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Asthma Flashcards

1
Q

What are the relievers of asthma?

A

Bronchodilators:
Short acting betan2 adreno receptors (SABAs)
Long acting “ (LABAs)
CysLT1 receptor antagonists
Methylxanthines

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2
Q

What are the controllers/prevent or of asthma?

A

Anti inflammatory agents that reduce airway inflammation:
Glucocorticoids
Humanised monoclonal IgE antibodies
Cromoglicate
Methylxanthines

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3
Q

Aerosol vs Oral therapy for asthma (NC come back to)

A

Aerosol:
Slow absorption and rapid systemic clearance
Low dose to achieve appropriate conc. in lungs - rapid
Low systemic conc. of drug
Low incidence of adverse effects
Distribution of drug reduced in severe airway disease

Oral:
Good absorption and slow systemic clearance
Need high dose to achieve appropriate conc. in lungs
High systemic conc. of drug
High incidence of adverse effects (but depends on drug)
Distribution of drug uneffected in airway disease

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4
Q

Beta 2-agonists

A
  • bronchodilators: relaxes smooth muscle in airways
  • stimulate bronchial smooth muscle beta2 receptors: increase cAMP
  • short acting: salbutamol
  • long acting: salmeterol/formoterol (twice a day), indacaterol/vilanterol/olodaterol (once daily)
  • combination inhalers - beclometasone/formoterol: MART (maintenance and reliever therapy)
  • used in asthma [as ICS/LABA dual or ICS/LABA/LAMA triple] and COPD [as triple or LAMA/LABA dual]
  • high therapeutic ratio when given inhaled route
  • Beta 2 down regulation and tachyphylaxis with chronic LABA
  • systemic beta 2 effects when given systemically or at high inhaled doses
  • high nebulised doses given in acute attack
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5
Q

What’s the the 2 classes of B2 adrenoreceptor agonists?

A

Short acting (SABA) - salbutamol
Long acting (LABA) - salmetrol, formoterol

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6
Q

What is the first line treatment for mild, intermittent asthma? (NC)

A

SABAs e.g salbutamol
Usually admitted by inhalation via dry powder …

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7
Q

What treatment is useful for nocturnal asthma (act for approx. 8 hours)?

A

long acting B2 adrenoreceptor agonists (LABA) - salmeterol, formoterol
LABAs must ALWAYS be co-administered with a glucocorticoid - used alone may worsen asthma and can increase risk of death
Never use alone

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8
Q

What does cysteinyl leukotrine (CysLT1) receptor antagonists do? (Check over)

A

Block CysLT1 receptors as when these receptors are activated is causes smooth muscle contraction, mucus secretion and oedema

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9
Q

Methylxanthines

A
  • Bronchodilator/anti-inflammatory
  • Oral theophylline for maintenance therapy
  • IV aminophylline for acute attacks
  • add to inhaled steroid as a complimentary non steroidal anti-inflammatory
  • non selective phosphodiesterase inhibitor (increase cAMP)
  • also act as adenosine antagonist
  • very narrow therapeutic window (therapeutic conc. can cause nausea, vomiting, abdominal discomfort)
  • low therapeutic ratio - P450 drug interactions 9eg. Erythromycin)
  • used in asthma
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10
Q

What type of drug is corticorticoids? What are the 2 major classes? (NC)

A

Anti-inflammatory
Glucocortocoids …
Mineralcorticoids - zona glomerusla ..

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11
Q

What do muscarinic (cholinergic) receptors do?

A
  • M1 receptors enhance the cholinergic reflex (innate immune response to injury, pathogens, and tissue ischemia)
  • M2 receptors inhibit acetylcholine release
  • M3 receptors mediate bronchoconstriction and mucus secretion
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12
Q

What are effort dependent tests?

A

Forced expiratory volumes and Forced expiratory Flow rates - spirometry

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13
Q

What is spirometry? NC

A

Taking a forced exilation from full inspiration
Volume (L) expired within first second should be close to full capacity - we measure the volume from the 1st second

  • Asthmatics get the same FVC as normal people but it just takes them longer - FVC conserved
  • In people with COPD FVC is not conserved/ is impaired ~ residual volume is higher (air can get in but cant get out/is trapped) FEV1:FVC ratio impaired/decreased
  • Restrictive curve is similar to normal pattern but is squashed down (people with interstitial lung disease) ratio of FEV1:FVC is not impaired, it is reduced but in proportion
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14
Q

