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

1
Q

Define nociception

A

neural process of encoding noxious stimuli

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2
Q

Define neuralgia

A

nerve pain

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3
Q

Define allodynia

A

pain from a stimulus that doesn’t usually cause pain

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4
Q

Define neuropathic pain

A

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

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5
Q

Define hyperalgesia

A

abnormal increased amount of pain from stimulus

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6
Q

Acute vs chronic pain disorders

A

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

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7
Q

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

A

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

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8
Q

Classify analgesics and anti-inflam agents

A

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

Anti-inflams: NSAID, glucocorticosteroids

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9
Q

List the endogenous opioid peptides

A

Endorphins
Enkephalins
Dynorphins

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10
Q

List the opioid receptors

A

Mu, kappa, delta

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11
Q

Purpose of strong agonists. Examples?

A

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

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

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12
Q

Purpose of mild-mod agonists. Examples?

A

used to treat mild-mod pain

Hydrocodone (hycodan)

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13
Q

Purpose of mixed agonists-antagonists. Examples?

A

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)

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14
Q

Purpose of antagonists. Examples?

A

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

Naloxone (narcan)
Naltrexone (ReVia, vivitrol)

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15
Q

Mechanism of pre synaptic effects of opioids

A

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

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16
Q

Mechanism of post synaptic effects of opioids

A

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

17
Q

Major CNS pharmacological effects of opioids (10)

A

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

18
Q

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

A

-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

19
Q

Major cause of opioid OD-induced death?

A

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

20
Q

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

A

tolerance, dependence, withdrawal, addiction

21
Q

What pharmacological effects of opioid develop tolerance (6)

A

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

22
Q

What pharmacological effects does not develop tolerance

A

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

23
Q

List out treatment options for opioid overdose and toxicity

A

Naloxone (narcan) = antidote for OD
Ventilation and oxygenation

24
Q

Purpose of COX-1

A

produces prostaglandins that mediate homeostatic fxns

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

25
Drugs that inhibit COX-1
diclofenac, ibuprofen, naproxen
26
Purpose of COX-2
produces prostaglandins that mediate inflam, pain and fever *pathologic - inflam, pain, fever, dysregulated proliferation*
27
Drugs that inhibit COX-2
diclofenac, ibuprofen, naproxen, celecoxib, rofecoxib
28
Acetaminophen MOA
inhibits COX enzyme, not fully understood and unclear why it doesn’t exert anticoagulant and anti-inflammatory effects
29
Acetaminophen serious AE
Hepatotoxicity and pain masking
30
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
31
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
32
Precursor for steroid biosynthesis
cholesterol
33
Name endogenous corticosteroids (glucocorticoids)
cortisol and corticosterone
34
Name endogenous corticosteroids (mineralocorticoids)
aldosterone
35
Pharmacological effects of corticosteroids
-Control glucose metabolism and body’s ability to deal w/ stress -Decrease inflammation -Suppress immune system
36
Clinical uses of corticosteroids (endocrine)
Endocrine: -Normalizes adrenal cortical hypofxn -Used as diagnostic tool to evaluate hormonal disorders
37
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)
38
AE of corticosteroids
-breakdowns of supporting tissue (inhibits collagen production) -mus atrophy -drug induced cushing syndrome (hypercortisolism) -adrenal crises/shock -osteoperosis