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BS - Respiratory System > Respiratory Pharmacology > Flashcards

Respiratory Pharmacology Flashcards

1
Q

What is the role of the cough?

A

It is a protective reflex that prevents the lungs from aspiration

Without the cough reflex, choking would cause death

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2
Q

What is a useless (unproductive cough)?

A

It is a persistent, dry cough which does not have any useful action for the body

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3
Q

What is used to suppress an unproductive cough?

Why is it suppressed?

A

It should be suppressed as it is not doing any use

It is suppressed with antitussives

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4
Q

What is the role of a productive (useful) cough?

A

It expels secretions, produces sputum and is involved in foreign body aspiration

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5
Q

Should a productive cough be suppressed?

Why?

A

It should NOT be suppressed as it is benefitting the body

It should only be suppressed if it is exhausting and may be causing respiratory compromises

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6
Q

Where are cough receptors located?

A
  1. larynx & supralaryngeal area
  2. trachea & bronchi
  3. ear canals and ear drums
  4. pleura, pericardium & diaphragm
  5. oesophagus & stomach
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7
Q

How are cough receptors stimulated?

How do they travel to the cough centre?

A
  1. Cough receptors stimulated mechanically or chemically
  2. Stimulus travels through the afferent vagus nerve
  3. It reaches the cough centre in the medulla
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8
Q

What happens after the stimulus reaches the cough centre in the medulla?

A

efferent nerves cause the contraction of the necessary muscles leading to forced expulsion of gases from the lungs

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9
Q

Which efferent nerves cause the contraction of which muscles in the cough reflex?

A
  1. spinal motor nerve causes contraction of expiratory muscles
  2. phrenic nerve causes contraction of the diaphragm
  3. vagus nerve causes contraction of the larynx, trachea and bronchi
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10
Q

When treating a dry cough, what is involved in addressing the afferent side of the reflex?

A

reducing stimuli

e.g. stopping smoking and linctuses

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11
Q

What are linctuses and where are they used?

A

They are a type of cough medication used above the larynx

They provide a protective layer to make the airways less stimulatory

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12
Q

Why are steam inhalation and nebulised local anaesthetics used to treat dry cough?

Where are they used?

A

They are used below the larynx

Local anaesthetics are used as cough reflexes to prevent anything entering the trachea

Steam soothes the respiratory epithelium n the trachea to relieve the cough

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13
Q

In treatment of a dry cough, how is the efferent side of the reflex addressed?

A

By taking antitussives that act on the medullary cough centre

this includes opioids, non-opioids and sedatives

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14
Q

What are the main opioids used to treat dry cough?

Which one is most commonly used and what is the most common side effect?

A

Codeine, methadone and pholcodeine

Codeine is most commonly used as it is unlikely to cause respiratory depression

Constipation is the main side effect of opioids

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15
Q

What are examples of non-opioids used to treat dry cough?

A

Dextromethorphan and noscapine

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16
Q

Why is dextromethorpan no longer used?

A

It has caused deaths in children under 5 years of age

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17
Q

What are examples of sedatives used to treat dry cough?

A

Diphenhydramine and chlorpheniramine

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18
Q

What are the two types of productive cough treatment?

A

Expectorants and mucolytics

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19
Q

What is the role of expectorants?

A

They increase the volume of the secretions which are expelled

This makes the secretions thinner

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20
Q

What are examples of expectorants and how frequently are they used?

A

Guaiphenesin, ipecacuanha and oils

rarely used as they have no added value

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21
Q

What is the role of mucolytics?

A

They decrease the viscosity of secretions

They break disulphide bonds in the mucous to make it thinner

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22
Q

What are examples of mucolytics?

Which condition are they often used to treat?

A

acetyl cysteine, carbocysteine, mecysteine and recombinant human DNASe

Often used to treat cystic fibrosis patients

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23
Q

In what condition is chronic cough one of the most common complaints?

A

obstructive pulmonary disease

COPD

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24
Q

What are the 4 most common causes of chronic cough?

