Clinical features of asthma in adulthood and children Flashcards

1
Q

_Describe the defining features and

A
  • “gasp for breath”
  • Complex disease- history of respiratory symptoms such as:
    o Expiratory Wheezing -KEY. WORD.
    o Shortness of breath
    o Coughing
    o Chest tightness
    o ^ all together with difficulty in expiration.
  • Define features include an increased responsiveness of the trachea and bronchi to various stimuli which results in airflow obstruction. It is manifested by a widespread narrowing of airways that changes in severity either spontaneously or a result of therapy.
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2
Q

epidemiology of asthma,

A

The NHS spends around 1 billion a year treating and caring for people with asthma. One in 11 children has asthma and it is the most common long-term medical condition. … The UK has among the highest prevalence rates of asthma symptoms in children worldwide

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3
Q

Describe the pathophysiology of asthma.

A
  • Very complex
  • Inflammation of the airways mediated by the immune system – causing:
     Widespread narrowing of airways
    • Changes in severity either spontaneously or in response to stimuli.
     Increased airway reactivity
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4
Q

Describe proven and putative aetiological factors.

A
  • Hereditary
    o Especially first degree family member has asthma or another atopic disease.
    o Maternal atopy most influential most influential (3* more than father)
    o Atopy is the body’s predisposition to develop an antibody called immunoglobulin (IgE) in response to exposure to environmental allergens and is an inheritable trait
    o Associated with asthma
-	Smoking:
o	Maternal smoking during pregnancy:
	Decrease in FEV1
	Increase in Wheezy illness
	Increase in airway responsiveness
	Increase in asthma
	Reduction in lung function
o	“Grandmother effect”
-	Occupation:
o	Underestimated (10-15% of adult onset asthma)
o	Interactions with smoking and atopy:
	Isocyanates (paints)
	Lab animals (rodent urinary proteins)
	Grains 
	Enzymes
	Drugs
	Shell fish
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5
Q

Triggers/provokes asthma

A

Different for each individual:

  • Pets
  • Tree or grass pollen
  • Cigarette smoke
  • Exercise
  • Drugs (aspirin/NSAIDS)
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6
Q

Different for each individual:

  • Pets
  • Tree or grass pollen
  • Cigarette smoke
  • Exercise
  • Drugs (aspirin/NSAIDS)
A

It is mostly about the history.
Clinical Test:
o Test for airway Obstruction
o Spirometry and bronchodilator reversibility
o FEV1/FVC ratio
o If they have normal spirometry, do not exclude asthma
o Reversibility to bronchodilator, corticosteroids
o Variable airflow obstruction: peak flow charts

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7
Q

If obstructed picture: Full pulmonary function testing. what does this exclude?

A

COPD/emphysema

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8
Q

Carbon monoxide gas transfer (transfer of CO to Hb across alveoli)

A

Gas transfer very important is differentiating between COPD and asthma.

good at identifying COPD

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9
Q

• _Contrast the management of asthma with strategies for management of COPD.

A

Initial treatments of COPD include bronchodilators, while initial treatments for asthma include inhaled corticosteroids

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10
Q

Oher useful investigations:

A
  • Chest X-Ray but it tends to look normal
    Hyperinflated, hyperlucent
    (no effusion, collapse, opacities, interstitial changes)
  • Skin prick testing (atopic status)
  • Total and specific IgE (atopic status)
  • Full blood count
    Eosinophilia (atopy)
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11
Q

Define the specific features to be included in the clinical history of asthma.

