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Respiratory Drugs > Drugs for Asthma & COPD > Flashcards

Drugs for Asthma & COPD Flashcards

1
Q

How is asthma categorized pathologically?

A

Lymphocytic/eosinophilic inflammation and remodelling of the bronchial mucosa

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2
Q

What are the clinical presentations of asthma?

A

Wheezing, dyspnea and cough
Mucus production
(Symptoms worsen at night)

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3
Q

What are the mast cell IgE mediators?

A

Histamine
Leukotrienes
Interleukins
Prostaglandins

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4
Q

What are the triggers of bronchoconstriction?

A

Cold Air
Exercise
Tobacco
Pollutants

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5
Q

What are the mediators that lead to airway inflammation?

A

Cytokines
Leukotrienes
Interleukins

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6
Q

Which are the inflammatory cells that infiltrate (asthma)?

A

Eosinophils
Leukocytes
Macrophages

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7
Q

What are the mediators for bronchoconstriction?

A

Prostanglionic postsynaptic muscarinic receptors (M3) that are activated by Ach

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8
Q

In order to prevent mast cell degranulation you would give:

A

Mast cell stabiliser
Prevents the release of mediators

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9
Q

What is the anti-antibody given in asthma?

A

Anti-IgE
To prevent degranulation

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10
Q

What do we give in case degranulation has already occurred and the mediators need to et inhibited?

A

PDE Inhibitors
Corticosteroids
Leukotriene modifiers

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11
Q

What are the bronchodilators that are given in asthma?

A

Beta agonists
Muscarinic antagonists
Methylxanthines

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12
Q

What are the anti-inflammatory agents given in asthma?

A

Release-inhibitors
Steroids
Slow-anti-inflammatory drugs
Antibodies

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13
Q

What are the leukotriene antagonists given in asthma?

A

Lipoxygenase inhibitors
Receptor inhibitors

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14
Q

What are the kind of drugs given in COPD?

A

Bronchodilators
Anti-inflammatory agents (steroids)
Antibiotics

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15
Q

The inhaled route is preferred for which kinds of drugs?
Why?

A

β2 agonists
corticosteroids

–> To reduce risk of systemic effects

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16
Q

Inhaled is the only possible route for which drugs?

A

Cromolyn
Anticholinergics

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17
Q

Which dosage would be higher to achieve the same effect, oral or inhaled?

A

Oral

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18
Q

Which patients are given drugs orally?

A

Those unable to use inhalers, small children, severe arthritis

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19
Q

Which drug is ineffective inhaled and has to be given systematically?

A

Theophylline

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20
Q

When is the parenteral route used ?

A

When the patient is severely ill, unable to absorb drugs via the GI route

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21
Q

Inhalation therapy deposits drugs directly where:

A

Lungs

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22
Q

The distribution of the inhaled drug is between which organs and depends on what?

A

Lungs and oropharynx,
Depends mostly on the particle size and efficiency of the delivery method

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23
Q

What happens to the largest percentage of inhaled drugs?

A

Swallowed and absorbed and will enter the systemic circulation –> first pass effect

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24
Q

How can inhaled drugs be given?

A

Metered-dose inhaler
Respimat
Nebuliser
Dry-powder inhaler

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25
Q

What is the distribution of the inhaled drug with the metered-dose inhaler?

A

10% to the lungs, 80% in the oropharynx and 10% in the device

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26
Q

What are Respimat inhalers?

A

Inhalers that deliver very fine mist –> extremely small particle size, decreased drug deposition in the mouth and the oropharynx

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27
Q

What does a nebuliser do?

A

It converts drug solution into mist –> smaller particle size –> less drug deposition in the mouth and oropharynx

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28
Q

What is the percentage distribution of the inhaled drug using the dry-powder inhaler?

A

20% in the lungs
Less than 80% in the oropharynx
Rest in the device

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29
Q

Which kind of inhaler requires hand coordination?

A

Metered-dose inhaler

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30
Q

Which inhaler cannot be used with a spacer?

A

Dry-powder inhaler

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31
Q

What is the function of a spacer?

