Exam Two - Pain Management Flashcards
NSAID stands for
Non-Steroidal Anti-Inflammatory Drugs
What are NSAIDs different classes?
- Salicylates
- Propionic Acid Derivatives
- Oxicams
- Acetic acid derivatives
- Cox-2 Inhibitor
Examples of salicylates
aspirin (ASA)
Examples of Propionic Acid Derivatives
Ibuprofen
naproxen
ketoprofen
fenoprofen
Examples of Oxicams
meloxicam
piroxican
Examples of acetic acid derivatives
indomethacin
sulindac
tolmetin
ketorolac
etodolac (COOH)
diclofenac (phenylacetic acid)
Examples of Cox-2 Inhibitors
celecoxib
Most NSAIDS inhibit the _________ AND ___________ pathways
COX-1
COX-2
COX-1 is responsible for…
cytoprotective prostaglandins
- protect gastric mucosa
- aid platelet aggregation
COX-2 is responsible for…
imflammatory prostaglandins
- recruit inflammatory cells
- sensitize skin pain receptors
- regulate hypothalamic temperature control
Adverse effects of NSAIDs
- increased GI bleed/ulcer risk
- decreased renal perfusion
- increased blood pressure
- increase CV event risk…. other than Aspirin
- increased bleeding risk
Which NSAIDs is safest to use in patients with CVD?
Naproxen
How close to surgery do you stop taking aspirin?
1 week
How close to surgery do you stop taking other NSAIDs?
1-2 days
Use NSAIDs with caution in patients with what diseases?
CVD, renal patients, HTN
How long can you use ketorolac (toradol)?
5 days! Black box warning
When we stay steroids, most often we’re referring to which kind?
Glucocorticoids
Uses of corticosteroids:
anti-inflammatory
anti-allergy
anti-rejection
Tx of Addisons DZ
Neonatology lung maturation
What are the routes of administration for corticosteroids
oral
inhaled
IV
IM
topical
eye drops
ear drops
rectal
intra-articular injection
Corticosteroids ____________ circulating lymphocytes
decrease
corticosteroids ___________ basophils, eosinophils, monocytes
decrease
corticosteroids ______ swelling.erythema/secretions
decrease
corticosteroids _____ PMN, Plts, RBCs, HGb/HCT
increase
corticosteroids ___ plasma glucose (GLC)
increase
increase hepatic HLC production
If you ______ mast cells, then you __________ histamine release
stabilize, decrease
if you __________ phospholipase A2, then you see a __________ in prostaglandins
inhibit, decrease
side effects for corticosteroids
hyperglycemia
increase appetite
steroid psychosis
impaired wound healing
hypertension and hypokalemia
risk of infection
osteoporosis
weight gain/fluid retention
common corticosteroids you should recognize:
prednisone (deltasone) 5mg
prednisolone (Pediapred) 5mg
Methyl-prednisolone (Solu-Medrol) 4mg
Dexamethasone (decadron) 1mg
triamcinolone (kenalog)
hydrocortisone (Solu-cortef)
betamethasone (celestone)
spasmolytic
agent to treat spasticity resulting from upper motor neuron lesions such as MS, CP, CVA, spinal cord injuries, etc.
anti-spasmodic
agent to treat spasms resulting from peripheral skeletal muscle conditions (local tissue injury)
spasms =
muscle weakness related to sustained involuntary contraction of skeletal muscles, stiffness, impaired movement and increased basal muscle tone. May interfere with mobility and/or speech
Spasmolytic agents you should know
- baclofen (lioresal)
- benzodiazepines (esp. diazepam)
- tizanidine (zanaflex) alpha-2 agonist
SE/risks of spasmolytics
fall, drowsiness/dizziness, N/V, impaired PT session
centrally-acting anti-spasmodic agents you should recognize
- cyclobenzaprine (flexeril)
- methocarbamol (robaxin)
- carisoprodol (Soma C-IV)
Which two centrally-acting anti-spasmodic drugs are strong CNS depressors, incite drug seeking behavior, works at brainstem level, and are ineffective on spasms related to spinal cord injury or CP?
