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Block 2 > Obstructive Airways Disease > Flashcards

Obstructive Airways Disease Flashcards

1
Q

What are the 2 main categories of obstructive airways disease?

A

Asthma

COPD

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2
Q

When is the onset of asthma most common?

A

Childhood

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3
Q

What are the 3 main causes of asthma?

A

Genetic factors (predisposition)

Environmental factors

Acute triggers

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4
Q

Name some specific causes and triggers of asthma

A

Environmental allergens:

  • Mould
  • Dust
  • Pet hair
  • Pollen

Occupational sensitisers:

  • Chemicals
  • Latex
  • Wood dust

Exercise

Atmospheric pollution

Drugs:

  • NSAIDs
  • B-blockers

Cold air

Emotion

Viral infections

Genetic predisposition

Irritant vapours

  • Perfumes
  • Cigarette smoke
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5
Q

What are the 2 broad types of asthma?

A

Extrinsic (atopic): The result of an inappropriate adaptive immune response to an inhaled antigen

  • Associated with atopy (e.g. eczema, hay fever)
  • Typical onset in childhood
  • Sensitisation and effector phases
  • Generally eosinophilic inflammation

Intrinsic (non-atopic):

  • No personal or family history of asthma/atopy
  • Typical onset in middle age
  • Often onset following upper airway infection
  • Generally neutrophilic inflammation
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6
Q

What histological changes occur in asthma?

A

Goblet cell hyperplasia

Thickening of basement membrane

Hypertrophy of smooth muscle (in response to hyper-reactivity)

Increase in inflammatory cells (macrophages, eosinophils, neutrophils, lymphocytes, mast cells)

Increase in size of mucus glands in submucosa

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7
Q

What is the sensitisation phase of asthma?

What is the effector phase?

A

Sensitisation phase

  • Allergen is taken up by dendritic (antigen presenting) cell
  • Presented to TH2 lymphocyte
  • Other immune cells (e.g. B-cells) primed to rapidly secrete IgE in presence of antigen.
  • B-cells secrete IgE

Effector phase:

  • IgE binds to mast cells (major effector)
    • On second major exposure to antigen this will respond.
  • Mast cells secrete a number of immune substances in response to antigen:
    • Histamine
    • Tryptase
    • LTC4
    • = ACUTE RESPONSE- BRONCHOCONSTRICTION
  • Also recruit inflammatory cells:
    • Eosinophils
    • T-lymphocytes
    • = LATE RESPONSE-
      • Mucus secretion
      • Vascular leak → oedema
      • Immune cell infiltration
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8
Q

Which immune cell predominates in atopic asthma?

A

Eosinophils

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9
Q

Which immune cell predominates in non-atopic asthma?

A

Neutrophils

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10
Q

Why are anticholinergic inhalers given in the acute phase of asthma?

A

To inhibit the cholinergic reflex brought about by irritatation of sensory nerves in the bronchi which leads to bronchoconstriction

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11
Q

What occurs in the immediate/early phase of asthma?

What occurs in the late phase?

A

Immediate/early phase

Mast cells activated by cross-linked IgE secrete substances such as histamine and tryptase which cause broncho constriction.

Late phase

Mast cells activated in the early phase also activated T-lymphocytes which secrete substances such as IL-3, IL-5, TNF which recruit neutrophils and eosinophils.

  • These substances, neutrophils and eosinophils cause vascular leak (oedema), increased mucus secretion and immune cell infiltration (inflammation).
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12
Q

What are the symptoms of chronic asthma?

A

History:

  • Quick onset, quick recovery of symptoms
  • Acute exacerbations (asthma attacks)
  • Cough
  • Wheeze (turbulent flow)
  • Chest-tightness
  • SOB often worse at night
  • Often associated atopy/allergens
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13
Q

What are the symptoms of an acute exacerbation of asthma?

A
  • Wheeze
  • Tachypnoea
  • Tachycardia
  • Inability to complete sentences
  • Use of accessory muscles
  • Reduced breath sounds if severe
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14
Q

How is asthma diagnosed?

