Presentation on theme: "Pathophysiology of COPD and Asthma"— Presentation transcript:
1 Pathophysiology of COPD and Asthma Fern White & tom Sutherland grant
2 Definition of AsthmaA chronic inflammatory disorder of the airways … in susceptible individuals, inflammatory symptoms are usually associated with widespread but variable airflow obstruction and an increase in airway response to a variety of stimuli. Obstruction is often reversible, either spontaneously or with treatment.Affects 5-8% of the UK population.Characterised by recurrent episodes of dyspnoea, cough, wheeze, caused by reversible airways obstruction.
3 Definition of COPDChronic obstruction of lung airflow that interferes with normal breathing and is not fully reversible. Traditionally regarded as a combination of smoking-related lung diseases - emphysema; chronic bronchitis.Common progressive disorder, affecting 10-20% of over 40s.
5 Pathophysiology of Asthma? Increase mucus production - from goblet hyperplasia, hypertrophy of mucus glands.Airway thickening - fibrosis of bronchial wall.Bronchoconstriction - smooth muscle hypertrophy.Three factors contribute to airway narrowing:Bronchial muscle contraction, triggered by various stimuliMucosal swelling / inflammation, caused by mast cell and basophil degranulation, resulting in release of inflammatory mediatorsIncreased mucus productionInflammation - mast cell degranulation, Eosinophil infiltration, inc. permeability, oedema.
7 Pathophysiology of COPD Blue bloaters: Decreased alveolar with a low pO2 and high pCO2. Irresponsive to CO2, therefore cyanosed and at risk of developing cor pulmonale.Pink puffers: Increased alveolar ventilation, near normal pO2 and normal – low pCO2. Over-responsive to CO2, therefore pink and tachypniac. Tend to be thin and at increased risk of type 1 respiratory failure.
8 How does smoking lead to lung disease? Loss of ciliaSquamous metaplasiaMucous hypersecretion (Goblet cell hyperplasia)Low grade alveolar inflammationNeutrophils counts in alveoli increasedProteinases released from inflammatory cells destroys alveolar wallsLeads to emphysemaFibrosis of small airways leads to small airways diseaseIndividual factors affect the extent and rate of these changes
9 What cells are involved? AsthmaCOPDCD4 T-lymphocytesMast cellEosinophilB cellCD8 T-lymphocytesMacrophagesNeutrophils
11 Clinical presentation AsthmaSigns/symptoms:WheezeCoughChest tightnessDyspnoeaDIBThings to look for on HxDate of onsetOther atopic diseaseFamily HxSmoking/Occupation/PetsProvocationThings to askDay time controlAmount of relieving meds requiredNight time controlCOPDSigns/SymptomsSputumSMOKINGWork HxFamily Hx (α1-antitrypsin)How long have they had a coughProductive coughClinical presentationDDX for a long-standing cough:- COPD- Asthma- V.long standing virus- Cancer
12 Diagnosing using spirometry and peak flow Asthma = Diurnal variation of >20% on 3 days a week for 2 weeks.Spirometry: Diagnose restrictive and obstructive airway diseases, using forced vital capacity (FVC) and forced expiratory volume in 1 second (FEV1).Predicted FEV1 and FVC used against Height, Weight, Age, Gender.FEV1/FVC ratios:<0.7 = obstructive lung disease (both asthma and COPD)>0.7 = restrictive lung diseaseTo diagnose asthma: an improvement in ratio should be seen following beta agonist trial.Contraindications: recent surgery, ENT disorders, recent pneumothorax, haemoptysis, communicable diseaseReversibilityGive salbutamol and retest FEV1. If increased after salbutamol it’s more likely to be asthma, not COPD
13 Know this graph! Black = Normal Blue = Obstructive (COPD) Red = RestrictiveObstructiveNarrowed airways, reduces the amount of air that can pass through at any timeReduces FEV1e.g. COPD and AsthmaRestrictiveLungs can’t expand as much, so FVC is reducede.g. Interstitial lung diseases, sarcoidosis, obesity
15 Acute asthma management O xygen high flowS albutamol nebuliserH ydrocortisone IVI pratropium bromideT heophyllineIf this isn’t working then intubate
16 Long term management of asthma Step 1: short acting beta 2 agonist (salbutamol)Step 2: Add low dose inhaled corticosteroidStep 3: Add long acting beta 2 agonistStep 4: Increase to high dose inhaled corticosteroidsStep 5: Add on therapies including oral corticosteroids
17 Management of COPDSmoking cessation advice - only way to prolong life expectancy.Bronchodilator therapy: short-acting ß2-agoinst (salbutamol); short-acting anticholinergic (ipratropium)Combination therapy: long-acting ß2-agonist (salmeterol); inhaled steroid (beclomethasone); long-acting anticholinergic (tiotropium)Oral theophylline: only if short and long-acting bronchodilators ineffective or inappropriateLong term oxygen therapy (LTOT)Infection prevention – flu jabRescue packs – steroids + antibiotics
18 Oxygen, salbutamol, hydrocortisone, ipratropium, theophilline QUIZ!Asthma is a chronic inflammatory disease that causes airway restriction, is variable and non-reversible. TRUE/FALSEThe immune cells involved in asthma are: B-cells, IgE, mast cells, eosinophils, cytokines and leukotrines TRUE/FALSEObstructive airway disease will have a FEV1/FVC ratio of > TRUE/FALSEAcute management of asthma?6. Chronic stepwise management of asthma?FALSETRUEFALSEOxygen, salbutamol, hydrocortisone, ipratropium, theophillineSalbutamol, low dose steroids, Salmeterol, high dose steroids, oral prednisolone
19 Quiz!CD8 T-lymphocytes, Macrophages, Basophils are all involved in COPD. TRUE/FALSEReversible component of COPD?Fibrosis and narrowing of the airways and loss of elastic recoil due to alveolar destruction are the irreversible causes of airflow obstruction in COPD. TRUE/FALSE.Asthma causes 3 airway pathologies What are they?FALSEBRONCHOCONSTRICTIONTRUEClassic triad of symptoms in asthma? Expiratory wheezeCoughSOB (dysnpnoea) especially at nightSmooth muscle dysfunctionAirway inflammationAirway remodelling
20 A lecherous reprobate, Shef Kirollos, 66, comes into your clinic complaining that his asthma has been getting worse. He was recently diagnosed with heart failure, and has been taking Propranalol for the condition.1. What type of drug is propranolol? (1)Beta Blocker2. What is the basic MoA of the above drug? (3)Blocks β1 receptors in the heartPrevents conversion of ATP to cAMP by adenylyl cyclase and activation of PKA, therefore reducing intracellular calciumNegative inotropic, chronotropic and dromotropic effect on the heart*Note there are β1 and β2 receptors in both lung and heart, but β1 strongly predominates in heart, and β2 strongly predominates in lungs3. Why might it be a bad idea to give someone with asthma propranolol?Propranalol has an antagonist effect on beta receptors in the lungs -> resulting in smooth muscle constriction -> further narrowing of already narrowed airways -> exacerbating the effects of asthma
21 Thank-you! Any questions? F.email@example.com
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