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Respiriatory: Airway Disease > Pharmacotherapy of airflow obstruction > Flashcards

Pharmacotherapy of airflow obstruction Flashcards

1
Q

What 2 categories can drugs for airflow obstruction be divided into?

A
  • Preventers (anti-inflammatory)

* Relievers (bronchodilators)

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2
Q

Describe an asthmatic inflammatory response to an allergen

A
  • Allergen digested into TSLP
  • TSLP digested and presented by dendritic cells
  • Dendritic cell travels to lymph node and presents antigen to CD4+ T cell via MHC II complex
  • Proliferate to form TH0 cells
  • TH0 cell proliferates to form TH2 cell
  • TH2 cell releases IL-4, which stimulates expansion of B cell population
  • TH2 also releases IL-5 which recruits eosinophils
  • B cells proliferate to form plasma cells, which secrete IgE
  • IgE binds to IgE receptors on mast cells, activating them
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3
Q

What do eosinophils do?

A

Release

  • Basic and cationic proteins
  • Leukotrienes
  • Cytokines
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4
Q

What causes hyper-secretion of mucous in asthma?

A

Leukotriene D4 acting on goblet cells

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5
Q

What cell releases Leukotriene D4?

A

Mast cells

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6
Q

When are monoclonal antibodies used to treat asthma?

A

When inhaled corticosteroids are ineffective in treating inflammation

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7
Q

What is a reliever drug for asthma?

A

Short-acting B2 agonist

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8
Q

What is the 1st line preventer for asthma?

A

Inhaled corticosteroids (e.g. cromoglycate)

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9
Q

What are examples of controllers?

2nd line additives to ICS

A
  • Theophyline
  • Leukotriene receptor agonist (LTRA)
  • Long-acting B2 agonist (LABA)
  • Long-acting muscarinic antagonists (LAMA)
  • Anti-IgE
  • Anti-IL5
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10
Q

What treatment is used for the most severe cases of asthma?

A

Oral corticosteroids

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11
Q

What combinations of treatment are used for severe asthma?

A
  • SABA
  • Inhaled corticosteroids
  • LABA/LAMA
  • LTRA/Theo/Anti-IgE/Anti-IL5
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12
Q

When is the only time LAMA and LABA can be used?

A

In addition inhaled corticosteroids

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13
Q

What is the disadvantage of using corticosteroids?

A

May predispose COPD sufferers to pneumonia

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14
Q

How do corticosteroids predispose COPD sufferers to pneumonia?

A
  • Local immune suppression

* Impaired mucocilliary clearance

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15
Q

Are oral steroids (e.g. prednisolone) used for maintenance of asthma?

A

No, only used for acute exacerbations

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16
Q

Why is prednisolone (oral steroid) only used for acute exacerbations and not maintenance therapy?

A

It has a very low therapeutic ratio

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17
Q

What is an example of an oral steroid used in asthma?

A

Prednisolone

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18
Q

What is an example of an inhaled corticosteroid?

A

Beclomethasone

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19
Q

Why are inhaled steroids used for maintenance monotherapy in asthma?

A

They have a high therapeutic ratio

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20
Q

When is the only time inhaled corticosteroids are effective in treating asthma?

A

In combination with LABA

not as monotherapy

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21
Q

What effect does an ICS/LABA combo have on COPD in ACOS?

A

If COPD sufferer has eosinophilia (>4%), reduces exacerbations in eosinophilic COPD (aka ACOS)

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22
Q

What is used to optimise lung delivery of inhaled corticosteroids?

A

Extra fine solution HFA/spacer

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23
Q

Why are doses of inhaled corticosteroids kept low in patients with ACOS?

A

Want to remove eosinophils but do not want to cause pneumonia

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24
Q

What is the safest inhaled corticosteroid to use in COPD?

A

Beclomethasone

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25
Q

Why are inhaled corticosteroids not effective in non-eosinophilic COPD?

