Asthma

Question 1

What is asthma?

Answer 1

Chronic inflammatory disorder of the airways resulting in episodes of reversible bronchospasm causing airflow obstruction

Question 2

Name 3 triggers of asthma

Answer 2

URTIs
Allergens (pet dander, house dust, moulds)
Irritants (cigarette smoke, air pollution)
Drugs (NSAIDs, beta-blockers)
Preservatives (sulphites, MSG)
Other (Emotion/anxiety, cold air, exercise, GORD)

Question 3

Explain the cellular pathophysiology of an asthmatic episode. Hint: What kind of hypersensitivity is it?

Answer 3

The immediate response if a Type 1 Hypersensitivity. IgE binding –> Mast cell degranulation –> Mediator release –> 3 acute phase components of response

The late phase response is a Type 4 Hypersensitivity.
Mediators released –> Eosinophils attracted to area –> release of mediators –> epithelial damage –> Increased airway hyperresponsiveness –> prolonged inflammatory response

Question 4

What are the three main components involved in the airway obstruction that occurs in an asthmatic episode?

Answer 4

1. Airway bronchospasm: constriction of airway smooth muscle
2. Increased mucus production
3. Increased vascular leak -> oedema

Question 5

What is physiology behind an asthma attack leading from the airway obstruction?

Answer 5

Airway Obstruction -> V/Q mismatch -> Hypoxemia -> Increased Ventilation -> Decreased PaCO2 -> Respiratory Alkalosis + Muscle Fatigue -> Decreased Ventilation + Increased PaCO2/Respiratory Acidosis …->… Status Asthmaticus

Question 6

What is involved in the chronic airway remodelling in chronic asthmatics? (obviously more in adults but i guess could happen in late teens with chronic severe asthma)

Answer 6

Goblet Cell hyperplasia
Collagen deposition and sub-epithelial fibrosis
Smooth muscle hypertrophy/hyperplasia
Increased Vascularity

Question 7

Explain the two mechanisms by which patients can get drug-induced asthma

Answer 7

1. Aspirin/NSAIDs promoted asthma: block COX pathway –> shift to lipoxygenase pathway –> increased leukotriene production –> bronchoconstriction
2. Beta-blocker induced asthma: Adrenaline acts on beta-2 adrenoceptors which causes bronchodilation. By using beta-2 receptor antagonists, bronchoconstriction can result in asthmatics

Question 8

List the clinical features associated with an asthmatic episode

Answer 8

Dyspnoea, expiratory wheeze, chest tightness, COUGH, sputum, nasal polyposis
Note: could be paroxysmal or persistent

Question 9

What are the 8 important questions/factors to know to determine if a patient’s asthma is well controlled?

Answer 9

1. Daytime Symptoms
2. Night-time Symptoms
3. Physical Activity
4. Exacerbations
5. Asthma-related absence from work/school
6. Beta-2 agonist use
7. FEV1 or PEF
8. PEF diurnal variation

Question 10

What is the gold standard when it comes to the diagnosis of asthma? What are you looking for?

Answer 10

• *Spirometry showing REVERSIBLE airway obstruction
  1. Decreased FEV1/FVC below lower limit of normal ( 12% (min 200ml in adults) after bronchodilator therapy or controller therapy

Question 11

What is another test being used now to determine the severity of a person’s asthma?

Answer 11

Bronchial Challenge Test
Directly or indirectly cause bronchoconstriction and assess severity by increasing doses of agents causing this obstruction.

Question 12

What is the basis of management of an asthmatic patient?

Answer 12

1. Assess (diagnosis, symptoms control etc.)
2. Adjust treatment (step up, step down or maintenance)
3. Review response (Asthma control, lung function etc.)

Question 13

How do you go about treating and managing ongoing treatment of an asthmatic patient?

Answer 13

**STEP WISE APPROACH
Assess the control of their asthma and evaluate based on flare-up frequency and lung function tests whether step up in treatment is required or if control is adequate whether is step down is necessary.

Question 14

In an acute exacerbation of asthma, what are 5 red flags you are looking for? (there are 8)

Answer 14

Severe Tachypnoea
Severe Tachycardia
Respiratory Muscle Fatigue
Diminished Expiratory Effort -> life threatening when PEFR

Question 15

In an acute exacerbation of asthma, what are 3 investigations you want to conduct?

