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3 - Respiratory > Asthma, COPD and Bronchiectasis > Flashcards

Asthma, COPD and Bronchiectasis Flashcards

1
Q

Define asthma

A
  • Asthma is a heterogeneous disease, usually characterized by chronic airway inflammation
  • Defined by history of respiratory symptoms such as wheeze, shortness of breath, chest tightness and cough that vary over time and in intensity, together with variable expiratory airflow limitation
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2
Q

What are the defining characteristics of asthma

A
  • Airway inflammation
    • Mainly eosinophilic but can also be non-eosinophilic or neutrophilic
  • Intermittent airflow obstruction
  • Bronchial hyper-responsiveness
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3
Q

Outline the pathogenesis of asthma

A
  • Asthma is a chronic inflammatory process driven by TH2 cells
  • Macrophage process and present antigens to T lymphocytes - activates TH2 cells
  • TH2 cells release cytokines which attract and activate inflammatory cells including mast cells and eosinophils
  • TH2 cells also activate B cells which produce IgE
  • Immediate response - type 1 hypersensitivity
    • Lasts about 20 minutes after antigen exposure
    • Allergens increase histamine and prostaglandin release from eosinophils and mast cells
      • Cause bronchial smooth muscle contraction leading to bronchoconstriction
  • Late phase response - type IV hypersensitivity
    • Occurs 3-12 hours after antigen exposure
    • Inflammatory cells including eosinophils, neutrophils and lymphocytes are attracted to the target site
      • Release cytokines which cause airway inflammation
        - Eosinophils release leukotriene and other mediators which are toxic to epithelial cells - causes shedding of epithelial cells
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4
Q

How does inflammation cause airway narrowing

A
  • Goblet cell hyperplasia causes mucus hypersecretion
  • Mucosal swelling (oedema) due to vascular leak
  • Thickening of bronchial walls due to infiltration by inflammatory cells
  • Epithelium shedding incorporated into the thick mucus
  • Smooth muscle hyperplasia stimulated by growth factor release and stimulates airway remodeling
    • Airways easier to constrict than remain constricted
      • Airway remodeling long term and also due to hypertrophy of mucus glands, thickening of basement membrane
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5
Q

Define specific allergen and give examples for asthma

A
  • Allergens cause body to develop specific IgE antibodies that target allergen
  • Pollen
  • Dust
  • Pets
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6
Q

Define non-specific allergen and give examples for asthma

A
  • Irritate airway without producing IgE antibodies
  • Perfume
  • Smoking
  • Weather changes
    • Thunderstorms - make pollen particles smaller
    • Cold - release of histamine which act as bronchoconstrictors
  • Exercise - increase oxygen demand and increases blood perfusion to lungs
  • Emotional distress
  • Drugs
  • Chemicals
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7
Q

What are the symptoms of asthma

A
  • Wheezing
  • Shortness of breath
  • Chest tightness
  • Cough
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8
Q

What tests could be used to test for asthma

A
  • Spirometry
  • Challenge test
  • Eosinophilic inflammation
  • Skin-prick test to find out if patient is allergic
  • Chest x-ray to rule out differential diagnosis
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9
Q

How is spirometry used to test for asthma

A
  • Low FEV1/FVC ratio (less than 0.70) with obstructive pattern on flow volume loop
  • Test before and after bronchodilator - if variation seen then probably asthma
    • If >15% improvement after bronchodilator, then asthma
    • If < 15% improvement after bronchodilator, could be COPD or other lung disease
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10
Q

Explain how the challenge test works

A
  • Histamine challenge airway hyper-responsiveness
  • Give doses of histamine and measure -FEV1 until it falls by 20%
  • If FEV1 does not fall significantly, then not asthma
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11
Q

Describe how eosiniphillic inflammation can be measured

A
  • Peripheral blood eosinophil count (FBC)
  • Induced sputum (eosinophils, neutrophils)
  • FeNO (exhaled nitric oxide) - marker for inflammation
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12
Q

