NSG 533 Advanced Pharmacology Exam 2 | COMPLETE QUESTIONS WITH 100%
GRADED CORRECT EXPERT SOLUTIONS| 2026 LATEST UPDATED | GET A+
1. pain: the most common symptom prompting patients to visit primary care providers. More than 80% of patients who
visit physicians report pain. Often remains under treated.
2. nociceptive pain: pain from a normal process that results in noxious stimuli being perceived as painful. Explained by
ongoing tissue injury. thermal, mechanical and chemical nociceptors that engage "withdrawal" reflex followed by
inflammatory response to protect injured tissue
3. functional pain: pain sensitivity due to an abnormal processing or function of the central nervous system in response
to normal stimuli
4. neruopathic pain: Pain caused by lesions or other damage to the nervous system.
5. Diabetic peripheral neuropathy: progressive deterioration of nerve function that results in loss of sensory perception
6. acute pain: is pain that occurs as a result of injury or surgery, under 3 months. Poorly treated acute pain can cause
psychological stress and compromise the immune system. Somatic acute pain is an injury to skin, bone, joint, muscle
and connective tissue. Visceral pain involves injury to nerves on internal organs. Treat aggressively. Examples: cut
hand, menstrual cramps.
7. chronic pain: can be intermittent or persistent, more than 3 months. Main affects include a) effects on physical
function b) psychological changes c) social consequences and d) societal consequences. Usually involving life
threatening diseases such as cancers, aids, progressive neurological diseases, end stage organ failure, dementia.
Management should be multimodal with cognitive interventions, physical manipulations, pharmacological agents,
surgical interventions, and regional or spinal anesthesia.
8. chronic malignant pain: Painn is associated with a progressive life-threatening disease like cancer, aids, neurologic
diseases, end stage organ failure, and dementia. Goal is pain alleviation and prevention. Dependence or addiction is
, not a concern. Pain not associated with life threatening disease and lasting more than 6 months beyond the healing
period is referred to as "chronic nonmalignant pain."
9. What are some non-pharmacological approaches to pain?: imagery, distraction, relaxation, psychotherapy,
biofeedback, cognitive behavioral therapy, support groups, and spiritual counseling. Physical therapy, heat, cold,
water, ultrasound, TENS, massage and therapeutic exercise.
10. WHO 3 step analgesic ladder: * 1- nonopioid
* 2 - opioid for mild to moderate pain
* 3 - opioid for moderate to severe pain
11. WHO first step pain ladder: mild pain/nonopioid analgesics such as NSAIDS or acetaminophen w/ or w/out
adjuvants (such as pregablin) .. "soreness." Med examples: apap 1000mg q 6hrs, ibu600mg q6 hrs
12. NSAIDs: Non-steroidal anti-inflammatory drugs. associated with several clinically significant contraindications
and drug interactions. NSAIDS are equally effective in analgesia, antipyretic and anti-inflammatory effects. Choice
should include STEPS (simplicity, tolerability, evidence, price, safety). If patient fails therapy with an agent from
one class of NSAIDs, use of an agent from another class is reasonable.
13. COX2 inhibitors: Celecoxib (Celebrex) selective agents (celecoxib) have ideal indication in patients with high
risk for GI bleed, high intolerance of non-selective NSAIDS, or treatment failure with non-selective agents. NSAIDs
are of minimal value in neuropathic pain. NSAIDs produce a flat dose response curve (celling effect) with higher
doses providing no greater efficacy than moderate doses.
14. Acetaminophen: Tylenol. blocks PG synthesis in CNS, inhibits peripheral pain impulses. APAP does not interfere
with COX 1 or COX2 and thus has no anti-inflammatory benefits.
