Obstructive diseases: Asthma, COPD, emphysema, bronchiectasis, chronic bronchitis Flashcards

1
Q

Pathophysiology of Asthma

A

(1.) Chronic conditions characterised by airways obstruction that is reversible. Acute exacerbation can occur in response to triggers.

(2. ) Three factors contribute to airway narrowing:
- Bronchial hyperresponsiveness/contraction = triggers by a variety of stimuli can narrow airways more
- Mucosal swelling/inflammation caused by mast cell and basophil degranulation
- Increased mucus production further narrows airways

(3. ) This leads to recurrent episodes of wheezing, dyspnoea, cough.
(4. ) Episodes are often reversible either spontaneously or with treatment

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2
Q

RF for asthma

A

(1. ) Hx of atopy (tendency to develop allergic disease such as eczema, hayfever)
(2. ) Fx of asthma, atopy
(3. ) Precipitating factors: weather, allergen, smoking, infection, stress etc
(4. ) Is it occupational, exercise or seasonal induced?

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3
Q

Clinical features of asthma

A

(1. ) Breathlessness
(2. ) Cough
(3. ) Wheezing
(4. ) Diurnal variation = worse in the morning than in the evening
(5. ) Look for precipitating factors

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4
Q

How do you assess severity of asthma? (3)

A

Can be achieved with ‘RCP3’ questions:

  • Recent nocturnal waking
  • Usual asthma Sx in day
  • Interference with ADLs? (activity of daily living)
  • > if one of these are positive, it indicates poorly controlled asthma
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5
Q

Ix and Dx of asthma (6)

A

DX = requires an obstructive pattern and reversibility. Spirometry is 1st line

(1. ) PFT = will show airway obstruction: reduced FEV1 or FEV1/FVC ratio
(2. ) 2w PEFR diary = >20% variation on >3/7d for 2w
(3. ) Bronchial challenge test (mannitol, methacholine) or exercise test, show FEV1 >15% decrease
(4. ) Reversibility testing: FEV1 = >12% increase (improved) after beta-agonist-bronchodilator/glucocorticoid
(5. ) Exhaled FeNO = marker of eosinophilic inflammation
(6. ) Skin prick test may be done to identify allergen (atopic IgE asthma)

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6
Q

what would indicate controlled asthma (7)

A

(1. ) No daytime symptoms
(2. ) No night-time walking
(3. ) No need for rescue medication
(4. ) No asthma attacks
(5. ) No limitations on activity including exercise
(6. ) Normal lung function (FEV1 and/or PEF >80% predicted or best)
(7. ) Minimal side effects from medication

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7
Q

If medication fails what must you consider

A

If medication doesn’t work before moving up in step-wise mx:

(1. ) Check adherence and inhaler technique
(2. ) Advising correct use of a spacer with ICS therapy (including mouth rinsing after)
(3. ) Are they using NSAIDs, b-blocker? this will provoke asthma

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8
Q

Conservative Mx of asthma?

A
  • Management of triggers
  • Smoking Cessation
  • Inhaler technique
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9
Q

Stepwise approach of asthma mx

A
  • Stepwise treatment based on symptoms, guided by pt’s preference and competence.
  • Move up or move down if control is good for >3months.

(1. ) SABA
(2. ) low-dose 200mg ICS

(3.) recheck technique + adherence
LTRA + low dose ICS
- If uncontrolled: LABA + ICS +/- LTRA
- If uncontrolled again: change to MART + ICS +/- LTRA
- MART contains ICS + fast-acting LABA
- If uncontrolled: inc MART ICS to 200-400mg and again to 800mg if fail -OR-

(4. ) High dose 2000mg ICS +/or trial fourth drug
- Fourth drug: muscarinic receptor antagonist (LAMA), SR theophylline or beta2agonist tablet

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10
Q

When would you offer an ICS for an asthmatic who’s currently using SABA only

A

Step-up in management is indicated if:

  • Experienced an exacerbation in the last two years
  • Used beta2-agonist inhaler more than three times per week.
  • Symptoms of asthma for more than three times per week
  • Waking due to asthma more than once per week
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11
Q

