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Pharm > Pain Management > Flashcards

Pain Management Flashcards

1
Q

Nociceptors

A
  • Found in somatic and visceral structures
  • Activated by mechanical, thermal and chemical impulses
  • Bradykinins, H+ and K+ ions, PGs, histamine, ILs, TNF, 5HT and substance P all activate nociceptors
  • Activation leads to action potential transmitted along afferent nerve fibers to the spinal cord
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2
Q

Acute pain

A
  • Begins suddenly
  • Usually sharp in quality
  • Warning of disease or threat
  • Disappears when injury heals or cause is treated
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3
Q

Chronic pain

A
  • May last yrs
  • Accompanied by muscle tightness, limited mobility, decreased energy
  • Persists after injury heals or cause is treated
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4
Q

WHO Pain ladder Adults

- initially for cancer pain

A
  1. Non-opiod (NSAIDs) +/- adjuvant
  2. Opiod for mild-moderate pain
  3. Opiod for moderate-severe pain +/- Non-opioid +/- adjuvant
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5
Q

WHO Pain treatment Peds

A
  • Mild pain: acetaminophen or ibuprofen (
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6
Q

Acetaminophen (Tylenol)

  • First Line for treatment of knee, hip osteoarthritis
  • MAX daily dose: 4g (adults), 5 doses* 50-75mg/kg (Peds
A
  • MOA: not well understood; centrally acting; may block cytokines in the dorsal horn; blocks PG release in CNS
  • Raises pain threshold
  • INDICATIONS: temporary relief of minor aches/pains; fever reduction
  • DRUG INTERACTIONS: P450 2E1 inducers
  • Analgesic, antipyretic
  • NOT an anti-inflammatory
  • LIVER warning (> 4g in 24 hrs, other acetaminophen drugs, >3 EtOH drinks per day; leading cause of acute liver failure in US)
  • Watch combo products!
  • Cmax 30-60 mins
  • T1/2= 2hrs
  • Metabolized to NAPQI– Toxic
  • Warning for severe liver injury, allergic rxn
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7
Q

Acetaminophen Toxicity

A

What could cause overdose

  • Acute dose > 7.5 g or repeat supratherapeutic doses
  • Hepatotoxicity at 10-15g (doses > 20g can be fatal)
  • Alcoholics
  • Drug interactions: P450 2E1 inducers
  • Fasting, malnutrition
  • Viral illness (dehydration)

After overdose:

  • Absorption w/in 2-3 hrs, PEAK 4 HRS
  • Nontoxic metabolic routs saturated–> formation of NAPQI by 2E1 increases
  • NAPQI increased (exceeds glutathione supply)
  • Excess NAPQI: covalent binding of cell proteins leads to cell death

Result:

  • Liver: Cell damage
  • Renal: acute renal tubular necrosis
  • Other organs: heart, pancreas, CNS

Clinical:

  • Sx may not develop for several hrs
  • Early s/sx: N/V, AMS, metabolic acidosis, increased PT/INR
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8
Q

4 Stages of APAP toxicity

A

Stage 1

  • No liver injury
  • Asymptomatic or early s/sx (N/V, diaphoresis, pallor, malaise)
  • Normal LFTs

Stage 2

  • Liver injury 24-36 hrs
  • AST elevated (may be >1000)
  • RUQ pain, hepatomegaly
  • Possible nephrotoxicity
  • Increased PT, bilirubin, sCr, BUN
  • Proteinuria, hematuria, casts

Stage 3

  • Max liver injury 72-96hrs
  • Hepatic failure: encephalopathy, coma, hemorrhage
  • N/V may return
  • High ammonia level
  • AST/ALT elevated > 10,000 IU/L
  • Abnormal PT, creatinine, glucose, pH, bilirubin, lactate
  • Fatality: usually 3-5 days after OD, multiorgan failure (hemorrhage, ARDS, sepsis, cerebral edema)