15. WHO pain ladder step 2: moderate pain: weak opioids (hydrocodone, codeine, tramadol) w/ or w/out nonopioid
analgesics w/ or w/out adjuvants "every time I do something, it hurts" med examples: apa325mg + cod 60mg q4 hrs
, 16. WHO pain ladder step 3: severe and persistent pain, potent opioids (morphine, tapentadol, oxycodone,
hydromorphone, fentanyl, w/ or w/out non-opioid analgesics and with or without adjuvants "no matter what I do it
hurts, theres a bone sticking out of my skin!" Examples; morphine 10mg q4 hrs, hydromorphone 4mg q4 hr
17. What is the mechanism of NSAIDs and precautions to use?: NSAIDS are either
nonselective (inhibit cox 1 and cox 2) or selective (inhibit cox 2). Cox 2 inhibition is responsible for anti-inflammatory
effects. - Cox 1 contributes to increased GI and renal toxicity assoc with nonselective NSAIDS. Use with caution in
patients with dyspepsia, peptic ulcers, bleeding, and patients taking corticosteroids. Nephrotoxicity can occur in the
elderly. A boxed warning is now required for prescription nonselective NSAIDs and Celecoxib due to the increase risk
of cardiovascular events and GI bleeding. Generally pts prescribed NSAIDS will need PPI's.
18. Managment for NSAID risks: Pts more pre-disposed to GI toxicity if pre-existing ulcer or dyspepsia, H Pylori
infection, older age, and some concurrent medications increase risk. Management options for GI side effects include
taking with food or milk, Switch to different NSAID with better safety profile, COX2 selective agent (celecoxib)
and/or gastroprotection (H2RA, PPI, misoprostol
19. Celecoxib: is recommended for patients at increased risk of gastrointestinal bleeding / ulcer who require a NSAID
-Side effects can also include htn, and worsening asthma symptoms.
20. Tordol (Ketorolac): 40mg, max 5 days.. huge bleeding risk beyond that!
21. When are NSAIDs indicated and is one NSAID better / safer than another
in a given patient?: Useful for mild to moderate pain that are mediated by prostaglandins (RA, menstrual cramps, and
postsurgical pain). Works well for pain assoc with bone metastasis. Will dose escalation provide greater benefits (i.e. is
there a ceiling effect)? Higher doses produce no greater efficacy than moderate doses.
22. What is the mechanism of acetaminophen?: Blocks prostaglandin synthesis in the CNS and block pain impulses
in the periphery.
GRADED CORRECT EXPERT SOLUTIONS| 2026 LATEST UPDATED | GET A+
1. pain: the most common symptom prompting patients to visit primary care providers. More than 80% of patients who
visit physicians report pain. Often remains under treated.
2. nociceptive pain: pain from a normal process that results in noxious stimuli being perceived as painful. Explained by
ongoing tissue injury. thermal, mechanical and chemical nociceptors that engage "withdrawal" reflex followed by
inflammatory response to protect injured tissue
3. functional pain: pain sensitivity due to an abnormal processing or function of the central nervous system in response
to normal stimuli
4. neruopathic pain: Pain caused by lesions or other damage to the nervous system.
5. Diabetic peripheral neuropathy: progressive deterioration of nerve function that results in loss of sensory perception
6. acute pain: is pain that occurs as a result of injury or surgery, under 3 months. Poorly treated acute pain can cause
psychological stress and compromise the immune system. Somatic acute pain is an injury to skin, bone, joint, muscle
and connective tissue. Visceral pain involves injury to nerves on internal organs. Treat aggressively. Examples: cut
hand, menstrual cramps.
7. chronic pain: can be intermittent or persistent, more than 3 months. Main affects include a) effects on physical
function b) psychological changes c) social consequences and d) societal consequences. Usually involving life
threatening diseases such as cancers, aids, progressive neurological diseases, end stage organ failure, dementia.
Management should be multimodal with cognitive interventions, physical manipulations, pharmacological agents,
surgical interventions, and regional or spinal anesthesia.
8. chronic malignant pain: Painn is associated with a progressive life-threatening disease like cancer, aids, neurologic
diseases, end stage organ failure, and dementia. Goal is pain alleviation and prevention. Dependence or addiction is
, not a concern. Pain not associated with life threatening disease and lasting more than 6 months beyond the healing
period is referred to as "chronic nonmalignant pain."