A
  1. upper airways cough syndrome (post nasal drip)
  2. bronchial asthma
  3. COPD
  4. gastroesophageal reflux disease
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25
Q

What leads to upper airways cough syndrome?

A

Irritation of the larynx and pharynx leads to constant coughing

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26
Q

What 3 factors act together to cause narrowing of the respiratory tract?

What conditions are these factors seen in?

A
  1. bronchoconstriction
  2. mucus plugs (secretions)
  3. inflammation

All chronic lung conditions see these 3 factors interacting

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27
Q

What is respiratory mucosal epithelium surrounded by?

A

Smooth muscle

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28
Q

What happens after inflammation of the respiratory mucosal eptihelium?

A

this causes more secretion to be produced (mucus plugs)

The smooth muscle in the bronchi then contracts (bronchoconstriction)

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29
Q

What are the 4 types of bronchial asthma?

A
  1. allergy-induced
  2. intrinsic
  3. exercise-induced
  4. asthma associated with COPD
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30
Q

What is the difference between allergy-induced and intrinsic asthma?

A

Allergy-induced is associated with type I hypersensitivity reactions and is associated with a specific type of allergen

Intrinsic is not associated with a specific allergen

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31
Q

In allergen-mediated asthma, what are the steps leading up to antibody production?

A
  1. allergen combines with an allergen-presenting cell
  2. allergen-presenting cell stimulates T cells
  3. T cells stimulate B cells
  4. B cells produce IgE antibodies
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32
Q

What is the role of IgE antibodies in allergen-mediated asthma?

A
  1. IgE activates mast cells and the complement system
  2. Mast cells release mediators
  3. Mediators attack the bronchi and lead to bronchoconstriction
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33
Q

What are the 4 mechanisms of treating asthma?

A
  1. non-specific reduction of bronchial hyper-reactivity
  2. dilatation of narrowed bronchi
  3. prevention of release of mediators
  4. antagonism of the released mediator
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34
Q

What is involved in non-specific reduction of bronchial hyper-reactivity?

A

Preventing the Ag:Ab reaction by preventing the patient from coming into contact with the allergen

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35
Q

What is the problem with trying to prevent asthma through preventing the Ag:Ab reaction?

A

It is sometimes too difficult to identify the allergen that gives rise to asthma

Total avoidance of the allergen is unlikely

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36
Q

What treatments/advice are given to a patient to help non-specific reduction of bronchial hyper-reactivity?

A
  1. stopping smoking
  2. losing weight
  3. corticosteroid treatment
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37
Q

What are the 2 ‘actions’ of corticosteroids?

A
  1. anti-inflammatory action

2. reduce bronchial reactivity to reduce asthma exacerbations

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38
Q

Why are corticosteroids not useful for someone suffering severe asthma?

A

They need time to work their effects

39
Q

What is a drawback of using corticosteroids to treat asthma?

A

They only work on the epithelium and do not relax the bronchial smooth muscle

40
Q

What are inhaled corticosteroids used for in asthma treatment?

When are they NOT useful?

A

they are the first line for regular therapy in treating mild to moderate asthma

They are not useful in acute severe asthma

41
Q

What are examples of inhaled corticosteroids and what type of inhaler are they found in?

A

Brown inhaler

fluticasone, flunisolide, triamcinolone

42
Q

What are oral corticosteroids used for in asthma treatment?

A

They are used to treat severe asthma/acute exacerbations

they are not used as regular therapy

43
Q

What are examples of oral corticosteroids?

A

prednisone

methylprednisolone

betamethasone

triamcinolone

44
Q

What are the 3 adverse effects of treatment with corticosteroids?

A
  1. Iatrogenic Cushing’s syndrome
  2. Inhibition of the hypothalamic-pituitary axis
  3. oropharyngeal candidiasis and hoarseness as they affect the vocal cords
45
Q

What are the symptoms associated with Cushing’s syndrome?

A

Carbohydrate intolerance which leads to:

  1. diabetes
  2. hypertension
  3. peptic ulcers
  4. psychosis
  5. delayed puberty
46
Q

What is oropharyngeal candidiasis?

