Pain Management Meds Flashcards
Pain meds
NON-OPIOIDS;
nonsteroidal anti-inflammatory drugs(NSAIDs)
Acteminophen
Antiepileptics, local anesthetics
OPIOIDS
NSAIDS
~ for mild to moderate pain, associated with inflammation, and temporary reduction of FEVER ( children)
~No evidence for management of neuropathic pain
~Some have other non-pain related indications ( aspirin is used for 2nd prevention of MI)
~ Remember: choice of agen depends on several factors; comorbidities, risk for bleeding
Recommendation Rx the lowest effective dose for each pt for the shortest pd.
COX-1
- constitutive “HOUSEKEEPING ENZYME” particularly in STOMACH
- Inducible activity (2-4X)
- Major product is thromboxane, induces platelet aggregation
- Inhibition of platelet COX-1 explains why aspirin effectively reduces cardiac events
COX-2
- Inducible enzyme in the INFLAMMATORY RESPONSE
- Inducible activity (10-20X)
- Kidney , lungs and inflammatory cells (macrophages)
- Both NSAIDs and GLUCOCORTICOIDS inhibit COX-2 gene expression; help reduce inflammation
NSAIDs MEDS (8)
- acetylated salicylates (aspirin
- non-acetylated salicylates (diflunisal),
- propionic acids (ibuprofen, naproxen),
- acetic acids (indomethacin, diclofenac),
- anthranilic acids (meclofenamate, mefenamic acid),
- enolic acids (meloxicam, piroxicam),
- naphthylalanine (nabumetone), and
- selective COX-2 inhibitors (celecoxib, etoricoxib).
NSAIDs MOA
Primary: inhibition of cyclooxygenase enzyme -> inhibiting prostaglandin synthesis
most inhibit both COX isoforms with little selectivity
Higher affinity to one or another (apirin, & coxibs) will exert anti-inflammatory, analgesic, and antipyretic effects at different degrees.
Low doses of aspirin= antiplatelet effect
High doses = analgesic effects
NSAIDS ADRs
-GI : Nausea, anorexia, dyspepsia, abdominal pain, ulcers, gastrointestinal hemorrhage, perforation, constipation, diarrhea **
-Cardiovascular: Hypertension, decreased effectiveness of anti- hypertensive medications, myocardial infarction, stroke, and thromboembolic events (last three with selective COX-2 inhibitors); inhibit platelet activation, propensity for bruising, and hemorrhage.
-Renal: Salt and water retention, deterioration of kidney function, edema, decreased effectiveness of diuretic medications, decreased urate excretion, hyperkalemia, analgesic nephropathy **
-CNS: Headache, dizziness, vertigo, confusion, depression, lowering of seizure threshold, hyperventilation (salicylates)
-Hypersensitivity: Vasomotor rhinitis, asthma, urticaria, flushing, hypotension, shock.
