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Respiratory block > Asthma > Flashcards

Asthma Flashcards

1
Q

True/false, asthma is an irreversible obstruction to the airways in response to substances (or stimuli)

A

False, asthma is a reversible obstruction to the airways in response to substances to stimuli and can be relieved by drugs

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2
Q

What are some causes of asthma attacks?

A
  • Allergens (in atopic individuals)
  • Exercise (cold, dry air)
  • Respiratory infections (eg. viral)
  • Smoke, dust, environmental pollutants
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3
Q

Symptoms of asthma attacks

A
  • Tight chest
  • wheezing
  • difficulty in breathing
  • cough
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4
Q

In chronic asthma, which pathological changes to the bronchioles are a result of long standing inflammation?

A
  • Increased mass of smooth muscle (hyperplasia and hypertrophy)
  • Accumulation of interstitial fluid (oedema)
  • Increased secretion of mucous
  • Epithelial damage (exposing sentry nerve endings)
  • Sub-epithelial fibrosis
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5
Q

Airway narrowing by inflammation and bronchoconstriction increase airway resistance, what does it decrease?

A

FEV1 and PEFR

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6
Q

What can be used as a diagnostic test for asthma?

A

can measure FEV levels and measure PEFR (pre respiratory flow rate)

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7
Q

Which pathological change contributes to hypersensitivity of the airways?

A

Epithelial damage exposing nerve endings

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8
Q

What are two components of Bronchial Hyper-responsiveness?

A
  • Hypersensitivity

- Hyper-reactivity

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9
Q

What are the two phases of an asthma attack?

A
  • Early phase (bronchospasm and acute inflammation)

- Late phase (bronchospasm and delayed inflammation)

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10
Q

Which type of Th is produced by atopic individuals? and what does it involve?

A

Th2, the immune response is antibody-mediated and involves IgE as it is due to an allergy to antigens

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11
Q

Which type of Th is produced by non-atopic individuals? and what does it involve?

A

Th1, the response is cell-mediated, involving IgG and macrophages

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12
Q

What does Th1 proliferation suppress?

A

Th2 production

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13
Q

What do Th2 cells mature and do with B cells?

A

Th2 cells mature proliferate and make physical contact with plasma B cells, this results in maturation and proliferation of B cells to plasma cells, and they produce immunoglobulin

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14
Q

Which interleukins do Th2 cells release and allow mast cells to express IgE receptors?

A

IL-4 and IL-13

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15
Q

Which interleukin is released from Th2 cells that signal for eosinophils to differentiate and activate?

A

IL-5

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16
Q

What is stimulated upon the cross-linkage of IgE receptors?

A

Stimulates (i) calcium entry into mast cells (ii) release of Ca2+ from intracellular stores

17
Q

What does calcium entry into mast cells and release of calcium from intracellular stores invoke?

A
  • The release of secretory granules containing preformed histamine and the production and release of other agents (e.g. leukotrienes LTC4 and LTD4) that cause airway smooth muscle contraction
  • release of substances [e.g. LTB4 and platelet-activating factor (PAF) and prostaglandins (PGD2)] that attract cells causing inflammation (e.g. mononuclear cells and eosinophils) into the area
18
Q

What is the treatment for an acute asthma attack?

A

SABAs (Beta2 agonists)

19
Q

When should an individual start controller-preventor therapy?

A

If they have more than 2 asthma attacks a week

20
Q

Which drug can be used to treat both acute and prolonged asthma?

A

Methylxanthines

21
Q

What do Beta2-adrenoceptor agonists act as?

A

They act as physiological antagonists of all spasmogens

22
Q

What are the different classes of Beta2-adrenoceptor agonists?

A
  • Short acting (SABA)
  • Long-acting (LABA)
  • Ultra long-acting (ultra-LABA)
23
Q

Examples of SABA

A

salbutamol aka albuterol, terbutaline

24
Q

Examples of LABA

A

salmeterol, formoterol

25
Q

What should LABA always be co-administered with?

A

LABAs must always be co-administered with a glucocorticoid

26
Q

What do Cysteinyl leukotriene (CysLT1) receptor antagonists do?

A

They act competitively at the CysLT1 receptor. CysLTs (LTC4, LTD4 and LTE4) derived from mast cells and infiltrating inflammatory cells cause smooth muscle contraction, mucus secretion and oedema

27
Q

How are CysLT1 receptor antagonists administered?

A

Orally

28
Q

True/false, Methylxanthines are first line drugs used in combination with beta2-adrenoceptor agonists and glucocorticoids

A

False, Methylxanthines are second line drugs

29
Q

How are Methylxanthines administered?

A

Orally

30
Q

Why is the inhalational route of glucocorticoid administration favoured in the treatment of mild, or moderate, asthma?

A

They are preferably delivered by the inhalational route to minimise adverse systemic effects

31
Q

Glucocorticoid Effects upon Gene Transcription

A
  • Glucocorticoids increase transcription of genes encoding anti-inflammatory proteins and decrease transcription of genes encoding inflammatory proteins. Transcription of genes encoding other proteins is also affected
  • Glucocorticoids recruit histone deacetylases (HDACs) to activated genes and switch off gene transcription
  • Expression of inflammatory genes is associated with acetylation of histones by histone acetyltransferases (HATs). Acetylation ‘unwinds’ DNA from histones allowing transcription
32
Q

Clinical uses of glucocorticoids in Asthma?

A
  • Glucocorticoids suppress the inflammatory component of asthma – (1) prevent inflammation and (2) resolve established inflammation
33
Q

Common adverse effects of glucocorticoids (due to deposition of steroid in the oropharynx) are:

A
  • dysphonia (hoarse and weak voice)

- oropharyngeal candidiasis (thrush)

34
Q

What are cromones?

A

They are second line drugs now infrequently used prophylactically in the treatment of allergic asthma (particularly children)

35
Q

Molecular mechanism of cromones?

A

They have an uncertain molecular mechanism of action that includes a weak anti-inflammatory effect . A decrease in the sensitivity of irritant receptors associated with sensory C-fibres that trigger exaggerated reflexes and reduction of cytokine release are potential mechanisms

36
Q

Molecular mechanism of cromones?

A

They have an uncertain molecular mechanism of action that includes a weak anti-inflammatory effect . A decrease in the sensitivity of irritant receptors associated with sensory C-fibres that trigger exaggerated reflexes and reduction of cytokine release are potential mechanisms

37
Q

Example of monoclonal antibodies that act against IgE

A

omalizumab

38
Q

Example of monoclonal antibodies that are directed at IL-5

A

mepolizumab

Respiratory block (7 decks)

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