NURS 4301 Exam 3 Multimodal Interventions For Pain
Management Learning Objectives Study Guide
Differentiate nociceptive pain - ANSWER caused by damage to somatic or visceral
tissue; normal processing of stimulus that damages normal tissue or has the potential to
do so if prolonged; usually responsive to non opioid and/or opioid drugs; includes
superficial somatic pain, deep somatic pain, and visceral pain
Differentiate neuropathic pain - ANSWER caused by damage to peripheral nerves or the
structures in the CNS; abnormal processing of sensory input by the peripheral or
central nervous system; usually includes adjuvant analgesics; includes central pain,
peripheral neuropathies, deafferentation pain, and sympathetically maintained pain
Differentiate acute pain - ANSWER sudden onset; lasts less than three months or as long
as normal healing takes to occur; mild to severe pain; usually has an identifiable cause;
pain decreases over time and goes away with recovery; manifestations can reflect
sympathetic nervous system activation
Differentiate chronic pain - ANSWER gradual or sudden onset; lasts longer than three
months or continues past normal time for recovery; mild to severe pain; cause may be
unknown or original cause may differ from mechanisms maintaining the pain; pain
typically doesn't go away and may have periods of increasing and decreasing severity;
manifestations include flat affect, decreased physical activity, fatigue, withdrawal from
social interaction; treatment focused on enhancing function and quality of life
Explain how the physiology of nociceptive pain relates to the selection of multimodal
interventions for pain relief - ANSWER there are many pathways that can be causing
nociceptive pain, so using two or more classes of analgesics takes advantage of various
mechanisms of action allowing for more broad relief of pain; different medications
impact different locations of the pain transmission pathway (transduction, transmission,
perception, modulation) so medications that target different pathway locations can be
used together for broader relief
Describe the mechanism of action for acetaminophen - ANSWER inhibit COX in CNS only
to reduce fever and pain (minimal effects on COX in peripheral sites)
, Describe the indication for acetaminophen - ANSWER analgesic, antipyretic (fever
reduction) (differ from NSAIDs: lack anti-inflammatory properties)
Describe the contraindications for acetaminophen - ANSWER concurrent alcohol use at
high doses may cause liver and kidney damage; warfarin; vaccines; undernourished;
liver disease
Describe the side effects for acetaminophen - ANSWER rare at therapeutic doses;
nausea, vomiting, hepatotoxicity at high doses (alcohol increases risk of liver damage)
Describe the recommended dose for acetaminophen - ANSWER 650 mg q4-6h
Describe the toxicity for acetaminophen - ANSWER 4,000 mg/day (3000 mg/day if used
long-term); hepatotoxicity from chronic dosing of more than 3 g/day, acute overdose, or
use by patients with severe preexisting liver disease; treat with acetylcysteine within 24
hours at the latest for protection
Antidote for acetaminophen overdose - ANSWER N-acetylcysteine, activated charcoal
Describe the nursing administration considerations for acetaminophen - ANSWER
maximum daily dose of 4000 mg, ceiling at 1000 mg; acute liver failure with acute
overdose; liver toxicity with chronic overdose; early toxicity symptoms include nausea,
vomiting, diarrhea, sweating, abdominal discomfort but only show up 48 to 72 hours
after hepatic injury has occurred; acetylcysteine can minimize liver damage
Describe the mechanism of action for nonsteroidal anti-inflammatory drugs (NSAIDs) -
ANSWER reversible nonselective inhibition of COX; COX-1 inhibition causes renal
function impairment, bleeding tendencies, GI irritation, ulceration, inhibit platelet
aggregation which protects against MI and stroke; COX-2 inhibition causes
anti-inflammatory effects such as vasoconstriction, reduced fever and inflammation,
analgesia, promote platelet aggregation which increases risk of MI and stroke
Management Learning Objectives Study Guide
Differentiate nociceptive pain - ANSWER caused by damage to somatic or visceral
tissue; normal processing of stimulus that damages normal tissue or has the potential to
do so if prolonged; usually responsive to non opioid and/or opioid drugs; includes
superficial somatic pain, deep somatic pain, and visceral pain
Differentiate neuropathic pain - ANSWER caused by damage to peripheral nerves or the
structures in the CNS; abnormal processing of sensory input by the peripheral or
central nervous system; usually includes adjuvant analgesics; includes central pain,
peripheral neuropathies, deafferentation pain, and sympathetically maintained pain
Differentiate acute pain - ANSWER sudden onset; lasts less than three months or as long
as normal healing takes to occur; mild to severe pain; usually has an identifiable cause;
pain decreases over time and goes away with recovery; manifestations can reflect
sympathetic nervous system activation
Differentiate chronic pain - ANSWER gradual or sudden onset; lasts longer than three
months or continues past normal time for recovery; mild to severe pain; cause may be
unknown or original cause may differ from mechanisms maintaining the pain; pain
typically doesn't go away and may have periods of increasing and decreasing severity;
manifestations include flat affect, decreased physical activity, fatigue, withdrawal from
social interaction; treatment focused on enhancing function and quality of life
Explain how the physiology of nociceptive pain relates to the selection of multimodal
interventions for pain relief - ANSWER there are many pathways that can be causing
nociceptive pain, so using two or more classes of analgesics takes advantage of various
mechanisms of action allowing for more broad relief of pain; different medications
impact different locations of the pain transmission pathway (transduction, transmission,
perception, modulation) so medications that target different pathway locations can be
used together for broader relief
Describe the mechanism of action for acetaminophen - ANSWER inhibit COX in CNS only
to reduce fever and pain (minimal effects on COX in peripheral sites)
, Describe the indication for acetaminophen - ANSWER analgesic, antipyretic (fever
reduction) (differ from NSAIDs: lack anti-inflammatory properties)
Describe the contraindications for acetaminophen - ANSWER concurrent alcohol use at
high doses may cause liver and kidney damage; warfarin; vaccines; undernourished;
liver disease
Describe the side effects for acetaminophen - ANSWER rare at therapeutic doses;
nausea, vomiting, hepatotoxicity at high doses (alcohol increases risk of liver damage)
Describe the recommended dose for acetaminophen - ANSWER 650 mg q4-6h
Describe the toxicity for acetaminophen - ANSWER 4,000 mg/day (3000 mg/day if used
long-term); hepatotoxicity from chronic dosing of more than 3 g/day, acute overdose, or
use by patients with severe preexisting liver disease; treat with acetylcysteine within 24
hours at the latest for protection
Antidote for acetaminophen overdose - ANSWER N-acetylcysteine, activated charcoal
Describe the nursing administration considerations for acetaminophen - ANSWER
maximum daily dose of 4000 mg, ceiling at 1000 mg; acute liver failure with acute
overdose; liver toxicity with chronic overdose; early toxicity symptoms include nausea,
vomiting, diarrhea, sweating, abdominal discomfort but only show up 48 to 72 hours
after hepatic injury has occurred; acetylcysteine can minimize liver damage
Describe the mechanism of action for nonsteroidal anti-inflammatory drugs (NSAIDs) -
ANSWER reversible nonselective inhibition of COX; COX-1 inhibition causes renal
function impairment, bleeding tendencies, GI irritation, ulceration, inhibit platelet
aggregation which protects against MI and stroke; COX-2 inhibition causes
anti-inflammatory effects such as vasoconstriction, reduced fever and inflammation,
analgesia, promote platelet aggregation which increases risk of MI and stroke
