community/GP Flashcards
what are the three characteristics of asthma ?
- airflow limitation - usually reversible spontaneously or with treatment
- airway hyper-responsiveness
- bronchial inflammation with T lymphocytes, mast cells, eosinophils with associated plasma exudation, oedema, small muscle hypertrophy, mucus plugging and epithelial damage
what are the two main types of asthma?
allergic/eosinophilic asthma (allergens e.g. fungal allergens and pets etc) and atopy
Non-allergic/non-eosinophilic - exercise, cold air and stress, smoking and non smoking associated, obesity associated.
what is atopy?
individuals who readily develop IgE against common environmental antigens such as house-dust mites, grass pollen and fungal spores leading to elevated IgE serum levels is linked to airway hyper-responsiveness and the prevalence of asthma
what environmental factors can influence asthma?
early childhood exposure to allergens and maternal smoking has a major influence on IgE production
growing up in a clean environment may predispose towards an IgE response to allergens where as growing up in a dirtier environment may allow the immune system to avoid developing allergic reaction
what are the risk factors for asthma?
personal history of atopy family history of asthma or atopy obesity inner-city environment premature birth socio-economic deprivation
what are precipitating factors for asthma?
occupational sensitizers such as wood dust, bleaches and dyes, isocyanates and latex can cause occupational asthma
- cold air and exercise
- atmospheric pollution and irritant dusts
- diet - more fruit and veg is protective
- drugs such as NSAIDs particularly aspirin which can trigger attacks, also beta-blockers have a direct parasympathetic innervation that results in bronchoconstriction which results in airflow limitation and potential attack - do not give beta blockers to someone who has asthma
- allergen induced asthma
what is the clinical presentation on asthma?
intermittent dyspnoea wheeze cough sputum symptoms worse at night episodic shortness of breath
during an asthma attack what would you see?
reduced chest expansion
prolonged expiratory polyphonic time
bilateral expiratory polyphonic wheeze
tachypnoea
what are the symptoms of uncontrolled asthma?
PEFR less than 50%
respiratory rate less than 25
pulse less than 110
normal speech
what are the symptoms of a severe asthma attack?
inability to complete sentences
pulse greater than 110 bpm
resp rate greater than 25/min
what are the symptoms of a life threatening asthma attack?
silent chest confusion and exhaustion cyanosis bradycardia PEFR less than 33%
how do you manage an acute asthma attack?
O SHIT ME
O - ocygen therapy to maintain sats at 94-98%
S - salbutamol - back to back nebulisers 5mg per hour
H - hydrocortisone or prednisolone
I - ipratropium nebulised - if there is poor response or if life threatening
T - theophylline - Aminophylline if unresponsive
M - magnesium sulphate
E- escalate care
ABG and repeat within 2 hours if severe attack or if the patient is detonating
CXR - if fails to respond to treatment
check PEFR within 15-30 mins/regularly
oximetry to ensure Sao2 is greater than 93%
what are some DD for asthma?
pulmonary oedema, COPD, large airway obstruction cause by foreign body/tumour, pneumothorax, bronchiectasis
what are the questions you would ask to try and help diagnose uncontrolled asthma?
RCP3 questions - recent nocturnal waking usual asthma? - usual asthma symptoms in the day? - is it interfering with you ADLs?
what are the methods you can use to see if asthma is controlled?
RCP3 questions
asthma control test (25=well controlled, 20-24 = on target, less than 20 = off target)
lung function tests
exercise tests
trial of corticosteroids
exhaled nitric oxide - means of eosinophilic inflammation and an index of corticosteroid response - used to assess the efficacy of corticosteroids
blood and sputum tests
skin prick tests to help identify allergic trigger factors
how can you distinguish between asthma and COPD?
COPD is a later disease and more dominantly smokers
more of a relentless progressive shortness of breath with wheeze as part of the symptom complex
less day-day variation
winter symptoms and sputum production in COPD overlap can occur
how is asthma treated?
first of all control extrinsic factors when specific allergen triggers are identified
- mild SABA - 2 puffs when required
- SABA + ICS (low dose)
- SABA + LABA or tiotropium + ICS (low or medium dose)
- SABA + LABA or tiotropium + ICS (medium)
- SABA + LABA or tiotropium + ICS (high dose) plus immunomodulator (omalizumab)
- oral corticosteroid + ICS (high dose) + LABA or tiotropium + immunomodulator + SABA
what are some examples of SABA?
salbutamol
Terbutaline
what are some examples of LABA?
salmeterol
formoterol
what is ipratropium and tiotropium?
muscarinic antagonists
what are some examples of inhaled corticosteroids that can be used?
beclomethasone, prednisolone, budesonide
what is COPD?
a disease state characterised by airflow limitation
NOT fully reversible
usually progressive and associated with abnormal inflammatory response of the lungs to noxious particles or gases
what is COPD associated with the envelopment of?
chronic bronchitis - cough with sputum for 3 months for 2 or more years
Emphysema - histologically its enlarged airspaces distal to terminal brocnhioles with destruction of alveolar walls
what are the causes of COPD?
