drugs for cough and cold Flashcards
what causes the cough and cold elements of infection
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
how to administer nasal drops and sprays
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
can you combine drugs of the same class
no because risk of additive AE
antihistamine-decongestant combinations
common antihistamine: chlorpheniramine
common decongestant: pseudoephedrine
common analgesic: paracetamol
MOA of antitussives
sensory inputs to brainstem nuclei regulate cough generation and anti-tussiv work in CNS to suppress cough
AE of codeine
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)
effect of CYP2D6 on codeine
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
AE of dextromethrophan
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)
properties of diphenhydramine
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
types of drugs to use for productive cough
expectorants like guaifenesin
mucokinetics
mucolytics
MOA of guaifenesin
promote coughing by increasing fluid in airways to stimulate more coughing
AE of guaifenesin (expectorant)
GIT disturbance
nausea
Contrindication
cannot for <2
caution for <6
impt thing to take note for guaifenesin
must take enough fluid to make secretions less viscous to increase secretion of fluids into airways
+ protect kidney function (kidney stones reported on overdose)
example of mucokinetic
bromhexine ->active metabolite is ambroxol
MOA of bromhexine
- 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
AE of bromhexine
allergic reaction
cutaneous AE
Contraindication
cannot use < 2, caution <6
history of peptic ulcer disease and asthma
example of mucolytic
acetylcysteine
carbocisteine (not for patients with peptic ulcer disease)
MOA of acetylcysteine
free sulphydryl group open disulfide bonds in mucoproteins
break down mucus -> decrease mucus viscosity
-> help mobilise and clear mucus from airways (enable productive cough)
AE of mucolytics
bronchospasm
anaphylaxis
GIT effects
Contraindication
elderly/ those with severe respiratory insufficiency
asthma (bronchospasm)
thing to take note of when taking anti-histamines
avoid taking with anti-depressants (CNS depressants) because can lead to respiratory depression
types of drugs to give for rhinorrhoea
mucoregulator
mast cell stabiliser
H1 antihistamines
nasal corticosteroids (anti-inflammatory)
example of mucoregulator
ipratropium
MOA of mucoregulator
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)
AE of mucoregulator
unpleasant taste
dry mouth
urinary retention in elderly (elderly more sensitive to AE -> urinary retention sign that too much ipratropium enter systemic circulation)
example of mast cell stabiliser
cromoglicic acid
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
AE of cromoglicic acid
nasal and throat irritation
dry mouth
cough
unpleasant taste
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
MOA of H1 antihistamines
reduce inflammation and nasal secretions by blocking effects of histamine (vasodilation and degranulation of mast cells)
thing to take note for mucolytic
strong sulphur smell and taste which can affect patient compliance
why is nasal corticosteroids administered intranasally
intranasal to reduce risk of systemic distribution and systemic AE
example of nasal corticosteroids
fluticasone -> rose water scent
mometasone
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
AE of nasal corticosteorids
nasal throat dryness and irritation
what causes nasal congestion
part of the inflammatory response
- decrease sympathetic vasoconstriction of submucosal blood vessel
- increase parasympathetic stimulation of mucus secretion
types of decongestants
nasal corticosteroids
adrenergic agonist
direct adrenergic agonists
alpha agonist: phenylephrine
non-selective: oxymetazoline, naphazoline
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
AE of adrenergic agonists
- rebound congestion upon withdrawal after prolonged used
- compensatory upregulation of parasympathetic system when intranasal adrenergic agonist is stopped -> excess parasympathetic activity continues, promoting mucosecretions - CNS stimulation -> if drug enter systemic circulation and cross BBB
- more likely to have systemic AE when take orally
(restlessness, tremors) - CVS stimulation -> adrenergic agonsits can cause vasoconstriction and increase BP
can intranasal delivery result in systemic AE
if adminsutered wrongly, drug can be swallowed and exposed to systemic circulation -> cross BBB
indirect adrenergic agonist
ephedrine -> more potent so delivered intranasally to reduce systemic AE
pseudoephedrine
