Lecture 5 asthma and copd

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SMS2053

Transcript of Lecture 5 asthma and copd

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SMS2053

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Overview

What is COPD?How do I know if I have COPD?How common is it?

– General population– Mining population

What increases my risk of developing COPD?

How can I prevent getting COPD?How is COPD treated?

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What is COPD?

A set of lung diseases that limit air flow and is not fully reversible.– COPD patients report they are “hungry” for air– Usually progressive and is associated with

inflammation of the lungs as they respond to noxious particles or gases

– Potentially preventable with proper precautions and avoidance of precipitating factors

– Symptomatic treatment is available

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Two Major Causes of COPD

Chronic Bronchitis is characterized by– Chronic inflammation and excess mucus

production– Presence of chronic productive cough

Emphysema is characterized by– Damage to the small, sac-like units of the lung

that deliver oxygen into the lung and remove the carbon dioxide

– Chronic cough

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What can cause COPD?

Smoking is the primary risk factor– Long-term smoking is responsible for 80-90 % of

cases Prolonged exposures to harmful particles and

gases from: – Industrial smoke, – Chemical gases, vapors, mists & fumes– Dusts from grains, minerals & other

materials

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Other Risk Factors for COPD

History of childhood respiratory infections

Genetic makeup

Increasing age

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Pathogenesis of Chronic Bronchitis and Emphysema

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Pathophysiology

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Emphysema Pathology (Histology)

– Hyperinflation of alveoli– Destruction of alveolar walls– Destruction of alveolar capillary walls– Narrowed airways– Loss of lung elasticity– Small bronchioles become obstructed as a result of

• Mucus• Smooth muscle spasm• Inflammatory process• Collapse of bronchiolar walls

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Emphysema Emphysema is an enlargement of air

spaces caused by destruction of alveolar walls.

Air spaces greater than one cm are bullae.

This photo shows apical bullous disease with relatively little involvement of the rest of the lung.

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Chronic BronchitisPathology (Histology)

Pathologic lung changes are: Hyperplasia of mucus-secreting glands in trachea and

bronchi Increase in goblet cells Disappearance of cilia Chronic inflammatory changes and narrowing of small

airways Hyperplasia of mucus glands Inflammatory swelling Excess, thick mucus

Altered of alveolar macrophages infections

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Normal versus Diseased Bronchi

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Chronic Bronchitis

Chronic bronchitis:Scarring or fibrosis of the walls of the bronchioles causing narrowing of the airway

Production of excessive quantities of thick mucus which further plugs the tubules and compromises breathing

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Primary Symptoms

Chronic Bronchitis– Chronic cough– Shortness of breath– Increased mucus– Frequent clearing of throat

Emphysema– Chronic cough– Shortness of breath– Limited activity level

Death from emphysema is related to:1. Pulmonary failure with respiratory acidosis, hypoxia and coma.2. Right-sided heart failure.

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Difference between COPD and Asthma

In COPD there is permanent damage to the airways. The narrowed airways are fixed, and so symptoms are chronic (persistent). Treatment to open up the airways, is therefore limited.

In asthma there is inflammation in the airways which makes the muscles in the airways constrict.

This causes the airways to narrow. The symptoms tend to come and go, and vary in severity from time to time.

Treatment to reduce inflammation and to open up the airways usually works well.

COPD is more likely than asthma to cause a chronic (ongoing) cough with sputum.

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Difference between COPD and asthma (cont…)

Night time waking with breathlessness or wheeze is common in asthma and uncommon in COPD.

COPD is rare before the age of 35 whilst asthma is common in under-35.

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COPD Diagnostic tests

SymptomsPhysical examinationSample of sputum Chest x-rayHigh-resolution CT (HRCT scan)Pulmonary function test (spirometery) Arterial blood gases testPulse oximeter

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Ways to prevent or slow the progression of COPD

Stop smoking, if you smoke, to prevent further damage to your body– Smoking cessation is critical for all severities of

COPD

Avoid or protect yourself from exposures to– Second-hand smoke and– Other substances such as chemical vapors,

fumes, mists, dusts, and diesel exhaust fumes that irritate your lungs

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How is COPD Treated?

