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
2
Q
Acute pain
A
- Begins suddenly
- Usually sharp in quality
- Warning of disease or threat
- Disappears when injury heals or cause is treated
3
Q
Chronic pain
A
- May last yrs
- Accompanied by muscle tightness, limited mobility, decreased energy
- Persists after injury heals or cause is treated
4
Q
WHO Pain ladder Adults
- initially for cancer pain
A
- Non-opiod (NSAIDs) +/- adjuvant
- Opiod for mild-moderate pain
- Opiod for moderate-severe pain +/- Non-opioid +/- adjuvant
5
Q
WHO Pain treatment Peds
A
- Mild pain: acetaminophen or ibuprofen; if less than 3 months old, take acetaminophen
- moderate pain: opioids, morphine DOC
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
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
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
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: severe liver damage in pts with levels > 300 microgram/mL at 4 hrs or 45 microgram/mL at 15 hrs
- Determines need for antidote
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
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
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)
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)
14
Q
NSAIDs Uses
A
- Acute or chronic pain (from any cause, caution with long term use)
- Cancer pain
- Anti-inflammatory
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)