-Hepatotoxicity**
NSAIDs CI
- HYPERSENSITIVITY is only major CI for NSAID use*
NSAIDS conditions demand AVOIDANCE, temporary SUSPENSION, or CAUTION
age >50 y.o
family hx of GI bleed/disorders
uncontrolled HTN
Renal disease
IBS, IBD
coronary artery & gastric bypass surgery
PREGNANCY => placental abruption
Stroke, TIA, MI ; excluding apirin
NSAIDS drug interaction with ACE inbitiors
severity: MODERATE
ADR: may decrease antihypertensive & natriuretic effects
Recommendation: monitor BP & cardiovascular function
NSAID drug interaction w/ LITHIUM
Severity: MODERATE
ADR: may increase Li plasma levels & decrease its clearance renally
Recommend: Monitor for lithium toxicity
NSAID drug interaction w/ WARFARIN
Severity: MODERATE
ADR: may result in increase risk of bleeding
Recommend: MOnitor PT & INR
NSAIDs drug interaction w/ METHOTREXATE
Severity: SEVERE
ADR: may result in increase risk of methotrexate toxicity
Recommend: DONT administer NSAIDS within 10 days of hihg dose methotrexate
NSAIDS nursing assessments
MONITOR:
NO need for routine monitoring of acute administration in healthy pts
*use chronically and pts at risk for toxicity should have evaluation including CBC, renal, & hepatic function test as a minimum
Most OD case are asymptomatic or develop insignificatnt self limiting GI symptoms
SERIOUS COMPLICATIONS: confusion, HA, nystagmus, drowsiness, blurred vision, diplopia, tinnitus, convulsion, matabolic acidosis, acute renal or liver failure, GI bleed, & coma
Acetaminophen (Tylenol)
~mild to moderate pain, moderate to severe pain, temporary reduction of FEVER
~ shouldnt be used for neuropathic pain there is no documented effect
~ Dose for ADULTS 650mg to 1000 mg Q4-6H, max of 4g/day*
Children dose 15mg/kg Q6H, up to 60mg/kg/day
~Administered PO, Rectally, IV
Acetaminophen MOA
Unclear to date, lacks anti-inflammatory properties & does not bind to the active site of either COX enzymes
HYPOTHESIS: inhibits a different variant of COX-1 AKA COX-3, remains uncomfirmed in human studies
~Diminished activity of the COX pathway leads to decreased prostaglandin synthesis in the central nervous system, thus inducing analgesia (serotonergic inhibitory pathways) and antipyresis (hypothalamic heat-regulating center)
Acetaminophen ADRs
Depends on route of administration
IV: Nausea, vomiting, pruritus, constipation, and abdominal pain.
Oral or rectal: acetaminophen may cause any of the following:
Rash or hypersensitivity reactions (toxic epidermal necrolysis, acute generalized exanthematous pustulosis, and SJS)
Hematological: anemia, leukopenia, neutropenia, pancytopenia
**Nephrotoxicity **
Metabolic and electrolyte disorders: Decreased serum bicarbonate, Hyponatremia, Hypocalcemia, Hyperammonemia, Hyperchloremia, Hyperuricemia, Hyperglycemia, Hyperbilirubinemia, Elevated alkaline phosphatase
Acetaminophen Considerations
Hypersensitivity to acetaminophen or any of its excipients, **severe hepatic impairment, or severe active hepatic disease. **
Pregnancy is not a contraindication for acetaminophen administration.
Acetaminophen Toxicity
develops at 7.5 g/day to 10g/day or 140mg/kg
* large amounts may cause severe liverdamage leading to liver
* Poisoning more frequent in children
* Adults present w/ more serious & fatal presentations
* serum levels must be drawn 4-24hrs since estimated time of ingestation to determine treatment modality
* Toxicity tool used is Rumack-Matthew Nomogram
* level greater than 140 mcg/ml at 4hrs from ingestation requires treatment w/ N-acetyl-cysteine (NAC)
* Activated charcoal avidly binds to acetaminophen & may be used w/in 1st hrs DONT administer to pts w/ increase risk of airway obstruction.
Neuropathic Med
(4)
Known for analgesic properties through MOA of lowering neurotransmitter release or neuronal firing.
* Gabapentin
* Pregabalin
* Oxcarbazepine
* Carbamazepine
Gabapentin treats…
Postherpetic neuralgia in adults & neuropathic pain
Pregabalin treats
neuropathic pain associated w/ diabetic peripheral neuropathy or spinal cord injury, postherpetic neuralgia and fibromyalgia.
Oxcarbazepine & Carbamazepine treats
trigeminal or glossopharyngeal neuralgia
Gabapentin & Pregabalin
MOA
Both are ligands to the αδ subunit of the voltage-dependent calcium channels, which overexpress in patients with neuropathic pain.
Reducing this calcium dependent release of excitatory neurotransmitters => decreases neuronal excitability.