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BS - Respiratory System > Respiratory Pharmacology > Flashcards

Respiratory Pharmacology Flashcards

(94 cards)

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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
What leads to upper airways cough syndrome?
Irritation of the larynx and pharynx leads to constant coughing
26
What 3 factors act together to cause narrowing of the respiratory tract? What conditions are these factors seen in?
1. bronchoconstriction 2. mucus plugs (secretions) 3. inflammation All chronic lung conditions see these 3 factors interacting
27
What is respiratory mucosal epithelium surrounded by?
Smooth muscle
28
What happens after inflammation of the respiratory mucosal eptihelium?
this causes more secretion to be produced (mucus plugs) The smooth muscle in the bronchi then contracts (bronchoconstriction)
29
What are the 4 types of bronchial asthma?
1. allergy-induced 2. intrinsic 3. exercise-induced 4. asthma associated with COPD
30
What is the difference between allergy-induced and intrinsic asthma?
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
31
In allergen-mediated asthma, what are the steps leading up to antibody production?
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
32
What is the role of IgE antibodies in allergen-mediated asthma?
1. IgE activates mast cells and the complement system 2. Mast cells release mediators 3. Mediators attack the bronchi and lead to bronchoconstriction
33
What are the 4 mechanisms of treating asthma?
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
34
What is involved in non-specific reduction of bronchial hyper-reactivity?
Preventing the Ag:Ab reaction by preventing the patient from coming into contact with the allergen
35
What is the problem with trying to prevent asthma through preventing the Ag:Ab reaction?
It is sometimes too difficult to identify the allergen that gives rise to asthma Total avoidance of the allergen is unlikely
36
What treatments/advice are given to a patient to help non-specific reduction of bronchial hyper-reactivity?
1. stopping smoking 2. losing weight 3. corticosteroid treatment
37
What are the 2 'actions' of corticosteroids?
1. anti-inflammatory action | 2. reduce bronchial reactivity to reduce asthma exacerbations
38
Why are corticosteroids not useful for someone suffering severe asthma?
They need time to work their effects
39
What is a drawback of using corticosteroids to treat asthma?
They only work on the epithelium and do not relax the bronchial smooth muscle
40
What are inhaled corticosteroids used for in asthma treatment? When are they NOT useful?
they are the first line for regular therapy in treating mild to moderate asthma They are not useful in acute severe asthma
41
What are examples of inhaled corticosteroids and what type of inhaler are they found in?
Brown inhaler fluticasone, flunisolide, triamcinolone
42
What are oral corticosteroids used for in asthma treatment?
They are used to treat severe asthma/acute exacerbations they are not used as regular therapy
43
What are examples of oral corticosteroids?
prednisone methylprednisolone betamethasone triamcinolone
44
What are the 3 adverse effects of treatment with corticosteroids?
1. Iatrogenic Cushing's syndrome 2. Inhibition of the hypothalamic-pituitary axis 3. oropharyngeal candidiasis and hoarseness as they affect the vocal cords
45
What are the symptoms associated with Cushing's syndrome?
Carbohydrate intolerance which leads to: 1. diabetes 2. hypertension 3. peptic ulcers 4. psychosis 5. delayed puberty
46
What is oropharyngeal candidiasis?
thrush that occurs in the mouth
47
What is used to reduce the risks of treatment with corticosteroids?
Cyclesonide is a prodrug which has less side effects
48
What are 2 examples of mast cell stabilisers?
1. cromolyn sodium | 2. nedocromil sodium
49
What is the role of mast cell stabilisers?
They inhibit the release of mediators from the mast cells
50
How are mast cell stabilisers taken and what are the side effects?
Administered by inhalation Side effects include: 1. throat irritation 2. cough 3. dermatitis 4. myositis 5. gastroenteritis
51
What are the drawbacks of using mast cell stabilisers?
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
What are mast cell stabilisers usually used to treat? Why are they not often used to treat asthma?
Allergic rhinitis and allergic conjunctivitis Not used regularly to treat asthma due to the long-term side effects
53
What is the role of leukotriene synthesis inhibitors?
They inhibit 5-lipooxygenase which is involved in converting arachidonic acid to leukotriene
54
Why are leukotriene synthesis inhibitors no longer used?
Zileuton was discontinued as it caused liver toxicity
55
Why is the action of leukotriene inhibited in asthma treatment?
leukotriene will bind to receptors and cause bronchospasm
56
What is the role of leukotriene receptor antagonists?
They prevent leukotriene from binding to the receptor This prevents bronchospasm
57
What are the most common leukotriene receptor antagonists? What are they most commonly used to treat?
Montelukast and Zafirlukast Used in allergen-induced and exercise-induced asthma as they reduce the frequency of exacerbations
58
Why are leukotriene receptor antagonists a good therapy for children with asthma?
They are only given orally
59
Why are leukotriene receptor antagonists not used in acute asthma?
