Acute Asthma Flashcards

1
Q

Asthma is a common obstructive chronic respiratory condition.

What is asthma characterised by?

A

Asthma is characterised by recurrent episodes of dyspnoea, cough and wheeze caused by a reversible airway obstruction.

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2
Q

What are the 3 main underlying pathology in asthma which lead to airway narrowing?

A
  1. Bronchial muscle contraction triggered by various stimuli => airflow limitation
  2. Mucosal inflammation caused by mast cell and basophil degranulation resulting in the release of inflammatory mediators
  3. Increased mucus production
    * In chronic asthma inflammation may be accompanied with irreversible airflow limitation due to airway wall remodelling.
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3
Q

Who does asthma affect?

A

Asthma commonly starts in childhood between 3-5 years => may worsen or improve during adolescence.

Westernised life-style / Developed countries

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4
Q

What is the atopic triad?

Who does this commonly affect?

A

Atopic triad:
=> Atopic Dermatitis,
=> Atopic Asthma,
=> Allergic Rhinitis

Atopic asthma is a childhood onset wheezing illness caused by inhaled allergic triggers.

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5
Q

What are the most common allergens in atopic asthma?

A

Dust mite

Animal danders particularly cats

Pollens

Fungi

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6
Q

Which age group does non-atopic asthma affect?

What extrinsic factors lead to asthma in this?

A

Middle aged individuals

Extrinsic causes:
Sensitisation to occupational agents
Intolerance to NSAIDs
Beta-adrenoreceptor blocking meds => block protective effect of endogenous catecholamines.

*Extrinsic causes must be considered in all cases of asthma and avoided.

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7
Q

What are the underlying theories behind allergic asthma?

Explain hygiene hypothesis in detail.

A
  1. Early childhood exposure to allergens and maternal smoking = major influence in IgE production
  2. Hygiene hypothesis: growing up in a ‘clean’ environment predispose towards IgE response to allergies

Conversely, growing up in a ‘dirtier’ environment allows the immune system to avoid allergic response

=> early life exposure to inhaled and ingested products of micro-organisms as seen in developing countries => reduces the risk of developing asthma/allergies.

*allergens involved in asthma similar to ones involved in rhinitis

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8
Q

What are the precipitating factors for asthma?

A

Exercise-induced

Cold air

Smoking & passive smoking

Emotions

Drugs i.e. NSAIDs, beta-adrenoceptor blocker

Environment exposure i.e. pollen, house dust-mite, fur

Irritants, dust, vapour, fumes

Atmospheric pollution

Viral infections i.e. rhinovirus, parainfluenza virus, RSV

Occupational sensitisers

Genetic factors

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9
Q

How does exercise or cold air induce asthma?

A

Exercise induced wheeze is driven by the release of histamine, prostaglandin and leukotrienes from mast cells.

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10
Q

Why are beta-adrenoceptor blockers contraindicated in asthma?

A

The airways have a direct parasympathetic innervation to produce broncho-constriction via beta2 receptors.

Non-selective beta-blockers i.e. propranolol => broncho-constriction and reduced airflow therefore, should be avoided in asthma.

Beta-1 receptor blockers may be given i.e. atenolol if needed in asthmatic patients

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11
Q

There are two broad types of occupational sensitisers.

I. Low molecular weight compounds i.e.
=> found in spray painting, welding, electronics industry,
=> wood dust,
=> bleaches and dyes,
=> complex metals i.e. nickel, platinum and chromium.

II. High molecular weight compounds
=> Antibiotics
=> Latex
=> Allergens from animals & insects inc. farmers, poultry workers, seafood processing industry, laboratory workers

A

INFO CARD

Occupational asthma depends on level of exposure.

Atopic individuals develop occupational asthma more quickly => development of specific IgE antibodies

Non-atopic individuals can also develop occupational asthma when exposed to occupational sensitisers for a longer time than atopic individuals.

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12
Q

What are the signs and symptoms of asthma?

A

Symptoms:

Wheezing attacks

Intermitted dyspnoea

Cough [nocturnal] => usually predominant feature in children and nocturnal cough may be the presenting symptom

Sputum

Signs:

Tachypnoea

Audible wheeze

Hyper-inflated chest

Hyper-resonant percussion

Reduced air entry

Widespread, polyphonic wheeze

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13
Q

What are the clinical features of a severe attack?

