respiratory (asthma, copd)

Question 1

how would you describe what asthma is

Answer 1

asthma is an chronic inflammatory airway disease characterised by intermittent reversible airway obstruction

Question 2

what is the pathophysiology of asthma

Answer 2

*ACh is involved in bronchoconstriction vs NO is involved in bronchodilation

airway hyperresponsiveness
- variable component: acute inflammatory events that release mediators which triggers cholinergic pathways that lead to release of ACh, ACh binds to muscarinic receptors on airway smooth muscle cells to cause vasoconstriction
- chronic component: chronic inflammation leads to structural and phenotypic changes leading to hyperplasia (increase amount) and hypertrophy (increase size) of airway smooth muscle cells

airway remodelling
- allergen leads to immune system activation and amplification
- release of paracrine signals that causes proliferation of cells by epithelial and immune cells
- triggers mesenchymal cells (fibroblasts and airway smooth muscle cells)
- increase mass and thickness of airway smooth muscles
- leads to narrowing of lumen and increases in airway resistance

airway inflammation
- allergen involves IgE allergic response whereby allergen is presented to allergen presenting cell - dendritic cell which presents it to TH2 cells and activates the immune system in releasing immune cells like mast cells, eosinophills, T lymphocytes that release inflammatory mediators like leukotrienes, histamine, prostaglandin and cytokines
- B cells are also activated, leading to antibody production including IgE, causing further activation of mast cells by IgE
- inflammatory mediators causes bronchoconstriction and excessive mucus secretion
- overall leading to airway obstruction

Question 3

what is the clinical symptoms of asthma

Answer 3

• breathlessness
• chest tightness
• coughing (that worsens at night or early morning)
• wheezing

Question 4

what are the risk factors of asthma

Answer 4

host factors
- genetics
- gender (M > F)
- obesity

environmental factors
- allergens (indoor/ outdoor)
- occupational sensitizers
- air pollution
- tobacco smoke
- respiratory infections
- socio-economic factors

Question 5

what are the factors that can cause asthma exacerbations

Answer 5

• allergens
• respiratory infections
• exercise and hyperventillation
• weather changes
• air pollution
• occupational sensitizers
• food and additives
• drugs
• GERD

Question 6

what is exercise induced bronchoconstriction

Answer 6

acute narrowing of airways in lungs triggered by exercise, defined as a decrease in FEV1 by 10% or more from pre-exercise value

Question 7

how is asthma assessed and diagnosed

Answer 7

1. hx of symptom pattern
   increased asthma probability
   - classic triad
   - worse at night or early morning
   - variable over time and in intensity
   - triggered by infections, allergens, pollutants, weather changes, exercise, strong smells, smoke and irritants

decreased ashtma probability
- isolated cough with no other respiratory symptoms
- chest pain
- chronic sputum production
- shortness of breath associated with dizziness or lightheadedness or peripheral tingling
- exercise induced dyspnea with noisy inspiration

2. evidence of variable airflow limitation
   - confirm presence of airflow limitation (document decrease in FEV1/FVC)
   - confirm variation in lung function greater than in healthy (using spirometry to compare FEV1 before using dilator vs 15-20mins after to determine excessive bronchodilator reversibility for diagnosis; peak flow meter is used for peak expiratory flow monitoring)

Question 8

what is the normal FEV1/FVC ratio

Answer 8

> 0.75-0.80 in healthy adults
0.90 in children

Question 9

what does FEV1 measure

Answer 9

measures volume of air exhaled forcefully in first second of maximal expiration

Question 10

what does FVC measure

Answer 10

maximum amount of air that can be exhaled when blowing out as fast as possible after full inspiration

Question 11

what does the FEV1/FVC ratio measure

Answer 11

measures the proportion of FVC that can be exhaled in first second of forced expiration

differentiates between obstructive and restrictive disease (FEV1/FVC decreases in obstructive disease but FEV1/FVC ratio may be maintained in normal range or even increased for restrictive disease as both FEV1 and FVC decreases)