the mast cells have already released the mediators, so they would have no effect
60
What are the minor adverse effects of leukotriene receptor antagonists?
1. headache 2. gastritis 3. flu-like symptoms 4. Cushing's syndrome
61
What controls relaxation of bronchial smooth muscle? How is this produced?
cyclic AMP causes bronchodilation cAMP is produced from ATP and adenylate cyclase
62
What enzyme breaks cAMP into AMP?
Phosphodiesterase
63
What causes constriction of bronchial smooth muscle?
Acetylcholine and adenosine They act directly on smooth muscle to cause bronchoconstriction
64
What is found in a blue inhaler?
beta agonists which act via B2 adrenoceptors
65
What are the 2 types of selective B2 agonist agents?
1. short-acting beta agonists (SABA) | 2. long-acting beta agonists (LABA)
66
What are examples of SABAs and what is their duration of action?
Salbutamol, terbutaline, fenoterol and metaproterenol They last for 3 - 6 hours
67
What are examples of LABAs and what is their duration of action?
Salmeterol and formetrol They last for 12 - 24 hours
68
What is the most common selective B2 agonist given? How is it administered?
Salbutamol It is administered by inhalation, nebulisation, oral or intravenous
69
What is an example of a a non-selective beta agonist? When is this used and how is it administered?
Adrenaline They are only used in an emergency and are administered as a subcutaneous injection or micro-aerosol
70
How are selective beta agonists administered?
Via metered dose inhalers or nebulisation
71
What is the onset and duration of non-selective beta agonists?
Immediate onset They peak after 15-30 minutes and their total duration of action is 3 - 4 hours
72
Why are beta agonists a first line of therapy in treating asthma?
They relax the bronchial smooth muscle directly
73
What are the side effects of beta agonists? Why do they come about?
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
What is the role of methylxanthines?
They inhibit phosphodiesterase and the action of adenosine This increases bronchial dilation through an increase in cAMP and reduction in adenosine
75
How are methylxanthines administered? What type of asthma therapy are they?
Orally or intravenously They are an adjuvant therapy in asthma
76
What are the side effects of methylxanthines?
1. cardiac arrhythmia, palpitations, hypotension 2. GI irritation through increased acid production 3. diuresis and hypokalaemia 4. anxiety, headache, seizures
77
What is the therapeutic window for methylxanthines? What happens outside of this window?
55 - 110 mmol/L Outside of this window they either have no effect or cause serious side effects
78
What is a commonly used methylxanthine as an adjuvant therapy in asthma? How is it administered?
Theophylline It is given orally and has a rapid and complete absorption
79
When taking theophylline, what is the mechanism that leads up to side effects occurring?
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
When is aminophylline given? How is it administered and why is it administered this way?
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
What is the other name for anticholinergic agents and how do they work?
Muscarinic antagonists They inhibit M3 muscarinic receptors, which acetylcholine acts on to cause bronchoconstriction
82
What are 3 examples of common selective muscarinic antagonist agents?
1. ipratropium 2. tiotropium 3. oxitropium
83
Why is tiotropium quite commonly used to treat asthma? What type of muscarinic antagonist is it?
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
What is the mechanism behind how anticholinergic agents work?
They inhibit the effects of vagus nerve stimulation Inhibiting parasympathetic nerves means that acetylcholine is not released
85
How are anticholinergic agents administered? When are they used clinically?
They are administered via inhalation They are part of adjuvant therapy in acute severe asthma and COPD
86
Why are there side effects when taking muscarinic antagonists? What are they?
They do not act exclusively on M3 receptor 1. airway irritation 2. anticholinergic effects 3. GI upset 4. urinary retention
87
What is the mechanism of action behind anti-IgE monoclonal antibodies? What is an example of one?
They inhibit the binding of IgE to mast cells to prevent the release of mediators from mast cells e.g. Omalizumab
88
What is seen with repeated administration of anti-IgE monoclonal antibodies?
They lessen asthma severity, reduce the magnitude of the response and lead to a reduced requirement of steroids
89
What is the negative consequence of using anti-IgE monoclonal antibodies?
The treatment is very expensive
90
What is ketotifen? What is it used for and what are its side effects?
Histamine receptor (H1) antagonist Some anti-asthma effects but no proven benefits Drowsiness is a side effect
91
In which patients is magnesium given to? How is it administered?
Patients who fail to respond to inhaled bronchodilators and patients in intensive care Given via intravenous infusion
92
When is ketamine prescribed to asthma patients?
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
How does ketamine work to treat asthma?
it has bronchodilator properties through sympathetic stimulation
94
What is the difference in treatment of COPD and asthma?
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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