A

Inability to finish sentences

Pulse >110bpm

Respiratory rate >25/min

Peak expiratory flow: 30-50% predicted

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14
Q

What are the clinical features of a severe life-threatening attack?

A

Silent chest

Confusion

Exhaustion

Cyanosis <92% O2 sats

Bradycardia

Peak expiratory flow <33% predicted

Near fatal = high CO2

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15
Q

What are the 7 important information to establish during history-taking a suspecting asthma patient?

A
  1. Diurnal variation: vary throughout the day but marked peak flow drop is common during morning
  2. Exercise: quantify tolerance
  3. Disturbed sleep: quantify as nights per week (sign of severe asthma)
  4. Acid reflux: 40-60% of people with asthma have reflux => treating it improves spirometry but not symptoms
  5. Other atopic disease: eczema, hay-fever or family Hx?
  6. Home (especially bedroom): pets? carpets? feather pillows or duvet? soft furnitures i.e. floor cushions?
  7. Job: 15% of cases are job related, more for paint sprayers, food processors, welders and animal handlers.

If symptoms get better during weekends or holidays then work may be the trigger => ask patient to measure their peak flow at intervals at work and at home (at the same time of day) to confirm

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16
Q

How is initial diagnosis of asthma made in children?

A

High probability of asthma => trial asthma treatment
=> if successful, continue at minimum effective dose
=> if unsuccessful, assess inhaler technique/compliance
=> no further improvement = refer

Intermediate probability => lung function tests/atopy
=> if lung function test +ve, start asthma trial
=> if lung function test -ve, investigate/treat other cause/refer

Low probability => consider alternative cause

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17
Q

How is initial diagnosis of asthma made in adults?

A

Clinical investigation i.e. spirometry or peak flow

High probability of asthma => asthma treatment
=> if successful, continue at minimum effective dose

Intermediate probability
=> FEV1/FVC <0.7 = asthma treatment
=> FEV1/FVC >0.7 = consider alternative cause / refer

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18
Q

Which clinical features increase the probability of asthma?

A

Wheeze, shortness of breath, chest tightness

Diurnal variation

Response to exercise, allergen, cold air

Symptoms after aspirin or B-blocker

Hx of atopy

Family Hx of atopy/asthma

Widespread wheeze on auscultation

Unexplained low FEV1 or peak expiratory flow

Unexplained peripheral blood eosinophilia

19
Q

Which clinical features lower the probability of asthma?

A

Prominent dizziness, lightheadedness, tingling

Chronic productive cough with no wheeze

Normal exam when symptomatic

Change in voice

Symptoms with colds only

Significant smoking hx >20 pack years

Cardiac disease

Normal peak expiratory flow when symptomatic

20
Q

Which investigations are carried out in acute asthma attack?

A

Peak expiratory flow

Sputum culture (sputum eosinophilia = diagnostic finding)

Bloods: FBC (peripheral eosinophilia), U&E, CRP, blood cultures

ABG: usually shows significantly reduced CO2 and a normal or slightly low O2 => hyperventilating

=> if O2 is normal but patient is hyperventilating then monitor carefully and repeat ABG later

=> if CO2 normal or high and patient is hyperventilating then transfer to ITU for ventilation => indicates respiratory failure

Chest X-ray: to exclude infection / pneumothorax (complication of asthma)

21
Q

Which investigations are carried out in chronic asthma attack?

A

Peak expiratory flow monitoring

Diurnal variation of >20% on >3days a week for 2wks

Spirometry: obstructive (reduced FEV1/FVC) => ~15% improvement in FEV1 after beta2 agonists or steroid trial.

Chest X-ray: hyper-inflation

Skin prick test: identify allergen

22
Q

What is the purpose of a lung function test?

What are the two main lung function tests?
Describe them.

A

Lung function tests help diagnose and assess asthma reversibility, treatment effectiveness and severity.

