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Asthma Flashcards

1
Q

What is Asthma?

A

Inflammatory disorder associated with recurrent, reversible & episodic airway obstruction in response to normal innocuous stimuli.

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2
Q

Is asthma reversible?

A

Yes

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3
Q

Is asthma obstructive or restrictive?

A

Obstructive

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4
Q

What causes airway narrowing

A
  1. Bronchial muscle contraction.
  2. Mucosal swelling/inflammation.
  3. Increased mucous production.
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5
Q

Pathological changes to bronchioles

A
  1. Hyperplasia & hypertrophy: increased mass of smooth muscle.
  2. Oedema: Accumulation of interstitial fluid.
  3. Increased secretion of mucus.
  4. Epithelial damage: Exposing sensory nerve endings.
  5. Sub-epithelial fibrosis.
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6
Q

Causes of Asthma attacks

A

Allergens, exercise, respiratory infections, smoke/dust/environmental pollutants.

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7
Q

Symptoms of Asthma

A
  • Intermittent dyspnoea (SOB)
  • Intermittent wheeze
  • Non-productive Cough (often nocturnal/diurinal)
  • Tight chest
  • Associated atrophy (rhinitis, conjunctivitis, eczema)
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8
Q

Signs of Asthma

A
  • Tachypnoea (rapid breathing)
  • Wheeze
  • Hyper resonant percussion note
  • Diminished air entry
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9
Q

Treatment for intermittent Asthma

A

Trigger avoidance, smoking cessation & salbutamol PRN.

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10
Q

Treatment for Chronic Asthma

A

Intermittent Reliever: SABA PRN.

Regular Preventer:

  1. Low dose ICS .
  2. Low dose ICS + inhaled LABA/
  3. Medium dose ICS or LTRA. If no response to LABA, consider stopping LABA.

If patient worsening refer for specialist care.

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11
Q

Treatment for Acute Asthma Attack

OSHITMAN

A
  1. Oxygen.
  2. Nebulised SABA (salbutamol) + Ipratropium Bromide.
  3. Prednisolone/Hydrocortisone.
  4. Magnesium Sulphate + refer to ICU/Anasthetist.
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12
Q

Development of Allergic Asthma

A

Initial presentation of antigen: initiates an adaptive immune response.

Subsequent presentation of antigen: cross links IgE receptors. Stimulates calcium entry into mast cells & release of Ca2+ from intracellular stores, evoking:

  • release of secretory granules containing preformed histamine & production & release of other agents that cause airway smooth muscle contraction.
  • Release of substances that attract cells causing inflammation into the area.
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13
Q

FEV1 in Asthma

A

<75%

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14
Q

FVC in Asthma

A

Normal

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15
Q

FER in Asthma

A

<75%

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16
Q

CXR in Asthma

A

Normal or hyper-inflation

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17
Q

FBC in Asthma

A

Normal or increased eosinophils

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18
Q

Tests in diagnosis of Asthma

A

Spirometry, CXR, FBC, provocation testing (bronchospasm), reversibility of salbutamol (>15%)

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19
Q

Moderate Asthma Attack

A

Increasing symptoms.

PEF > 50-75%.

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20
Q

Severe Asthma Attack

A

Inability to complete sentences.

PEF 33-50%, Resp rate > 25, HR > 110.

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21
Q

Life-Threatening Asthma Attack

A

Silent chest, Cyanosis, Bradycardia, poor Resp effort, exhaustion, altered conscious level, hypotension.

PEF < 33%, SpO2 < 92%, PaO2 < 8kPa.

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22
Q

Bronchial hyper-responsiveness in Asthma

A

Epithelial damage, exposing sensory nerve endings contributes to increased sensitivity of the airways to bronchoconstrictor influences.

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23
Q

Two phases of an asthma attack

A

Immediate (Type I hypersensitivity) & Late Phase (Type IV hypersensitivity)

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24
Q

Immediate Phase

A

Type I Hypersensitivity: Bronchospasm & Acute Inflammation

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25
Q

Late Phase

A

Type IV Hypersensitivity: Bronchospasm & Delayed Inflammation

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26
Q

Key events of Immediate Phase

A

Eliciting Agent (Stimulus) => Mast cells, mononuclear cells

  • Smasmogens, CysLTs, Histamine => Bronchospasm, Acute inflammation.
  • Chemotaxins, Chemokines
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27
Q

Key events of Late Phase

A

Chemotaxins, Chemokines => Infiltration of cytokine releasing TH2 cells & monocytes, activation of inflammatory cells, particularly eosinophils (also TH1 involvement in severe asthma) =>
- Mediators, CysLTs & others.
- Eosinophil major basic & cationic proteins => Epithelial damage
=> Airway inflammation, airway hyper-responsiveness, Bronchospasm, wheezing, mucus oversecretion, cough.