A

Cannot melt away neutrophils

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26
Q

What are the most dangerous steroids for COPD?

A
  • Fluticosone proprionate

* Flucticosone furoate

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27
Q

Why are fluticosone proprionate and flucticosone furoate the most dangerous steroids for COPD?

A

Stay in the lungs for a long time causing immuno-suppression (greater risk for pneumonia)

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28
Q

Why do inhaled corticosteroids have a large therapeutic ratio?

A

Directly delivered to site of tissue action (lungs) – do not require large doses

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29
Q

What is eosinophilia?

A

> 4% eosinophils in the blood

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30
Q

How to corticosteroids work?

A

Not bronchodilators - they target eosinophilic inflammation

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31
Q

What is the effect of inhaled corticosteroid on peak flow in asthma sufferers?

A
  • Increases peak flow

* Variability of peak flow diminishes

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32
Q

What size must particles be to get delivered past the carina?

A

They must be less than 5um (microns)

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33
Q

How many times does the bronchial tree divide?

A

23

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34
Q

What is a spacer?

A

Plastic holding chamber

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35
Q

What are the advantages of a spacer?

A
  • Requires less coordination
  • Decreases particle size and velocity
  • Reduces oropharyngeal and laryngeal side effects
  • Reduces systemic absorption from swallowed fraction
  • Acts as a holding chamber for aerosol
  • Improves lung deposition
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36
Q

What are dry powder inhalers?

A

Emit dry powder, not pressurised aerosol

37
Q

What is the advantage of dry powder inhalers?

A
  • Easy to use - do not require coordination
38
Q

What are the disadvantages of dry powder inhalers?

A
  • Particle size is large - stuck in airways, poor lung deposition
  • Can cause oropharyngeal candidiasis if deposited in oropharynx
39
Q

What are cromones used to treat?

40
Q

What is the function of cromones?

A
  • Mast cell stabiliser

* Weak anti-inflammatory properties

41
Q

How are cromones administered?

A

Inhaled route only

42
Q

Why are cromones not used much?

A

Poor efficacy

43
Q

What do LTRAs do?

A

Block cysteinyl leukotriene D4

44
Q

What are prostaglandins and thromboxanes blocked by?

45
Q

What do prostaglandins and thromboxanes do?

A
  • Prostaglandins - cause pain

* Thromboxanes - platelet aggregation (clotting)

46
Q

What does LD4 do?

A
  • Promotes mucous secretion (hyper-secretion)
  • Mucocilliary dysfunction
  • Increases vascular permeability (oedema)
  • Amplifies cascade
  • Promotes smooth muscle contraction
47
Q

What are LTRAs used to treat?

48
Q

What is the function of LTRAs in treating asthma?

A

Anti-inflammatory

49
Q

What is an example of an LTRA?

A

Monteleukast

50
Q

Are LTRAs the 1st line treatment for inflammation in asthma?

A

No, the are 2nd line treatment - complementary to inhaled corticosteroid

51
Q

Are LTRAs steroids?

A

No, but still anti-inflammatory

52
Q

What is an example of an anti-IgE monoclonal antibody?

A

Omalizumab

53
Q

What does omalizumab do?

A
  • Inhibits the binding to the high-affinity IgE receptor

* Inhibits TH2 response and associated mediator release from basophils/mast cells

54
Q

What is the function of anti-IgE monoclonal antibodies and anti-IL5 drugs?

A
  • Prevent exacerbations - do not improve lung function
55
Q

Are anti-IgE monoclonal antibodies and anti-IL5 drugs effective in COPD?

A

No, asthma only

56
Q

What are examples of anti-IL5 drugs?

A
  • Mepolizumab

* Resilizumab

57
Q

What do anti-IL5 drugs do?

A

Block the effects of IL-5 which is responsible for eosinophilic inflammation in asthma

58
Q

What do B2-agonists do?

A
  • Bronchodilators - stimulate bronchial smooth muscle B2-receptors
  • Increase cAMP levels
59
Q

What is an example of a short-acting B2-agonist?

