Wilkes University
2 MAXE · 335 GSN
W
Passan School of Nursing
EST. 1933
UNITY AMIDST DIVERSITY
NSG 533 Advanced Pharmacology Exam 2
PA I N M A N AG E M E N T, O P I O I D S , H E A DAC H E D I S O R D E RS & A DJ UVA N T A N A LG E S I CS
INSTITUTION Wilkes University COURSE CODE NSG 533
PROGRAM Advanced Pharmacology — EXAM Exam 2 — Pain & Headache
Graduate Nursing Pharmacology
EXAM TITLE NSG 533 Advanced Pharmacology TOTAL QUESTIONS 85 Questions
Exam 2
COURSE TITLE Advanced Pharmacology FORMAT Multiple Choice — Select the
Single Best Answer
EXAMINATION INSTRUCTIONS
▸ Select the single best answer for each question.
▸ Pain pathophysiology, WHO analgesic ladder, NSAIDs, acetaminophen, opioids, adjuvant analgesics,
migraine/cluster headaches, and opioid safety are all testable content.
▸ Correct answers and clinical rationales appear below each question.
▸ All content reflects NSG 533 Advanced Pharmacology course objectives.
, SECTION I — PAIN & HEADACHE PHARMACOLOGY Questions 1 – 85
1. What is the most common symptom prompting patients to visit primary care providers?
A. Fatigue
B. Pain — more than 80% of patients who visit physicians report pain, yet it often remains
undertreated
C. Nausea
D. Dizziness
CORRECT ANSWER B — Pain; >80% of patients report pain; often undertreated
RATIONALE Pain is the most common symptom prompting primary care visits — over 80% of
patients who see physicians report pain. Despite its prevalence, pain often
remains UNDERTREATED. Pain can be nociceptive (normal tissue injury response
— thermal, mechanical, chemical stimuli triggering withdrawal reflex and
inflammatory response), neuropathic (damage to nervous system — diabetic
peripheral neuropathy, postherpetic neuralgia), or functional (abnormal CNS
processing of normal stimuli). Acute pain lasts <3 months; chronic pain persists >3
months. The NSG 533 emphasizes aggressive treatment of acute pain to prevent
chronic pain development.
,2. The WHO three-step analgesic ladder begins with which step for mild pain?
A. Potent opioids like morphine
B. Nonopioid analgesics such as NSAIDs or acetaminophen, with or without adjuvants —
e.g., APAP 1000mg q6h or ibuprofen 600mg q6h
C. Weak opioids like codeine
D. Surgical intervention
CORRECT ANSWER B — Step 1: Nonopioid analgesics (NSAIDs or APAP) ± adjuvants for mild
pain
RATIONALE WHO analgesic ladder: Step 1 (mild pain — "soreness") = nonopioid analgesics
(NSAIDs or acetaminophen) with or without adjuvants. Examples: APAP 1000mg
q6h, ibuprofen 600mg q6h. Step 2 (moderate pain — "every time I do something it
hurts") = weak opioids (hydrocodone, codeine, tramadol) ± nonopioid analgesics
± adjuvants. Step 3 (severe pain — "no matter what I do it hurts") = potent opioids
(morphine, oxycodone, hydromorphone, fentanyl) ± nonopioid analgesics ±
adjuvants. Adjuvants include pregabalin, gabapentin, TCAs, and SNRIs.
, 3. What is the mechanism of NSAIDs and what are the key precautions?
A. Block opioid receptors; no GI risk
B. Inhibit COX-1 and COX-2 (nonselective) or COX-2 only (selective); COX-2 = anti-
inflammatory; COX-1 inhibition = GI/renal toxicity; boxed warning for CV events and GI
bleeding; often require PPI gastroprotection
C. Block serotonin receptors; safe in all patients
D. Activate GABA receptors; no contraindications
CORRECT ANSWER B — COX inhibition; COX-2 = anti-inflammatory; COX-1 = GI/renal toxicity;
boxed warning for CV/GI risk
RATIONALE NSAIDs inhibit cyclooxygenase enzymes: COX-2 inhibition produces anti-
inflammatory, analgesic, and antipyretic effects. COX-1 inhibition (by nonselective
NSAIDs) causes GI toxicity (dyspepsia, ulcers, bleeding) and renal toxicity. All
NSAIDs now carry a boxed warning for increased cardiovascular events and GI
bleeding. Management: take with food/milk, switch to COX-2 selective agent
(celecoxib) for high GI risk, or add gastroprotection (PPI, H2RA, misoprostol).
NSAIDs produce a CEILING EFFECT — higher doses provide no greater efficacy
than moderate doses. Ketorolac is limited to 5 days maximum due to bleeding
risk.
