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

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
Q

Drugs that inhibit COX-1

A

diclofenac, ibuprofen, naproxen

26
Q

Purpose of COX-2

A

produces prostaglandins that mediate inflam, pain and fever

pathologic - inflam, pain, fever, dysregulated proliferation

27
Q

Drugs that inhibit COX-2

A

diclofenac, ibuprofen, naproxen, celecoxib, rofecoxib

28
Q

Acetaminophen MOA

A

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

29
Q

Acetaminophen serious AE

A

Hepatotoxicity and pain masking

30
Q

Serious AE of NSAIDs (4)

A

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

31
Q

PT considerations of NSAIDs

A

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
Q

Precursor for steroid biosynthesis

A

cholesterol

33
Q

Name endogenous corticosteroids (glucocorticoids)

A

cortisol and corticosterone

34
Q

Name endogenous corticosteroids (mineralocorticoids)

A

aldosterone

35
Q

Pharmacological effects of corticosteroids

A

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

36
Q

Clinical uses of corticosteroids (endocrine)

A

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

37
Q

Clinical uses of corticosteroids (nonendocrine)

A

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
Q

AE of corticosteroids

A

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

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