9. What are some non-pharmacological approaches to pain?: imagery, distraction, relaxation, psychotherapy,
biofeedback, cognitive behavioral therapy, support groups, and spiritual counseling. Physical therapy, heat, cold,
water, ultrasound, TENS, massage and therapeutic exercise.
10. WHO 3 step analgesic ladder: * 1- nonopioid
* 2 - opioid for mild to moderate pain
* 3 - opioid for moderate to severe pain
11. WHO first step pain ladder: mild pain/nonopioid analgesics such as NSAIDS or acetaminophen w/ or w/out
adjuvants (such as pregablin) .. "soreness." Med examples: apap 1000mg q 6hrs, ibu600mg q6 hrs
12. NSAIDs: Non-steroidal anti-inflammatory drugs. associated with several clinically significant contraindications
and drug interactions. NSAIDS are equally effective in analgesia, antipyretic and anti-inflammatory effects. Choice
should include STEPS (simplicity, tolerability, evidence, price, safety). If patient fails therapy with an agent from
one class of NSAIDs, use of an agent from another class is reasonable.
13. COX2 inhibitors: Celecoxib (Celebrex) selective agents (celecoxib) have ideal indication in patients with high
risk for GI bleed, high intolerance of non-selective NSAIDS, or treatment failure with non-selective agents. NSAIDs
are of minimal value in neuropathic pain. NSAIDs produce a flat dose response curve (celling effect) with higher
doses providing no greater efficacy than moderate doses.
14. Acetaminophen: Tylenol. blocks PG synthesis in CNS, inhibits peripheral pain impulses. APAP does not interfere
with COX 1 or COX2 and thus has no anti-inflammatory benefits.
15. WHO pain ladder step 2: moderate pain: weak opioids (hydrocodone, codeine, tramadol) w/ or w/out nonopioid
analgesics w/ or w/out adjuvants "every time I do something, it hurts" med examples: apa325mg + cod 60mg q4 hrs
, 16. WHO pain ladder step 3: severe and persistent pain, potent opioids (morphine, tapentadol, oxycodone,
hydromorphone, fentanyl, w/ or w/out non-opioid analgesics and with or without adjuvants "no matter what I do it
hurts, theres a bone sticking out of my skin!" Examples; morphine 10mg q4 hrs, hydromorphone 4mg q4 hr
17. What is the mechanism of NSAIDs and precautions to use?: NSAIDS are either
nonselective (inhibit cox 1 and cox 2) or selective (inhibit cox 2). Cox 2 inhibition is responsible for anti-inflammatory
effects. - Cox 1 contributes to increased GI and renal toxicity assoc with nonselective NSAIDS. Use with caution in
patients with dyspepsia, peptic ulcers, bleeding, and patients taking corticosteroids. Nephrotoxicity can occur in the
elderly. A boxed warning is now required for prescription nonselective NSAIDs and Celecoxib due to the increase risk
of cardiovascular events and GI bleeding. Generally pts prescribed NSAIDS will need PPI's.
18. Managment for NSAID risks: Pts more pre-disposed to GI toxicity if pre-existing ulcer or dyspepsia, H Pylori
infection, older age, and some concurrent medications increase risk. Management options for GI side effects include
taking with food or milk, Switch to different NSAID with better safety profile, COX2 selective agent (celecoxib)
and/or gastroprotection (H2RA, PPI, misoprostol
19. Celecoxib: is recommended for patients at increased risk of gastrointestinal bleeding / ulcer who require a NSAID
-Side effects can also include htn, and worsening asthma symptoms.
20. Tordol (Ketorolac): 40mg, max 5 days.. huge bleeding risk beyond that!
21. When are NSAIDs indicated and is one NSAID better / safer than another
in a given patient?: Useful for mild to moderate pain that are mediated by prostaglandins (RA, menstrual cramps, and
postsurgical pain). Works well for pain assoc with bone metastasis. Will dose escalation provide greater benefits (i.e. is
there a ceiling effect)? Higher doses produce no greater efficacy than moderate doses.
22. What is the mechanism of acetaminophen?: Blocks prostaglandin synthesis in the CNS and block pain impulses
in the periphery.
