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Human Diseases > 18.1 Asthma and COPD > Flashcards

18.1 Asthma and COPD Flashcards

1
Q

Describe what asthma is.

A

A chronic inflammatory disease of the airways characterised by variability of symptoms and reversible airway obstruction.
Airways become narrowed due to bronchoconstriction and mucous hypersecretion.

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2
Q

What are the clinical symptoms of asthma?

A
  • Wheeze
  • Chest tightness
  • Cough
  • Mucous production
  • Shortness of breath
  • Airway hyper-responsiveness = twitchy/sensitive airways e.g. bronchospasm after entering a room filled with smoke
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3
Q

How does airway obstruction reverse in asthma?

A

Can reverse spontaneously or due to treatment with beta-2-agonists or anti-inflammatory agents (corticosteroids)

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4
Q

What factors influence the variability of asthma?

A
  • Allergens
  • Cigarette smoke
  • Respiratory infection
  • Exercise and hyperventilation
  • Weather changes
  • Air pollutants
  • Food, additives, drugs
  • Cold/damp
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5
Q

Describe the epidemiology of asthma.

A
  • Very common, affects at least 300 million people worldwide
  • Responsible for 1 in every 250 deaths worldwide
  • 15% prevalence in Western world
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6
Q

What are some hypotheses for why asthma is becoming more common?

A
  • Hygiene hypothesis (less bacteria, immune system less busy resulting in autoimmune response)
  • Dust mites
  • Pollution
  • Polyunsaturated fats
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7
Q

What are some risks for developing asthma?

A
  • Genetics
  • Maternal smoking
  • Viral infections in infancy
  • Pre-term birth
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8
Q

Provide a simple overview of the pathophysiology of asthma.

A

More than 1 inflammatory pathway, more than 1 phenotype.
- Early onset asthma: associated with allergy, inflammation mediated by antigen binding to serum IgE
- Late onset asthma: non-allergy related, mediated by eosinophils and neutrophils

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9
Q

Describe early onset asthma (allergy).

A
  • Antigen binds to IgE
  • Degranulation of mast cells
  • Histamine release
  • Leukotrine release
  • Inflammation in airways
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10
Q

Describe the cells involved in the pathophysiology of asthma.

A
  • Neutrophils, mast cells, eosinophils, Th2 cells work together and upregulate inflammatory mediators
  • Upregulates mucous secretion
  • Sensory nerve activation = bronchoconstriction and hypertrophy of the smooth muscle
  • Plasma leakage and oedema, also contributes to bronchoconstriction
  • Over time, epithelial shedding occurs, can cause epithelial fibrosis if asthma is left untreated- permanent airway damage
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11
Q

Summarise the causes of smooth muscle dysfunction and airway inflammation in asthma.

A
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12
Q

How can airway obstruction be measured?

A
  • Peak flow meter
  • Spirometry
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13
Q

How is asthma diagnosed?

A

There isn’t one test that accurately diagnoses asthma.
Thorough history is required.
Investigations are used to help to confirm a diagnosis.

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14
Q

What is the typical presentation of a patient with asthma?

A
  • History of intermittent and variable wheeze, cough, breathlessness
  • Tend to get worse with exertion and specific triggers
  • Symptoms tend to be worse at night as cortisol drops (anti-inflammatory and bronchodilator)
  • Improves with salbutamol short term, steroids long term
  • May have a history of atopy (rhinitis, eczema etc), family history
  • Ask about occupation e.g. baker, paint sprayer, construction
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15
Q

What investigations are carried out to support an asthma diagnosis?

A
  • Ask patient to keep diary and record peak flow measurements
  • Spirometry before and after salbutamol (beta 2 agonist), if FEV1 improves by 200ml and 15% they likely have asthma
  • Exercise testing with pre and post spirometry
  • Skin prick tests
  • Blood tests (IgE levels/RAST)
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16
Q

What are FEV1 and FVC?

A

FEV1 = forced expiratory volume in 1 second
FVC = forced vital capacity (the amount of air that can be forcibly exhaled from your lungs after taking the deepest breath possible)

FEV1 and FVC ratio is important, measured using spirometry.

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17
Q

What are the aims of asthma management?

A
  • No daytime symptoms
  • No night-time awakening due to asthma
  • No need for rescue medication
  • No exacerbations
  • No limitations on daily activity including exercise
  • Normal lung function
  • Minimal side effects from medication
18
Q

What are the consequences of poor asthma control?

A
  • Exacerbations
  • Development of chronic, irreversible asthma
  • Epithelial fibrosis
19
Q

What closed questions should be asked by a dentist to an asthma patient?

A
  • Have you had any daytime asthma symptoms recently?
  • Have you needed to use your blue inhaler recently?
  • Do you wake up in the middle of the night due to your asthma?
  • Have you had an attack or needed emergency medical attention recently?
20
Q

What inhaled medication is used to manage asthma?

A
  • Inhaled steroids are used as a long term preventer (e.g. beclamethasone- brown inhaler)
  • Beta-2-agonist for immediate relief (e.g. salbutamol- blue inhaler)
  • Pts begin with a low dose corticosteroid inhaler and the dose is increased if symptoms persist
21
Q

What non-inhaler treatment is used to manage asthma?

