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Respiratory physiology > Lecture 12 - Respiratory Pharmacology > Flashcards

Lecture 12 - Respiratory Pharmacology Flashcards

1
Q

What is a cough

A

symotom of a respiratory disease

Protective reflect: prevents lungs from aspiration

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2
Q

What is a useless cough

A

persistent and unproductive: dry

eg. ashtma, oesophageal reflux, sinusitis and psychogenic

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3
Q

Should a useless cough be suprressed?

A

yes it should
cough supressants are called - antitussives
always treat underlying cause as cough is a symptom

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4
Q

What is a useful cough?

A

expels secretions i.e sputum - productive

eg. chest infection

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5
Q

Should a useful cough be suppressed?

A

No

yes if it is exhausting and dangerous

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6
Q

Mechanism of a cough

A

Cough receptors in nose or upper airways (lung irritant receptors detected. goes to the
cough centre in the medulla which leads to stimulation leading to cough

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7
Q

How do dry cough - cough suprressants act? and what drugs act to reduce that afferent side

A

On the afferent side: reduce stimuli
- above larynx - linctuses
Below larynx - steam inhalation, nebulised local anaesthetics
Treat cause: stop smoking

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8
Q

What happens on the efferent side: in dry cough suppressants?

A

Medullary cough centre - antitussives

  • opiods (codeine, methadone, pholcodeine)
  • non opiods (dextromethorphan, noscapine)
  • sedatives: diphenhydramine, chlorpheniramine
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9
Q

Efferemt side antitussives

A 
Opiods (codeine, methadone, pholcodeine) 
Non opiods (dextromethorphan, noscapine)
Sedatives: diphenhydramine, chlorpheniramine
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10
Q

Productive cough

A

Expectorants which increase volume of secretion and mucolytics which decrease the viscosity

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11
Q

Examples of expectorants

A

Guaiphenesin, ipecacuanha

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12
Q

Examples of mucolytics

A

Acetyl cysteine, recombinaant humane DNase

used for cystic fibrosis

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13
Q

What is the best treatment for a productive cough that shouldn’t be suppressed?

A

antibiotics

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14
Q

3 common causes of a chronic caugh

A

upper airways cough syndrome - post nasal drip
bronchial asthma/COPD
Gastrooesophageal reflux disease

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15
Q

Treatment for upper airways cough syndrome - post nasal drip?

A

anti- allergics, and nasal decongestants

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16
Q

Gastroesophageal reflux disease

A

anti-reflux therapy with PPi’s

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17
Q

What are the causes of chronic obstructive lung diseases

A

inflammation, bronchoconstriction and secretions (mucus plugs)

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18
Q

What are the types of bronchial asthma

A

associated with allergic reactions - Type 1 hypersensitivity
not associated with specific allergen
exercise induced asthma
asthma associated with COPD

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19
Q

Describe the pathology of allergen mediated asthma

A

Antigen is presented through TH 2 cell to a B cell which induces IgE production and Mast cell activation. This mediates the release of mediators (histamine) and causes the pharmacological effects - bronchoconstriction

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20
Q

Treatment of asthma

A

non-specific reduction of bronchial hypersensitity -
non - pharmacological : stop smoking, weight reduction
pharmacological: corticosteroids
Dilation of narrowed bronchi
mimicking dilators: sympathomimetics
direct acting bronchodilators: methylaxines
Blockade of constrictor transmitter: Anti-cholinergics
Prevention of release of transmitter
- mast cell stabilisers
Antagonism of released transmitter
- leukotriene receptor antagonists

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21
Q

How to prevent an antigen:antibody reaction

A

avoidance of allergen

  • difficult to find
  • insufficient evidence
  • avoidance of tobacco and weight reduction
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22
Q

What do corticosteroids do

A

anti-inflammatory - inhibit influx of inflamm cells, reduce microvascular leakage - decreased oedema
reduce bronchial reactivity - reduce asthma exacerbations and do not relax bronchial smooth muscle

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23
Q

What are the different types of corticosteroids?

A

inhaled and oral

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24
Q

Inhaled corticosteroids - first line for asthma

A

beclomethasone, budesonide
fluticasone, flunisolide, triamcinolone
first line regular therapy - mild to mod asthma

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25
Q

oral corticosteroids - for sever asthma

A

Prednisolone, methylprednisolone
Betamethasone and triamcinolone
for severe asthma

26
Q

What are the adverse effects of corticosteroids

A

Iatrogenic Cushings syndrome
- diabetes, hypertension, peptic ulcer, psychosis, delayed puberty
Inhibition of hypothalamic pituitary axis
Other side effects
-oropharyngeal candidiasis
-hoarseness: direct effect vocal cords

27
Q

Which corticosteroid produces less side effects

A

cyclesonide - prodrug

28
Q

How do mast cell stabilisers work and examples?

