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antitussives use
for cough (aka cough suppressant)
antitussives contradinications
concurrent MAOI use (antidepressant) = hypertensive crisis
antitussive MOA
blocking cough centrally and peripherally (in brain or sooths throat/chest)
antitussives central agents MOA
blocks cough center in the brain & elevates cough threshold
antitussives using central agents examples
dextromethorphan (DM)
codeine and hydrocodone (opiates)
antitussives peripheral agents MOA
numbs the local nerve endings and demulcents (sooths)
antitussives using peripheral agents examples
menthol (vicks vapor rub)
benzonatate (tessalon perles)
antitussives onset/duration
quick onset: 15-30 min w/ duration of 3-6 hours
antitussives side effects
DM: drowsiness, nausea, dizziness
Opiates: sedation, constipation
why DM vs codeine for antitussives
DM = 1st choice
- has less side effects, minimal euphoria, available OTC
cautions w/ DM (antitussive)
high doeses can cause dissociative effects like PCP
if high enough for dissociation = high enough to cause toxicity - high BP, HR, lower RR
expectorants are used for
loosening mucous from respiratory tract (thins secretions here)
contraindications of expectorants
none
expectorants MOA
increases the amount of fluid in respiratory tract - thins everything out - allows for better movement of fluids - clears out irritants and decreases mucus thickness
expectorant example
guaifenesin (duratuss, robitussin)
guaifenesin (expectorant) side effects
usually well tolerated!
nasuea, drowsiness, vomiting @ high dose
considerations w/ antitussives
-lower dose codeine gives you less respiratory depression but will still affect peds
-high dose opioids via IV can induce cough
-older gen antihistamines can be used as cough meds
considerations w/ expectorants
-not much data on efficacy w/ all ages (not recomended w/ peds)
-multisystem products = risk of overdose from duplicated ingredients
-other expecterants (not guaifenesin) can lead to acidosis, nasuea, vomiting
decongestants are used for
nasal congestion (stuffy nose)
contraindications of decongestants
used w/ MAOIs = hypertensive crisis
severe hypertension and coronary disease due to vasoconstriction
decongestants MOA
vasoconstriction = reduces hydrostatic pressure
nasal congestion is reduced as result of constriction of vessels that decrease capillary pressure, blood flow, and volume
decongestants examples (2 types)
Direct agonists - sudafed PE , afrin
indirect agonists - sudafed
direct agonist decongestant examples
phenylephrine (sudafed PE, dimetapp)
oxymetazoline (afrin)
indirect agonist decongestant example
pseudoephedrine (sudafed)
decongestant onset/duration
oral onset: 30 min w/ 4-6 hr duration
topical agents: faster onset of action w/ fewer systemic effects
decongestant side effects
CNS stimulation = agitation (hyperstimulated) , anxiety, insomnia
**Increased heart rate and palpitations
-rebound nasal congestion
-dry mouth
-sweating
-local irritation/nostril burning
considerations w/ decongestants
Rhinitis medicamentosa = rebound nasal congestion w/ chronic spray use
pseudoephedrine has precurser ingridents to meth so it is behind the counter and monitered how much you buy
H1 histamine antagonists are used for
allergic rhinitis, urticaria (itchy rashes) , nasal symptoms from common cold, nausea (1st gen)
contraindications of H1 antagonists
none
H1 histamine antagonists MOA
blocks allergic response meditated by histamine - blocks histamine receptor from releasing allergy cascade = helps w/ allergy symptoms
anticholinergic effects w/ 1st gens = used for nausea
1st gen H1 antagonists examples
diphenhydramine (benadryl)
chlorpheniramine (chlortrimeton)
hydroxzyine (atarax)
cyproheptadine (periactin) - common in kids
2nd gen H1 antagonists examples
Loratadine (claritin)
cetirizine (zyrtec)
fexofenadine (allegra)
considerations w/ antihistamines
*sedation w/ 1st gen mostly
-not used for acute anaphylactic reactions bc it can't control hypotension & bronchoconstriction
other use of H1 antagonists
for insomnia bc of sedative effects
doxeoin
a TCA antidepressant but has potent antihistamine activity
mast cell stabilizers are used for
conditions w/ allergy component and adjuct therapy (can't be used alone/must be used prior to allergen exposure)
-ashtma, rhinitis, conjunctivitis, systemic mastocytosis
contraindications of mast cell stabilizers
none
mast cell stabilizers MOA
prevents degranulation of mast cells = blocks release of proinflammatory factors
mast cell stabilizers example
cromolyn sodium (nasal crom)
side effects of cromolyn sodium (mast cell stabilizer)
well tolerated but can get cough from throat irritation and nose irritation bc it's inhaled
considerations for cormolyn sodium (mast cell stabilizer)
doesn't give bronchodialation = NOT useful for ashtma attack or allergy symptoms that have already started
leukotriene receptor antagonist (LTRAs) are used for
prevention of persistent asthma (but not 1st line)
exercise induced asthma/bronchospasm
allergic rhinitis
leukotriene receptor antagonist contraindication
acute liver disease/ any impaired liver functioning
not for asthma - prevention only
leukotriene receptor antagonist MOA
inhibits enzyme responsible for producing inflammation response to leukotriene = reduces bronchoconstriction and decreases inflammation
leukotriene receptior antagonist example
montelukast (singulair)
intranasal steroids are used for
allergic rhinitis - congestion, sneeze, itchy, rhinorrhea
nasal congestion - good alternative for pts who cannot use decongestants bc of hypertension/palpitations
contraindications of intranasal steroids
hypersensitivity, but usually well tolerated in all ages
intranasal steroid MOA
inhibits cells that contribute to inflammation (mast cells, eosinophils, basophils, lymphocytes, macrophages)
intranasal steroid examples
fluticasone (flonase/veramyst)
mometasone (nasonex)
considerations w/ intranasal steroids
minimal systemic absorption = not bad side effects
slower response than antihistamines and requires continuous dosing - especially when using for rebound congestion