Pain meds Flashcards

1
Q

Pain Meds

A

NON-OPIOIDS:
* nonsterioidal anti-inflammatory drugs (NSAIDs)
* Acetaminophen
* Antiepilieptics
* Local anesthetics
OPIOIDS

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2
Q

NSAIDs

facts

A
  • for mild-to-moderate pain
  • associated w/ inflammation
  • temporary reduction of fever (children)
  • No evidence for management of neuropathic pain
  • Some have non-pain related indications (aspirin;2nd prevention use for MI)
    Remember: choice of agent depends on several factors (comorbities, risk for bleeding)
    *recommend Rx lowest effective dose for shortes pd.
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3
Q

COX-1

A
  1. Housekeeping enzyme primarly in the stomach
  2. inducible activity (2-4X)
  3. major product is thromboxane => induces platelet aggregation
  4. inhibition of platelet COX-1 explains why aspiring effectively reduces cardiac events
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4
Q

COX-2

A

1. Inflammatory Response
2. inducible activity (10-20X)
3. Kidney, lungs, inflammatory cells (macrophages)
4. both NSAIDs & glucocorticoids inhibit COX-2 gene expression => help reduce inflammation

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5
Q

NSAIDs Meds

(8) generic (13) trade

A
  1. Acetylated salicylates (aspirin)
  2. Non-acetylated salicylates (diflunisal)
  3. Propionic acids (ibuprofen, naproxen)
  4. Acetic acids (indomethacin, diclofenac)
  5. Anthranilic acids (meclofenamate, mefenamic acid)
  6. Enolic acids (meloxicam, piroxicam)
  7. Naphthylalanine (nabumetone)
  8. Selective COX-2 inhibitors (celecoxib, etoricoxib)
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6
Q

NSAIDs MOA

A
  • inhibits cyclooxygenase => inhibits prostaglandin synthesis
  • most inhibit both COX isoforms w/ little selectivity
  • Higher affinity to one or another ( aspirin & coxibs) will exert antiinflammatory, analgesic, & antipyretic effects @ different degress
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7
Q

NSAIDs ADRs

A

GI: N/C/D, anorexia, dyspeppsia, abd pain, ulcers, GI hemorrhaeg, perforation
Cardiovascular: HTN, decrease antihypertensive med effectiveness, MI, stroke, & thromboembolitic events (last 3 w/ selective COX-2 inhibitors) inhibit platelet activation, propensity for bruising & hemorrage
RENAL: salt & water retention, deterioration of kidney function, edema, decrease diuretic med effectiveness, urate excretion, hyperkalemia, analgesic nephropathy
CNS: HA, dizziness, vertigo, confusion, depression, lowering seizure threshold, hyperventilation (salicylates)
Hypersensitivity: vasomotor rhinits, asthma, urticaria, fluching, hypotension, shock
HEPATOTOXICITY

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8
Q

NSAIDs CI

A

Hypersensitivity
only major CI

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9
Q

NSAIDs conditions that demand AVOIDANCE, temporaty SESPENSION or CAUTION

A
  • age >50 y.o.
  • family hx of GI bleed/disorder
  • uncontrolled HTN
  • RENAL DISEASE
  • IBS, IBD
  • Coronary artery & gastric bypass surgery
  • PREGNANCY => placental abruption
  • STROKE, TIA, MI (excluding aspirin)
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10
Q

NSAIDs drug interaction w/ ACE inhibitos

A

Severity: MODERATE
ADR: may decrease antihypertensive & natriuretic effects
Recommendation: monitor BP & cardiovascular function

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11
Q

NSAIDs interaction w/ LITHIUM

A

Severity: MODERATE
ADR: may increase lithium plasma level & deccrease its clearance renally
Recommendation: monitor for lithium toxicity

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12
Q

NSAIDs interaction w/ WARFARIN

A

Severity: MODERATE
ADR: may result in increase risk of bleeding
Recommendation: monitor PT & INR

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12
Q

NSAIDs interaction w/ METHOTREXATE

A

Severity: SEVERE
ADR: may result in increase risk of methotrexate toxicity
Recommendation: DONT administer NSAIDs w/in 10 days of high dose methotrexate

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13
Q

NSAIDs Nursing Assessment

A

MONITOR:
pts w/ chronical use & at risk for toxicity; should have evaluationg including CBC, RENAL, HEPATIC function test as a minimum
Most OD case are asymptomatic or develop insignificant self limiting GI symptoms
SERIOUS COMPLICATIONS: confusion, HA, nystagmus, drowsiness, blurred vision, diplopia, tinnitus, convulsion, metabolic acidosis, acute renal or liver failure, GI bleed, coma

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14
Q

Acetaminophen (tylenol)

A

mild-to-moderate or moderate-to- severe pain
temporary reduction of FEVER
SHOULDNT be used for neuropathic pain theres no doc effect
Dose for ADULTS 650-1000mg Q4-6H, max 4g/day
Children dose 15mg/kg Q6H, up to 60mg/kg/day
Administer PO, Rectally or IV

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15
Q

Acetaminophen MOA

A

Dimished activity of the COX pathway leads to decrease prostaglandin synthesis in the CNS =>inducing analgesia (serotonergic inhibitory pathways) & antipyresis (hypothalamic heat-reduction center)
* Unclear to date
* Lacks anti-inflammatory properties & DOESNT bind to the active site of either COX enzymes
* Hypothesis: inhibits different variant of COX-1 AKA COX-3; remains uncomfirmed in human studies

16
Q

Acetaminophen ADRs

A

depends on route of administration
* IV: N/C, pruritis, abd pain
* ORAL or RECTAL: may cause Rash or Hypersensitivity reaction ( TEN, acute generalized exanthematous pustulosis, & SJS)
* Hematological: anemia, leukopenia, neutropenia, pancytopenia
* Nephrotoxicity
* Metabolic & electrolyte disorders: decreased serum bicarbonate, hyponatremia, hypocalcemia, hyperammonenia, hyperchloremia, hyperuricemia, hyperglycemia, hyperbilirubinemia, elevated alkaline phosphate

17
Q

Acetaminophen CI

A

Hypersensitivity,
Severe hepatic impairment or disease

* Pregnancy is not a CI

18
Q
A