Unit 13 Week 1 Flashcards
What is asthma
- characterized by paroxysmal (fits of) and reversible obstruction of the airways
- now increasingly understood as an inflammatory condition
- combined with bronchial hyperresponsiveness such as bronchospasm and excessive production of secretions
“Chronic eosinophilic bronchitis”
What are the types of asthma (8)
Allergic or atopic
Seasonal
Occupational
Non-allergic
Exercise induced
“difficult asthma”
Asthma COPD overlap
Cough variant
allergic or atopic asthma
triggered by allergens such as pollen, pets and dust, most commonly these patients will also suffer from hay fever, eczema and food allergies alongside this
Atopy = the genetic tendency to develop allergic disease
Eosinophillic – typically high levels of eosinophils and IgE in the blood
Doesn’t always involve eosinophils – neutrophilic and basophilic asthma
Seasonal asthma
flare ups during certain times of the year such as during hay fever season or when it is cold
Occupational asthma
usually first diagnosed as an adult and symptoms improve the days that they are not at work
non allergic asthma
often develops later in life and can be more severe, but causes are not well understood
“difficult asthma”
symptoms do not go away even with high doses of medication, frequent asthma attacks
Asthma can also be categorised by its onset (2)
Adult
Childhood
What is the staging system for asthma
Mild intermittent asthma – mild symptoms of asthma occur no more than two days per week to two times per month
- Mild persistent asthma – mild symptoms occur more often than twice per week
- Moderate persistent asthma – increasingly severe symptoms of asthma occur daily and at least one night each week – flare ups also last several days
- Severe persistent asthma – symptoms occur several times per day almost every day
Allergenic triggers for asthma
mediated by IgE responses leading to mediator release causing inflammation, capillary leakage into the airways, increase in mucus secretion and bronchial smooth muscle contraction
- Dust mite faeces
- pollen
- pet fur
- Food stuffs
- etc.
Non-allergenic triggers for asthma
mediated by bronchospasm due to increased parasympathetic vagal tone
- Cold/ dlu symptoms
- cigarette smoke
- air pollution
- meteorologiocal changes- changes in temperature
- occupation exposures- e.g., working in a bakery or carpenters
- drugs- analgesics, NSAID’s
- Stress and emotional disturbance
- exercise
- time of day- natural dip in peak flow overnight may lead to nocturnal waking
Symptoms of asthma
Variable with time and intensity
Wheezing
shortness of breath
chest tightness
cough
diurnal episodes (waking up at night due to worsening)
between exacerbations most patients are asymptomatic
Pathophysiology of asthma 1st exposure
Type 1 hypersensitivity
Harmless primary exposure
- Allergen is phagocytosed by an antigen presenting cell (e.g., a dendritic cell at a mucosal surface) and presented on MHC II.
- Presented to naive T cells causing them to become Th2
a) T cells release cytokines (Il-4) which cause B cells to class switch to produce IgE
b) They also release Il-5 which stimulates locally recuited eosinophils
c) IL-13 – stimulates mucous secretion from bronchial submucosal glands and promote IgE production from B cells.
- T cells and epithelial cells secrete chemokines that recruit more T cells and eosinophils – this exacerbates the reaction
- IgE specific to that antigen binds to Fc receptors of submucosal mast cells.
- Allergen is cleared from the body mainly by IgE
Pathophysiology of asthma 2nd exposure
- Antigen binds to the variable region on IgE molecules on mast cells surfaces
- Cross-linking of multiple IgE molecules which enhances signalling into mast cell.
- Mast cell releases its granule contents which have immediate effect.
- Mast cells also synthesise other inflammatory mediators
Early phase hypersensitivity reaction
Dominated by:
by bronchoconstriction – triggered by direct subepithelial vagal receptors through both central and local reflexes triggered by mediators produced by mast cells and other cells in the reaction.
o increased mucus production
o variable degrees of vasodilation
o increased vascular permeability.
Late phase hypersensitivity
dominated by:
o Recruitment of leukocytes – eosinophils, neutrophils, and T cells
o Th17 cells recruit neutrophils.
Substances that cause bronchoconstriction
- Leukotrienes- C4, D4, E4 (also increase mucous secretions and vascular permeabilty)
- Acetylcholine- released from transpulmonary parasympathetic neurones by stimulating smooth muscarinic receptors
- Histamine
- Porstaglandin- also vasodilates
- Platelet activating factor- aggregation of platelets
As the inflammation goes on it causes airway dysfunction and through the release of chronic inflammatory mediators causes remodeling of the airway wall. Name some of those changes:
Mucous gland enlargement
Smooth muscle hyperplasia
Angiogenesis
Fibrosis
What 2 things contribute to reversible airway narrowing?
Bronchospasm- smooth muscle contraction
Inflammation- increase in exudate, mucous, oedema
Lifetyle changes to manage asthma
Identify and eliminate exposure to triggers where possible
Weight loss through diet and increased physical activity
Stop smoking
Dietary changes- move away from western diet
Diagnosis of asthma
- Take a structured clinical history
- Use clinical judgement to determine diagnosis
- Presence of more than one variable symptom of wheeze, cough, breathlessness and chest tightness (symptoms are episodic and diurnal)
- Look at personal and family history of other atopic conditions (e.g., eczema)
- Results of fractional exhaled nitric oxide (FeNo) IN OVER 17’s
- Provocative testing
Results of objective tests to detect airway obstruction:
- Spirometry
- Bronchodilator reversibility test
- Variable peak flow findings
Differential diagnosis of asthma
COPD
Cystic fibrosis
Chronic rhinosinusitis
Vocal cord dysfunction
etc.
