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(Edited) Respiratory System > S8) Asthma > Flashcards

S8) Asthma Flashcards

1
Q

What is asthma?

A

Asthma is a chronic inflammatory disorder of the airways, wherein widespread but variable airflow obstruction and increased airway responsiveness to a variety of stimuli occurs

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2
Q

Identify 5 defining characteristics of asthma

A
  • Chronic inflammatory process
  • Susceptibility
  • Variable airflow obstruction
  • Airway hyper-responsiveness
  • Reversibility
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3
Q

Airways obstruction is a feature of both Asthma and Chronic Obstructive Pulmonary Disease (COPD).

How can one distinguish between the two conditions?

A
  • Asthma: airway obstruction is often reversible (> 15% improve spontaneously, with bronchodilators/steroids)
  • COPD: airway obstruction is not fully reversible (< 15% improve with treatment)
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4
Q

Identify the most influential cells in asthma

A

Asthma is a chronic inflammatory process driven by TH2 cells

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5
Q

What do TH2 cells do?

A
  • Release cytokines, which attract and activate inflammatory cells (incl. mast cells and eosinophils)
  • Activate B cells, which produce IgE
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6
Q

In a sensitised atopic asthmatic, exposure to antigen results in a 2 phase response.

Briefly, identify and describe these 2 phases

A
  • Immediate response (< 20 mins)
  • Late phase response (3 – 12 hours later)
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7
Q

What type of immune response is the immediate response to asthma?

A

The immediate response is an example of type 1 hypersensitivity

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8
Q

In 5 steps, describe the immediate response to asthma

A

⇒ Allergen interacts with specific IgE antibodies

⇒ Mast cell degranulation occurs

⇒ Mediators are released (histamine, prostaglandin D2, leukotriene)

⇒ Bronchial smooth muscle contracts

⇒ Bronchoconstriction occurs

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9
Q

What type of immune response is the late phase response to asthma?

A

The late phase response is an example of type IV hypersensitivity

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10
Q

The late phase response to asthma involves inflammatory cells.

What do they do?

A

Inflammatory cells release mediators and cytokines which cause airway inflammation

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11
Q

Identify 4 inflammatory cells involved in the late phase response to asthma

A
  • Eosinophils
  • Mast cells
  • Lymphocytes
  • Neutrophils
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12
Q

What do eosinophils do in the late phase response to asthma?

A

Eosinophils release Leukotriene C4 and other mediators, some of which are toxic to epithelial cells, and causes shedding of epithelial cells

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13
Q

Identify 5 events which causes the airway narrowing observed in asthma as a result of inflammation

A
  • Mucosal oedema due to vascular leak
  • Bronchial wall thickening due to inflammatory cell infiltration
  • Mucous over-production
  • Smooth muscle contraction
  • Epithelium shedding
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14
Q

Identify 6 major precipitating factors for asthma

A
  • Allergens e.g. pollen, animals hair/dander
  • Cold air (airway hyper-responsiveness)
  • Exercise
  • Irritants e.g. car exhaust fumes, smoke, strong smells
  • Emotional distress
  • Viral infections
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15
Q

Identify 6 signs and symptoms of asthma

A
  • Expiratory wheeze
  • Cough
  • Diurnal variability (worse at night & morning)
  • Breathlessness
  • Chest tightness
  • Exercise induced wheeze
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16
Q

What 3 questions can one ask a patient to ascertain asthma?

A
  • Have you had difficulty sleeping because of your asthma symptoms?
  • Have you had your usual asthma symptoms during the day?
  • Has your asthma interfered with usual activities?
17
Q

What is the most common test used to confirm a diagnosis of asthma?

A

Spirometry

18
Q

What do the spirometry tracings in an asthmatic patient usually show?

A

Obstructive condition – FEV1/FVC is reduced

19
Q

Which further test can be used to confirm an asthma diagnosis if the spirometry tracing is normal?