Question 12

what are the non-pharmacological management of asthma

Answer 12

• avoidance of tobacco smoke
• increase physical activity (general health benefits and advice on how to manage exercise induced bronchoconstriction)
• occupational asthma
• dealing with emotional stress through relaxation strategies
• breathing exercises
• vaccinations
• avoiding medications like NSAIDs and BB
• sublingual immunotherapy

Question 13

what is the goals of therapy of asthma

Answer 13

• symptom control: achieve good control of symptoms and maintain normal activity level
• risk reduction: minimise future risks of asthma-related mortality, exacerbations, persistent airflow limitation and s/e

Question 14

what is the pharmacological management for asthma

Answer 14

reliever
- SABA
- ICS-formoterol
- SAMA (less frequently used)

controller
- ICS
- ICS-formoterol
- ICS-LABA
- LTRA
- LAMA (used less frequently)

Question 15

what are the benefits of long term use of corticosteroids

Answer 15

• most effective anti-inflammatory medication for persistent asthma
• reduce asthma symptoms
• reduce use of reliever
• improve QoL
• improve lung function
• control airway inflammation
• reduce airway hyperresponsiveness
• reduce frequency and severity of exacerbations
• reduce asthma mortality

Question 16

what are the s/e of corticosteroids

Answer 16

inhaled
- cough, dysphonia, oral thrush

systemic
- osteoporosis, skin thinning, immunosuppression, easy bruising, HTN, DM, muscle weakness

Question 17

what are the s/e of beta agonists

Answer 17

• tachycardia, palpitation, HA, tremor

Question 18

what are the s/e of montelukast

Answer 18

• N, HA, neuropsychiatric events (depression, agitation, insomnia, suicidal, restlessness)

Question 19

what are the s/e of LAMA

Answer 19

• dry mouth

Question 20

what are the s/e of theophylline

Answer 20

• GI: N/V
• CNS: insomnia, HA, seizures
• CV: flutter, tachycardia

Question 21

how to manage asthma exacerbations

Answer 21

1. initial assessment (ABC: airway, breathing, circulation)
2. further triage by clinical status
3. assess clinical progress frequently and measure lung function in all patients 1hr after initial treatment (discharge if FEV1 or PEF is 60-80%; continue treatment and assess frequently if FEV1 or PEF <60%)

Question 22

how to further triage by clinical status

Answer 22

mild-moderate if
- talks in phrases
- prefers sitting or lying
- not agitated
- RR increased
- accessory muscles not used
- O2 saturation >90-95%
- PR 100-120
PEF >50%

manage with SABA, ipatropium (consider combi of both), short course OCS to speed up recovery

severe if
- talks in words
- sits hunched forward
- agitated
- RR >20
- accessory muscles used
- PR >120
- O2 saturation<90%
- PEF 50% or less

manage with SABA, ipatropium, IV/PO corticosteroids, consider IV magnesium

Question 23

what is the follow-up and monitoring duration for asthma

Answer 23

• exacerbations TCU in 1w
• monitoring TCU 1-3m after initiation, q3-12m after

Question 24

what is part of a written asthma plan

Answer 24

• asthma triggers
• medications (reliever, controller, administration techniques, for other comorbs)
• symptom monitoring (signs of well-controlled vs warning signs)
• emergency action plan for exacerbations (use of reliever, when to contact HCP or emergency care)
• follow ups

Question 25

how would you explain what is copd

Answer 25

copd is a chronic inflammatory lung disease characterised by progressive, largely irreversible airway obstruction

Question 26

what are the risk factors of copd

Answer 26

- smoking - environmental tobacco smoke - hx of TB - occupational hazards - exposure to biomass burning - alpha1-antitrypsin deficiency

Question 27

what are the main pathological features

Answer 27

- obstructive bronchiolitis, fibrosis - emphysema (alveolar wall destruction) - chronic bronchitis, mucus hypersecretion

