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Respiratory > Obstructive Airway Disease > Flashcards

Obstructive Airway Disease Flashcards

1
Q

What are the 2 Obstructive Airway Diseases?

A

Asthma & COPD

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2
Q

Asthma:

Prevalence?

A

inc prevalence

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3
Q

Why is Asthma Prevalence increasing?

A

Hygiene hypothesis and inc in genetic hypersensitivity predisposition

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4
Q

What are the different classes of asthma?

A

Allergic, non-allergic, acute exacerbation

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5
Q

What is Asthma…

A

Reversible airway obstruction, inflammation of airways due to airway hyper-responsiveness

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6
Q

What is the pathophysiology of asthma?

A

Bronchoconstriction due to chronic airway inflammation & airway remodelling…

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7
Q

What drives inflammation in asthma pathophysiology?

A

TH1 & TH2 lymphocytes activate mast cells and eosinophils

  • Mast Cells: release pro-inflam mediators which act on mucus secreting cells & ASM
  • Eosinophils: release proteins that are toxic to epithelial cells
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8
Q

What does airway inflammation cause as a repercussion in asthma?

A

Airway remodelling; structural changes which alter airway physiology causing symptoms

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9
Q

Give 2 examples by which the airways are remodelled?

A
  • depositions of proteins and cellular infiltration causing swelling of the submucosa resulting in airway narrowing
  • swelling outside ASM layer causes a reduction in retractile forces of alveoli so airways close more
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10
Q

Asthma triggers (aetiology)?

A

atmospheric pollution, cold air, allergen, occupational sensitisers, drugs, irritants, viral, emotion, associated atopy (e.g. eczema), not using inhaler properly

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11
Q

Presenting symptoms of asthma…

A

wheezing, SOB, nocturnal exacerbations, non-productive cough

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12
Q

Asthma investigations…

A 
blood test (eosinophilia >4%) 
PFTs (PEFR, spirometry) 
Exercise test, exhaled NO, skin test for allergen
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13
Q

Asthma treatment…

A

Avoid allergen

  1. SABA (occasional symptoms)
  2. SABA & Inh Corticosteroids (CS) + xanthine (e.g. theophylline)/ cromone (daily symptoms)
  3. LABA & Inh CS + CysLT1/ xanthine (severe)
  4. inc dose of inh CS & LABA & SABA/CysLT1/ xanthine (severe but not responding to 3)
  5. step 4 + oral CS (e.g. prednisolone) (severe and deteriorating)
  6. Hospital Admission
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14
Q

Presentation of acute exacerbation of asthma (AEoA)

A

progressive shortening of breath, accessory muscles engaged, tachypnoea

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15
Q

Grading of AEoA…

A

PEFR
Moderate: 75-50%
Severe: 50-30%, RR >25/min, HR> 100/min, can’t finish sentences
Threatening: <33%, stats <92%, CHEST criteria

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16
Q

What is the CHEST criteria?

A 
Cyanosis 
Hypotension 
Exhausted 
Silent chest
Tachycardic arrhythmias
17
Q

Treatment of AEofA

A

Moderate: 100% O2, nebulised SAMA/SABA, CS (oral: prednisolone, IV: hydrocortisone)
Severe: O2, IV SABA, & ^
Threatening: intubation, IV Magnesium Sulphate Infusion

18
Q

Prevalence of COPD…

A

10-20% of smokers develop COPD, dec in prevalence

19
Q

Class of COPD…

A

chronic & acute exacerbation of COPD (AEoCOPD)

20
Q

What is COPD…

A

chronic bronchitis and emphysema

21
Q

What is Chronic bronchitis and how does it occur?

A

Inflammation of bronchi

  • inflammation of airways resulting in ulceration & fibrosis of airways narrowing them
  • also inc in mucus secreting goblet cells resulting in mucus hyper secretion and blockage of airways (COPD has dysfunctional mucociliary escalator)
22
Q

What is emphysema and how does it occur?

A

Damaged alveoli

  • abnormal permanent enlargement of alveoli due to destruction of their wall causing impaired gas exchange
  • No bronchial support due to bronchitis so loss of lung recoil so small airways collapse and rapid closure of airways during expiration
23
Q

What are the main points for the pathophysiology of COPD?

A

inflammation & scarring, loss of lung elasticity, inc mucus secretion= airway narrowing
air trapping= hyperinflation= inc work of breathing

24
Q

COPD triggers…

A

smoking, long term exposure to toxins, not using inhaler properly

25
Q

COPD presentation…

A

breathlessness worsening with time, productive cough, frequent exacerbations, crackles, reduced breath sounds

26
Q

What is the COPD cascade?

A

fixed airway obstruction> impaired gas exchange> respiratory failure (inc CO2)> pulmonary HT> right ventricular hypertrophy (due inc work of breathing)> death

27
Q

COPD ix…

A

PFTs (FEV1:FVC ratio dec, PEFR low)
Imaging: cxr (flattened abdomen/hyperinflation), HRCT
ABGs: hypoxia/hypercapnia

28
Q

COPD Tx…

A

smoking cessation!!

  1. SABA
  2. LABA
  3. combo LABA & LAMA/SAMA
  4. step 3 + theophylline & inhaled corticosteroids
29
Q

What is COPD treatment expressed as?

A

Palliative as no possibility of resolution

30
Q

Causes of AEoCOPD?

A

Viral/ bacterial infection

31
Q

Ix for AEoCOPD?

A

ABGs (high bicarbonate)

32
Q

Tx for AEoCOPD?

A

Home: regular inhalers, oral prednisolone
Hospital: nebulised SABA & SAMA, prednisolone, antibis, 24-28% O2 (monitor PaCO2- can’t rise above 7kPa)
Severe: intubation

33
Q

True/False:

Asthma-COPD Overlap can be identified by COPD patient with eosinophilia >4%?

A

True

Respiratory (19 decks)

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