A

cromolyn sodium, nedocromil sodium

- inhibit release of mediators - histamine

29
Q

How are mast cell stabilisers administered

A

by inhalation and very poorly absorbed
no effect on bronchial smooth muscle
no use in acute bronchospasms

30
Q

When are mast cell stabilisers useful

A

when taken prophylactically (as a preventative defensive measure)
main uses: allergy rhinitis, allergic conjunctivitis
side effects: throat irritation, cough, dermatitis, myositis and gastroenteritis

31
Q

What do Leukotriene pathway inhibitors do?

A

prevents bronchospasms.
arachidonic acid produces leukotrienes and prostaglandins. 5 They inhibit Lipoxygenase which cause leukotriene synthesis and leukotriene receptor antagonists block receptors from causing bronchospasms.

32
Q

Inhibition of leukotriene synthesis occurs by

A

inhibition of 5-lipoxygenase

zileuton - discontinued liver toxicity

33
Q

Inhibition of leukotriene receptors done by

A

inhibit binding of leukotriene to receptor

34
Q

leukotriene receptor inhibitors

A

montelukast, zafirlukast

35
Q

When are leukotriene receptor antagonists used?

A

allergen induced asthma, exercise induced asthma
reduce frequency of exacerbations
given orally: good for children.

36
Q

Are leukotriene receptor anatagonists useful in acute asthma

A

nope

37
Q

side effects of leukotriene receptor anatagonists

A

headache, gastritis, flu-like symptoms

38
Q

commonly used leukotriene receptor anatagonists

A

montelukast - receptor blocker

39
Q

How is bronchial tone controlled

A 
Theophylline and muscarinic antagonists cause bronchodilation.
bronchial dilator drugs
sympathomimetics
parasymptholytic agents
- anticholinergic drugs
Methylxanthines
40
Q

Sympathomimetic

A
  • Act via B2 adrenoceptors
    selective B2 agonist agents
    -short acting
    albuterol, salbutamol - most common terbutaline, fenoterol, metaproterenol
    Long acting - salmetrol, formetrol
    Non-selective - adrenaline - use in emergency as subcutaneous injection
41
Q

Selective B2 agonists

A 
dose inhalers or nebulisation
onset - immediate
peak 15-30 mins
duration 3-4 hours
first line therapy
albuterol-salbutamol
42
Q

Side effects of selective B 2 agonists

A

due to b2 receptors in heart muscle and other tissues

- palpitations, tachycardia, cardiac arrhythmias tremor, restlessness, nervousness, hypokalaemia

43
Q

What role do Phosphodiesterase inhibitors play in bronchodilation

A

decrease in breakdown of cAMP and hence cause dilation

44
Q

Methylxanthines

A

oral or IV

adjuvant therapy in asthma

45
Q

Adverse effects of methylxanthines

A 
palpitations, cardiac arrhythmia, hypotension
GI irritation
diuresis, hypokalaemia
anxiety, headache, seizures
therapeutic window - 55-110 mmol/l
46
Q

Theophylline

A

methylxanthine
oral: rapid and complete absorption
90% metabolised
adjuvant therapy

47
Q

Aminophylline is used for?

and how is it administered?

A

intravenous

sever asthma

48
Q

What do anti-cholinergic agents do

A

act via inhibiting musarinic receptors
selective type: ipratropium, tiotropium, oxitropium
inhibits effects of vagus nerve stimulation

49
Q

How are anti-cholinergics administered and what are the adverse effects?

A 
inhalation
adjuvant therapy in acute sever asthma, COPD
Adverse effects:
- airway irritation
-anticholinergic effects
-GI upset, urinary retention
50
Q

long acting anti-cholinergics

A

tiotropium

51
Q

anti cholinergic - colour

A

green inhalers

52
Q

corticosteroids - colour

A

brown inhalers

53
Q

Selective short acting B2 agonists colour

A

blue inhalers

54
Q

Anti IgE monoclonal antibody

A 
Omalizumab 
inhibits binding of IgE to mast cells
Repeat administration 
- lessens asthma severity
-reduces magnitude of response
-reduced requirement of steroids
-very expensive
55
Q

Anti IgE monoclonal antibody example

A

Omalizumab

56
Q

Ketotifen

A

Histamine receptor antagonist
some anti-asthma effect
side effects: drowsiness
no proven benefit

57
Q

Magnesium

A

patients who fail to respond to inhaled bronchodilators

IV infusion

58
Q

Ketamine/ volatile anaesthetic agents

A

anaesthetic agents
bronchodilator properties
no role in routine management
used in life threatening or near fatal asthma

59
Q

is asthma reversible?

A

yes it is

60
Q

COPD reversibility

A

incompletely reversible airway obstruction

61
Q

COPD characteristics

A

occurs in older patients

progressive worsening over age

62
Q

COPD treatment

A

approach same as for asthma
Anti-muscarinics - more effective than b2 agonists in COPD
Smoking cessation - major role in COPD

Respiratory physiology (12 decks)

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