Question 28

what is the pathophysiology of copd

Answer 28

obstructive bronchiolitis, fibrosis - smoke and irritants interact with epithelial cells which triggers release of profibrotic mediator (a growth factor) that acts of fibroblast to produce matrix protein leading to peribronchiolar fibrosis (scarring of tissue) - structural change results in narrowing of small airways thus obstructive bronchiolitis emphysema (alveolar wall destruction) - imbalance between protease and anti-protease activity - irritants trigger activation of immune system - neutrophils and macrophages release protease like neutrophil elastase and MMP9 that causes break down of elastic fibers important for alveoli attachment that hold airway open chronic bronchitis, mucus hypersecretion - goblet cell hyperplasia - mucosal edema - mucus hypersecretion - proteases produced by macrophages also involved in mucus production and causes a build up of mucus air trapping - attributed to premature closure of small airways upon expiration due to fixed narrowing of airways resulting from fibrosis, mucus hypersecretion and loss of alveolar attachments - can cause lung hyperinflation and dynamic hyperinflation (leading to reduced exercise tolerance as next inhale starts before fully exhaling) - already hypoxemia (low PO2) due to airway narrowing and obstruction, but air trapping reduces volume of CO2 escaping thus causing hypercapria (increased PCO2) but partial pressures of gases important for gas exchange via diffusion and major changes will affect efficient gas exchange in airways oxidative stress - mainly mediated by ROS - ROS increases inflammation and contribute to bronchitis and bronchiolitis - worsens tissue damage and causes copd progression

Question 29

compare asthma with copd

Answer 29

age of onset - asthma: any age but usually childhood - copd: >40yo patterns of sx - asthma: shortness of breath, wheezing, cough, chest tightness; variable; worse at night or early morning - copd: dyspnea, chronic cough, sputum; usually continuous hx - asthma: allergies, personal hx of childhood asthma/ FHx - copd: exposure to risk factors lung function - asthma: variable airflow limitation, may be normal between sx - copd: persistent airflow limitation (FEV1/FVC <0.7) chest xray - asthma: normal - copd: severe hyperinflation time course - asthma: no worsening over time, may improve spontaneously - copd: slowly worsen over time (years), sx improve with treatment but progression is usual

Question 30

how is copd assessed

Answer 30

using spirometry GOLD 1 (mild): FEV1 ≥80% GOLD 2 (moderate): 50% ≤ FEV1 <80% GOLD 3 (severe): 30% ≤FEV1<50% GOLD 4 (very severe): FEV1<30% based on symptoms (mMRC questionnaire) 0 (none) if only breathlessness with strenuous exercise 1 (mild) if SOB when hurrying or walking up a slight hill 2 (moderate) if walks slower than age group or has to stop for breath when walking on level ground at own pace 3 (severe) if stops for breath after walking 100m or a few minutes on level ground 4 (very severe) if breathless when dressing/ undressing or too breathless to leave the house symptoms also can be assessed based on CAT assessment, an 8 item measure of health status impairment in COPD

Question 31

what is the classification of copd

Answer 31

A (less sx, low risk) if GOLD1-2 and mMRC 0-1 or CAT<10 B (more sx, low risk( if GOLD 1-2 and mMRC 2-4 or CAT ≥10 C (less sx, high risk) if GOLD 3-4 and mMRC 0-1 or CAT <10 D (high sx, high risk) if GOLD 3-4 and mMRC 2-4 or CAT ≥10

Question 32

what is a copd exacerbation

Answer 32

an acute worsening of respiratory symptoms that result in additional therapy, classified as high risk and low risk high risk if ≥2 exacerbations in the past 1 yr or ≥1 leading to admission low risk if 0/1 exacerbation but not leading to admission

Question 33

what are the goals of therapy of copd

Answer 33

- reduce symptoms (relieve symptoms, improve exercise tolerance, improve health status) - reduce risk of exacerbations (prevent disease progression, prevent and treat exacerbations, reduce mortality)