Summary of lung function pattens - obstructive vs restrictive NC

MUST KNOW

A

Obstructive - asthma, COPD
FEV1 response to B2 antagonist >12%
<12% due to airway muscle hypertrophy so doesn’t react the same way to bronchodilators

Restrictive- interstitial lung disease

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15
Q

Bronchial challenge testing

A

Induce bronchoconstriction by excercise
- fall in FEV1 or PEF after exercise, also activated by cold air ~ asthma
- fall in SaO2 during exercise in interstitial lung disease (good for monitoring treatment response)
- full CArdiopulmoary exercise test (CPET) - differentiate cardiac vs resp dyspneo (rarely used and if so tends to be in athletes)

Induce bronchoconstriction by methacholine/histamine/mannitol
- Marker of Airway hyper-responsiveness - twitchiness (must have to have asthma)
- Conc. to produce a 20% fall in FEV1

Induce bronchoconstriction by allergen/chemicals
- early and late responses
- diagnose of occupational asthma

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16
Q

Transfer factor (differing capacity) NC come back to!!

A

DLCO always preserved in asthma
DLCO not preserved in COPD
DLCO also decreased in…

Used to measure how much emphysema a patient has got or monitor treatment response with patients with interstitial lung disease

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17
Q

Asthma: Type 2 high vs low

A

High
- early onset
- atopic (allergy)
- extrinsic

Low
- late onset
- non-atopic
- intrinsically

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18
Q

What is the asthma triad?

A
  • reversible airflow obstruction
  • T2 airway inflammation
  • Airway hyperresponsiveness
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19
Q

What is the dynamic evolution of asthma?

A

Bronchoconstricton > T2 airway inflammation > airway remodeling

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20
Q

What are the hallmarks of airway remodelling on asthma?

A
  • Basement membrane thickening
  • submucosa collagen disposition
  • smooth muscle hypertrophy
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21
Q

Presence of one or more of what biomarkers = type 2 high asthma?

A
  • presence of cytokines IL4/5/13
  • blood/sputum eosinophilia
  • raised FeNO
  • raised total or specific IgE

T2 high responds well to corticosteroids and biologics

22
Q

Inflammatory cascade in asthma and corresponding treatments

A

Inherited or aquired factors: genetic predisposition, viral, allergen or chemical
-> avoidance of precipitant

Eosinophilic inflammation
-> anti-inflammatory medication: cortocosteroids, theophylline

Mediators, Th2 cytokines
-> antileukotrienes or antihistamines, monoclonal antibodies: anti-IgE, anti-interleukin-5/R(alpha), anti-IL4R(alpha) AntiTSLP

Twitchy smooth muscle (hyperreactivity)
-> bronchodilators: Beta 2 agonists, muscarinic antagonists

23
Q

Severe asthma under the microscope

A
  • Alive epithelial shedding -desquamation
  • Autopsy - mucus plugging
24
Q

Asthma triggers - worsening of symptoms in the presence of

A

Allergens
- animal dander
- dust mites
- pollens
- fungi

Others
- exercise
- viral infection
- smoke
- cold
- chemicals
-drugs (NSAIDS, beta-blockers)

