pain management Flashcards
what are the 5 classes of drugs used in pain management
- opioids
- alpha- 2 agonists
- non steroidal anti-inflammatory drug
- NMDA antagonists
- infiltrative and local anesthetics
what are opioid drugs commonly used for
- analgesia
- sedation
- restraint
- anesthetics
- antitussive
what are advantages of opioids?
- rapid onset of action
- safe
- reversible (with a reversal drug)
- potent analgesia
what are the 3 opioid receptors
mu, delta, kappa
what is an agonist?
drugs with high level of affinity and efficacy that causes a physiological activity
what is an antagonist?
drugs that block another drug from combining with a receptor
what are the 4 classes of opioids?
- pure agonists
- partial agonists
- agonist-antagonist
- antagonist
what is a pure agonist?
they bind on receptors and produce the desired therapeutic effect
what is a partial agonist?
binds on receptors but are unable to elicit the maximal response of the receptor system. still have some analgesic effect)
what is a agonist-antagonist
mixed effect. able to bind on one type of receptor while blocking another type of receptor
what is an antagonist?
binds on receptor but produces no effect, mainly function as a competitor to block other opioids from attaching to the receptors
what are the major side effects of opioids?
- respiratory depression (at a high dose)
- bradycardia
- histamine release (can be prevented by slow injection)
- vomiting
- urine retention
- constipation
- patients
how are opioids metabolized? and caution in which patients?
- metabolized by the liver and excreted via kidneys
- caution in patients with renal or hepatic disease
what are alpha 2 agonists?
they bind to alpha 2 receptors - they inhibit release of norepinephrine activation -> of antinociceptive system (dampen pain)
what are the analgesic effects of alpha 2 agonists?
- good visceral pain
- dose dependent (20 min to 2 hrs)
- rapid onset (5 to 15 min)
how long does the sedative effect last for with alpha 2 agonists?
30 to 90 min
what are 3 commonly used alpha 2 agonists?
xyazine, medetomidine, dexmedetomidine
what are some negative side effects of alpha 2 agonists
cardiovascular effects, vomiting, transient hyperglycemia
what does NSAID stand for?
non-steroidal anti-inflammatory drug
what patients do you not use alpha 2 agonists in
geriatric, cardiac, increased intracranial pressure patients
pros of NSAIDS
- readily available
- easy to give
- long duration of action
- inexpensive
list 5 common NSAIDs in North America
Meloxicam, Carprofen, Deracoxib, Ketoprofen, Robenacxib
what do NSAID act as inhibitors to
Cyclooxygenase enzymes (COX)
which inflammatory mediators are produced upon production/activation of COX
prostaglandins, prostacyclin, thromboxane
how many types are there of cyclooxygenase enzymes
2, COX-1 and COX-2
what is a COX-1 enzyme, what does it produce
it is a constitutive enzyme, produces prostaglandins that deal with normal physiologic functions
- secretion of protective gastric mucus
- perfusion of gastric mucosa
- maintenance of renal blood flow
- maintenance of platelet function
what is a COX-2 enzyme, what does it produce
it is an inducible enzyme, prostaglandins that deal with clinical signs of inflammation
- vasodilation
- amplify nociception
- amplify transmission of pain
list side effects of tramadol
- may decrease seizure threshold in high dose
- use a lower dose for patients with hepatic and renal deficiencies
when should be cautioned with tramadol
patients with seizures and increased intracranial pressure
what is tramadol
a synthetic product that provides mild to moderate analgesia
list the 2 dissociative agents
ketamine, tramadol
what are the cardiovascular side effects of ketamin
sympathomimetics effects
- increased heart rate and blood pressure
- positive inotropic, which increases cardiac workload and myocardial oxygen consumption
what are some side effects of ketamine
- potential to increase cerebral metabolic activity
- may increase cerebral blood flow and intracranial pressure
- contraindicated for patients with intracranial disease or high intracranial pressue
what is ketamine
a good somatic analgesia but poor visceral analgesia, not popular can cause rough recoveries, hallucinations, not good in humane medicine either
which drug has a proposed dual mechanism as an opioid and as a non-opioid
tramadol
what does being a proposed opioid for tramadol mean
it suggest that it selectively interacts with mu receptors and induces analgesia
what does being a proposed non - opioid for tramadol mean
it suggests that it inhibits central norepinephrine and serotonin reuptake and blocks nociceptive impulses at the spinal level
which patients should we use caution in for NSAIDs
renal insufficiency, hypotensive/hypovolemia, peri-operative use, avoid NSAIDs for patients receiving steroids
why should a patient receiving steroids not be given an NSAID
because it will further decrease the production of protective gastric secretions and cause a severe GI ulcer
why should NSAIDs be given with food
to avoid GI irritations
what are the side effects of NSAIDs
gastric irritation/ulercation, decreased renal blood flow (may damage the kidneys), decreased platelet activity (may decrease level of thromboxane(used for platelet aggregation)
what are the 3 generations of NSAIDs
COX -1 preferential
COX-2 preferential
COX-2 selective
what does the COX-1 preferential do? example?
it has a higher affinity and blocks COX-1 enzyme
Aspirin
what does the COX-2 preferential do? examples (4)?
it has a higher affinity and blocks COX-2 enzyme
Carprofen, Meloxicam, Ketoprofen, Etodolac
what does COX-2 selective do? examples (3)?
it may block the negative side effects of COX-2 with minimal effect on COX-1
Deracoxib, Robenacoxib, Firocoxib
