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respi drugs > drugs for cough and cold > Flashcards

drugs for cough and cold Flashcards

1
Q

what causes the cough and cold elements of infection

A

due to histamine release by mast cells

sore throat -> inflammation irritating throat
post-nasal dip -> excess mucus drip down back of throat, causing irritation and cough (result in rhinorrhoea)
excess mucus production -> nasal congestion

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2
Q

how to administer nasal drops and sprays

A

LABA+iCS (combined inhaler)
1. gently blow nose
2. tilt head forward or all the way back (for spray not needed becase fine mist distributes drugs to nasal lining ->less risk of gravity redistributing meds)
3. insert spray bottle nozzle and press pump steadily and firmly
4. breather gently through nose and avoid blowing nose for 2-3min

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3
Q

can you combine drugs of the same class

A

no because risk of additive AE

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4
Q

antihistamine-decongestant combinations

A

common antihistamine: chlorpheniramine
common decongestant: pseudoephedrine
common analgesic: paracetamol

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5
Q

MOA of antitussives

A

sensory inputs to brainstem nuclei regulate cough generation and anti-tussiv work in CNS to suppress cough

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6
Q

AE of codeine

A

opioid antitussive

potential for abuse
CNS: sedation
respiratory depression on overdose

Contrindicated for <18
- respiratory centres in brain not fully developed so more sensitive to respiratory depression
- liver not fully developed so higher level of drug in body (codeine cleared by liver)

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7
Q

effect of CYP2D6 on codeine

A

CYP2D6 are ultra rapid metabolisers
- codeine is a pro drug converted to more potent opioid, morphine
- with CYP2D6, codeine converted to morphine faster -> greater risk of AE

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8
Q

AE of dextromethrophan

A

most potent non-opioid anti-tussives

  • CNS: drowsiness, dizziness
    insomnia, excitement, nervousness at higher dose
    -GIT effects
    potential for abuse at higher dose (dissociative anaesthetic like effect)
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9
Q

properties of diphenhydramine

A

MOA: antihistamine
(used as anti-tussive and anti-histamine)

no risk of addiction

AE:
sedative -> cross BBB

anticholinergic effects -> dry mouth, urinary retention, tachycardia

alpha adrenergic antagonism: hypotension, dizziness, reflex tachycardia
*1st gen antihistamines have ANS effect because block both alpha adrenergic and cholinergic receptors

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10
Q

types of drugs to use for productive cough

A

expectorants like guaifenesin
mucokinetics
mucolytics

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11
Q

MOA of guaifenesin

A

promote coughing by increasing fluid in airways to stimulate more coughing

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12
Q

AE of guaifenesin (expectorant)

A

GIT disturbance
nausea

Contrindication
cannot for <2
caution for <6

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13
Q

impt thing to take note for guaifenesin

A

must take enough fluid to make secretions less viscous to increase secretion of fluids into airways
+ protect kidney function (kidney stones reported on overdose)

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14
Q

example of mucokinetic

A

bromhexine ->active metabolite is ambroxol

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15
Q

MOA of bromhexine

A
  • promote mucus clearance by stimulating surfactant production to prevent mucus from sticking
  • local anaesthetic by blocking voltage gated Na channel to alleviate sore throat
  • anti inflammatory
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16
Q

AE of bromhexine

A

allergic reaction
cutaneous AE
Contraindication
cannot use < 2, caution <6
history of peptic ulcer disease and asthma

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17
Q

example of mucolytic

A

acetylcysteine
carbocisteine (not for patients with peptic ulcer disease)

18
Q

MOA of acetylcysteine

A

free sulphydryl group open disulfide bonds in mucoproteins

break down mucus -> decrease mucus viscosity

-> help mobilise and clear mucus from airways (enable productive cough)

19
Q

AE of mucolytics

A

bronchospasm
anaphylaxis
GIT effects

Contraindication
elderly/ those with severe respiratory insufficiency
asthma (bronchospasm)