A
  • Antihistamines
  • Steroid tablets
  • Aminophylline (bronchodilator)
  • Montelukast
  • Nebuliser
  • Omalizumab injection (biological theropy which ‘mops up’ IgE)
22
Q

What may cause difficult asthma/poorly controlled asthma?

A
  • Lack of compliance with inhalers
  • Poor inhaler technique
  • Incorrect diagnosis
  • Peristent exposure to allergen or trigger?
  • Concomitant allergic rhinitis
  • Other drugs making asthma control worse e.g. beta blockers, NSAIDs
  • Smoking, pollution, stress, occupation
23
Q

What is an asthma exacerbation?

A
  • Sustained worsening of symptoms, usually accompanied by a fall in peak flow
  • Either due to poor control or viral illness
  • Can often lead to hospital admission
24
Q

What is chronic obstructive pulmonary disease?

A

A treatable and preventable condition, characterised by airflow obstruction, which is usually progressive- not fully reversible and does not change markedly over several months (unlike asthma which is a variable condition).

  • Airflow obstruction is associated with an abnormal inflammatory response in the lungs in response to noxious stimuli
  • Primarily affects the lungs but also produces systemic consequences
25
Q

What other systemic conditions are associated with COPD?

A
  • Osteoporosis
  • Loss of fat free mass (cachexia)
  • Type 2 diabetes
  • Peptic ulcers
  • Cardiovascular disease
  • Chronic renal impairment
26
Q

What are the differences between chronic bronchitis, emphysema and COPD?

A

Doesn’t necessarily include asthma, but asthma and COPD are likely to exist together.

27
Q

Describe the multi-component disease process of COPD.

A
  • Noxious particles set up a cascade of epthileal damage
  • Direct inflammation of airway
  • Loss of elastic recoil
  • Airway obstruction
  • Difficult to get air out
28
Q

What are the consequences of COPD inflammation?

A
  • Fixed airway obstruction, narrowing
  • Impaired gas exchange as alveoli are affected
  • Reduced exercise tolerance
  • Progressive deconditioning and disability
  • Recurrent infections and exacerbations
  • Respiratory failure (chronically low oxygen levels)
  • Pulmonary hypertension
29
Q

Describe the fatality rates of COPD.

A
  • 3rd biggest killer worldwide
    Causes of death in COPD:
  • Pulmonary cause
  • Cardiovascular cause
  • Cancer
  • Other
30
Q

How is a COPD diagnosis made?

A

COPD diagnosis is considered in patients over 35 who:
- Are smokers or ex-smokers
- With symptoms including exertional breathlessness, chronic cough, regular sputum production, frequent winter ‘bronchitis’, wheeze
- Have evidence of airflow obstruction on spirometry
- Have no clinical features of asthma

31
Q

COPD vs asthma diagnosis.

A
32
Q

What are the differences in the inflammatory processes behind COPD vs asthma?

A
  • Asthma: humoral immune pathway
  • COPD: cellular immune pathway
33
Q

At what age does FEV1 peak?

A

Age 25, then gradually decreases for the rest of your life.

34
Q

How is COPD severity graded?

A

Stage 1-4

35
Q

How is COPD managed?

A
  • Smoking cessation
  • Inhaled therapy
  • Beta-2-agonists
  • Anti-cholinergic drugs
  • Combination inhalers
  • Oxygen therapy
36
Q

Explain smoking cessation in COPD management.

A
  • Most beneficial and cost effective measure
  • Nicotine replacement therapy e.g. patches, lozenges
  • Bupropion can be prescribed but has severe side effects
  • Varenicline (Champix) can be prescribed to assist smoking cessation
37
Q

Describe the inhalers that can be used to manage COPD.

A
  • Main treatment is bronchodilators e.g. beta-2 agonists: salbutamol (short term relief/SABA) salmeterol (longer term relief/LABA)
  • Anti-cholinergic drugs: ipratropium (SAMA) and tiotropium (LAMA)
  • Combination inhalers: inhaled corticosteroid + LABA. Indicated for frequent exacerbations. Potential risk of pneumonia.
38
Q

Describe oxygen therapy in the management of COPD.

A
  • For pts with low oxygen levels, NOT for breathlessness
  • Over-prescribed, can be dangerous
  • Not to be given to smokers, fire hazard
39
Q

What other treatments can be used for COPD?

A
  • Oral steroids
  • Theophylline
  • Mucolytics
  • Diuretics for cor pulmonale (right side heart failure)
40
Q

What are acute exacerbations of COPD?

A
  • Increased severity of cough
  • Change in sputum volume and purulence
  • Increased dyspnoea
  • Wheeze, fatigue, oedema
  • 70-80% of cases due to infection
  • 20% idiopathic or due to air pollution
41
Q

Why are acute exacerbations of COPD important?

A
  • Increased lung function loss
  • Worse health status
  • Patients experiencing frequent exacerbations have a worse prognosis
  • Approx. 40% of patients admitted to hospital due to exacerbation die within a year
  • Higher risk of mortality of COPD exacerbation compared to heart attack
42
Q

How is acute COPD exacerbation treated?

A
  • Good supportive care, hydration, nutrition
  • Regular bronchodilation using short acting beta-2 agonist
  • Chest physiotherapy with mucolytic agents if mucous plugging is an issue
  • If they are hospitalised, they will be given oral steroids
  • Antibiotics not given needlessly (greener sputum = more likely antibiotics necessary)

Human Diseases (47 decks)

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