A

thrush that occurs in the mouth

47
Q

What is used to reduce the risks of treatment with corticosteroids?

A

Cyclesonide is a prodrug which has less side effects

48
Q

What are 2 examples of mast cell stabilisers?

A
  1. cromolyn sodium

2. nedocromil sodium

49
Q

What is the role of mast cell stabilisers?

A

They inhibit the release of mediators from the mast cells

50
Q

How are mast cell stabilisers taken and what are the side effects?

A

Administered by inhalation

Side effects include:

  1. throat irritation
  2. cough
  3. dermatitis
  4. myositis
  5. gastroenteritis
51
Q

What are the drawbacks of using mast cell stabilisers?

A
  1. they are poorly absorbed
  2. they have no effect on smooth muscle so are not useful in acute bronchospasm
  3. only valuable if taken prophylactically
52
Q

What are mast cell stabilisers usually used to treat?

Why are they not often used to treat asthma?

A

Allergic rhinitis and allergic conjunctivitis

Not used regularly to treat asthma due to the long-term side effects

53
Q

What is the role of leukotriene synthesis inhibitors?

A

They inhibit 5-lipooxygenase which is involved in converting arachidonic acid to leukotriene

54
Q

Why are leukotriene synthesis inhibitors no longer used?

A

Zileuton was discontinued as it caused liver toxicity

55
Q

Why is the action of leukotriene inhibited in asthma treatment?

A

leukotriene will bind to receptors and cause bronchospasm

56
Q

What is the role of leukotriene receptor antagonists?

A

They prevent leukotriene from binding to the receptor

This prevents bronchospasm

57
Q

What are the most common leukotriene receptor antagonists?

What are they most commonly used to treat?

A

Montelukast and Zafirlukast

Used in allergen-induced and exercise-induced asthma as they reduce the frequency of exacerbations

58
Q

Why are leukotriene receptor antagonists a good therapy for children with asthma?

A

They are only given orally

59
Q

Why are leukotriene receptor antagonists not used in acute asthma?

A

the mast cells have already released the mediators, so they would have no effect

60
Q

What are the minor adverse effects of leukotriene receptor antagonists?

A
  1. headache
  2. gastritis
  3. flu-like symptoms
  4. Cushing’s syndrome
61
Q

What controls relaxation of bronchial smooth muscle?

How is this produced?

A

cyclic AMP causes bronchodilation

cAMP is produced from ATP and adenylate cyclase

62
Q

What enzyme breaks cAMP into AMP?

A

Phosphodiesterase

63
Q

What causes constriction of bronchial smooth muscle?

A

Acetylcholine and adenosine

They act directly on smooth muscle to cause bronchoconstriction

64
Q

What is found in a blue inhaler?

A

beta agonists which act via B2 adrenoceptors

65
Q

What are the 2 types of selective B2 agonist agents?

A
  1. short-acting beta agonists (SABA)

2. long-acting beta agonists (LABA)

66
Q

What are examples of SABAs and what is their duration of action?

A

Salbutamol, terbutaline, fenoterol and metaproterenol

They last for 3 - 6 hours

67
Q

What are examples of LABAs and what is their duration of action?

A

Salmeterol and formetrol

They last for 12 - 24 hours

68
Q

What is the most common selective B2 agonist given?

How is it administered?

A

Salbutamol

It is administered by inhalation, nebulisation, oral or intravenous

69
Q

What is an example of a a non-selective beta agonist?

When is this used and how is it administered?

A

Adrenaline

They are only used in an emergency and are administered as a subcutaneous injection or micro-aerosol

70
Q

How are selective beta agonists administered?

A

Via metered dose inhalers or nebulisation

71
Q

What is the onset and duration of non-selective beta agonists?

A

Immediate onset

They peak after 15-30 minutes and their total duration of action is 3 - 4 hours

72
Q

Why are beta agonists a first line of therapy in treating asthma?

A

They relax the bronchial smooth muscle directly

73
Q

What are the side effects of beta agonists? Why do they come about?