  1. Peak respiratory flow rate (PEFR) measurements on walking, prior to taking a bronchodilator, before bed and after a bronchodilator

=> Demonstrates variable air-flow restriction which characterises asthma

=> Diurnal variation in PEFR = a good measure of asthma activity

  1. Spirometry assess reversibility => asthma can be diagnosed by showing >15% improvement in FEV1 or PEFR after inhaling bronchodilator
23
Q

When should skin prick tests be performed?

What is the alternative and when should this test be performed?

A

Skin prick tests should be performed in all cases of asthma to help identify allergic triggers.

Alternative: allergen specific IgE measurement in serum.

This should only be performed if skin-prick test is not available, if patient taking anti-histamines or no suitable antigen extracts are available.

24
Q

What is allergen provocation test for?

A

Allergen inhalation challenge ONLY indicated for patients suspected with occupational asthma, NOT ordinary asthma.

25
Q

What are the differential diagnosis for asthma?

A

Pulmonary oedema (cardiac asthma)

COPD

Superior vena cava obstruction (wheezing/dyspnoea not episodic)

Pneumothorax

Pulmonary embolism

Bronchiectasis

Obliterative bronchiolitis (elderly)

26
Q

What lifestyle changes are required to help improve asthma?

A

Stop smoking

Avoid triggers

Stop beta-blockers and NSAIDS

Weight loss if overweight

27
Q

What specific advice is given to patients about asthma management?

A

Correct inhaler technique

Teach use of peak flow meter to monitor peak expiratory flow twice a day

Educate to enable self-management by altering their medications depending on their symptoms

Written plan on how to act in an emergency

Consider teaching relaxed breathing technique to avoid dysfunctional technique (Papworth method - use stomach area for breathing, not chest)

28
Q

Which drugs are used for asthma management?

A

Beta-adrenoceptor agonists (short acting & long acting)

Inhaled & oral corticosteroids

Leukotriene receptor antagonists

Anti-muscurinic (anti-cholinergic) bronchodilators

Anti-inflammatory drugs

Monoclonal antibodies

29
Q

What is the mechanism of action for Beta2-adrenoceptor agonists?

What are the two types of beta2-adrenoceptor agonists?
Examples?

What are the side effects?

A

Beta2-adrenoceptor agonists are selective for respiratory tract (doesn’t stimulate beta1 adrenoceptors of the myocardium).

=> They help relax the bronchial smooth muscles and help relieves symptoms by increasing CAMP

=> They have no affect on the underlying inflammation => only symptomatic control!!

2 types of beta2-adrenoceptor agonists:

=> Short-acting Beta agonists (SABA) : 2 puffs/day and can be taken as and when required i.e. salbutamol 100ug ; terbutaline 250ug

=> Long-acting Beta agonists (LABA) : once or twice daily by inhalation can help with nocturnal symptoms & reduce morning dips - effective up to 12h e.g. salmeterol => can be used as an alternative to increasing steroid dose

They should be given in combination with an inhaled corticosteroid e.g. salmeterol + fluticasone

Side effects: tachyarrythmias, decreased K+, tremor, anxiety + LABA = paradoxical breathing

30
Q

What is the mechanism of action for corticosteroids? Examples?

When do you need oral corticosteroid?

A

Act over days to decrease bronchial mucosal inflammation i.e. Beclomethasone, fluticasone => inhaled to minimise systemic effects.

For all patients with symptoms, even mild.

Rinse mouth after inhaled steroids to prevent mouth candidiasis

Inhaled corticosteroid dose should be lowered once asthma is controlled

Oral corticosteroid is needed for acute exertions (high dose) and for long term use (small dose) when other meds don’t work e.g. prednisolone

31
Q

What is the mechanism of action for leukotriene receptor antagonist? Examples?

A

Targets cysteinyl LT1 recceptor => blocking the effects of cysteinyl leukotrienes in the airway e.g. montelukast

=> only effective on a small proportion of asthma patients
=> should be trialled for 4 weeks before deciding on effectiveness

Leukotriene receptor antagonist should be tried on patients whose asthma is not controlled on low-medium dose of inhaled steroids

32
Q

What is the mechanism of action for anticholinergic (anti-muscuric) broncho-dilators? Examples?

