Week 4 Flashcards
What is COPD
Chronic obstructive pulmonary disease - common preventable and treatable disease that is characterised by persistent respiratory symptoms and airflow limitation due to airway/alveola abnormalities. Usually consists of - air limitations - abnormal gas exchange - overproduction of mucous - pulmonary hypertension
Includes emphysema - destruction of alveoli
Chronic bronchitis - presence of cough/sputum production for at least 3 months
Risk factors for COPD
Smoking Genetic Increased age Female Exposure to particles Pollution Lower social economic class He of respiratory disease
Symptoms of COPD
Main - sputum production, chronic productive cough and dyspnoea
Other
- pursed lip breathing to help reduce WOB by keeping airway open
- chest tightness
- hypoxaemia (has trap)
- hypercapnia (gas trap)
- Fatigue
Pathophysiology of COPD
- Noxious stimuli
- Abnormal/prolonged inflammatory response
- Increased neutrophils/macrophages/lymphocytes/cytokines leading to:
- Fatigue/weight loss
- breakdown in lung parenchyma/enlargement of air space -destruction of alveoli wall/loss of elastic recoil
- bronchial irritation/inflammation = hypertrophic/hyperplasia of goblet cells = bronchial oedema + mucous hypersecretion/airway remodelling - Leads to gas trapping = hyperinflation/airflow limitations/gas exchange abnormalities
- Dyspnoea/cough/hypoxemia/hypercapnia/for pulmonale
How does gas trapping work?
Problems with air movement on expiration.
Force of Air moving in expands bronchial wall, with air going around mucous plug
During expiration, bronchial wall collapse + mucous secretion block airway. Gas can’t escape
Complications of COPD
Pulmonary hypertension Cor pulmonale - airway remodelling/gas trapping —> reduced gas exchange —> increased paco2 = hyperventilation —> can’t maintain —> hypoxemia —> pulmonary vasoconstriction to compensate reduced perfusion —> pulmonary hypertension —> R ventricle and atrium overworked = become enlarged —> cor pulmonale HF Ischemic heart disease HF Osteoporosis
Management of COPD
Smoking cessation
Reduce/eliminate risk factors
Vaccinations - flu
Pharmacology - bronchodilators/corticosteroids/combination therapy
Pulmonary rehabilitation - exercise/self management
Long term o2 therapy
Non-invasive ventilation - CPAP/BIPAP
Can be managed to decrease disease progression but not cure
Differentiate reliever and preventer
Reliever- as needed
Preventer - prevent exacerbation and control symptoms
What are the two types of relievers in asthma
Short acting beta 2 agonist (SABA)
Anticholinergic/anti muscarinic (short acting muscarinic antagonist) - SAMA
Example of a SABA, how it works and it’s adverse effect
Salbutamol - ventolin
MOA - stimulates B2 receptors found in smooth muscle of airways inhibits bronchial smooth muscle = relaxation of airway muscles
- increase airway diameter + reduce resistance + increase gas exchange + reduce work of breathing
Adverse effects : tachycardia, palpitations, tremors, fishing, headaches, HT
Example of SAMA, how it works and adverse effects
Ipratropium - atrovent
MOA: binds to muscarinic chollinergic receptors that blocks acetylcholine which inhibits bronchial smooth muscle and produces airway relaxation
- increase airway diameter + reduce resistance + increase gas exchange + reduce work of breathing
Adverse: urinary retention, dry mouth, constipation, tachycardia
What are 4 preventer medications in asthma
- Corticosteroids
- Leukotrine receptors antagonist/antileukotrine
- Mast cell stabalisers
- Long acting beta 2 agonists (LABA)
Examples of corticosteroids, it’s MOA and adverse effects
Budesonide, fluticasone, prednisolone - these are potent anti-inflammatory drugs used to decreased airway inflammation
MOA: inhibit synthesis of chemical mediators at cellular level —> inhibits PLA2 enzyme —> No PGs, leukotrines, histamine —> reduced asthma signs/symptoms
Adverse effects:
Inhaled - hoarseness, URTI, pharyngitis, rhinitis, thrush
Oral -headache, nausea, dizziness, insomnia, liver dysfunction
Examples of leukotrine receptor antagonist/antileukotrine, MOA and adverse effects
Montelukast + zafirlukast - causes bronchodilation through direct action on bronchial muscles
MOA - inhibit leukotrines which function is to trigger contraction in the smooth muscle lining in bronchioles, production is from the release of histamine/prostaglandins
Adverse che, nausea, dizziness, insomnia, gastric upset
Examples of mast stabiliser cells, MOA and adverse effects
Nedocromil (tilade) + cromoglycate (intal)
MOA: inhibit the release of allergic mediators from mast cell (histamine) - prevent bronchospasm.
Adverse- headaches, dry mucosa, nausea
