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PHA223 (2023) > Asthma > Flashcards

Asthma Flashcards

1
Q

What is asthma?

A

Inflammatory condition in which there is recurrent reversible airways obstruction in response to irritant stimuli. Chemical mediators are released by mast cells in airways; bronchoconstriction, mucosal oedema, hypersecretion of mucus

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2
Q

What are the symptoms of asthma?

A

wheezing, tight chest, cough - especially at night

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3
Q

What is asthma cause by?

A

genetics
animal allergens
pollen
infections
chemicals
drugs - NSAIDs
smoking
emotions stress
exercise
cold weather

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4
Q

Describe the onset of asthma?

A
  • Cases begin in childhood and can develop later in life
  • Late onset: non-T2-type (absence of allergy) - such as NAIDs intolerance, rhino-sinusitis
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5
Q

What are the two onset sub-types?

A

T2 - allergy, exercise - induced, aspirin exacerbation.
Non-T2 - obesity associated, smoking related

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6
Q

What are the two phases of asthma?

A

Immediate
Late

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7
Q

What are the 3 features of airway hyper-responsiveness?

A
  • Airway wall inflammation involving neutrophils, T cells (CD8+) alveolar dendritic cells and macrophages. Dendritic cell recruit T cells (CD4+) in the alveolar air spaces and eosinophils in bronchioles
  • Luminal obstruction of the airways by mucus caused by hyper-secretion of bronchial mucous glands and infiltration by inflammatory cells.
  • Vasodilation of bronchial microvasculature with increases vascular permeability and oedema.
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8
Q

What is hypersensitivity?

A

Bronchial hyper reactivity is abnormal sensitivity to a stumli - bronchoconstriction.

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9
Q

What is the 1st phase of Th2 response?

A

Attract inflammatory granulocytes (eosinophils) to the mucosal surface.

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10
Q

What is the 2nd phase of Th2 response?

A

IL-5 and granulocyte -macrophage colony stimulating factor prime eosinophils to produce cysteinyl leukotrienes to release granule proteins that damage the epithelium.
- This damage is a cause of bronchial hyper - responsiveness

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11
Q

What is the 3rd phase of Th2 response?

A

Promote IgE synthesis and responsiveness in some asthmatics.
- IL-4 and 13 switch B cells to IgE synthesis and cause expression of IgE receptors on mast cells and eosinophils - enhance adhesion of eosinophils to endothelium.

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12
Q

List the bronchodilators used in the treatment of asthma.

A

SABA
LABA
Anticholinergics
Methylxanthines

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13
Q

List the anti-inflammatories used in the treatment of asthma

A
  • ICS
  • LTRA
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14
Q

Describe the adrenergic receptors

A

All are typical G protein-coupled receptors

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15
Q

What are the 2 categories of adrenergic receptors?

A
  • alpha - adrenergic receptors - 2 sub types
  • beta - adrenergic receptors - 3 sub types
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16
Q

Where are beta1 receptors found?

A

mainly in the heart and responsible for effects of catecholamines

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17
Q

Where are beta2 receptors found?

A

mainly in the lungs and responsible for causing smooth muscle relaxation in many other tissues

18
Q

Describe SABAs MOA and give examples.

A

MOA - activates B2-R which relaxes smooth muscle and widens airway to relieve symptoms.
- Patients with symptomatic asthma should be given SABA2A
- Well absorbed and does not cross BBB

Examples: Salbutamol, Terbutaline

19
Q

Describe LABAs MOA

A

MOA: bind to 2 sites (exo & active) on R - longer duration of effect (12hours) - use x2 a day
- Patients with uncontrolled asthma by SABA alone
- Improve lung function and decreases asthma symptoms
- Must be used in combo with ICS

20
Q

State examples of LABAs

A

Fostair - formoterol/ beclometasone
Duoresp - formoterol/ budesonide
Seretide - salmeterol/ fluticasone
Relvar - vilanterol/ fluticasone

21
Q

Describe anticholinergics MOA and give examples.

A

MOA: block effects of acetylcholine and inhibit muscarinic GPCR leading to muscle relaxation.
- used in addition to SABA and LABA - rarely used in asthma

Examples:
SAMA - ipatropium
LAMA - tiotropium

22
Q

Describe Methylxanthines MOA and give examples.