25
Clinical symptoms of asthma?
Episodic symptoms and signs Diurnal variability - nocturnal/early morning Non-productive cough, wheeze Triggers Associated T2 comorbidities (allergic rhinoconjunctivitis, chronic rhinosinusitis with nasal polyps, atopic dermatitis, eosinophilic esophagitis, urticaria - hives>red itchy rashes) Responsive to steroids or beta-agonists Family history of asthma Wheezing due to turbulent airflow
26
Diagnosis of asthma
History and examination Diurnal variation of peak flow rate (morning/night) Reduced forced expiratory ratio (FEV1/FVC <75%) Reversibility to inhaled salbutamol (>15%) Provocation testing -> bronchospasm - Exercise - Histamine/methacholine/mannitol
27
Diagnosis - what is the history?
Factors increasing pre-test probability of asthma -variable symptoms of: > wheezing > breathlessness > cough and phlegm > triggered by external factors (e.g cold, virus, exercise) > history of atopy (atopic dermatitis) > family history Factors reducing pre-test probability of asthma -constant symptoms of: > no variation > monosymptomatic cough > no effect of asthma medications
28
What are the diagnostic tests of asthma?
Demonstration of variable airflow obstruction: - spirometer with reversibility testing (improvement of FEV1 of 12% and at least 200ml) -peak flow diary (20% variation between the minimum and maximum, 2 weeks) - bronchial challenge testing (exercise:10%, mannitol test: 15%, methacholine test:20%)
29
When do you get asthma symptom control?
Symptoms more than twice a week (e.g. GINA, ACQ, ACT) Lung function less than 80% Exacerbations
30
What are the risk factors for future adverse outcomes? (I.e. exacerbations, loss of lung function, side-effects of asthma medications)
- uncontrolled symptoms - tendency to exacerbations - low lung function - high T2 biomarker - exposures (e.g Tabacco) - comorbidities - high SABA use Determines need for treatment and treatment intensity
31
What are the inflammatory biomarkers and clinical phenotyping for asthma?
Allergic asthma: - allergic sensitisation to aeroallergens (skin prick test or specific IgE) - symptoms of allergic rhinoconjunctivitis T2 biomarker: - FeNO more than 25ppb - blood eosinophils equal to or more than 300 cells per ul - sputum eosinophils equal to or more than 3% Predicts effect of treatment guides individualised management
32
What is asthma COPD overlap syndrome (ACO)
- COPD with blood eosinophilia >30/ul - Responds better to ICS with respect to exacerbation reductions - More reversible to salbutamol - Difficult to distinguish ACO from Type 2 asthmatic smokers who have airway remodelling (ie reduced FVC)
33
Asthma VS COPD
ASTHMA - Non smokers - Early or lat onset - Intermittent symptoms - Non-productive cough - Non-progressive - Eosinophilic inflammation - Diurnal variability - Good corticosteroid response - Good bronchodilator response - Preserved FVC and DLCO - Normal gas exchange COPD - Smokers - Non allergic - Late onset - Chronic symptoms - Productive cough - Progressive decline - Neutrophilic inflammation* - No diurnal variability - Poor corticosteroid response* - Poor bronchodilator response - Reduced FVC and DLCO - Impaired gas exchange *except in ACO with Eos COPD
34
What is the asthma treatment pyramid?
Reliever: SABA prn - taken as required Controller (preventer) 1st line: inhaled corticosteroid (ICS) Controller 2nd line (added on to ICS): LTRA, LABA, LAMA, Theophylline 3rd line: oral steroids (shorts burst only), Biologics (long term)
35
What is the controller and preferred reliever treatment to the corresponding steps 1-5
*for all steps reliever: as needed low-dose ICS-formoterol* Steps 1-2: as-needed low dose ICS-formoterol Step 3: low dose maintenance ICS-formoterol Step 4: medium dose maintenance ICS-formoterol Step 5: add-on LABA. Refer for assessment of phenotype. Consider high dose maintenance ICS-formoterol. +/- anti-IgE, anti-IL5/5R, anti-IL4R, anti-TSLP
36
What is the controller and alternative reliever treatment to the corresponding steps 1-5?
*for all steps reliever: taken as needed short-acting beta2-agonist (SABA)* Step 1: take ICS whenever SABA taken Step 2: low dose maintenance ICS Step 3: low dose maintenance ICS-LABA Step 4: medium/high dose maintenance ICS-LABA Step 5: add-on LAMA. Refer for assessment of phenotype. Consider high dose maintenance ICS-LABA. +/- anti-IgE, anti-IL5/5R, anti-IL4R, anti-TSLP
37
Preventer/controllers vs relievers
Preventer/controllers: anti-inflammatory Relievers: bronchodilators
38
What is the treatment of acute asthma?
- oral prednisolone (or IV hydrocortisone) - Nebulised high dose salbutamol, +/- Neb ipratropium, +/- aminophylline/magnesium - at least 60% O2 - ITU assisted mechanical intubated ventilation if falling PaO2 (ie low PaO2/FiO2 ratio) and rising PaCO2
39
What is the treatment of persistent asthma?
*aim: abolish symptoms, min. SABA use, normalise FEV1, reduce PEF variability, reduce exacerbations and prevent long term airway remodelling* - avoid triggers - suppress inflammatory cascade with inhaled steroid +/- LTRA - +/- stabilise smooth muscle with LABA/LAMA
