Pain and Analgesic (opioids), NSAIDs, and Steroidal Anti-Inflams Flashcards
Define nociception
neural process of encoding noxious stimuli
Define neuralgia
nerve pain
Define allodynia
pain from a stimulus that doesn’t usually cause pain
Define neuropathic pain
damage to the neurons and somatosensory NS due to disease, condition, or lesion
Define hyperalgesia
abnormal increased amount of pain from stimulus
Acute vs chronic pain disorders
acute: pain lasting < 3 months
chronic: pain lasting > 3 months
Treatments for mild, mod, and severe pain as per WHO analgesic ladder
Mild: PT, OT, NSAID, non-opioid analgesics
Moderate: PT, OT, weak opioids
Severe: PT, OT, strong opioids
Classify analgesics and anti-inflam agents
Analgesics: opioid (narcotics), non-opioid (NSAID, acetaminophen)
Anti-inflams: NSAID, glucocorticosteroids
List the endogenous opioid peptides
Endorphins
Enkephalins
Dynorphins
List the opioid receptors
Mu, kappa, delta
Purpose of strong agonists. Examples?
used to treat severe pain; interact primarily with μ opioid receptors
Morphine (MS contin)
Methadone (dolophine)
Oxycodone (oxycontin)
Hydromorphone (dilaudid)
Purpose of mild-mod agonists. Examples?
used to treat mild-mod pain
Hydrocodone (hycodan)
Purpose of mixed agonists-antagonists. Examples?
have the ability to act differently at specific classes of opioid receptors; activate 𝛋 receptors → kappa receptor agonists, partially activate μ receptors → μ receptor antagonists or partial agonists
Buprenorphine (buprenex)
Purpose of antagonists. Examples?
block all opioid receptors with particular affinity for mu variety; used to treat opioid OD and addiction
Naloxone (narcan)
Naltrexone (ReVia, vivitrol)
Mechanism of pre synaptic effects of opioids
Opioids close voltage-gated Ca2+ channels on presynaptic nerve terminals → reduce transmitter release (glutamate and substance P)
Mechanism of post synaptic effects of opioids
Opioids open K+ channels on postsynaptic neurons and hyperpolarize them → inhibit postsynaptic neurons
Major CNS pharmacological effects of opioids (10)
Analgesia
Euphoria
Sedation
Respiratory depression
Cough suppression
Miosis (pupil constriction)
Truncal rigidity (trunk)
Nausea and vomiting
Body temp
Sleep disturbances
Major PNS pharmacological effects of opioids (6 systems w/ S/S)
-CV system: bradycardia, hypotension, increase cerebral BF, increase intracranial pressure
-GI system: constipation (opioids don’t develop tolerance to constipating factors)
-Biliary (bile) tract: biliary colic (stone in cystic duct, GB to small intestine)
-Renal: decrease renal fxn, antidiuretic effect, urinary retention
-Endocrine: decrease testosterone w/ chronic use, decrease libido, energy and mood
-Pruritus (“itching” of skin): flushing and warming skin, sweating, urticaria (hives), itching, increase peripheral histamine release
Major cause of opioid OD-induced death?
Opiate toxicity triad: CNS depression (coma), respiratory depression (cyanosis), pupillary miosis
Common and serious AE of opioids (not sure if this is the right answer)
tolerance, dependence, withdrawal, addiction
What pharmacological effects of opioid develop tolerance (6)
Tolerance: analgesic, sedating, respiratory depressant, antidiuretic, emetic, hypotensive
What pharmacological effects does not develop tolerance
Doesn’t develop tolerance: miotic, convulsant, constipating actions
List out treatment options for opioid overdose and toxicity
Naloxone (narcan) = antidote for OD
Ventilation and oxygenation
Purpose of COX-1
produces prostaglandins that mediate homeostatic fxns
homeostatic: protect gastric mucosa, platelet activation, renal fxns, macrophage differentiation
Drugs that inhibit COX-1
diclofenac, ibuprofen, naproxen
Purpose of COX-2
produces prostaglandins that mediate inflam, pain and fever
pathologic - inflam, pain, fever, dysregulated proliferation
Drugs that inhibit COX-2
diclofenac, ibuprofen, naproxen, celecoxib, rofecoxib
Acetaminophen MOA
inhibits COX enzyme, not fully understood and unclear why it doesn’t exert anticoagulant and anti-inflammatory effects
Acetaminophen serious AE
Hepatotoxicity and pain masking
Serious AE of NSAIDs (4)
-pain masking
-GI effects (bleeding or discomfort)
-CV risks: physical exertion may exacerbate risks w/ long term use
-renal impairment
PT considerations of NSAIDs
Therapy timing → maximize pain relief during exercises but be cautious of over exertion
Pt education → impact of meds on therapy, risks of over reliance and importance of not exceeding recommended dosages
Monitoring for side effects → regularly assess for dizziness, fatigue or other symps that can impair pt’s ability to safely perform exercises
Precursor for steroid biosynthesis
cholesterol
Name endogenous corticosteroids (glucocorticoids)
cortisol and corticosterone
Name endogenous corticosteroids (mineralocorticoids)
aldosterone
Pharmacological effects of corticosteroids
-Control glucose metabolism and body’s ability to deal w/ stress
-Decrease inflammation
-Suppress immune system
Clinical uses of corticosteroids (endocrine)
Endocrine:
-Normalizes adrenal cortical hypofxn
-Used as diagnostic tool to evaluate hormonal disorders
Clinical uses of corticosteroids (nonendocrine)
Nonendocrine:
-Work on various conditions as anti-inflammatory or immunosuppressive effects
-Primary conditions = RA, myositis, tenosynovitis, collagen diseases
-Injections help localize effects of drugs and minimize systemic side effects (ex. Carpal tunnel)
-Repeated injection not recommended (can cause breakdown of structure; limit 4 or less per year in a joint)
AE of corticosteroids
-breakdowns of supporting tissue (inhibits collagen production)
-mus atrophy
-drug induced cushing syndrome (hypercortisolism)
-adrenal crises/shock
-osteoperosis