A

MOA:
- Relaxes smooth muscle of bronchial airways and pulmonary blood vessels which leads to low responsiveness to histamines, metchacholine, adenosine and allergens.
- Competitively inhibits PDE which is the enzyme responsible for breakdown of cAMP in smooth muscle resulting in bronchodilation.

Examples; theophylline

23
Q

Describe the MOA of ICS and give an example

A
  1. Restrain clonal proliferation of the Th cell by decreasing transcription of the IL-2 gene and decreases cytokine formation. Th2 cytokines recruit and activate eosinophils. They are responsible for promoting production of IgE and expression of IgE-R.
  2. Glucocorticoids inhibit the generation of vasodilators PGE2 and PGI2 by inhibiting COX-2.
  3. Activate GR & inhibit inflammatory stimuli to decrease inflammation.

Example: beclometasone diproprionate by brand - QVAR or Clenil

24
Q

Describe the MOA of LTRA and give and examples

A
  1. CysLT (LTC4,LTD4,LTE4) are eicosanoids released by mast cells and eosinophils.
  2. CysLT bind to CysLT type 1 receptor on respiratory airway smooth muscle cells, airway macrophages & pro-inflammatory cells e.g. eosinophils
  3. Decreases sputum eosinophilia

Examples: montelukast, zafirlukast

25
Q

Why are corticosteroids used in asthma?

A

Inhibit mediators involved in airway inflammation
Oral - predisnolone for severe attack

26
Q

What is the MART regime?

A

Maintenance And Reliever Therapy - one inhaler used as reliever and preventer ICS/LABA - LABA must be rapid acting.

27
Q

What are the requirements for MART regime?

A
  • 18+
  • Pt prefers one inhaler
  • Continued poor control after regular, preventative therapies.
28
Q

How is the MART regime used?

A
  • Twice a day - am and pm
  • Reliever dose throughout the day
  • up to 6 puffs a day MAX 8 a day
29
Q

What are the licensed MART products?

A
  • Fostair 100/6
  • Duoresp 160/4.5
  • Symbicort 100/6 or 200/6
30
Q

What are the benefits of MART?

A
  • Decreases airway inflammation
  • Relives symptoms - breathlessness, tight chest
  • Quickly manages symptoms - decreases risk of asthma attack and decreases hospital admission.
  • Freq use will decrease due to extra anti inflammatory effects of ICS providing LT control.
31
Q

What are the different types of asthma?

A

Moderate - PEF >50-75%
Acute - PEF 33-50%
Life-threatening - PEF <33%

32
Q

Describe the spirometry test

A
  • Positive results : improvement in FEV1 of more than or equal to 12% and increase in vol of 200mL
  • Improvement in FEV1 of more than or equal to 400mL this suggest asthma
33
Q

Describe Peak Low test

A

Estimate in variability of airflow
- repeat 2x a day fir 2 weeks
- take an average of best readings am and pm
- take highest and lowest readings & express as a % - 20% difference suggest asthma

34
Q

How is PF test performed?

A
  • deep breath in
  • hold for 2s
  • rapidly breath out
  • record value
  • repeat 3x am and pm, records best from each
35
Q

What are examples from reliever?

A

bronchodilators
SABAs
SAMAs
Theophylline

36
Q

What are examples of preventers?

A

Anti-inflammatory drugs - ICS

37
Q

What suggests poor control?

A
  • Asthma attack in last 2 years
  • Using SABA 3 times a week
  • Symptomatic 3x a week +
  • Waking 1 night a week
  • Asthma affecting daily activities
38
Q

What to you check in an asthma review?

A
  • Adherence
  • Technique - ask Pt to show you
  • Symptoms - daytime, night time, activities
  • Asthma control questionnaire
  • PEF
  • Triggers/ smoking status
  • Does Pt have a personal asthma action plan (PAAP)
39
Q

What shows high probability of asthma?

A

wheeze heard by HCP
history

40
Q

How do you confirm an asthma diagnosis

A
  • Code Pt as ‘suspected asthma’
  • 6 weeks treatment trail of ICS & SABA
  • Assess response; asthma control questionnaire, LFTs - spirometry and PEF
  • Improvement following 6 wk treatment strongly suggests asthma.
41
Q

How is asthma diagnosed?

A
  1. Investigations - spirometry - compare results when pt is symptomatic or asymptomatic.
  2. Structured clinical assessment: episodic symptoms, atopic history, confirmed wheeze by HCP on auscultation, diurnal variability.

PHA223 (2023) (22 decks)

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