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synergy drug treatment
interaction of 2 or more drugs when their combined effect is greater than the sum of the effects seen when each drugs is given alone
lower doses/drug used to create an effect(to reduce the side effect)
higher dose= more/higher chance of side effects
treatment at PNS
high efficacy if inflammation is present
NSAIDs
Glucocorticoids
inflammation increases volume which increases pressure
this increases pain due to pressure on nociceptors
so if we decrease inflammation we decrease pain
treatment at CNS
opioids→ potency(mg or mcg)
tylenol(acetaminophen)
acetaminophen(Tylenol)
centrally(CNS) acting analgesic
#1 for antipyretic
synergy that combines into >600 combination medications e.g. opioid Tramacet
not an anti-inflammatory(is not an NSAID)
Mechanism of action:
many theories most common one→ believes it interferes with prostaglandins(PGs) but not at the peripheral level(making it not an anti-inflammatory)
agonizes cannabinoid receptors which have an inhibitory affect on the brain
fever-pyrexia
is a hypothalamic non-specific response to pyrogens with the goal of responding to endogenous and exogenous threats both
exogenous→ bacteria produced e.g. endotoxins
endogenous→ inflammatory mediators e.g. cytokines
aim is to destroy pathogen by high temperature
high temperature increases Basal metabolic rate(BMR)
decreases cellular function which can make fever a bad thing
and can be uncomfortable
because it is a non-specific response we need to find the threat
antipyretics
goal is to comfort patient, decrease Basal metabolic rate(BMR) , and decrease cellular function
Drugs:
acetaminophen(Tylenol)→ 1st choice, best efficacy
NSAIDs(Ibuprofens, ASA)→ antiinflammatory reduce cytokines(no ASA in pediatrics)
other Tx:
treatment of the cause(e.g. infection)
hydration→ patient hydration status needs to be checked
congestion, cough, rhinitis
acetaminophen(Tylenol) as an antipyretic
1st choice, best efficacy
MOA: induces hypothalamic→ peripheral vasodilation(inhibit PGE2) which leads to heat loss
safe in pediatrics(mg/kg) and in pregnancy
NSAIDS(Ibuprofen and ASA) as an antipyretic
anti-inflammatories reduce cytokines which causes a decrease in pyrogenic stimuli
remember NO ASA IN PEDIATRICS
antitussives
medications used to suppress or relieve coughing
CNS depression of cough reflex
however is not always desirable→ coughing= protective innate response
drugs:
codeine(opioid)→ causes CNS sedation
Dextromethorphan(Robituzel)→ non-opioid that causes some CNS depression
congestion treatment
adrenergic agonist(sympathomimetic)
Sympathetic nervous system stimulation decreases nasal secretions
Drugs:
Ephedrine
Pseudoephedrine
cough reflex
protective mechanism that uses forceful loud expiration to help clear mucus and irritants from airways(review this flashcard)
afferent impulses from the cough center are sent to the medulla
vagus nerve→ stimulates mechano/chemoreceptors in the upper/lower airways
efferent impulses to diaphragm/lungs/intercostals= cough
anti-tussive work against this reflex
benylin(daytime)
contains acetaminophen and provides relief of
sinus pain
nasal congestion→ by decreasing sinus pressure
headache→ if headache was cause by sinus pressure release in nasal congestion and sinus pressure
fever→ antipyretic piece of acetaminophen
Benylin( nighttime)
most likely a 1st generation antihistamine added which makes a person sleepy
fast relief of:
runny nose→ decreases when we decrease nasal congestion
sneezing
sinus pain
nasal congestion
headache
menthol as an analgesic
mechanism of action→ activates cold sensing receptors
has cooling effect which gives sensory receptors the effect of being cool
free nerve ending(receptor for hot and cold) activating them works on he gate control theory of pain
sensation of coolness activated receptors closes the gate on the pain signaling
inhibitory interneuron signal back and override the sensation of pain
Robaxacet
combination drug of acetaminophen and muscle relaxant
Robax=muscle relaxant(methocarbamol)
acet=acetaminophen
Mechanism of action is unclear but it is a CNS depressant→ depressing CNS stimulation of the somatic nervous system
Side effects: patient can be more sleepy, be careful of other CNS depressants
Robaxisal
combination drug of ASA and methocarbamol with some acetaminophen mixed in a
acts a muscle relaxant that helps relieve:
pain sensation
back and muscle pain
psychological addiction
change in behavior to have a substance as much as possible
4 C’s:
cravings
compulsions to use
loss of control over use
Use despite harmful consequences
chronic pain
causes in alteration in pain pathway but not the same way as acute pain
repetitive and altered Sympathetic NS initiation of responses leads to chronic inflammation and chronic pain cycle
increased inflammation leads to increased pain
complex regional pain syndrome(CRPS)
develops after injury or surgery
The pain is way more intense than expected for the injury and lasts longer than normal healing time
the pain triggers another response establishing a cycle of pain and swelling
can lead to:
allodynia→ painful response to a non-painful stimulus
muscle pr joint stiffness
skin changes to the injured area→ hair loss, temperature changes, colour changes
treatment of chronic pain
cognitive behavioral therapy(CBT)
physiotherapy
Occupational therapy(OT)→ optimize ability of patient to live with injury
CNS drugs→ but opioids are not the 1st line in chronic pain
drugs that decrease excitatory neurotransmitters(Tx for chronic pain)
Gabapentin(gabrone)
NMDA antagonists
inhibit glutamate from binding
NMDA receptors binds glutamate which is an excitatory neurotransmitter
tx of chronic pain→ serotonin
some antidepressants will increase serotonin will be used to modulate pain
serotonin=mood stabilizing neurotransmitter in the brain\
it modulates pain endogenously
balance is needed to optimize mood
side effects of excessive use→ tachycardia, tachypnea