20
Q

thing to take note of when taking anti-histamines

A

avoid taking with anti-depressants (CNS depressants) because can lead to respiratory depression

21
Q

types of drugs to give for rhinorrhoea

A

mucoregulator
mast cell stabiliser
H1 antihistamines
nasal corticosteroids (anti-inflammatory)

22
Q

example of mucoregulator

A

ipratropium

23
Q

MOA of mucoregulator

A

decrease mucus hypersecretion from goblet cells and submucosal glands

*not for acute cough and cold but reserved for more severe cases of rhinorrhoea
- inhaled bronchodilator for subacute/chronic cough (Eg post infection persistent cough)

24
Q

AE of mucoregulator

A

unpleasant taste
dry mouth
urinary retention in elderly (elderly more sensitive to AE -> urinary retention sign that too much ipratropium enter systemic circulation)

25
Q

example of mast cell stabiliser

A

cromoglicic acid

26
Q

MOA of mast cell stabiliser

A

PK: intranasal

control Cl- channels to inhibit cellular activation
- decrease mast cell degranulation induced by IgE mediated FceRI cross linking
-decreased secretion of inflammatory mediators
- increase annexin A1 (anti-inflammatory mediator) -> inhibit prostaglandin and leukotriene production

27
Q

AE of cromoglicic acid

A

nasal and throat irritation
dry mouth
cough
unpleasant taste

28
Q

types of H1 antihistamines

A

1st gen: Dont cook the pig
Diphenhydramine
Chlorpheniramine
Tripolidine
Promethazine

2nd gen:
(30% sedation) cetrizine -> levocetirizine
(no sedation) loratadine -> desloratadine
fexofenadine

29
Q

MOA of H1 antihistamines

A

reduce inflammation and nasal secretions by blocking effects of histamine (vasodilation and degranulation of mast cells)

30
Q

thing to take note for mucolytic

A

strong sulphur smell and taste which can affect patient compliance

31
Q

why is nasal corticosteroids administered intranasally

A

intranasal to reduce risk of systemic distribution and systemic AE

32
Q

example of nasal corticosteroids

A

fluticasone -> rose water scent
mometasone

33
Q

MOA of nasal corticosteroids

A

increase expression of anti-inflammatory genes (eg annexin A1)
decrease pro-inflammatory genes (eg Cox-2)

decrease inflammation -> decrease congestion and mucus secretion

34
Q

AE of nasal corticosteorids

A

nasal throat dryness and irritation

35
Q

what causes nasal congestion

A

part of the inflammatory response
- decrease sympathetic vasoconstriction of submucosal blood vessel
- increase parasympathetic stimulation of mucus secretion

36
Q

types of decongestants

A

nasal corticosteroids
adrenergic agonist

37
Q

direct adrenergic agonists

A

alpha agonist: phenylephrine
non-selective: oxymetazoline, naphazoline

38
Q

MOA of alpha agonist

A

oral/intranasal more effective

alpha adrenoceptors on submucosal blood vessels promote vasoconstriction to counteract vasodialtion occuring as partof inflammatory response

+ reduce blood supply to nose to reduce activity of secretory cells -> less secretions

39
Q

AE of adrenergic agonists

A
  1. rebound congestion upon withdrawal after prolonged used
    - compensatory upregulation of parasympathetic system when intranasal adrenergic agonist is stopped -> excess parasympathetic activity continues, promoting mucosecretions
  2. CNS stimulation -> if drug enter systemic circulation and cross BBB
    - more likely to have systemic AE when take orally
    (restlessness, tremors)
  3. CVS stimulation -> adrenergic agonsits can cause vasoconstriction and increase BP
40
Q

can intranasal delivery result in systemic AE

A

if adminsutered wrongly, drug can be swallowed and exposed to systemic circulation -> cross BBB

41
Q

indirect adrenergic agonist

A

ephedrine -> more potent so delivered intranasally to reduce systemic AE
pseudoephedrine

respi drugs (2 decks)

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