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28
Q

Relievers

A

Function: Act as bronchodilators.

SABAs, LABAs, CysLT1 receptor antagonists & methylxanthines.

29
Q

Controllers/Preventors

A

Function: Act as anti-inflammatory agents that reduce airway inflammation.

Glucocorticoids, Cromoglicate, humanised monoclonal IgE antibodies, methylxanthines.

30
Q

B2-Adrenoceptor Agonists

A

Physiological antagonists of all spasmogens.
- Airway smooth muscle relaxation: Reduction of intracellular Ca2+ conc & activation of large conductance K+ channels.

31
Q

Types of B2-Adrenoceptor Agonists

A

Short-acting (SABA), Long-acting (LABA), ultra long-acting (ultra LABA)

32
Q

SABAs

A

Reliever/Bronchodilator.

E.g. Salbutamol.

First line treatment for mild, intermittent asthma. Relievers taken as needed.

Route of Administration: Inhaled via metered dose dry powder device (inhalers), oral (in children) or IV (emergency).

Functions:

  • Act rapidly to relax bronchial smooth muscle.
  • Increase mucus clearance & decrease mediator release from mast cells & monocytes.
33
Q

Adverse effects of SABA

A

Fine tremor, tachycardia, cardiac dysrhytmia & hypokalaemia.

34
Q

LABAs

A

Reliever/Bronchodilator.

e.g. Salmeterol, Formoterol.

Useful for nocturnal Asthma (act for 8 hours)

Used as an add-on therapy in asthma inadequately controlled by other drugs. Must always be co-administered with Glucocorticoids.

35
Q

SABA or LABA for acute relief of bronchospams

36
Q

What should LABA be co-administered with?

A

Glucocorticoids

37
Q

CysLT1 Receptor Antagonists

A

Reliever/Bronchodilator.

E.g. Montelukast, Zafirlukast)

Act competitively at the CysLT1 receptor => relax bronchial smooth muscle.

Effective against antigen & exercise induced asthma.

Mild/Persistent Asthma: Effective as add-on therapy against early & late bronchospasm.

Severe: Effective in combination with other medications, including ICS.

38
Q

What do CysLTs do?

A

CysLTs derived from mast cells & infiltrating inflammatory cells cause smooth muscle contraction, mucus secretion & oedema.

39
Q

Route of administration of CysLT1 receptor antagonists.

40
Q

Side effects of CysLT1 receptor antagonists.

A

Headache & GI upset.

41
Q

Xanthines

A

Reliever & Preventer: Bronchodilator & anti-inflammatory.

E.g. Methylxantines: theophylline & aminophylline.

Uncertain molecular MOA: May involve inhibition of i so forms of Phosphodiesterases that inactivate cAMP and cGMP.

Functions:

  • Combine bronchodilator & anti-inflammatory actions
  • Inhibit mediator release from mast cells
  • Increase mucus clearance
  • Increase diaphragmatic contractility & reduce fatigue => improve lung ventilation.
42
Q

Theophylline

A

Methylxanthine.

Activates HDAC which may potentiate the anti-inflammatory action of glucocorticoids.

43
Q

What are methylxanthines used in combination with?

A

SABA/LABAs & glucocorticoids.

44
Q

Adverse effects of Methylxanthines

A

Dysrhythmia, seizures, hypotension, nausea, vomiting, abdominal discomfort & headache.

Have numerous drug interactions involving CYP450s (particularly antibiotics).

45
Q

Corticosteroids

A

Preventer: Anti-inflammatory agent.

Glucocorticoids & mineralocorticoids.