Outline the treatment of asthma

A
  • ß2 agonists used to relieve symptoms of asthma - cause bronchodilation
    • Short acting bronchodilator - salbutamol
    • Long acting bronchodilator - formoterol
  • Corticosteroids used to treat inflammation of airways and prevent attacks
    • Inhaled corticosteroids - budesonide
      • Preferred as directly enter the target site
      • Oral corticosteroids - prednisolone
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13
Q

Describe the signs and symptoms of acute severe asthma

A
  • Worsening symptoms - cough, breathlessness, wheeze, chest tightness, chest pain
    • High respiratory rate ≥ 25/min
    • High heart rate ≥ 110/min
    • Inability to complete sentences on one breath
    • Peak expiratory flow - 33-50% best
  • Increase in pCO2 - body unable to cope with hyperventilation (life threatening asthma)
    • Possible transition from type 1 to type 2 respiratory failure
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14
Q

Describe the treatment of severe acute asthma

A
  • High flow oxygen - aim to keep sats at 94-98%
  • Nebulised salbutamol - continuous if necessary
  • Oral prednisolone (corticosteroid)
  • If still not responding, give nebulised ipratropium bromide and IV magnesium as bronchodilators
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15
Q

Describe the causes of COPD

A
  • Smoking (90%)
    • Approximately only 15% who smoke get COPD
  • Alpha-1-antitrypsin deficiency - deficiency leads to imbalance of proteinases and antiproteinases
    • Leads to destruction of alveolar walls and emphysema
  • Occupational exposure - coal dust
  • Pollution
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16
Q

Define emphysema

A
  • Swelling of alveoli loses its elasticity and causes them to permanently enlarge
  • Impairment of gas exchange
17
Q

Describe the pathogenesis of emphysema

A
  • Inflammation of the alveoli walls triggered by irritants such as cigarette smoke
    • Immune cells attracted which causes release of proteases and other inflammatory mediators
    • Proteases breakdown structural proteins such as collagen and elastin, which give lungs its elastic nature
  • When exhaling, low pressure within the alveoli/tubule and high pressure in the chest pull the walls inwards
    • Loss of elastin means walls are pulled inwards and collapse in exhalation
  • Makes lungs more compliant, as walls are able to expand more and contain more air - hyper-inflation
    • Leads to large airspaces in acinus called bullae
  • Alpha-1 antitrypsin - protease inhibitor to protect against collapse of airsacks
18
Q

Describe the pathogenesis of chronic bronchitis

A
  • Caused by inflammation in the large airways leading to proliferation of mucus producing cells
    • Goblet cells replace ciliated respiratory epithelium
  • Loss of ciliary function
  • Leads to chronic productive cough and frequent respiratory infections
  • Results in airflow obstruction due to remodelling and narrowing of the airways
19
Q

Describe hoe COPD can lead to peripheral oedema

A
  • Progressive hypoxia causes pulmonary vasoconstriction and vascular muscle thickening due to increased pulmonary resistance
    • Leads to pulmonary hypertension and right heart failure (cor pulmonale)
20
Q

Describe the symptoms of COPD

A
  • Cough and sputum production
  • Progressive breathlessness
  • Breathless on exertion
21
Q

Describe the signs of COPD

A
  • Purse lip - increases the pressure within airways and keeps airways from collapsing
    • Typical of emphysema
  • Tachypnoea - increased respiratory rate to compensate for hypoxia and hypoventilation
  • Use of accessory muscles of respiration - bending down to aid breathing
  • Barrel chest - due to hyperinflation and air trapping secondary to incomplete expiration (emphysema)
  • Hyper-resonance on percussion - air trapping
  • Reduced intensity breath sounds - caused by barrel chest, hyperinflation and air trapping
  • Reduced air entry - loss of lung elasticity and lung tissue breakdown
  • Wheezing and crackling
22
Q