A

Strong suspicion of asthma:

  • Trial of treatments and assess response
  • Good response = asthma
  • Poor response =
    • Spirometry before and after salbutamol (bronchodilator reversibility)
    • Diurnal variation of peak flow monitoring
    • Histamine challenge tests (asthmatics require small amounts to intiate bronchoconstriction)
    • FeNO (fraction of exhaled)
    • Blood oesinophils
    • Skin prick test
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15
Q

What occurs in the remodelling (chronic) phase of asthma?

A
  • Smooth muscle and epithelial cell hyperplasia
  • Smooth muscle hypertrophy
  • Basement membrane thickening
  • Goblet cell hypertrophy, excess mucous production
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16
Q

What are the classifications of acute asthma?

A

Moderate

  • Increasing symptoms
  • PEF >50-75% best of predicted
  • No features of acute severe asthma

Acute Severe Asthma

  • Any one of:
    • PEF 33-50% best or predicted
    • Respiratory rate >25/min
    • Heart rate >110/min
    • Inability to complete sentences in one breath

Life Threatening Asthma

  • Any one of:
    • Altered conscious level
    • Exhaustion
    • Arrhythmia
    • Hypotension
    • Cyanosis
    • Silent chest
    • Poor respiratory effort
    • SpO2< 92%
    • PEF <33% of best or predicted
    • pO2<8kPa (CO2 normal)

Near fatal asthma:

  • Symptoms of life threatening asthma + pCO2 raised or requiring mechanical ventilation.
17
Q

Why is pCO2 often normal in patients with life threatening asthma?

A

Hyperventilation leads to excretion of CO2 causing hypocapnia. As bronchoconstriction gets worse and air trapping worsens, pCO2 rises and reaches a point where it is normal before it becomes raised.

18
Q

How is an acute asthma exacerbation managed?

A

Oxygen

  • sats 94-98%

B2 agonist bronchodilators

  • Salbutamol or terbutaline (nebs/spacers) every 15-30 mins

Corticosteroids

  • To address inflammation
  • Prednisolone PO or IV hydrocortisone
  • Minimum 5 days

Anticholinergics

  • Ipratropium- add to nebulisers if poor initial response to bronchodilators
19
Q

What is used to treat the immediate/early phase acute asthma?

A

B2 agonists

Anticholinergics

Leukotreine antagonists

20
Q

What is used to treat the late/inflammatory phase of asthma?

A

Glucocorticoids

21
Q

What is COPD?

What are the 2 main types?

A

Chronic, irreversible, obstructive airway changes.

  • Chronic bronchitis
  • Emphysema
22
Q

What is emphysema?

A

Occurs in peripheral bronchioles and alveoli:

  • Alveolar wall destruction
  • Air space enlargement
23
Q

What is chronic bronchitis?

A

Occurs in larger airways (bronchi, bronchioles)

  • Mucus gland hypertrophy and hyperplasia = mucus hypersecretion
24
Q

What are the causes of COPD?

A
  • Smoking
  • a1-antitrypsin deficiency (genetic predisposition)
  • Pollutants (e.g. asbestos)
25
Q

What are the causes of airway obstruction in COPD?

Which of these are reversible and which are irreversible?

A

Reversible:

  • Accummulation of plasma exudate, inflammatory cells and mucus in the bronchi
  • Smooth muscle contraction in peripheral and central airways
  • Dynamic hyperinflation during exercise

Irreversible:

  • Fibrosis and narrowing of airways
  • Loss of elastic recoil due to alveolar destruction
  • Destruction of alveolar support that maintains patency of small airways
26
Q

What are the clinical symptoms of COPD?

A
  • Productive cough (sputum)
  • Wheeze
  • Dyspnoea
  • Frequent infective exacerbations with purulent sputum production
  • Signs of respiratory failure, cor pulmonale
27
Q

How is COPD diagnosed?

A

Spirometry: reduced FEV1 : FVC ratio

CXR: may show hyperinflation but may also be normal.

Haemoglobin may be raised in chronic hypoxia

28
Q

How is COPD managed?

A

Bronchodilators:

  • Short acting B2 agonists (salbutamol, terbutaline)
  • Anticholinergics (ipratropium bromide)

Smoking cessation

Combination therapy:

  • Long acting B2 agonist (salmeterol, formoterol) + inhaled corticosteroid (beclometasone, fluticasone)

Home oxygen

Pulmonary rehabilitation (MDT management)

Vaccinations: pneumococcal, influenza

Block 2 (46 decks)

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