46
Q

MOA of Glucocorticoids

A

Signal via nuclear receptors (GRa):

  1. Glucocorticoids enter cells across plasma membrane.
  2. Combine with GRa.
  3. Produce dissociated of inhibitory heat shock proteins. Activated receptor trans locates to nucleus, aided by ‘Importins’.
  4. Within nuclear activated receptor monomers assemble into homodimers. & bind to GREs in promotor region of specific genes.
  5. Transcription of specific genes switched off or on to alter mRNA levels & rate of synthesis of mediator proteins.
47
Q

Glucocorticoid effects on Gene transcription

A
  1. Increase transcription of genes encoding anti-inflammatory proteins & decrease transcription of genes encoding inflammatory proteins.
  2. Expression of inflammatory genes associated with acetylation of histones by HAT. Glucocorticoids recruit HDACs to activated genes and switch off gene transcription.
48
Q

Glucocorticoid effects on inflammation

A
  1. Decrease formation of TH2 cytokines => cause apoptosis.
  2. Prevent allergen-induced influx into lung => cause apoptosis.
  3. Prevent production of IgE antibodies.
  4. Reduce number of cells & decrease FcE expression.
49
Q

Cellular effects of Glucocorticoids

A

Inflammatory cells:
- Decreased number of eosinophils, mast cells & dendritic cells.
- Decreased cytokines from T-lymphocytes & macrophages.
Structural cells:
- Decreased cytokines and mediators from epithelial cells.
- Decreased leak from endothelial cells.
- Decreased B2 receptors & cytokines from airway smooth muscle.
- Decreased mucus secretion from mucus gland.

50
Q

Clinical use of Glucocorticoids in Asthma

A

E.g. Beclomethasone, budesonide, flluticasone, prednisolone.

Suppress inflammatory component of Asthma:

  • Prevent inflammation.
  • Resolve established inflammation.

Long-term treatment effective (in combination with LABA).

51
Q

Adverse effects of Glucocorticoids

A

Due to deposition of steroid in oropharynx: Dysphonia (hoarseness) & oropharyngeal candidiasis (thrush).

52
Q

Route of administration of Glucocorticoids.

A

Mild/Moderate Asthma: Inhalation from metered dose inhaler.
- Efficacy develops over several days.

Severe/Chronic Asthma:
- Oral Prednisolone, in combination with inhaled steroid.

53
Q

Cortisol

A

Main hormone in man - regulates numerous essential processes such as decreasing inflammatory & immunological responses.

54
Q

Why are synthetic derivatives or cortisol instead of cortisol?

A

They are glucocorticoids with little/no mineralocorticoid activity => used for their anti-inflammatory effect.

55
Q

What treatment should be used in prophylaxis of Asthma?

A

Glucocorticoids.

56
Q

Are glucocorticoids effective in relieving bronchospasm?

A

No, they have no bronchodilator action.

57
Q

Cromones

A

Reliever & Anti-inflammatory.

E.g. Sodium Cromoglicate.

Used prophylactically in treatment of allergic asthma (particularly in asthma).

Mast Cell stabilisers.

Weak anti-inflammatory effect & can reduce both phases of asthma attack.

58
Q

Route of administration of Cromones

A

Inhalation

59
Q

Who is sodium cromoglicate more effective for?

A

Children & young adults.

60
Q

Monoclonal antibodies directed against IgE

A

E.g. Omalizumab.

Functions:

  • Binds IgE via Fc to prevent attachment to Fce receptors - suppresses mast cell response to allergens.
  • Reduces expression of Fce receptors on various inflammatory cells.
61
Q

Route of administration of Omalizumab

62
Q

Asthma triad

A
  1. Reversible Airflow obstruction.
  2. Airway inflammation.
  3. Airway hyperresponsiveness.
63
Q

Evolution of Asthma

A
  1. Bronchoconstriction -> Brief Symptoms.
    => 2. Chronic Airway inflammation -> Exacerbations AHR.
    => 3. Airway Remodelling -> Fixed Airway Obstruction.
64
Q

Hallmarks of Remodelling in Asthma

A
  1. Basement membrane thickening.
  2. Submucosa collagen deposition.
  3. Smooth muscle hypertrophy.
65
Q

Inflammatory cascade in asthma

A

Inherited (genetic predisposition) or acquired factors (viral/allergen/chemical) => Eosinophilic inflammation => Mediators & TH2 cytokines => Twitchy smooth muscle (hyperreactivity)

66
Q

Treatment at Factor stage

A

Avoidance of precipitant

67
Q

Treatment at Eosinophilic inflammation stage

A

Anti-inflammatory medication

  • Corticosteroids
  • Cromones
  • Theophylline
68
Q

Treatment at mediators/TH2 cytokines stage

A

Antileukotrines, antihistamines, monoclonal antibodies.

69
Q

Treatment at twitchy smooth muscle (hyperreactivity) stage

A

Bronchodilators

  • B2 agonists.
  • Muscarinic antagonists.

Respiratory System (35 decks)

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