Methocarbamol (Robaxin) and carisoprodol (Soma C-IV)
Which centrally acting anti-spasmodic drug has high abuse rates and patients ask for it by name?
Carisoprodol (Soma-IV)
What is the MOA for centrally-acting anti-spasmodic agents?
still don’t know… general CNS depression?
opiate
drug derived from the alkaloids of the opium poppy
opioid
drugs that includes opiates, opiopeptins, and all synthetic/semisynthetic drugs that mimic the action of opiates
opioid peptides
endogenous peptides that act on opioid receptors
opioid agonist
drug that activates some or all opioid receptors and does not block any
opioid partial agonist
drugs that can activate an opioid receptor to elicit a submaximal response
opioid antagonist
drug that blocks some or all opioid receptors
mixed agonist-antagonist
drug that activates some opioid receptors and blocks others
narcotic
psychoactive compound with sedative properties, used in legal context to refer to substances with abuse/addictive potential
What are the 3 types of opioid receptors?
mu
kappa
delta
Mu receptors are responsible for…
analgesia
respiratory depression
euphoria
sedation
physical dependence
glowed GI tract
miosis
modulation of hormone & NT release
kappa receptors are responsible for
analgesia
minimal respiratory depression
dysphoria
mild sedation
glowed GI transit
miosis
psychomimetic effects
delta receptors responsible for
analgesia
modulation of hormone and &NT release
Opiate overdose can kill why?
respiratory depression
What are some CNS effects of opiates?
analgesia
euphoria
sedation
respiratory depression
cough suppression
miosis
truncal rigidity
N/V
reduced shivering
may increase ICP
what are some PNS effects of opiates
bradycardia
hypotension
constipation
biliary colic
urinary retention
prolong labor
stimulate release of ADH, prolactin, somatotropin, and inhibit release of LH
pruritus (itching)
hives (increase HA release)
What are the strong morphine like side effects?
respiratory depression
constipation
sedation
emesis N/V!
elevation of intracranial pressure
urinary retention
orthostatic hypotension
miosis (pinpoint pupils)
pruritus
Morephine mnemonic stands for…
miosis
orthostatic hypotension
respiratory depression
physical dependency
histamine release
increased ICP
Nausea
Euphoria
Sedation
Tolerance
a higher dose of drug is needed to achieve the same response
What side effects of opiates have low tolerance build?
miosis and constipation
Physical dependence
withdrawal symptoms occur if drug is abruptly stopped, should taper
Opioid antagonist MOA?
antagonists at mu and kappa receptors
What are examples of opioid antagonists?
naloxone (narcan) - short acting
naltrexone (ReVia) - oral
nalmefene (Revex) - long acting
What are examples of common types of chronic neuropathic pain?
- diabetic neuropathy
- post-herpectic neuralgia
- phantom limb pain
- fibromyalgia
What drugs are used to help chronic neuropathic pain?
- TCA: tri-cyclic anti-depressants
- SSRI (anti-depressant)
-SNRI (anti-depressant) - Pregabalin (lyrica) anti-epileptic
- Gabapentin (Neurontin) anti-ep
Which drug has the longest track history in treating neuropathic pain?
TCA
Which drugs are most commonly prescribed for neuropathic pain today?
pregabalin (lyrica) and gabapentin (neurontin)
What is the MOA of TCA?
blocks re-uptake of NE, also blocks 5HT, alpha, HA and muscarinic receptors, analgesic actions still not clear
- Fall risks and narrow TI
gabapentin (Neurontin) MOA?
increases CNS GABA availability
SE of gabapentin?
DZ, ataxia, sedation, mood changes, tremors
Pregabalin (lyrica) MOA
MOA: similar to gabapentin
How is pregabalin (lyrica) different from gabapentin?
much better bioavailability (F) = 0.9
SNRIs appear ______ than SSRIs for chronic pain
more effective
MOA: inhibit reuptake of 5HT and NE