- cigarette smoking is the major cause of COPD
- chronic exposures to: pollutants at work, outdoor air pollution, inhalation of smoke from biomass fuels used in heating and cooking in poorly ventilated areas
- alpha-1 antitrypsin deficiency causes early onset COPD
what is alpha-1 antitrypsin deficiency?
causes early onset COPD (due to proteolytic lung damage)
a rare cause of cirrhosis (due to an accumulation of the abnormal protein in the liver mutations in the alpha-1 antitrypsin gene on chromosome 14 lead to reduced hepatic production of alpha 1 antitrypsin which normally inhibits proteolytic enzyme - neutrophil elastase
what is chronic bronchitis?
airway narrowing - hypertrophy and hyperplasia of mucus secreting glands of the bronchial tree, bronchial wall inflammation and mucosal oedema
inflammation is followed by scarring and thickening of the walls which narrows the small airways
chronic bronchitis = blue bloaters
what is emphysema?
dilatation and destruction of the lung tissue distal to the terminal bronchioles
results in loss of elastic recoil, which normally keeps the airways open during expiration
leads to expiratory airflow limitation and air trapping
patients with emphysema are referred to as the pink puffers
what do patients with COPD get V?Q (ventilation/perfusion) mismatch?
mismatch is partly due to damage and mucus
plugging of smaller airways from the chronic inflammation and partly due
to rapid closure of smaller airways in expiration owing to the loss of
elastic support
what does V/Q mismatch cause?
- this mismatch leads to a fall in PaO2 and increased
work or respiration - CO2 excretion is less affected and many patients will have normal PaCO2 due to increasing alveolar ventilation in an attempt to correct their hypoxia (pink puffers)
- other patients fail to maintain their resp efforst and their PaCO2 levels increase - in the long term this can cause these patients to become insensitive to CO2 and come depend of hypoxaemia to drive ventilation - such patients appear less breathless and because of renal hypoxia they start to retain fluid and increase erythrocyte production which can lead to polycythaemia - typical appearance of a blue bloater
what is the presentation of COPD ?
Characteristic symptoms are productive cough with white or clear
sputum, wheeze and breathlessness, usually following many years of a
smokers cough
cold seem to settle on the chest and frequent infective exacerbations occur with purulent sputum
symptoms can be worsened by cold or damp weather and atmospheric pollution
what are some systemic effects of COPD?
hypertension osteoporosis depression weight loss reduced muscle mass with general weakness
what would you see on examination of someone with COPD?
breathless at rest with prolonged expiration, chest expansion is poor and the lungs are hyper inflated
pursed lips
DD fir COPD?
asthma CHF bronchiectasis allergic fibrosing alveolitis pneumoconiosis asbestos
how is COPD diagnosed?
- based on history of breathlessness and sputum production in a chronic smoker
lung function tests show progressive airflow limitation with increasing severity and breathlessness - post bronchodilator FEV1/FEV of <70% on spirometry
CXR - may be normal or may show evidence of hyperinflated lungs
High res CT
ABG
BMI
how is COPD staged?
breathlessness
• FEV less than 80% predicted value
• FEV1/FVC less than 0.7 - airway obstruction
• Stages:
- Stage 1 - FEV1 less than 80% of predicted value
- Stage 2 - FEV1 50-79%
- Stage 3 - FEV1 30-49%
- Stage 4 - FEV1 less than 30% of predicted value
• Multiple peak flow measurements may be necessary to exclude
asthma
how is COPD treated?
smoking cessation is the most useful - even in advanced disease it may slow down the rate of deterioration
encourage exercise
influenza and pneumococcal vaccination, pulmonary rehab
PRN SABA - salbutamol or short acting antimuscarinic - ipratropium
if severe combine LABA or combo of B2 agonist and corticosteroid e.g. Symbicort (budesonide plus formoterol)
anti mucolytic agents can help by reducing sputum viscosity
diuretic can be used to treat oedema
good diet
reduce weight and obesity
