Pain and Analgesic (opioids), NSAIDs, and Steroidal Anti-Inflams

Question 1

Define nociception

Answer 1

neural process of encoding noxious stimuli

Question 2

Define neuralgia

Answer 2

nerve pain

Question 3

Define allodynia

Answer 3

pain from a stimulus that doesn’t usually cause pain

Question 4

Define neuropathic pain

Answer 4

damage to the neurons and somatosensory NS due to disease, condition, or lesion

Question 5

Define hyperalgesia

Answer 5

abnormal increased amount of pain from stimulus

Question 6

Acute vs chronic pain disorders

Answer 6

acute: pain lasting < 3 months
chronic: pain lasting > 3 months

Question 7

Treatments for mild, mod, and severe pain as per WHO analgesic ladder

Answer 7

Mild: PT, OT, NSAID, non-opioid analgesics
Moderate: PT, OT, weak opioids
Severe: PT, OT, strong opioids

Question 8

Classify analgesics and anti-inflam agents

Answer 8

Analgesics: opioid (narcotics), non-opioid (NSAID, acetaminophen)

Anti-inflams: NSAID, glucocorticosteroids

Question 9

List the endogenous opioid peptides

Answer 9

Endorphins
Enkephalins
Dynorphins

Question 10

List the opioid receptors

Answer 10

Mu, kappa, delta

Question 11

Purpose of strong agonists. Examples?

Answer 11

used to treat severe pain; interact primarily with μ opioid receptors

Morphine (MS contin)
Methadone (dolophine)
Oxycodone (oxycontin)
Hydromorphone (dilaudid)

Question 12

Purpose of mild-mod agonists. Examples?

Answer 12

used to treat mild-mod pain

Hydrocodone (hycodan)

Question 13

Purpose of mixed agonists-antagonists. Examples?

Answer 13

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)

Question 14

Purpose of antagonists. Examples?

Answer 14

block all opioid receptors with particular affinity for mu variety; used to treat opioid OD and addiction

Naloxone (narcan)
Naltrexone (ReVia, vivitrol)

Question 15

Mechanism of pre synaptic effects of opioids

Answer 15

Opioids close voltage-gated Ca2+ channels on presynaptic nerve terminals → reduce transmitter release (glutamate and substance P)

Question 16

Mechanism of post synaptic effects of opioids

Answer 16

Opioids open K+ channels on postsynaptic neurons and hyperpolarize them → inhibit postsynaptic neurons

Question 17

Major CNS pharmacological effects of opioids (10)

Answer 17

Analgesia
Euphoria
Sedation
Respiratory depression
Cough suppression
Miosis (pupil constriction)
Truncal rigidity (trunk)
Nausea and vomiting
Body temp
Sleep disturbances

Question 18

Major PNS pharmacological effects of opioids (6 systems w/ S/S)

Answer 18

-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

Question 19

Major cause of opioid OD-induced death?

Answer 19

Opiate toxicity triad: CNS depression (coma), respiratory depression (cyanosis), pupillary miosis

Question 20

Common and serious AE of opioids (not sure if this is the right answer)

Answer 20

tolerance, dependence, withdrawal, addiction

Question 21

What pharmacological effects of opioid develop tolerance (6)

Answer 21

Tolerance: analgesic, sedating, respiratory depressant, antidiuretic, emetic, hypotensive

Question 22

What pharmacological effects does not develop tolerance

Answer 22

Doesn’t develop tolerance: miotic, convulsant, constipating actions

Question 23

List out treatment options for opioid overdose and toxicity

Answer 23

Naloxone (narcan) = antidote for OD
Ventilation and oxygenation

Question 24

Purpose of COX-1

Answer 24

produces prostaglandins that mediate homeostatic fxns

homeostatic: protect gastric mucosa, platelet activation, renal fxns, macrophage differentiation

Question 25

Drugs that inhibit COX-1

Answer 25

diclofenac, ibuprofen, naproxen

Question 26

Purpose of COX-2

Answer 26

produces prostaglandins that mediate inflam, pain and fever *pathologic - inflam, pain, fever, dysregulated proliferation*

Question 27

Drugs that inhibit COX-2

Answer 27

diclofenac, ibuprofen, naproxen, celecoxib, rofecoxib

Question 28

Acetaminophen MOA

Answer 28

inhibits COX enzyme, not fully understood and unclear why it doesn’t exert anticoagulant and anti-inflammatory effects

Question 29

Acetaminophen serious AE

Answer 29

Hepatotoxicity and pain masking

Question 30

Serious AE of NSAIDs (4)

Answer 30

-pain masking -GI effects (bleeding or discomfort) -CV risks: physical exertion may exacerbate risks w/ long term use -renal impairment

Question 31

PT considerations of NSAIDs

Answer 31

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

Question 32

Precursor for steroid biosynthesis

Answer 32

cholesterol

Question 33

Name endogenous corticosteroids (glucocorticoids)

Answer 33

cortisol and corticosterone

Question 34

Name endogenous corticosteroids (mineralocorticoids)

Answer 34

aldosterone

Question 35

Pharmacological effects of corticosteroids

Answer 35

-Control glucose metabolism and body’s ability to deal w/ stress -Decrease inflammation -Suppress immune system

Question 36

Clinical uses of corticosteroids (endocrine)

Answer 36

Endocrine: -Normalizes adrenal cortical hypofxn -Used as diagnostic tool to evaluate hormonal disorders

Question 37

Clinical uses of corticosteroids (nonendocrine)

Answer 37

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)

Question 38

AE of corticosteroids

Answer 38

-breakdowns of supporting tissue (inhibits collagen production) -mus atrophy -drug induced cushing syndrome (hypercortisolism) -adrenal crises/shock -osteoperosis