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MPharm 2 - PH2113 > PH2113 - Asthma > Flashcards

PH2113 - Asthma Flashcards

1
Q

What is asthma caused by?

A

Lung inflammation

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2
Q

What are the steps in asthma development?

A
  • sensitisation
  • exposure
  • inflammatory response
  • bronchoconstriction (asthma attack)
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3
Q

Describe the airways during an asthma attack

A

During an asthma attack, the airway is constricted due to smooth muscle contracting

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4
Q

What is resistance to air flow proportional to?

A

1 / airway radius^4

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5
Q

What is mucus plugging?

A

Airways completely blocked by mucus

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6
Q

What causes a decreased airway diameter?

A

Airway smooth muscle contraction + increased mucus production

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7
Q

What does airway resistance affect?

A

Airflow

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8
Q

What determines airflow?

A

Respiratory drive

- metabolism

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9
Q

How is airflow measured?

A

Spirometry

  • peak flow
  • FEV1 - the amount of air you can force from your lungs in one second
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10
Q

What generates the pressure gradient in the lungs?

A

At rest - diaphragm

During exercise - diaphragm, internal and external intercostals

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11
Q

What is resistance to airflow determined by?

A

Airway diameter

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12
Q

What is peak flow?

A

Maximum rate of exhalation

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13
Q

What is FEV1?

A

Volume of air that can be forcibly exhaled in 1 second

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14
Q

What is the function of a reliever inhaler?

A
  • cause bronchodilation (relieve acute asthma symptoms)

- no anti-inflammatory action (does not affect disease progression)

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15
Q

What is the function of a preventer inhaler?

A
  • do not cause bronchodilation (no acute relief from symptoms)
  • anti-inflammatory action (limits disease progression)
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16
Q

Which class of drugs are primarily in preventer inhalers?

A

Corticosteroids

  • beclametasone
  • fluticasone
17
Q

What is a combi-inhaler?

A
  • contains both preventer (steroid) and reliever (long acting beta-agonist)
  • provides long-term bronchodilation and prophylaxis
18
Q

How many people in the UK have asthma?

A

5.4 million people

19
Q

What proportion of households are affected by asthma?

A

1/5

20
Q

How many people die each day from asthma?

A

3 people a day die from asthma

21
Q

What percentage of asthma hospital admissions are avoidable?

A

75%

22
Q

What percentage of asthma deaths are preventable?

A

90%

23
Q

Why are asthma statistics so bad?

A

Poor asthma control
- increase rates of morbidity and mortality
Asthma is controlled by preventers (corticosteroids)
- corticosteroids are not effective? (steroid resistance)
- patients do not take their medication (poor adherence)
- as low as 50%
- confuse anabolic steroids and corticosteroids
- patients do not take their medication correctly (poor inhaler technique)
- needs to go to the bottom of the lung

24
Q

What type of hypersensitivity reaction is asthma?

A

Type 1

25
Q

What are the two main types of asthma phenotype?

A

Extrinsic
- allergen induced
Intrinsic
- non-allergen induced

26
Q

Give examples of extrinsic asthma triggers

A
  • pollen
  • house dust mite
  • mould
  • ragweed
27
Q

Give examples of intrinsic asthma triggers

A
  • viral infection
  • cold, dry air
  • environmental pollution
  • aspirin
  • cigarette smoke
  • exercise
28
Q

What are the two phases of an asthma attack?

A
  • early phase

- late phase

29
Q

What happens in the early phase of an asthma attack?

A

Immediate response to release of inflammatory mediators from mast cells

30
Q

What happens in the late phase of an asthma attack?

A

Continuation of inflammation characterised by an influx of eosinophils into the lungs

31
Q

What is hyperresponsiveness?

A

Increased response of the target cells (receptors)

32
Q

How does asthma sensitisation take place?

A 
An allergen (foreign protein) triggers a dendritic cell (resident in the lungs) which migrates into the lymph nodes
The dendritic cell presents the antigen to the Th0 helper lymphocytes which differentiate into Th2 lymphocytes
This activates B cells which generates IgE antibodies

Upon re-exposure, the IgE receptors on mast cells in the lungs bind the IgE which starts the inflammation process

33
Q

What happens to mast cells when they are activated by an allergen binding to IgE?

A

Degranulation

- release of histamine and other mediators

34
Q

Describe the process of sensitisation

A
  • allergen is recognised as foreign by dendritic cell
  • dendritic cells migrate to lymph nodes where they display the allergen to undifferentiated population of T cells
  • This then causes the T cells to differentiate into TH2 lymphocytes which then activate B cells.
  • B cells generate IgE immunoglobulins
  • IgE then binds to high affinity receptors on mast cells
  • preexposure of the allergen causes cross linking between multiple IgE binded to the mast cell which triggers mast cell degranulation
35
Q

What are the outcomes of the inflammatory cascade?

A
  • bronchoconstriction
  • vasodilation
  • increased mucus production
  • increased vascular permeability
  • leukocyte recruitment
36
Q

What are the late phase responses of an asthma attack?

A

Continuation of the inflammatory response

  • oedema begun during early phase is more prominent
  • sensory nerve fibres release inflammatory agents that can cause bronchoconstriction
  • increased parasympathetic activation ACh and M3 receptors which cause bronchoconstriction
37
Q

What causes and drives asthma progression?

A

Inflammation

38
Q

What is airway remodelling?

A

Airway remodelling is an ongoing structural change caused by asthma that leads to thickened airway walls and the narrowing of the airway

Driven by chronic inflammation
Generally makes airway thicker
- reducing diameter of airway
- increased obstruction of airway
- increased resistance to airflow
Lung less stretch
- reduced capacity of lung
- reduced elastic rebound when exhaling
Chronic inflammation
- more mucus from goblet cells
Pulmonary angiogenesis
- new blood vessels
Smooth muscle hypertropy

MPharm 2 - PH2113 (50 decks)

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