A

Salbutamol

60
Q

What are examples of long-acting B2 agonists?

A
  • Salmeterol

* Formoterol

61
Q

What is SMART?

A

Single maintenance and deliver therapy

62
Q

What drugs are used in SMART for asthma?

A

Beclometasone and formoterol in combination inhalers

63
Q

Should salmeterol and formoteral (LABAs) be given on their own?

A

No, only with corticosteroids

64
Q

What do M3 receptors on airway smooth muscle cells mediate?

A
  • Bronchoconstriction

* Mucous secretion

65
Q

What are muscarinic antagonists?

A

Bronchodilators - block M3 receptors

66
Q

What is an example of a short-acting muscarinic antagonist?

A

Ipratropium

67
Q

What are examples of long-acting muscarinic antagonists?

A
  • Tiotropium
  • Glycopyronium
  • Umeclidinium
68
Q

What are muscarinic antagonists used for?

A
  • To reduce exacerbations in COPD

* Used in combination with ICS to treat asthma

69
Q

What is the problem with administering B2 agonists regularly?

A

Body adapts - B2 receptors internalise, meaning there are less receptors available to mediate effect of adrenaline

70
Q

What are methylxanthines?

A
  • Bronchodilators

* Anti-imflammatory

71
Q

What is an example of a methylxanthine?

A

Theophyline (oral)

72
Q

What are the functions of methylxanthines?

A
  • Prevent nocturnal dips (peak flow falls at night)
  • Inhibits phosphodiesterase enzymes, increasing cAMP
  • Adenosine antagonist
73
Q

What are methylxanthines used to treat?

A

Asthma and COPD

74
Q

What are PDE4 inhibitors?

A

Anti-Inflammatory drugs (minimal effect on FEV1)

75
Q

What is an example of a PDE4 inhibitor?

A

Roflumilast

76
Q

What are PDE4 inhibitors used for?

77
Q

What are the adverse effects of PDE4 inhibitors?

A
  • Nausea
  • Diarrhoea
  • Headache
  • Weight loss
78
Q

What are examples of mucolytics?

A
  • Carbocisteine

* Erdosteine

79
Q

What is the function of mucolytics?

A

To reduce sputum viscosity and so reduce exacerbations in COPD

80
Q

What is the treatment for chronic asthma?

A
  • Inhaled corticosteroid - suppress inflammatory cascade
  • Plus non-steroid anti-inflammatory therapy e.g. theophylline, anti-leukotriene, cromoglycate
  • Plus LABA/LAMA - stabilise smooth muscle
81
Q

What are inhaled steroids not used to treat?

A

Acute asthma

82
Q

What is the treatment of acute asthma?

A
  • Oral prednisolone or IV hydrocortisone
  • Nebulised high dose salbutamol
  • At least 60% O2
  • Assisted mechanical intubated ventilation if falling PaO2 and rising PaCO2
83
Q

What should never be used in the treatment of asthma?

A

Respiratory stimulants

84
Q

What happens to FEV1 over the course of an individual’s life?

A

Will fall continuously and smoothly

85
Q

What is the effect of smoking of rate of FEV1 fall over an individual’s lifetime?

A

Much sharper decline

86
Q

What is the effect of stopping smoking on the rate of FEV1 fat over an individual’s lifetime?

A

Stopping smoking will never restore the lost FEV1, but the subsequent rate of loss may revert to normal

87
Q

What is the treatment of acute COPD?

A
  • Nebulised high dose salbutamol + ipratropium
  • Oral prednisolone
  • Antibiotic if infection
  • 24-28% O2 titrated against PaO2/PaCO2
  • Physiotherapy to aid sputum expectoration
  • Non-invasive ventilation to allow higher FiO2
  • Intubated assisted ventilation only if reversible component e.g. pneumonia
88
Q

What is never used to treat acute COPD?

A

Inhaled corticosteroids

Respiriatory: Airway Disease (10 decks)

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