Answer 15

1. PEF or FEV1
2. Oxygen Saturation
3. Short-acting Bronchodilator response trial

Question 16

What 5 steps are used to manage a patient with an acute exacerbation of asthma?

Answer 16

1. Inhaler beta-2 agonist + O2
2. Systemic steroids
3. Anticholinergic therapy with/without magnesium sulphate
4. Rapid sequence intubation in life-threatening cases
5. SC/IV Adrenaline, IV Salbutamol if unresponsive

Question 17

In terms of acute management of asthma, there are 4 grades of severity; mild, moderate, severe and critical. Discuss the signs of severity of a mild asthma attack. (mental state, work of breathing, HR, ability to talk)

Answer 17

Normal mental state
Subtle or no increased work of breathing accessory muscle use/recession.
Able to talk normally

Question 18

What is the management of a mild asthma attack?

Answer 18

Salbutamol with MDI + spacer - once and review after 20 mins
if good response - discharge on beta2-agonist PRN
if poor response - manage as moderate

Oral pred if no response to bronchodilator and continue for following days depending on salbutamol requirement.
Important for reassessment of asthma action plan

Question 19

What are the signs of severity of a moderate asthma attack? (mental state, work of breathing, HR, ability to talk)

Answer 19

Normal mental state
Some increased work of breathing accessory muscle use/recession
Tachycardia
Some limitation of ability to talk

Question 20

What is the management of a moderate asthma attack?

Answer 20

Oxygen if O2 saturation is less than 92%. Need for Oxygen should be reassessed.

Salbutamol by MDI + spacer - 1 dose every 20 minutes for 1 hour ; review 10-20 min after 3rd dose to decide on timing of next dose.

Oral prednisolone - 2 mg/kg (max 60 mg) initially, only continuing with 1 mg/kg daily for further 1-2 days if there is ongoing need for regular salbutamol.

Question 21

What are the signs of severity of a severe asthma attack? (mental state, work of breathing, HR, ability to talk)

Answer 21

Agitated/distressed
Moderate-marked increased work of breathing accessory muscle use/recession.
Tachycardia
Marked limitation of ability to talk

Note: wheeze is a poor predictor of severity.

Question 22

What is the management of a severe asthma attack?

Answer 22

Oxygen if O2 less than 92%

Salbutamol by MDI + spacer - 1 dose every 20 minutes for 1 hour; review ongoing requirements 10-20 min after 3rd dose.
If improving, reduce frequency.
If no change, continue 20 minutely.
If deteriorating at any stage, treat as critical.

Ipratropium by MDI/ spacer - 1 dose every 20 minutes for 1 hour only.

Aminophylline If deteriorating or child is very sick. Loading dose: 10 mg/kg i.v. (maximum dose 500 mg) over 60 min.
Unless markedly improved following loading dose, give continuous infusion or 6 hourly dosing.

Magnesium sulphate for intravenous administration

Oral prednisolone ; if vomiting give IV methylprednisolone

Question 23

What are the signs of severity of a critical asthma attack? (mental state, work of breathing, HR, ability to talk)

Answer 23

Confused/drowsy 
Maximal work of breathing accessory muscle use/recession 
Exhaustion 
Marked tachycardia 
Unable to talk 

SILENT CHEST, wheeze may be absent if there is poor air entry.

Question 24

What is the management of a critical asthma attack?

Answer 24

O2
Continuous Nebulised Salbutamol
Nebulised ipratropium
Methylprednisolone
Aminophylline
Magnesium Sulphate
May consider IV salbutamol but be weary of salbutamol toxicity with tachycardia, tachypnoea and metabolic acidosis.

Question 25

What is important to discuss in terms of spacer use in the management of asthma?

Answer 25

A spacer is required to distribute the medication down into the lower airways rather than the back of the pharynx.

Question 26

What are the discharge requirements for a child who had an asthma attack?

Answer 26

Improvement 1hr following initial therapy and if clinically well.
Adequate oxygenation
Adequate oral intake
Asthma action plan