Management of acute asthma

A
  • determine severity*
    (1. ) Controlled oxygen
    (2. ) Nebulised/inhaler SABA
    (3. ) 30-40mg PO prednisolone
    (4. ) Monitor oxygen saturation, heart rate, respiratory rate
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12
Q

How would you classify asthma attacks

A

(1.) Determine the severity based on consciousness, signs of exhaustion, resp rate, pulse rate, chest, BP, PEFR, oxygen saturation

(2. ) Moderate
- PEFR >50%, RR <25, <110bpm
- normal speech

(3. ) Severe
- PEFR 33-50%, RR >25, HR >110bpm
- inability to complete sentences

(4. ) Life-threatening
- PEFR <33%, SpO2 <92%
- altered consciouness, cyanosis, hypotension, silent chest

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13
Q

Preventer therapies in asthma

A

(1. ) ICS e.g. beclometasone

(2. ) Leukotriene receptor agonists

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14
Q

What is COPD?

A

(1. ) Chronic obstructive airway condition (or airway limitation) with acute exacerbations
(2. ) It is progressive with little/no reversibility
(3. ) It includes: emphysema, chronic bronchitis, small airway fibrosis

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15
Q

What is Acute COPD?

A

(1.) Usually occur due to a trigger (e.g., bacterial or viral pneumonia, environmental irritants) or in winter (cold air, virus).

(2. ) Sudden worsening of COPD Sx
- Wheezing with cough and breathlessness may become worse and may have more sputum

(3.) Change of Tx may be needed or hospitalisation.

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16
Q

Rf for COPD

A

(1. ) Male
(2. ) >35y
(3. ) Smoking
(4. ) Second-hand smoking (occupational, exposure)
(5. ) Genetic = AATD
(6. ) Low socioeconomic background

17
Q

Clinical Features of COPD (8)

A

(1. ) Chronic + productive cough
(2. ) Progressive dyspnoea
(3. ) Wheeze
(4. ) Cachexia (wt loss, muscle wasting)
(5. ) Hyper-inflated chest
(6. ) Pursed lip breathing, use of accessory muscles
(7. ) Cor pulmonale Sx
(8. ) Cyanosis

18
Q

Describe the progression of dyspnoea in COPD (MRC scale)

A

Grade 1 - breathless during exercise/exertion

Grade 2 - SoB when walking up hill

Grade 3 - SoB on walking

Grade 4 - SoB and pausing during walks

Grade 5 - SoB is distressing, housebound

19
Q

Dx of COPD

A

(1.) Based on typical clinical features supported by spirometry (post bronchodilator: FEV1/FVC <0.7).

(2. ) Suspect COPD in >35y with risk factors (smoking, occupational or environmental exposure) and one or more of the following symptoms:
- Breathlessness
- Chronic/recurrent cough
- Regular sputum production
- Frequent LRTI
- Wheeze
- Other Sx = wt loss, anorexia, fatigue, waking at night with breathlessness, etc

20
Q

Ix for COPD

A

(1. ) Spirometry and SABA/SAMA
- FEV1 = <80%
- FEV1/FVC = <0.7
- Severity assessed with FEV1

Extra tests:

(2. ) CXR
- hyperinflation, flattened diaphragm
- may see bullae if emphysema

(3. ) ECG
- Cor Pulmonale = peaked p wave, right axis deviation

(4. ) ABGs
- if very low FEV1 and dyspnoea

21
Q

How is severity of COPD assessed?

A
  • Severity of airflow limitation can be assessed with FEV1
  • Stage 1 Mild = >80%
  • Stage 2 Moderate = 50-79%
  • Stage 3 severe = 30-49%
  • Stage 4 Very severe = <30%
22
Q

What are the aims of Tx in COPD

A

Reduce Sx

  • Relieve Sx
  • Improve exercise intolerance
  • Improve health status
  • Improve QoL
  • Reduce exacerbations

Reduce risk

  • Prevent/slow down disease progression
  • Prevent and treat exacerbations
  • Reduce mortality
23
Q

How is acute COPD managed?