A

There are B2 receptors in the heart, muscles and other tissues

Side effects in the heart are palpitations, tachycardia and cardiac arrhythmias

Muscle tremors

restlessness, nervousness and hypokalaemia

74
Q

What is the role of methylxanthines?

A

They inhibit phosphodiesterase and the action of adenosine

This increases bronchial dilation through an increase in cAMP and reduction in adenosine

75
Q

How are methylxanthines administered?

What type of asthma therapy are they?

A

Orally or intravenously

They are an adjuvant therapy in asthma

76
Q

What are the side effects of methylxanthines?

A
  1. cardiac arrhythmia, palpitations, hypotension
  2. GI irritation through increased acid production
  3. diuresis and hypokalaemia
  4. anxiety, headache, seizures
77
Q

What is the therapeutic window for methylxanthines?

What happens outside of this window?

A

55 - 110 mmol/L

Outside of this window they either have no effect or cause serious side effects

78
Q

What is a commonly used methylxanthine as an adjuvant therapy in asthma?

How is it administered?

A

Theophylline

It is given orally and has a rapid and complete absorption

79
Q

When taking theophylline, what is the mechanism that leads up to side effects occurring?

A

90% of the theophylline is metabolised until it reaches saturable metabolism

After a certain dose, plasma levels suddenly start to rise

The liver can no longer metabolise the drug so side effects begin to appear

80
Q

When is aminophylline given?

How is it administered and why is it administered this way?

A

It is used in severe asthma

It is given intravenously

A loading dose is initially given and then there is a continuous infusion to maintain plasma concentration within the therapeutic window

81
Q

What is the other name for anticholinergic agents and how do they work?

A

Muscarinic antagonists

They inhibit M3 muscarinic receptors, which acetylcholine acts on to cause bronchoconstriction

82
Q

What are 3 examples of common selective muscarinic antagonist agents?

A
  1. ipratropium
  2. tiotropium
  3. oxitropium
83
Q

Why is tiotropium quite commonly used to treat asthma?

What type of muscarinic antagonist is it?

A

It is longer acting

A once-daily dose of 18 mcg will last for 24 hours

It is a LAMA - long-acting muscarinic antagonist

84
Q

What is the mechanism behind how anticholinergic agents work?

A

They inhibit the effects of vagus nerve stimulation

Inhibiting parasympathetic nerves means that acetylcholine is not released

85
Q

How are anticholinergic agents administered?

When are they used clinically?

A

They are administered via inhalation

They are part of adjuvant therapy in acute severe asthma and COPD

86
Q

Why are there side effects when taking muscarinic antagonists?

What are they?

A

They do not act exclusively on M3 receptor

  1. airway irritation
  2. anticholinergic effects
  3. GI upset
  4. urinary retention
87
Q

What is the mechanism of action behind anti-IgE monoclonal antibodies?

What is an example of one?

A

They inhibit the binding of IgE to mast cells to prevent the release of mediators from mast cells

e.g. Omalizumab

88
Q

What is seen with repeated administration of anti-IgE monoclonal antibodies?

A

They lessen asthma severity, reduce the magnitude of the response and lead to a reduced requirement of steroids

89
Q

What is the negative consequence of using anti-IgE monoclonal antibodies?

A

The treatment is very expensive

90
Q

What is ketotifen?

What is it used for and what are its side effects?

A

Histamine receptor (H1) antagonist

Some anti-asthma effects but no proven benefits

Drowsiness is a side effect

91
Q

In which patients is magnesium given to?

How is it administered?

A

Patients who fail to respond to inhaled bronchodilators and patients in intensive care

Given via intravenous infusion

92
Q

When is ketamine prescribed to asthma patients?

A

It has no role in routine management and is used in intensive care

Acts as an anaesthetic agent used in life-threatening or near-fatal asthma

93
Q

How does ketamine work to treat asthma?

A

it has bronchodilator properties through sympathetic stimulation

94
Q

What is the difference in treatment of COPD and asthma?

A

The approach to treatment is the same in COPD and asthma

Antimuscarinics are more effective than beta agonists in COPD

BS - Respiratory System (20 decks)

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