COPD can be managed, but not cured

Treatment is different for each individual and is based on severity of the symptoms

Early diagnosis and treatment can– Slow progress of the disease– Relieve symptoms– Improve an individual’s ability to stay active– Prevent and treat complications– Improve quality of life

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When should you see your doctor?

If smoker, see doctor for baseline evaluation of your lungs

When first experiencing shortness of breath or having other lung symptoms

When your symptoms get worse

Seek emergency medical treatment if: Breathing suddenly becomes more difficult

If diagnosed with chronic bronchitis, emphysema or COPD, see doctor 1-2 times yearly to review your treatment plan

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What medications are used to treat symptoms?

Short-acting bronchodilator inhalers such as salbutamol and terbutaline

Long-acting bronchodilator inhalers such as salmeterol (Seretide), formoterol (flutiform)

Bronchodilators – Theophylline tablets Relaxes muscles around airways

Oxygen therapy Helps with shortness of breath

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long-acting β2 agonist and inhaled corticosteroid

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Chronic Obstructive Pulmonary Diseases

Bronchial asthmaChronic relapsing inflammatory disorder

characterized by hyperactive airways leading to episodic, reversible bronchoconstriction owing to increased responsiveness of the tracheobronchial tree to various stimuli.

It has been divided into two basic types:1. Extrinsic asthma.2. Intrinsic asthma.

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Extrinsic AsthmaInitiated by type 1

hypersensivity reaction induced by exposure to extrinsic antigen like food, pollen, dust, etc.

Subtypes include:a. atopic (allergic) asthma.b. occupational asthma.c. allergic bronchopulmonary aspergillosis.

Develop early in life

Intrinsic Asthma

• Initiated by diverse, non-immune mechanisms, including ingestion of aspirin, pulmonary infections, cold, inhaled irritant, stress and exercise.• No personal or family history of allergic reaction.• Develop later in life

CLASSIFICATION OF ASTHMA

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**Some Potential Asthma Triggers**Allergens — Pollen, pet dander, fungi, dust mitesCold airFragrances and chemicalsFood and drinksPollutantsCigarette smokeStrong emotionsExerciseRespiratory tract infections

Bronchial asthma

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Extrinsic Asthma

Atopic (allergic) asthma is the most common form, begins in childhood

Other allergic manifestation: allergic rhinitis, urticaria, eczema.

Other family member is also affected

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Pathogenesis of Bronchial AsthmaExaggerated Bronchoconstriction Two components:

1. Chronic airway inflammation.2. Bronchial hyperresponsiveness.

The mechanisms have been best studied in atopic asthma.

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Pathogenesis

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Pathogenesis of Atopic Asthma• IgE-mediated reaction to inhaled allergens

elicits: 1. acute response (within minutes) 2. a late phase reaction (after 4-8 hours)

In the airway – initial sensitization to antigen (allergen) with stimulation of TH2 type T cells and production of cytokines (IL-4, IL- 5, and IL-13).

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Pathogenesis of Atopic AsthmaAcute-phase response Begin 30 to 60 minutes after inhalation of antigen.Mast cells on the mucosal surface are activated.Mediator produced are :

Leukotrienes C4, D4 & E4 (induce bronchospasm, vascular permeability & mucous production)

Prostaglandins D2, E2, F2 (induce bronchospasm and vasodilatation) Histamine ( induce bronchospasm and increased vascular permeability) Platelet-activating factor (cause agggregation of platlets and release of

histamine) Mast cell tryptase (inactvate normal bronchodilator).

Mediators induce bronchospasm, vascular permeability & mucous production.