A
  • Compatible Symptoms: wheezing, chest tightness, breathlessness, coughing. Occasionally sputum (BUT more common in COPD)
  • Past medical history:
    o Childhood asthma, bronchitis or wheeze in infancy
    o Eczema
    o Hayfever
  • Drugs:
    o Have they been on any treatment for asthma and what has its effect been?
    o Current inhalers (check technique!), compliance
    o -blockers, aspirin, NSAIDS
    o Effects of previous drugs/inhalers
  • Family history:
    o Asthma and other atopic disease
-	Social history:
o	Tobacco, recreational drugs, vaping
o	Pets
o	Occupation (past and present)
o	Psychological aspects- stress can make asthma worse
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12
Q

Probably not asthma if:

A
  • Finger clubbing
  • Stridor- inspiratory wheeze (large airways)
  • Asymmetrical expansion, dull percussion note (collapse/effusion)
  • Crepitations
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13
Q

What else could it be if its not asthma?

A
  • Generalised airflow obstruction
    o COPD (irreversible AFO)
    o Bronchiectasis
    o Cystic Fibrosis
  • Localised airway obstruction: inspiratory stridor= large airways
    o Tumour
    o Foreign body
  • Cardiac
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14
Q

• _list the factors to assess the severity of acute, severe asthma.

A

Assess it via Objective parameters>subjective

  • Ability to speak
  • Heart rate
  • Respiratory rate
  • PEF
  • Oxygen saturation / Arterial blood gases
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15
Q

• _Explain how to assess the severity of acute, severe asthma.

moderate

A
Moderate:
Essentially increasing symptoms, 
-	Able to speak, complete sentences
-	HR < 110
-	RR < 25
-	PEF 50 - 75% predicted or best
-	SaO2 ≥ 92% (no need for ABG)
-	PaO2 ≥ 8kPa
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16
Q

• _Explain how to assess the severity of acute, severe asthma.

severe

A
Severe:
Any one of 
-	Inability to complete sentences in one breath
-	HR ≥110
-	RR ≥25
-	PEF  33 - 50% predicted or best
-	SaO2 ≥ 92% 
-	PaO2 ≥ 8kPa
17
Q

• _Explain how to assess the severity of acute, severe asthma.

life threatening

A
Life threatening:
Any one of
-	Grunting
-	Impaired consciousness, confusion, exhaustion
-	Bradycardia/ arrhythmia/ hypotension
-	PEF < 33% predicted or best
-	Cyanosis
-	Silent chest
-	Poor respiratory effort
-	SaO2 < 92% (definitely needs blood gas!)
-	PaO2 < 8kPa
-	PaCO2 normal (4.6 - 6.0kPa)
18
Q

• _Explain how to assess the severity of acute, severe asthma.

near fatal

A

Near Fatal:

  • Raised PaCO2
  • Need for mechanical ventilation
19
Q

asthma children lecture:

Near Fatal:

  • Raised PaCO2
  • Need for mechanical ventilation
A
  • Genes
  • Host response to environment
  • Infection is important, especially in paediatrics
  • Physiology is abnormal before symptoms
20
Q

There are many inconsistencies:

A
  • “Transient” vs persistent
  • VIW versus asthma/MTW
  • Different severities
  • Different age at onset
  • Heterogeneity in response- not just a single asthma gene, there are 10 variants with the two most common ones being ADAM33 and ORMDL3
  • Different triggers
21
Q

Allergy usually does not cause asthma.

A
  • Primary epithelial abnormality (of the skin/airway/gut) results:
    o Excema/asthma
    o Allergy -> allergy then fuels eczema/asthma
22
Q

When is it asthma in children?

A
  • Always at the doctor for a wheezy cough

- Shortness of breath at rest

23
Q

When is it not asthma?

A
  • Under 18 months, most likely infection

- Over 5 years, highly likely asthma

24
Q

Asthma treatment

A
  • Inhaled corticosteroids for 2 months- if its not asthma then it has no bad effect anyway.
  • Remember “false positive responses”- holiday
25
Q

Asthma vs VIW (Viral induced wheeze)

A

The difference between asthma and viral-induced wheeze is that children with asthma will wheeze at times other than when they have a cold – often with exercise or when they are exposed to particular ‘triggers’ like house dust mites or pets.
VIW is usually during a cold.

Most children with viral-induced wheeze will stop wheezing as they get older and will not develop asthma.