A

Muscurinic receptors are found in respiratory tract:
large airways = M3 receptors
Peripheral lung tissue = M1 & M3 receptors

=> nebulised short-acting antimuscurinic drug e.g. Ipratropium may be used in acute severe exacerbation of asthma

33
Q

What is the mechanism of action for monoclonal antibodies? Examples?

A

Omalizumab, monoclonal antibody, directed against IgE to downregulate its number and activity of mast cells and basophils.

=> Given as subcutaneous injection every 2-4 weeks
=> Effective in eosinophilic asthma

34
Q

What is cromoglicate and when can it be used?

A

Cromoglicate is a mast cell stabiliser (inhaled)

Can be used as prophylaxis in mild and exercise induced asthma in children

35
Q

What is the prognosis for asthma?

A

Most childhood asthma improves by adolescence or is less severe as adults.

Significant number develop chronic asthma later in life.

36
Q

In an acute severe asthma attack patients often present with acute breathlessness and wheeze.

What other features are present in a life-threatening attack?

A

Peak expiratory flow <33% of predicted or best

Silent chest, cyanosis, feeble respiratory effort

Arrhythmia or hypotension

Exhaustion, confusion or coma

ABG: normal/high CO2 ; low O2

37
Q

What investigations should be done for a acute asthma attack?

A

Peak expiratory flow - may be difficult to obtain

ABG if O2 sats <92% or life-threatening features

Chest X-ray if suspicion of pneumothorax, infection or life-threatening attack

FBC, U&E

38
Q

How do you manage acute asthma attack?

A

Assess severity of attack - warn ICU if severe or life-threatening

Immediate treatment:
O2 - maintain between 94-98%

Salbutamol 5mg nebuliser with oxygen

If severe/life-threatening, add in Ipratropium 0.5mg/6h to nebuliser

Hydrocortisone 100mg IV or prednisolone 40mg orally

=> Reassess every 15 mins

If peak expiratory flow <75% repeat salbutamol nebuliser every 15-30mins

Add Ipratropium if not already given

Monitor ECG for arrhythmias

Consider single dose of magnesium sulphate IV => in patients with severe/life-threatening features without good response to therapy (only done by senior)

39
Q

How do you manage acute asthma attack?

A

Assess severity of attack - warn ICU if severe or life-threatening

Immediate treatment:
O2 - maintain between 94-98%

Salbutamol 5mg nebuliser with oxygen

If severe/life-threatening, add in Ipratropium 0.5mg/6h to nebuliser

Hydrocortisone 100mg IV or prednisolone 40mg orally

=> Reassess every 15 mins

If peak expiratory flow <75% repeat salbutamol nebuliser every 15-30mins

Add Ipratropium if not already given

Monitor ECG for arrhythmias

Consider single dose of magnesium sulphate IV => in patients with severe/life-threatening features without good response to therapy

40
Q

What is the next step in management of acute asthma attack if patient is improving within half an hour of initial management?

A

Continue nebuliser salbutamol every 4-6h (+ipratropium if started)

Prednisolone for 5-7 days

Monitor peak flow and O2 (94-98%)

If peak expiratory flow >75% 1h after initial treatment, consider discharge with follow up appt

41
Q

What is the next step in management of acute asthma attack if patient is not improving with initial management?

A

Refer to ITU for ventilatory support and additional meds i.e. aminophylline, IV salbutamol if patient has the following signs:

=>Deteriorating peak expiratory flow 
=>Persistent/worsening hypoxia 
=>Hypercapnia 
=>ABG shows low pH, high H+
=>Exhaustion, feeble respiration 
=>Drowsiness, confusion, altered conscious level
=>Respiratory arrest
42
Q

What are the differential diagnoses for acute asthma attack?

A

Acute infective exacerbation of COPD

Pulmonary oedema

Upper respiratory tract obstruction

Pulmonary embolus

Anaphylaxis

43
Q

What steps should be met in a patient who was admitted for acute asthma attack before discharge?

A

Discharge patient once:

=> stable on discharge meds for 24h
=> inhaler technique checked
=> peak flow rate >75%
=> steroid (inhaled and oral) and bronchodilator therapy
=> their own peak flow meter and written management plan

=> GP appt within 2 days
=> respiratory clinic appt within 4wks