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
example of mast cell stabiliser
cromoglicic acid
26
MOA of mast cell stabiliser
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
AE of cromoglicic acid
nasal and throat irritation dry mouth cough unpleasant taste
28
types of H1 antihistamines
1st gen: Dont cook the pig Diphenhydramine Chlorpheniramine Tripolidine Promethazine 2nd gen: (30% sedation) cetrizine -> levocetirizine (no sedation) loratadine -> desloratadine fexofenadine
29
MOA of H1 antihistamines
reduce inflammation and nasal secretions by blocking effects of histamine (vasodilation and degranulation of mast cells)
30
thing to take note for mucolytic
strong sulphur smell and taste which can affect patient compliance
31
why is nasal corticosteroids administered intranasally
intranasal to reduce risk of systemic distribution and systemic AE
32
example of nasal corticosteroids
fluticasone -> rose water scent mometasone
33
MOA of nasal corticosteroids
increase expression of anti-inflammatory genes (eg annexin A1) decrease pro-inflammatory genes (eg Cox-2) decrease inflammation -> decrease congestion and mucus secretion
34
AE of nasal corticosteorids
nasal throat dryness and irritation
35
what causes nasal congestion
part of the inflammatory response - decrease sympathetic vasoconstriction of submucosal blood vessel - increase parasympathetic stimulation of mucus secretion
36
types of decongestants
nasal corticosteroids adrenergic agonist
37
direct adrenergic agonists
alpha agonist: phenylephrine non-selective: oxymetazoline, naphazoline
38
MOA of alpha agonist
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
AE of adrenergic agonists
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
can intranasal delivery result in systemic AE
if adminsutered wrongly, drug can be swallowed and exposed to systemic circulation -> cross BBB
41
indirect adrenergic agonist
ephedrine -> more potent so delivered intranasally to reduce systemic AE pseudoephedrine