Question 34

what is the pharmacological management of copd

Answer 34

SABA - salbutamol LABA - indacaterol - formoterol - olodaterol SAMA - ipatropium LAMA - tiotropium - glycopyrronium - umeclidinium ICS-LABA - budesonide/formoterol - fluticasone/salmeterol - fluticasone/vilanterol LAMA-LABA - umeclidinium/vilanterol - glycopyrronium/indacaterol - tiotropium/olodaterol ICS METHYL XANTHINES (theophylline) PDE4i ABX (azithromycin)

Question 35

what is the GOLD's recommended initial pharmacotherapy for each classification of copd

Answer 35

A: SAMA/SABA B: LAMA/LABA (LAMA>LABA) C: LAMA D: LAMA or LAMA-LABA or ICS-LABA

Question 36

what is the non-pharmacological management of copd

Answer 36

- reduce exposure to risk factors including smoking cessation - vaccination (flu, pneumococcal, pertussis) - self-management on breathlessness, energy conservation and stress management - written action plan - increase physical activity - oxygen therapy - end of life care - pulmonary rehab (patient education, exercise training, nutritional support, psychosocial support) - surgery

Question 37

what does the written action plan comprise of

Answer 37

- severity - medications - symptom monitoring - smoking cessation (if applicable) - pulmonary rehab programme (if applicable) - breathlessness, energy preservation and relaxation techniques - exacerbation management (avoidance of aggravating factors, contact number in the event of an exacerbation)

Question 38

what is the follow up for copd

Answer 38

based on dyspnea - LABA/LAMA --> LABA+LAMA --> consider switching inhaler device and identifying and treating other causes of dyspnea - LABA+ICS --> LABA+LAMA+ICS --> consider switching inhaler device and identifying and treating other causes of dyspnea (or trying LABA+LAMA) and exacerbation - LABA/ LAMA --> LABA+LAMA --> (if eos ≥100cells/µ, else skip) ICS+LABA+LAMA --> azithromycin (esp in ex smokers) - LABA/LAMA --> ICS+LABA --> LABA+LAMA or ICS+LABA+LAMA --> azithromycin (esp in ex smokers)

Question 39

what are the criterias that support use of ICS

Answer 39

- exacerbation leading to hospitalisation - ≥2 exacerbations/ year - eos ≥300cells/µL (indicates esosinophil inflamm) - hx of concom asthma

Question 40

what are the criterias supporting the use of triple therapy

Answer 40

- severely symptomatic - moderate to very severe airway obstruction - history of frequent and/or severe exacerbations

Question 41

what is the presentation of an exacerbation

Answer 41

- increase sputum production - worsening dyspnea - worsening cough - drowsiness - fatigue - decreased exercise tolerance

Question 42

what are the 5 As of smoking cessation

Answer 42

- ask about use of tobacco - advise to quit - assess willingness and rationale - assist in quitting - arrange for follow-up

Question 43

what are the vaccinations

Answer 43

- influenza - pneumococcal (PCV13, PPSV23) - Tdap - COVID19

Question 43

what are the components of pulmonary rehabilitation

Answer 43

- patient education about disease and treatment options - exercise training - nutritional support - psychosocial support

Question 44

what are the differential diagnosis for copd exacerbations

Answer 44

- pneumonia (chest radiograph, assess CRP and/or procalcitonin) - pneumothorax (chest radiograph/ ultrasound) - pleural effusion ie. water buildup in lungs (chest radiograph/ ultrasound)

Question 45

what is the goal of therapy for copd exacerbations

Answer 45

- minimise impact of current exacerbation - prevent development of subsequent exacerbations

Question 46

what is the management of copd exacerbations

Answer 46

- SAMA (combi with BA as first line) - SABA - oxygen therapy - vitamin D supplement for severe vitD deficiency of <10ng/ml - OCS (prednisolone) x5d - abx (augmentin, macrolide, cefuroxime, FQ) *controversial use - respiratory support