A

Decrease particle size and increase speed –> less drug distribution to mouth and oropharynx –> less drug swallowed –> less drug absorbed from the GI –> limiting systemic effects

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32
Q

Which is the bronchodilator drug of choice when it comes to asthma?
Why?

A

β2 adrenergic agonists
They are long acting due to their high solubility

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33
Q

How do β2 agonists work?

A

Open Ca2+ activated K+ channels –> hyperpolarization

Decreased phosphoinositide hydrolysis –> increased Na+/K+ exchange, increased Na+, Ca2+ ATPase

Decreased myosin light chain kinase activity –> reduce contraction

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34
Q

Mechanism of Action of β2 agonists?

A

They activate the β2 receptors in the smooth muscle of the bronchial tree
They promote vasodilation and relieve bronchospasm
Suppress histamine release in the lungs and increase cilary motility

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35
Q

What are the examples of β2 agonists?

A

SABA & LABA
SABA: albuterol and salbutamol
LABA: salmeterol and formoterol

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36
Q

What is the duration of action of both kinds of β2 agonists?

A

SABA: 3 to 6 hours duration of action
LABA: >12hours duration of action

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37
Q

Clinical use for SABA?

A

Used as required based on symptoms and not on a regular basis, increased use –> more anti-inflammatory therapy

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38
Q

Which is the drug of choice in acute severe asthma?

A

SABA

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39
Q

What is one advantage of LABA over SABA?

A

Improved asthma control due to long duration

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40
Q

What is a contraindication of LABA?

A

They should never be used alone without ICS

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41
Q

What are the combination inhalers?

A

LABA + ICS
Salmeterol + Fluticasone (ADVAIR)

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42
Q

Why are combination inhalers used?

A

There is evidence of synergism and simplifies therapy

Ensures delivery of both ICS & LABA to the same cells

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43
Q

What are the side effects of β2 agonists?

A

Muscle tremor
Tachycardia and QT prolongation
Hypokalaemia
Hypoxemia
Metabolic effects
Tolerance/Resistance

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44
Q

What are the metabolic effects thatβ2 agonists can cause?

A

Hyperglycemia
Increased free fatty acids

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45
Q

Which kinds of drugs aren’t recommended as monotherapy for asthma and why?

A

β2 agonists
They have no anti-inflammatory action

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46
Q

What are the examples of muscarinic receptor antagonists ?

A

SAMA & LAMA
SAMA: ipratropium
LAMA: tiotropium

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47
Q

What is the mechanism of action of SAMA?

A

Blocks all M subtypes including M2, which increases the risk of bronchoconstriction

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48
Q

How can SAMA cause bronchoconstriction?

A

M2 (which is blocked by SAMA) causes inhibition of Ach release,
Increase in acetylcholine –> constriction

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49
Q

Mechanism of action for LAMA?

A

Block M1& M3 and a little M2

50
Q

Which other respiratory disease are LAMA approved for?

A

COPD

51
Q

What are the side effects of anticholinergics?

A

Dry mouth
Irritation of pharynx
Increased intraocular pressure
Blurred vision
Constipation
Urinary retention
Tachycardia
Tolerance & Withdrawal

52
Q

Side effects of ipatropium?

A

Bitter taste
The nebulised version can cause glaucoma
Paradoxical bronchoconstriction

53
Q

When are muscarinic anticholinergics given in asthma?

A

If there is intolerance to inhaled β2 agonists

In status asthmaticus: additive effects with β2 agonists

54
Q

What are the examples of methylxanthines?

A

Theophylline, Aminophylline, Caffeine

55
Q

When are methylxanthines used in terms of sequence?

A

2nd line after LABA

56
Q

Why are methylxanthines not used so often?

A

Need for plasma level monitoring, there is increase in side effects and poorly absorbed

Low therapeutic index !!

57
Q

Sites of pharmacological effect of methylxanthines?

A

CNS
Cardiovascular
Pulmonary
GI
Renal
Skeletal

58
Q

Main mechanism of action of methylxanthines?

A

Non-selective PDE inhibition
Adenosine receptors antagonism

59
Q

What is the point of PDE inhibition with methylxanthines?

A

Increase in cAMP and cGMP –> bronchodilation

60
Q

What is the benefit of adenosine receptor antagonism?

