% of normal

Hypoxia is a universal finding but

frank ventilatory failure is relatively uncommon(10-15%)

Hypocapnia and respiratory alkalosis

Normal PaCO2 tends to be associated with quite severe levels of obstruction(impe

nding respiratory failure)

Normal ventilation and perfusion

Ventilation/perfusion mismatch in asthma

Clinical Features

Triad : dyspnea, cough, wheezingNocturnal awakening with dyspnea and/or wheezingProlonged expirationTachypnea, tachycardia, mild systolic hypertensionOverinflated lungsUse of accessory muscles , Paradoxical pulse Extremely valuable in indicating the severity of the obstructionCough/sputum Curschmann’s spirals, eosinophils, Charcot-Leyden crystalsAtelectasisSpontaneous pneumothorax/pneumomediastinum

Mild asthma Moderate Severe

Verysevere

Sentences

Words None

Stethosco-pic rhonchi

Audible wheezinessBreathless at rest

Speech

Use of accessory muscles

Pulsus paradoxus

Cyanosis

Confusion, loss of consciousness

Clincal signs and severity of asthma

Pulsus paradoxus

Differential Diagnosis

1. Upper airway obstruction by tumor or laryngeal edema stridor, harsh respiratory sounds localized to tracheal area absent of diffuse wheezing throughout both lung fields indirect laryngoscopy or bronchoscopy2. Glottic dysfunction narrow glottis during inspiration and expiration occasional PaCO2 retention but preserved PaO2

3. Endobronchial disease(tumor, bronchial stenosis, foreign body) persistent localized wheezing 4. Acute left ventricular failure5. Chronic bronchitis no true symptom-free periods, chronic cough,sputum 6. Recurrent pulmonary emboli lung scan, pulmonary angiography7. Carcinoid tumor8. Eosinophilic pneumonias9. Systemic vasculitis

Diagnosis

History : personal or family history of allergic diseases (eczema, rhinitis, urticaria), occupation, contact with animals

Reversible airway obstruction

≥ 15% in FEV1 following beta-adrenergic agonist

Provocation test (methacholine, histamine, cold air) ≥ 20% in FEV1

Skin tests Sputum and blood eosinophiliaSerum IgE levelsChest X-ray : hyperinflation

Questions to an asthma patient1. Do any of your patents, siblings or children have childhood eczema, asthma or h

ay fever?2. Have you ever had eczema or hay fever?3. Do you smoke/have you smoked?4. What is your occupation?5. Are you in contact with animals?6. Can you tolerate acetylsalicylic acid?7. How old were you when the disease strarted?8. Did the disease first strart with :episodes of wheezing(asthma) daily productive

cough(bronchitis), breathlessness on effort(emphysema)?9. Is there any difference between asthma : indoors/outdoors, at home/at pla

ce of work, in spring/summer/autumn/winter?10. What factors start or worsen your asthma?11. Are you ever completely free from chest symptoms?12. Have you ever been treated with steroid tablets for asthma?13. How often do you use your bronchodilator spray?14. How many days/times per month: do you have asthma symptoms? Do you wake

with asthma? Do you stay home from school/work?

Atopic dermatitis : Eczema

Keratoconjunctivits

Papillary hypertrophy in upper tarsal conjunctiva

Atopic kerato-conjunctivitis

Thickened lid margins

Eczematous skin

Allergic rhinitis

Diagnosis

History : personal or family history of allergic diseases eczema, rhinitis, urticaria, atopy

Reduced PEF

PEF varies ≥ 20%PEF varies ≥ 20%

Normal lung functionreduced lung function

PEF falls ≥ 20%PEF increases ≥ 20%

Dyspnea, cough

PEF increases ≥ 15%

Normal PEF

The diagnosis is

Asthma

Beta 2 inhaler

Diary with PEF for 14days

Corticosteroid in 14days

Diary with PEF for 14days

Bronchoprovocation

Not asthma

Yes Yes

Diagnosis

History : personal or family history of allergic diseases eczema, rhinitis, urticaria, atopy

Treatment

1. Elimination of the causative agents from the environment of an allergic ast

hmatics

2. Desensitization or immunotherapy with extracts of the suspected allergen

3. Drug treatment

⑴ Adrenergic stimulants (epinephrine, beta2 agonist)

⑵ Methylxanthines (theophylline)

⑶ Anticholinergics (ipratropium bromide)

⑷ Glucocorticoids

⑸ Mast cell-stabilizing agents (cromolyn sodium, nedocromil)

⑹ Leukotriene antagonist

Prognosis and clinical course

Mortality rate from asthma is small.

Good prognosis for 50-80% of all patients, particularly whose disease is mild and

develops in childhood.

26-78% still have asthma 7-10 years after initial Diagnosis.

6-19% continue to have severe disease

20% spontaneous remission

Asthma is not progressive unlike other airway diseases such as chronic bronchitis.

Asthma developing irreversible changes in lung function : comorbid stimuli such as

cigarette smoking

Bronchial Athma Yoon Jung Oh, M.D. The Departments of Pulmonary and Critical care Medicine Ajou...

Documents