36. Asthma Flashcards Preview

Year 1 - Term 2: Carriage of Oxygen > 36. Asthma > Flashcards

Flashcards in 36. Asthma Deck (11):
1

What is asthma, and what are it's 3 main features?

A disease of airway inflammation. 

1) hypertrophy of airway wall muscle

2) increased mucous production

3) inflammatory cell infiltration

Produces a wheeze cough and breathlessness. 

(20% in kids, 15% adults)

2

How do allergens resut in the symptoms of asthma?

What does late onset allergic asthma occur via?

List 5 things that cause asthma.

Allergens activate Th2 cells -> produce IL4 and mediators. B cells activated by IL4, 13 -> produce IgE -> release mediators of inflammation including histamine, PGD3, LTC4 and kinins. Eosinophils release the same. Mediators activate nerve endings, make mucus, produce airway wall oedema, and cause bronchoconstriction.

Cholinergic bronchoconstriction

Genetics, allergens, irritants, infection, exercise (cools airway, activates nerves in wall -> bronchospasm)

3

When might a wheeze not be asthma?

What respiratory test would you do to monitor asthma compared to COPD?

Bronchiolitis in kids (common lower respiratory tract viral infection)

Upper airway obstruction (e.g. acute epiglottis) and stridor

Upper airway dysfunction

COPD (fixed narrowing of airways, usually chronic smokers)

 

Asthma: peak flow COPD: spirometry

COPD and asthma symptoms can overlap!

4

What happens to flow during an asthma attack?

What effect does a broncodilator have to have for an asthma diagnosis?

How are the vital capacity and total lung capacity affected by asthma?

All indices of expiratory flow are reduced, peak flow, FEV1/FVC all fall.

FEV1 increaes by >15% or >200ml after 400mg salbutamol inhaler (or 2.5mg via nebuliser, or 30mg/day of steroids for 14 days)

VC reduced becuase of airway closure but TLC increased with increased RV

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5

What is the difference between restictive and obstructive lung disease and what would the FEV1 look like on a volume-time graph for each?

Restrictive e.g. fibrosis - can't fully fill lungs with air but airways function. Graph: lower VC, plateaus.

Obstructive: volume may not be reduced as much but difficulty exaling all air from lungs due to damage or narrowing. Graph: Steeper.

 

 

 

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6

Why is gas exchange impaired in asthma?

What is the general day-to-day peak flow pattern in an asthmatic?

What findings in a peak expiratory flow rate (PEFR) diary would imply asthma?

How might peak flow increaese naturally?

Where are the 2 kinds of airflow found in the lungs?

V/Q mismatch, plugged bronchi, hypoxic pulmonary vasoconstriction

Lowest in morning and highest in evening. Saw tooth pattern. 

20% diurnal variation for 3 days/week for 2 weeks.

With respiratory training e.g. brass instrument

Central flow is lamina, but around ramifications of trachea/small airways it's turbulent

7

What is challenge testing?

What is bronchial hyperreactivity?

What happens between asthma attacks?

Use PEFR over time and environment to observe whether history correct e.g. pets. Stimulus challenges e.g. histamine, metacholine, cold air.

Often after infection, physical and irritant stimuli provoke cough, wheeze and breathlessness. NO ALLERGY - NOT ASTHMA.

Lung function may be normal. If chronic - some changes persist. Air trapping after bronchoconstriction due to airway closure lasts several days.

8

What are some common asthma allergens, and how soon is asthmatic's reaction?

What are some common asthma irritants?

How does the following affect asthma:

a) infection?

b) occupation?

c) exercise?

Dust, dust mite, grasses, pollen, fur, urine. Most reactions are soon after but can get late reaction and nocturnal wheeze.

Sulphur dioxide, nitrogen dioxide, ozone, cigarette smoke, particulate matter, wood smoke, burned hydrocarbons, rape pollen and dust (cause wheeze as irritants not allergens).

a) Viral infection with most upper respiratory tract viruses worsen asthma, symptoms may persis for weeks after infection

b) Can produce irritant fumes e.g. epoxy resins, grain dusts, flour/yeast, lab workers

c) Increased ventilation -> cooling -> spasm b/c receptors in bronchial wall. Breathing training may help e.g. through nose only. Treat before exercise.

9

What happens to asthma at night?

Is asthma affected by gender?

How is asthma assessed?

What happens if asthma is not treated?

Worsens - acid reflux works via vagal afferents -> cough/spasm, post nasal drip, bed allegens, inhaler compliance?

Female = changing hormone levels, menstural asthma, rarely severe, may affect 30%

History (+family, env, job, allergies), examination for wheeze, peak flow and PF monitoring, inhaler technique, compliance and puff counting

Poor control -> long term fixed airway changes via airway remodelling, and COPD outcome. 

10

List the 5 steps of asthma treatment.

1) Salbutamol inhaler as required

2) Regular inhaled steroids

3) Add long-acting bronchodilators, increase inhaled steroids, consider leukotriene antagoists

4) Theophyllines (methylxanthine), leukotriene antagonists, whatever you have not used before e.g. anticholinergics

5) Oral steroids, review diagnosis

Consider anti IgE therapy (monoclonal antibody against IgE), steroid sparing agents, thermoplasty

11

What is acute severe asthma?

How does smoking affect asthma?

What is laryngeal dysfunction?

Life threatening, 1200 die/yr, need immediate treatment with inhaled high dose bronchodilators, O2, steroids (24h delay). If pCO2 normal/raised = v. severe, need ITU and stay in hospital until off nebulisers. 999.

Causes oxidative stress by increasing NF kB and blocks steroid response by HDAC2 which can be activated by theophyllines. = Blocks some of the anti-inflammatory pathways and some inhaled steroid.

Lyrangeal 'closes down', supraglottic narrowing in inspiration, "asthma"? Test via continous laryngoscopy on exercise.

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