A

Adenosine causes bronchoconstriction by the release of histamine and leukotrienes

61
Q

How does the release of IL-10 due to methylxanthine play a role in asthma?

A

IL-10 is an anti-inflammatory and is reduced during asthma, theophylline increases the release of IL-10.

62
Q

What does NF-KB induce and why is it inhibited?

A

Induces pro-inflammatory genes, so theophylline inhibits the translocation of NFKB to the nucleus

63
Q

What is the main role of adenosine?

A

Balances O2 need and availability

64
Q

Which kind of drug is Adenosine inhibited by?

A

Methylxanthine

65
Q

Which receptors does adenosine bind to?

A

A1& A2

66
Q

What is the effect of adenosine on the lungs?

A

It releases histamine and leukotrienes –> causes bronchoconstriction

67
Q

What are the side effects of theophylline?

A

Inhibition of phosphodiesterase
Blockage of adenosine receptors
Release of intracellular calcium

68
Q

What happens if there is inhibition of phosphodiesterase?

A

Increase in HR and contractility
Relaxation of systemic arterioles
Nausea, vomiting and gastric discomfort

69
Q

What happens if there is blockage of the adenosine receptors?

A

CNS stimulation
Increase HR & contractility
Diuretic effect

70
Q

What happens if there is release of intracellular calcium?

A

increase in skeletal tone –> tremor

71
Q

What increases the clearance of theophylline?

A

Enzyme induction, mainly CYP1A2 by co-administered drugs and smoking

72
Q

What decreases clearance of theophylline?

A

CYP1A2 inhibition
Liver disease
Old age

73
Q

Does theophylline have a high or low therapeutic index?

A

Low therapeutic index

74
Q

What are two other examples of xanthine phosphodiesterase inhibitors?

A

Sildenafil (Viagra)
Pentoxyphilline (Trental)

75
Q

Details about sildenafil?

A

PDE5 Inhibitor
Erectile dysfunction use

76
Q

Details about pentoxyphilline?

A

Non-selective PDE inhibitor
Peripheral vascular disease use

77
Q

What is the main purpose of corticosteroids in the treatment of asthma?

A

Mainly prophylactically as controller therapy

78
Q

When do the benefits of ICS start?

A

Within 1 week but continue up to several months, their effects are more on a gene expression level thus it would take longer to appear.

79
Q

What to do if asthma is not controlled by the dosage of ICS prescribed?

A

Add LABA

80
Q

The adrenal cortex produces 3 classes of corticosteroids:

A

Glucocorticoids: cortisol
Mineralocorticoids: aldosterone
Adrogens: testosterone

81
Q

The therapeutic indications of the corticosteroids produced by the adrenal cortex?

A

Endocrine: low dose; physiologic effect
Non-endocrine: high doses; pharmacologic effect

82
Q

What are the therapeutic indications for non-endocrine glucocorticoids?

A

Rheumatologist Disorders
Allergic Conditions
Asthma
Dermatologic
Neoplasms
Allograft Rejection Suppression

83
Q

Mechanism of action of non-endocrine glucocorticoids (ICS)?

A

Decreased synthesis and release of inflammatory mediators (histamine, leukotrienes and PG)
Decreased infiltration and activity of inflammatory cells (eosinophils and leukocytes)
Decreased edema (decrease in vascular permeability)

84
Q

The sequence of events of the mechanism of action of ICS?

A
  1. Corticosteroids bind to the glucocorticoid receptor (GR)
  2. Receptor- ligand complexes translocate to the nucleus
  3. Bind to coactivators
  4. Inhibit HAT & recruit HDAC2
  5. Reverse histone acetylation
  6. Suppress activated inflammatory genes
85
Q

What are the physiologic effects of ICS at higher systemic doses?

A

Hyperglycemia
Decreased muscle mass, myopathy
Thinning of skin
Potbelly, moon face, buffalo hump

86
Q

What happens to the ICS dosage if there is increased stress?

A

Increase dosage

87
Q

What are the local side effects of ICS?

A

Vocal cords atrophy –> hoarseness and dysphonia
Reflex cough and bronchospasm
Oral candidiasis

88
Q

How do you prevent the local side effects of the ICS?