Role of asthma clinic
Clinic that has access to all specialists and tests
Led by specialist respiratory physicians
Role of allergy clinic
Safely test for suspected allergies
- Skin prick testing
- Blood tests
- Patch tests
- Elimination testing
- Challenge testing
Wheeze breath sound
Higher pitched whistling sound
Most noticable on breathing out but also present on inhalation
Casused by narrowing of airways due to bronchospasm
Found in asthma and COPD
Stridor breathing sound
- A type of wheeze
- Harsh
- High pitched
- Vibrating sound
- Comes from upper airways
- Occurs when there is disrupted airflow or obstruction
Ronchi breathing sound
- Low pitched
- rattling
- Snoring sound
- Often cleared with a cough
- Indicative of a lower respiratory tract infection
- COPD, pneumonia, cystic fibrosis
Coarse crackles/ rales
- Short explosive sounds
- Sounds like bubbling, talling, clicking
- Most heard on inhalation
- Heard in the smallest airways when there is fluid in them
Fine crackles/ rales
- Fine crackles are shorter and higher in pitch than cparse crackles
- pneumonia, pulmonary fibrosis, acute bronchitis
What can cause the feeling of chest tightness? (2)
Airway obstruction
Bronchospasm
What should a healthy spirometry (flow volume loop) look like
- Volume as Y axis
- Flow as X axis
- Roughly an oval rhough +ve and -ve axis, higher than wide
- Expiration on top
- Inspiration on bottom
What does an obstructive flow volume loop look like
Pre bronchodilator:
Treatment of asthma (5)
- control of triggers
- Drug therapy (maintenance and reliever therapy MART)
- monitoring
- patient education
- treatment of acute exacerbations
Treatment objectives
- Minimise impairment and risk, including preventing exacerbations
- Minimizing chronic symptoms (inc. nocturnal waking’s)
- Minimize need for emergency department visits
- Maintain baseline pulmonary function
- Avoid adverse treatment effects.
- Control of triggering factors
Medication for asthma (brief)
- Short acting beta agonists (SABAs) and LABAs.
- Corticosteroids inhaled and then oral corticosteroids if severe asthma
- Immunomodulators if exacerbations are linked to an allergy
6 stepped management plan of asthma
Step 1- intermittent asthma- SABA for acute exacerbations
Step 2→6 more persistent and increasingly severe
Step 2- add low dose ICS as a preventor at start of day. If not tolerated choose leukotriene receptor antagonists
Step 3- SABA + LABA +low-dose ICS
Step 4- SABA + LABA +med dose ICS
Step 5- SABA + LABA + high dose ICS + possible immunomodulator
Step 6- SABA + LABA + High dose ICS +oral ICS + immunomodulator
What is a nebuliser
Machines that turn the liquid from short acting bronchodilator medications into a fine mist
Inhaler technique for standard inhalers
- remove cap
- shake inhaler
- breathe out gently
- place mouthpiece between lips
- breathe in slowly and deeplu while pressing button
- hold breathe for 5-10 seconds then breathe out
- wait a few seconds then repeat the proces
- replace the inhaler cap
Why would someone do a spirometry test?
assess airflow limitation- wehther theyre constricted or not
constricted gives a lower FEV1/FVC ratio (value of <50% suggests severe obstruction)
Used to diagnose obstructive lung diseases (asthma, COPD, emphysema)
How would the FEV1/FVC ratio (spirometry) be affected by a restrictive lung disease?
pulmonary fibrosis and oedema
normal ratio
how do you perform a spirometry (brief)
- Patient takes a maximum inspiration followed by forced expiration (breathe out as hard as they can for as long as they can) into the spirometer.
- Process repeated several times to obtain an accurate result.
- The spirometer measures forced expiratory volume in one second (FEV₁) and the total volume of exhaled gas (FVC).
- These are then combined as the FEV₁/FVC ratio which is expressed as a percentage.
What % from a FEV1/FVC ratio is borderkine for healthy lungs
>0.7 (70%)
What is a reversibility test
- Normal spirometry is measured
- Patient is then given a bronchodilator
- Spirometry again 15 minutes later
*note* patients should not use their inhaler in the time immediate to completing spirometry
Presence of reversibilty (improvement in FEV1/FVC) suggestive of diagnosis of asthma whereas absence would suggest fixed obstructive disaese like COPD
Peak flow test for asthma
Patients take a full inspiration then blow out forcefully (as hard as possible) into the peak flow meter – repeat 3 times and record the best attempt.
This similar to spirometry measures the amount and rate of air that can be forcefully breathed out of the lungs and can be used in diagnosis of asthma. A reading of around 200-400 L/min is indicative of asthma.
Can also be used to monitor asthma in a patient.
Sputum eosinophil count
Best test for identifying eosinophilic asthma
Your doctor gives you a nebulizer with salt water to help you cough up a sample, then the sample is tested for eosinophils.
Blood total IgE
helps identidy type 1 hypersensitivity i.e. asthma
Nitric oxide test
This test measures the levels of nitric oxide gas in an exhaled sample of breath. Nitric oxide is produced throughout the body, including in the lungs, to fight inflammation and relax tight muscles. High levels of exhaled nitric oxide in your breath can mean that your airways are inflamed; this is one sign of asthma.
Also useful as it lets you know how useful steroid medications would be