Outline the investigation of COPD patients

A
  • Spirometry - obstructive pattern with FEV1/FVC ratio < 0.70
    • Both FEV1 and FVC decrease but FEV1 decreases more
    • Limited reversibility following treatment with bronchodilators
    • Normally sufficient in diagnosing COPD alongside good history
  • Decreased diffusing capacity of the lung for carbon monoxide shows emphysema
  • Chest x-ray - hyper-inflated lungs may result in flattened diaphragm, hyperlucent lungs, increased antero-posterior diameter of the chest
    • Rule out other pathologies such as lung carcinoma
  • Pulse oximetry and arterial blood gas
    • Carried out in acutely unwell patients to assess for hypoxia and hypercapnia
  • Alpha-1 antitrypsin level
    - Checked if suspicion of positive family history and atypical COPD (young patients who do not smoke)
23
Q

Outline the treatment of COPD

A
  • Smoking cessation
  • Patient education
  • Monitor patient weight, nutrition, physical activity
  • Bronchodilators and inhaled corticosteroids
  • Pulmonary rehabilitation - many patients avoid exercise because of breathlessness
    • Leads to muscle weakness, depression and social isolation
    • Pulmonary rehabilitation aims to break this cycle and suggest exercise and nutritional advice
  • Long term oxygen treatment - extended periods of hypoxia cause pulmonary hypertension
  • Surgical interventions - removal of large bullae, lung volume reduction
  • Check inhaler technique
  • Non invasive ventilation - for acute exacerbation of COPD with type II respiratory failure (when patient fails to hyperventilate)
24
Q

Describe what bronchiectasis is

A
  • Chronic dilation of one or more bronchi

- Bronchi exhibit poor mucus clearance and there is predisposition to recurrent or chronic bacterial infection

25
Q

Describe the investigation of bronchiectasis

A
  • High resolution CT scan - bronchial dilation bigger than the adjacent blood vessel
  • Bronchial wall thickening
  • Signet ring sign
26
Q

List the symptoms of bronchiectasis

A
  • Chronic cough
  • Daily sputum production
  • Breathlessness on exertion
  • Intermittent hemoptysis
  • Nasal symptoms
  • Chest pain
  • Fatigue
27
Q

Describe potential causes of bronchiectasis

A
  • Post-infection - whooping cough, TB
  • Immune deficiency - low immunoglobulin levels
  • Mucociliary clearance defects - genetic causes
    - Cystic fibrosis
28
Q

Describe the management of bronchiectasis

A
  • Treat underlying cause
  • Physio/airways clearance - mucus clearance
  • Sputum sampling - antibodies according to sputum cultures
29
Q

Describe the pathophysiology of cystic fibrosis

A
  • Autosomal recessive disorder
  • Chromosome 7 defect leads to cystic fibrosis transmembrane conductance regulator (CFTR) gene mutation
    • CFTR pumps secretes chloride ions which drives water out through osmosis
  • Mutation leads to ineffective cell surface chloride transport
  • Leads to thick, dehydrated body fluids in organs which have CFTR as water is not drawn out
    - Reduced mucus movement through cilia means that bacteria can more likely infect airways
30
Q

Describe how to diagnosis cystic fibrosis

A
  • History of CF in sibling
  • Positive newborn screening test results
  • Increased sweat chloride concentration - sweat test
    • Chloride cannot be reabsorbed
  • Genotyping - identification of two CF mutations
31
Q

Describe the presentation of cystic fibrosis

A
  • Meconium ileus - thickened meconium causing bowel obstruction in newborn
  • Intestinal malabsorption - pancreatic enzyme insufficiency
    • Thick secretions block pancreatic ducts
  • Chest infections
32
Q

Describe the management of cystic fibrosis

A
  • Maintain lung health and nutritional state
  • No smoking
  • Pancreatic enzyme supplements
  • Bronchodilators
33
Q

Distinguish between COPD and asthma

A
  • COPD has persistent, productive cough, Asthma has intermittent and usually non-productive cough
  • COPD typically due to smoking
  • COPD presents with breathlessness at night, asthma has coughing and wheezing at night
  • Asthma more common in family history
  • COPD mainly neutrophils and macrophages, asthma mainly eosinophils and mast cells
  • COPD irreversible in spirometry, asthma reversible

3 - Respiratory (16 decks)

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