A

Decrease with spacer and mouth rinsing after inhalation

89
Q

What is ciclesonide?

A

Pro-drug activated in brachial epithelia

90
Q

Mechanism of action of ciclesonide?

A

When absorbed in the circulation, it binds to the serum proteins and has little access to receptors in the skin, eyes –> less side effects

91
Q

What is the function of leukotriene modifiers?

A

They inhibit:
Bronchoconstrictiomm
Eosinophil infiltration
Mucus secretion
Airway edema

92
Q

What are the examples of leukotriene modifiers?

A

5-LO Inhibitors
LT Antagonists

5-LO Inhibitors: Zileutron
LT Antagonists: Montelukast, Pranlukast, Zafirlukast

93
Q

What is the function of zileuton?

A

Inhibits leukotriene synthesis

94
Q

What is the function of zafirlukast & montelukast?

A

Leukotriene receptor blockers, the leukotriene has already been produced but they prevent it from binding to its receptors

95
Q

What are the side effects of zileuton?

A

Liver injury,
Neuropsychiatric effects
CYP Interactions

96
Q

What are the side effects of zafirlukast and montelukast?

A

Headaches and Gi
Liver injury (zafirlukast)
Churg-Strauss vasculitis

97
Q

What is an example of Anti-IgE?
What is it?

A

Omalizumab
Humanised monoclonal antibody

98
Q

How is Omalizumab given?§

A

Subcutaneously

99
Q

What is the mechanism of action of Omalizumab?

A

Blocks the binding of IgE to high-affinity IgE receptors on mast cells and other inflammatory cells –> no degranulation

100
Q

What are the common side effects of Omalizumab?

A

Injection-site reactions
Sinusitis, pharyngitis, headache
Cardiovascular (rare)
Anaphylaxis risk

101
Q

What is the main risk factor of COPD?

A

Smoking

102
Q

What is the FEV1/FVC ratio like?

A

Reduced

103
Q

What is the difference between asthma and COPD?

A

COPD is irreversible and progressive

104
Q

COPD comprises of:

A

Chronic bronchitis and emphysema

105
Q

What is the pharmacotherapy for COPD

A

Smoking cessation!!
Bronchodilators
Corticosteroids
PDE4 Inhibitors
Mucolytics

106
Q

Which bronchodilators are approved for COPD?

A

β2 agonists and inhaled anti-muscarinic drugs

107
Q

Which drug are used to target nicotinic acetylcholine receptors and help smoking cessation?

A

Bupropion: antagonist
Varenicline: partial antagonist

108
Q

When is bupropion prescribed?

A

1 to 2 weeks before quitting

109
Q

When is varenicline prescribed?

A

1 week before quitting

110
Q

What is the mechanism of action of the nicotine replacement drugs?

A

Allow for some or none of the sodium to pass through –> allow some or none of the smoking sensation (based on the degree of antagonism)

111
Q

What is one risk of ICS when it comes to COPD?

A

May increase the risk of pneumonia / lower tract infections

112
Q

Why can’t ICS be used as mono therapy in COPD?

A

ICS are not effective in suppressing the inflammation of chronic bronchitis

113
Q

When are ICS used in COPD?

A

Acute exacerbations

114
Q

What is the example of PDE 4 Inhibitor?

A

Roflumilast: oral PDE 4 Inhibitor

115
Q

When is roflumilast used?

A

To reduce exacerbations in patients with severe chronic bronchitis

116
Q

Side effects of roflumilast?

A

GI disturbances and headache

117
Q

What kind of drug is roflumilast?

A

An anti-inflammatory (increases cAMP levels)

118
Q

What are mucolytics?

A

Drugs that breakdown the mucoprotein files in sputum, and decease viscosity making the sputum easier to be cleared

119
Q

Examples of mucolytics?

A

Bromhexine, carbocysteine, erdosteine, acetylcysteine

120
Q

What is the PK route of mucolytics?

A

Orally

121
Q

What is the only exception of mucolytic PK route?

A

Acetylcysteine –> can also be given through a nebulizer

Respiratory Drugs (4 decks)

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