Stage 4
- Recovery: hepatic regeneration, several days-weeks

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9
Q

Diagnosis of Acetaminophen overdose

A
  • Rumack-Matthew Nomogram
  • Acetaminophen level: single, acute overdose in pt > 12yrs old; 4-24 hrs post ingestion
  • Predicts likelihood of toxicity
  • Determines need for antidote
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10
Q

NAC (N-acetylcysteine)

- APAP Antidote

A
  • Prevents hepatic injury by limiting formation of NAPQI
  • Glutathione precursor (increased glutathione availability, combines with NAPQI)
  • Must be administered w/in 8 hrs of overdose
  • Use with possible or probable risk of hepatotoxicity
  • Preg cat B
  • Can use IV or oral (Fewer side effects with oral)
  • IV anaphylaxis possible: rash, urticaria, pruritus; flushing; N/V; Bronchospasms (potentially fatal, may need antihistamines, steroids, beta agonist, epi)

Treatment Protocol

  • IV NAC 20 hr protocol
  • Oral NAC 72 hr protocol: ADRS (N/V/abd pain)
  • Kids
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11
Q

APAP Toxicity Treatment

A
  • Chronic or multiple ingestions
  • Cannot use nomogram
  • NAC if: dose > 150-200mg/kg in 24 hrs; elevated LFTs; Acetaminophen level > 10mcg/ml
  • Stop treatment 24-36 hrs after last APAP dose if PT/INR and LFTs normal
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12
Q

NSAIDS

A
  • Nonsteroidal Anti-inflammatory drugs
  • Inhibit cyclooxygenase enzymes (COX)
    1. Prostaglandin synthase enzymes
    2. COX-1: physiologic, constitutive (found in nearly all cells at constant level)
    3. COX-2: pathologic, inducible (released in response to cell mediators;pyretic, pain, inflammatory actions)
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13
Q

COX action

A
  • PGs help maintain renal blood flow in compromised kidneys
  • Risk of renal ischemia with chronic NSAID use in pts with renal insufficiency, CHF or cirrhosis
  • PGs induce uterine contractions during labor
  • Indomethacin used to help prevent premature labo
  • Avoid NSAIDs in 3rd trimester (may cause premature closure of PDA)
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14
Q

NSAIDs Uses

A
  • Acute or chronic pain (from any cause, caution with long term use)
  • Cancer pain
  • Anti-inflammatory
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15
Q

NSAIDs Risks

A

GI

  • Common ADRs: N/D/abd pain/dyspepsia/anorexia/flatulence
  • Take with food or milk (enteric coated products should not be taken with milk or antacids)

GI Bleed:

  • Increased risk in elderly, h/o peptic ulcer or GI bleed, CVD
  • Incidence of gastric ulcer, duodenal ulcer, complications (perfusion, obstruction, bleed)
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16
Q

NSAID ulcer prevention/treatment

A

PPIs: reduce risk of gastric and duodenal ulcers

Double dose H2RAs: reduced gastric and duodenal ulcers; reduced abd pain

17
Q

G6PD deficiency

A

d

18
Q

Misoprostol (Cytotec)

A
  • Synthetic prostaglandin E1 analog
  • Inhibits gastric acid secretion (Basal, nocturnal and in response to stimuli)
  • Protects GI mucosa
  • Reduces incidence of gastric and duodenal ulcers
  • ADR: D/N/abd pain
  • Abortiacient: induction of labor or uterine rupture after 8th week of pregnancy
  • Teratogenic: CATEGORY X (deformities if used during 1st trimester)

Documentation

  • Advise pts of potential for abortion
  • Warn pts not to share the drug with others
  • Negative serum pregnancy test w/in 2 weeks prior to beginning therapy
  • Pt capable of complying with effective contraceptive measures
  • Pt has received both oral and written warnings of the hazards of misoprostol, the risk of possible contraception failure, and the danger to other women of childbrearing potential should the drug be taken by mistake
  • Pt will begin misoprostol only on the second or third day of the next normal menstrual period
19
Q

NSAIDs cardiovascular risk

A
  • Primarily with COX-2 inhibitors
  • Celecoxib (Celebrex) and Diclogenac increase CV events
  • Slight increase with ibuprofen
  • No increase with Naproxen (naprosyn)
  • NSAIDs shouldn’t be used for pain control for cardiac surgery
  • ALL NSAIDs can increase BP
20
Q