A

Methacholine / histamine challenge to determine airway hyper-responsiveness

20
Q

Identify 3 investigations used to measure the airway inflammation in asthma

A
  • Peripheral blood eosinophil count (FBC)
  • Induced sputum (eosinophils, neutrophils)
  • FeNO (exhaled nitric oxide)
21
Q

Identify 5 aims of asthma management

A
  • No daytime symptoms
  • No night-time awakening due to asthma
  • No asthma attacks
  • No limitations on activity
  • Normal lung function
22
Q

Identify and describe 3 factors which affect asthma treatment

A
  • Pharmacological management: incorrect or suboptimal prescribing
  • Clinical factors: environmental (triggers), medication, co-existing condition
  • Behavioural factors: sub-optimal adherence, poor inhaler technique, smoking
23
Q

Outline the principles of asthma treatment

A
  • Smoking cessation
  • Inhaler technique
  • Monitoring
  • Pharmacotherapy
  • Lifestyle
  • Education
24
Q

Identify the 5 stages in asthma treatment

A
  1. Regular preventer
  2. Initial add-on therapy
  3. Additional add-on therapies
  4. High dose therapies
  5. Continuous/frequent use of oral steroids
25
Q

What is the regular preventer in asthma treatment? (first line)

A

Low dose inhaled corticosteroid (ICS)

26
Q

What is the initial add on therapy in asthma treatment? (second line)

A
  • Low dose inhaled corticosteroid (ICS)
  • Inhaled long acting β2 agonists (LABA)
27
Q

What are the additional add on therapies in asthma treatment? (third line)

A

If no response / inadequate control from LABA:

  • Increase ICS dose + continue LABA
  • Continue LABA + ICS and trial LTRA, LAMA or theophylline

(LTRA = leukotriene receptor antagonists)

28
Q

What are the high dose therapies in asthma treatment? (fourth line)

A
  • Increase to high-dose ICS
  • Addition of 4th drug (LTRA, theophylline, LAMA, β2-agonist tablet)
29
Q

Describe the continuous/frequent use of oral steroids in asthma treatment (last line)

A
  • Low dose steroid tablet
  • Maintain high dose ICS
  • Refer to specialist care
30
Q

Describe the treatment of acute severe asthma

A
  • Oxygen (high flow, 94-98%)
  • Nebulised salbutamol
  • Oral prednisolone (Steroids)
  • Admit them?
31
Q

Describe the treatment of life threatening asthma

A
  • Nebulised ipratropium bromide (add to acute treatments)
  • IV magnesium and/or IV aminophylline (add to acute treatments)
  • Discuss with senior doctor and ICU
  • If treatment is not working CXR to check for other pathology - asthmatic patients are prone to pneumothorax
32
Q

Describe the difference in symptoms betwen asthma COPD

A
  • Asthma: - Dry cough, wheeze, history of atropy, typically children/young people, obstructive pattern - Good reversibility
  • COPD: - Productive cough, wheeze, history of smoking, typically older adults, obstructive pattern - Poor reversibility
33
Q

How does management depend on probability of asthma?

A
  • High probability:
    • start on treatment
  • Low probability:
    • Investigate/rule out other causes
    • Refer for further investigations
  • Intermediate probability:
    • Spirometry with reversibility testing
34
Q

What are the signs of acute severe asthma?

A

ABCDE assessment (sort of):

  • Airways: might not be abel to complete sentences as out of breath
  • Breathing: oxygen saturation might be low but wont typically drop below 92%, RR >= 25, ± wheezing on auscultation
  • Circulation: High HR
  • Peak expiratory flow rate 33-55% of the best or predicted value
35
Q

What are the signs of life threatening asthma?

A

All the features of acute severe asthma but any of the following instead of or as well as:

  • cyanosis
  • drowsy, poor respiraotry effort
  • O2
  • PEFR < 33% of predicted or best value
  • Arrhytmia, hypotension
36
Q

What are the ABG results in an acute severe asthma attack?

A
  • Hyperventilating → hypocapnia → ↓ pH = Respiratory alkalosis
  • Hypoxic
  • Bicarbonate would be normal

= Type 1 respiratory failure

37
Q

What are the ABG results in an acute severe asthma attack?

A

Might appear normal:

  • potentially due to treatment working
  • Or due to patient deterorating and CO2 is ↑ as RR is ↓ as they are starting to tire
  • These pateitns may need ventilation and ITU suppport

(Edited) Respiratory System (19 decks)

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