A

(1. ) Emergency Admission: Severe breathlessness, Rapid onset of Sx, Confusion, impaired consciousness etc
(2. ) Inc inhaled SABA/SAMA dose (short-acting bronchodilators)
(3. ) Consider Oral corticosteroids

(4. ) PO Abx (amoxicillin, doxycycline, clarithromycin) if infection present:
- Change in sputum: colour, thickness, volume
- Previous sputum culture and susceptibility results.

(5. ) Identify triggers
(6. ) Non-invasive ventilation (NIV): Improves resp acidosis, dec RR, severity of dyspnoea

24
Q

Mx of COPD

A

Non-pharmacological

(1. ) Smoking cessation
(2. ) Pulmonary rehabilitation
(3. ) Flu and pneumococcal vaccines
(4. ) Optimise tx for comorbidities

Pharmacological, if above fails

(1. ) Offer SABA or SAMA
(2. ) If still limited by Sx or has exacerbations:
(a. ) Offer LABA + LAMA (if FEV >50%, no asthmatic features)
(b. ) Offer LABA + ICS (if <50%, asthmatic features)

(3. ) Consider 3-month ICS if
- still no response to above
- day-to-day sx that impact QoL
- 1 severe or 2 moderate exacerbations within a year

25
Q

When is long-term oxygen therapy indicated in COPD pts?

A

(1. ) Pts with chronic resp failure, failure of tx, pulmonary HTN, oedema, polycythaemia
(2. ) SATS <93%, PaO2 <7.3, FEV1 <30%
(3. ) CI = smokers

26
Q

What differences are there between asthma and COPD?

A

(1. ) Age
- COPD >35y, Asthma: <35y

(2. ) RF
- COPD = smoking, second hand smoking, Fx AATD
- Asthma = pollen, exercise, smoke, stress etc, Fx asthma, atopy

(3. ) Clinical features
- COPD = productive cough, progressive breathlessness, minimal variation
- Asthma = non-productive cough, intermittent breathlessness, diurnal variation

(4. ) Spirometry post bronchodilator
- COPD: FEV1/FVC <0.7
- Asthma: FEV1 improves (reversibility)

27
Q

What would you see on a spirometry for restrictive and obstructive lung disease?

A

(1. ) Both present with low FEV1 <80%
(2. ) FVC = reduced (restrictive), close to normal (obstructive)
(3. ) FEV1/FVC = >0.8 (restrictive), <0.7 (obstructive)
(4. ) Examples = Restrictive - IPF, Obstructive - asthma, COPD

28
Q

Bronchiectasis: patho, Sx, complications

A

(1. ) Dilation of bronchi due to inflammation
(2. ) Inflammation, secretion, infections causes obstruction
(3. ) Lung tissue can’t absorb as much oxygen due to this damage

(4. ) Sx = chronic cough, large quantities of foul smelling sputum +/- blood
(5. ) Complications = recurrent pneumonia, fungal infection, metastatic abscess e.g. brain, heart, cor pulmonale

29
Q

Chronic Bronchitis: patho, Sx, complications

A

(1. ) Chronic inflammation and mucus hypersecretion with bronchial mucous gland hypertrophy leading to squamous metaplasia.
(2. ) Productive cough (cough and sputum) for 3m in 2 consecutive years. Other Sx = hypercapnia, hypoxia, cyanosis, RHSF +/- resp failure etc
(3. ) RF = smoking-induce (tobacco or environment), middle aged
(4. ) These individuals are prone to recurrent bronchial infections

30
Q

Emphysema: patho, Sx, aetiology, complications

A

(1. ) Enlargement of alveolar airspaces with destruction of elastin -> bullae
(2. ) This has a ‘gas trapping’ effect i.e. prevent full exhalation of air [obstructive disease], leading to progressive loss of lung functionality
(3. ) Aetiology: cigarette smoke, coal dust exposure, cadium toxicity, alpha-1-antitrypsin deficiency
(4. ) Complications: NO inc cancer risk, but instead pulmonary HTN, poor oxygen delivery to tissues