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Pathogenesis of Atopic Asthma Late phase reaction:

Recruitment of leukocytes mediated by product of mast cells including:

1. Eosinophil and neutophil chemotactic factors 2 . IL-4 & IL-5 and induceTH2 subset ofCD4+ T cells

3. Platelet-activating factor 4. Tumor necrosis factor.Other cell types are involved: activated epithelial cells,

macrophages and smooth muscle.

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Pathogenesis of Atopic AsthmaLate phase reaction:The arrival of leukocytes at the site of mast cell

degranulation lead to: 1. Release of more mediators to activate more mast cells2. Cause epithelial cell damage .

Eosinophils produce major basic protein, eosinophilic cationic protein and eosinophil peroxidase ( toxic to epithelial cells).

These amplify and sustains injury without additional antigen.

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Non-Atopic AsthmaTriggered by respiratory tract infection

including viruses and inhaled air pollutants e.g. sulfur dioxide, ozone.

Positive family history is uncommon.Serum IgE – normal.No other associated allergies.Skin test – negative.Hyperirritability of bronchial tree.Subtypes:

1. Drug-induced asthma. 2. Occupational asthma.

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Morphology of Asthma

Grossly: - Lung over distended (over inflation), occlusion of bronchi and bronchioles by thick mucous.

Histological finding: mucous contain Curschmann

spirals, eosinophil and Charcot-Leyden crystals.

Thick BM.Edema and inflammatory

infiltrate in bronchial wall.Submucosal glands increased.Hypertrophy of the bronchial

wall muscle.

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Normal

Asthma patient

Epithelial remodelingApoptosis

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Curschmann spiralsCoiled, basophilic plugs of mucus formed in the lower

airways and found in sputum and tracheal washings

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Clinical signsClassic asthmatic attack – Dyspnea, Persistent/recurrent coughWheezingChest tightnessDifficult expiration, progressive hyperinflation of lung and

mucous plug in bronchi. Status asthmaticus – severe cyanosis and

persistent dyspnea, may be fatal.May progress to emphysema.

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DiagnosisSpirometry

Breathing test which measures the amount and rate at which air can pass through the airways

Bronchodilator Reversibility TestingRelaxing tightened muscles around the airways and opening up

airways quickly to ease breathingOther pulmonary function testing

Diffusion capacityChest X-rayArterial Blood Gas

Shows oxygen level in blood

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Asthma Medications: Bronchodilators2-adrenergic agonists

Rapid onset: quick relief of bronchoconstriction Acts in minutes, lasts 4 to 8 hoursTreatment of choice for acute attacks If used too much causes tremors, anxiety, tachycardia, palpitations,

nausea Short-acting

Albuterol(Proventil, Ventolin); metaproterenol (alupent); bitolterol (tornalate)

Continuous -adrenergic agonist nebulizer therapy may be given

Bronchodilators : Theophylline (relaxing bronchial smooth muscle, anti-inflammatory effects)

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AsthmaDrug Therapy

Antiinflammatory drugsCorticosteroids (e.g., beclomethasone, budesonide)

Suppress inflammatory response Inhaled form is used in long-term control Systemic form to control exacerbations and manage

persistent asthma

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Emphysema: Dilated air spaces beyond respiratory arteriols

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Chronic Bronchitis: Persistent productive cough for at least 3 consecutive months in at least 2 consecutive years, smoking related

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Asthma: Dyspnea and wheezing

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Case Study A 64 year old gentleman presents to emergency

department with shortness of breath, cyanosed lips and cough productive of thick, green sputum. He has a past medical history of asthma as well he has smoked 20 cigarettes a day for the past 40 years. Physical examination showed heart rate 144, respiratory rate 40, PaO2/Fio2=.21. .O/E he is using his accessory muscles to breathe, bilateral diffuse coarse crepitations and widespread wheeze.

Identify the diagnosis of the disease and describe the pathogenesis of both condition.

Describe the pathological changes in lung section. Describe the treatment options for the patient.

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