NSAIDs renal risk

- Renal adjust or avoid for renal insufficiency

A
  • Acute renal insufficiency; Tubulointerstitial nephropathy; Renal papillary necrosis; Hyperkalemia
  • Clinical signs: increased sCr, BUN, K+; increased BP; Peripheral edema; wt gain
  • High risk pts: chronic renal insufficiency, CHF, severe hepatic dz, nephrotic syndrome, elderly, meds (diuretics, ACEI, cyclosporine, aminoglycosides)
21
Q

NSAIDs warning

A
  • Avoid in 3rd trimester due to premature closure of PDA
  • Liver impairment: primarily metabolized in liver, minor renal elimination
  • SJS
22
Q

NSAIDs drug interactions

A
  • ASA: ibuprofen blocks antiplatelet effects
  • Anticoagulants
  • Antihypertensives, diuretics
  • Hypoglycemics
23
Q

NSAIDs classes

A 
Salicylates 
Proprionic Acids
Carboxylic acids
Enolic Acids
COX-2 inhibitors
24
Q

Salicylates

A

Aspirin

25
Q

Aspirin (Acetylsalicylic Acid)

- MAX daily dose 4 g

A
  • Nonselective COX inhibitor
  • Suicide inhibitor (irreversible)
  • Antiplatelet, analgesic, antiinflammatory
  • Anticancer?
26
Q

Aspirin OVERDOSE?

A

Bicarb

27
Q

Proprionic acids

A

Ibuprofen (Advil, motrin): Max dose 3200 mg/daily
Ketoprofen (Orudis)
Naproxen (Aleve): Max dose 1500 mg/daily
- Naproxen sodium: cross reactive with ASA allergy

28
Q

Carboxylic acids (~ac)

A 
Ketorolac (Toradol)
Etodolac (Lodine)
Diclofenac (Voltaren, Flector, Zipsor, Pennsaid)
Sulindac (Clinoril)
Idomethacin (Indocin)
Nabumetone (Relafen)
29
Q

Diclofenac

A

COX-2 side

Three strikes

  1. Increases risk of cardiac events as much as rofecoxib or high dose celecoxib
  2. Causes more liver toxicity than most NSAIDs
  3. Causes more GI toxicity than celecoxib, etodolac, nabumetone, or meloxicam
  • For oral NSAIDs: use ibuprofen or naproxen instead
30
Q

Ketorolac (Toradol)

A
  • Concern raised over painkiller’s use in sports
31
Q

Idomethacin (Indocin)

- First Line for gout flares

A
  • First line for gout: usual pain improvement/relief w/in 24 hrs (Naproxen also approved for use)
  • Used to close PDA in neonates: usually given after other treatments fail; must be used w/in first 14 days of life (IV ibuprofen another option)
32
Q

Enolic Acids

- Semi selective COX2 inhibitors (possible less GI ADRs)

A

Meloxicam (Mobic)

Piroxicam (Feldene)

33
Q

Meloxicam (Mobic)

- Relief of signs and symptoms of Osteoarthritis and Rheumatoid arthritis

A
  • RENAL adjust
34
Q

Piroxicam (Feldene)

- Symptomatic treatment of acute and chronic RA and OA

A
  • HEPATIC adjust
  • Monitoring parameters: occult blood loss, hemoglobin, hematocrit, periodic renal and hepatic function tests, periodic eye exams with chronic use
35
Q

COX-2 Inhibitors

A

Celecoxib (Celebrex)

36
Q

Celecoxib (Celebrex)

- Indicated for prevention of familial adenomatous polyposis (colon cancer)

A
  • Selective COX 2 inhibitor
  • USE: acute pain, osteoarthritis, rheumatoid arthritis
  • Minimizes GI ADR: may lose this effect if given with ASA; still associated with potential for ulcer
  • Watch for CV effects
  • HEPATIC adjust

Pharm (9 decks)

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