2 MAXE · 335 GSN
W
Passan School of Nursing
EST. 1933
UNITY AMIDST DIVERSITY
NSG 533 Advanced Pharmacology Exam 2
PA I N M A N AG E M E N T, O P I O I D S , H E A DAC H E D I S O R D E RS & A DJ UVA N T A N A LG E S I CS
INSTITUTION Wilkes University COURSE CODE NSG 533
PROGRAM Advanced Pharmacology — EXAM Exam 2 — Pain & Headache
Graduate Nursing Pharmacology
EXAM TITLE NSG 533 Advanced Pharmacology TOTAL QUESTIONS 85 Questions
Exam 2
COURSE TITLE Advanced Pharmacology FORMAT Multiple Choice — Select the
Single Best Answer
EXAMINATION INSTRUCTIONS
▸ Select the single best answer for each question.
▸ Pain pathophysiology, WHO analgesic ladder, NSAIDs, acetaminophen, opioids, adjuvant analgesics,
migraine/cluster headaches, and opioid safety are all testable content.
▸ Correct answers and clinical rationales appear below each question.
▸ All content reflects NSG 533 Advanced Pharmacology course objectives.
, SECTION I — PAIN & HEADACHE PHARMACOLOGY Questions 1 – 85
1. What is the most common symptom prompting patients to visit primary care providers?
A. Fatigue
B. Pain — more than 80% of patients who visit physicians report pain, yet it often remains
undertreated
C. Nausea
D. Dizziness
CORRECT ANSWER B — Pain; >80% of patients report pain; often undertreated
RATIONALE Pain is the most common symptom prompting primary care visits — over 80% of
patients who see physicians report pain. Despite its prevalence, pain often
remains UNDERTREATED. Pain can be nociceptive (normal tissue injury response
— thermal, mechanical, chemical stimuli triggering withdrawal reflex and
inflammatory response), neuropathic (damage to nervous system — diabetic
peripheral neuropathy, postherpetic neuralgia), or functional (abnormal CNS
processing of normal stimuli). Acute pain lasts <3 months; chronic pain persists >3
months. The NSG 533 emphasizes aggressive treatment of acute pain to prevent
chronic pain development.
,2. The WHO three-step analgesic ladder begins with which step for mild pain?
A. Potent opioids like morphine
B. Nonopioid analgesics such as NSAIDs or acetaminophen, with or without adjuvants —
e.g., APAP 1000mg q6h or ibuprofen 600mg q6h
C. Weak opioids like codeine
D. Surgical intervention
CORRECT ANSWER B — Step 1: Nonopioid analgesics (NSAIDs or APAP) ± adjuvants for mild
pain
RATIONALE WHO analgesic ladder: Step 1 (mild pain — "soreness") = nonopioid analgesics
(NSAIDs or acetaminophen) with or without adjuvants. Examples: APAP 1000mg
q6h, ibuprofen 600mg q6h. Step 2 (moderate pain — "every time I do something it
hurts") = weak opioids (hydrocodone, codeine, tramadol) ± nonopioid analgesics
± adjuvants. Step 3 (severe pain — "no matter what I do it hurts") = potent opioids
(morphine, oxycodone, hydromorphone, fentanyl) ± nonopioid analgesics ±
adjuvants. Adjuvants include pregabalin, gabapentin, TCAs, and SNRIs.
, 3. What is the mechanism of NSAIDs and what are the key precautions?
A. Block opioid receptors; no GI risk
B. Inhibit COX-1 and COX-2 (nonselective) or COX-2 only (selective); COX-2 = anti-
inflammatory; COX-1 inhibition = GI/renal toxicity; boxed warning for CV events and GI
bleeding; often require PPI gastroprotection
C. Block serotonin receptors; safe in all patients
D. Activate GABA receptors; no contraindications
CORRECT ANSWER B — COX inhibition; COX-2 = anti-inflammatory; COX-1 = GI/renal toxicity;
boxed warning for CV/GI risk
RATIONALE NSAIDs inhibit cyclooxygenase enzymes: COX-2 inhibition produces anti-
inflammatory, analgesic, and antipyretic effects. COX-1 inhibition (by nonselective
NSAIDs) causes GI toxicity (dyspepsia, ulcers, bleeding) and renal toxicity. All
NSAIDs now carry a boxed warning for increased cardiovascular events and GI
bleeding. Management: take with food/milk, switch to COX-2 selective agent
(celecoxib) for high GI risk, or add gastroprotection (PPI, H2RA, misoprostol).
NSAIDs produce a CEILING EFFECT — higher doses provide no greater efficacy
than moderate doses. Ketorolac is limited to 5 days maximum due to bleeding
risk.