40
what are the anti-inflammatory treatments for asthma?
- corticosteroids - leukotriene receptor antagonsits - biologics: anti-IgE, anti-IL5 (mepo) or anti-IL5Ralpha (Benra), anti-IL4Ralpha, anti-TSLP - methylxanthines (also a bronchodilator)
41
What are the bronchodilator treatments?
- beta 2 agonists - muscarinic antagonists (aka anticholinergics) - methylxanthines (also anti-inflammatory)
42
Corticosteroids
- Anti inflammatory - used in asthma and COPD: may cause pneumonia in COPD due to local immune suppression & impaired mucociliary clearance & altered microbiome - oral steroid (prednisolone) - low therapeutic ratio: only used in short bursts for acute exacerbations *NOT LONG TERM MAINTENANCE* - inhaled steroid (e.g beclomethasone) - high therapeutic ratio - used in mono therapy or combination in asthama (only in combination in COPD) - reduces exacerbations in eosinophilic asthma and COPD (aka ACO) - optimise lung delivery - extra fine solution HFA/spacer
43
Leukotriene receptor antagonists
- only used in asthma (A-I) - montelukast: oral route once daily, high therapeutic ratio - less potent anti-inflammatory than inhaled steroid - 2nd line: complimentary non steroidal anti-inflammatory additive to inhaled steroid - effective in exercise induced bronchoconstriction (EIB) and allergic rhinitis (with anti-histamine)
44
Benefits of using a Pressurized metered-dose inhalers (pMDI) used in conjunction with a spacer
- avoids coordination problem with pMDI - reduces oropharyngeal and laryngeal side effects from ICS - reduces systemic absorption from swallowed fraction with ICS - acts as a holding chamber for aerosol - reduces particle size and velocity - improves lung deposition
45
What are the monoclonal antibodies (biologics) for type 2 inflammation in sever asthma?
- anti-IgE - anti-IL5 (mepo) or anti-IL5Ralpha (Benra) - anti-IL4Ralpha - anti-TSLP IgE, blood eosinophils and FeNO - all type 2 biomarkers
46
Anti-IgE biologics treatment for T2 asthma summary
- anti-IgE monoclonal antibody : * Omalizumab*(brand name: Xolair) - Omalizumab inhibits the binding to the high affinity IgE receptor,therefore, inhibits TH2 response and associated mediator release from basophils/mast cells - injection every 2-4 weeks (for asthma only) - patients with severe persistent asthma have raised IgE despite maximum therapy (step 5) - also used for Chronic spontaneous urticaria (CSU) and Chronic rhinosinusitis with nasal polyps (CRSwNP) - very expensive with little effect on pulmonary function but reduces exacerbations - not used much now
47
Anti-IL5 (mepo) or Anti-IL5alpha (Benra) biologics treatment for T2 asthma summary
- mepolizumab (Nacala)/Benralizumab (Fasenra) - blocks the effects of the TH2 cytokine IL-5 which is responsible for eosinophilic inflammation in asthma - injections every 4-8 weeks (for asthma only) - this is for patients with sever refractory eosinophilic asthma (raised blood eos >300/ul) - despite max. Therapy (step 5) - Mepo suppresses Eos where as Benra depletes Eos - very expensive - little effect on pulmonary function but reduces exacerbations and oral steroid sparing effect
48
Anti-IL4alpha biologics treatment for T2 asthma summary
- Dupilumab (Dupixent) - blocks IL4/13 signaling - injection every 2 weeks (for asthma only) - for patients with severe asthma with either raised blood Eos>150/ul and raised FeNO >25ppb despite max therapy (step 5) - suppresses FeNO and IgE - also used for AD, CRSwNP and eosinophilic esophagitis (EE) - rate adverse events of eosinophil escape with Dupixent - very expensive - better on pulmonary function than anti-IL5, also effective at reducing exacerbations and oral steroid sparing
49
Anti-TSLP biologics treatment for T2 asthma summary
- Tezepelumab - blocks upstream epithelial alarmin TSLP and hence inhibiting downstream T2 cytokines IL4/5/13 - ie broad spectrum - injection every 4 weeks (for asthma only) - for patients with severe asthma irrespective of biomarkers but best for T2 high patients (step 5) - avoids eosinophil escape which may rarely occur with Dupixent (suppression of IL-5) - very expensive - better effect on pulmonary function than anti-IL5, reduces exacerbations
50
Muscarinic antagonists (aka Anticholinergics)
- block M3 receptors - short acting non-selective: Ipratropium (four times a day) - long acting M3 selective: Tiotropium (once daily), Glycopyrronium (once or twice daily) or Umeclidinium (once daily) - inhaled route only - high therapeutic ratio - used mostly in COPD to reduce exacerbations and improve symptoms - LAMA/LABA dual: Glycopyrronium/Indacaterol or Vilanterol/Umeclidinium - ICS/LABA/LAMA triple for eosinophilic COPD: Beclometasone/Formoterol/Glycopyrronium - also used in asthma as triple therapy at step 5: ICS/LABA/LAMA - High nebulised doses of Ipratropium used in acute COPD and acute asthma

Respiratory (31 decks)

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