Graduate Nursing Program
1 MAXE · 335 GSN
★ ★
Rx College of Nursing — Advanced Practice
PHARM
PHARMACOLOGY · CLINICAL REASONING · SAFE PRESCRIBING
NSG 533 Advanced Pharmacology — Exam 1 Comprehensive Review
G E R D/ P U D , D I A B E T E S , T H Y R O I D , CO N T RAC E PT I O N , M E N O PAUS E , B P H / E D , A N T I D E P R E SS A N TS ,
A N X I O LYT I CS , I N S O M N I A & P R E G N A N CY S A F E TY
INSTITUTION Graduate Nursing Program PROGRAM MSN — Advanced Practice Registered Nurse
COURSE CODE NSG 533 COURSE TITLE Advanced Pharmacology Across the Lifespan
ACADEMIC YEAR EXAM TITLE NSG 533 Advanced Pharm Exam 1 —
Comprehensive Review
TOTAL QUESTIONS 200 Questions FORMAT Multiple Choice — Select the Single Best Answer
EXAMINATION INSTRUCTIONS
▸ Select the single best answer for each question.
▸ Content spans GERD/PUD, diabetes mellitus, thyroid disorders, contraception, menopause/HRT, BPH/ED, antidepressants,
anxiolytics, insomnia, and pregnancy medication safety.
▸ Questions reflect NSG 533 Advanced Pharmacology Exam 1 content and competency expectations.
▸ Correct answers and clinical rationales appear below each question for comprehensive test preparation.
▸ Questions have been randomized to promote active recall and simulate authentic testing conditions.
SECTION I — NSG 533 ADVANCED PHARMACOLOGY COMPREHENSIVE
Questions 1 – 200
EXAMINATION
1. What is the underlying pathophysiology of GERD?
A. Overproduction of gastric acid with normal LES function
B. Lower esophageal sphincter dysfunction including transient relaxations and low tone, often with hiatal hernia,
delayed gastric emptying, or increased intra-abdominal pressure
C. Autoimmune destruction of esophageal mucosa
D. Bacterial infection of the lower esophagus
CORRECT ANSWER B — Lower esophageal sphincter dysfunction including transient relaxations and low tone
RATIONALE GERD results from dysfunction of the lower esophageal sphincter (LES) — including transient relaxations
and low basal tone — that allows gastric contents to reflux into the esophagus. Contributing factors
include hiatal hernia (promotes reflux), delayed gastric emptying, and increased intra-abdominal pressure
(obesity, pregnancy). The injury to esophageal mucosa is caused by acid and pepsin exposure; severity
relates to exposure time and clearance. GERD is not primarily caused by acid overproduction,
autoimmune disease, or infection.
,2. Which of the following worsens GERD by reducing LES tone?
A. Fiber supplements
B. Chocolate, peppermint, caffeine, and fatty meals
C. Proton pump inhibitors
D. H2 receptor antagonists
CORRECT ANSWER B — Chocolate, peppermint, caffeine, and fatty meals
RATIONALE Multiple dietary and lifestyle factors reduce LES tone and worsen GERD: chocolate, peppermint (relaxes
LES), caffeine, alcohol, smoking, obesity, late meals, and large/fatty meals. Medications that worsen GERD
include anticholinergics, calcium channel blockers, nitrates, theophylline, and progesterone. PPIs and
H2RAs are treatments for GERD — they do not worsen it. Fiber supplements are generally neutral or
beneficial for GI health.
3. What are ALARM symptoms in GERD that warrant endoscopy rather than an empiric PPI trial?
A. Mild heartburn occurring less than once weekly
B. Dysphagia, odynophagia, weight loss, and GI bleed/anemia
C. Occasional regurgitation after large meals
D. Chronic cough that improves with antacids
CORRECT ANSWER B — Dysphagia, odynophagia, weight loss, and GI bleed/anemia
RATIONALE ALARM symptoms in GERD indicate potential complications (malignancy, stricture, erosive disease,
bleeding) and require prompt endoscopy, NOT an empiric OTC trial. These include: dysphagia (difficulty
swallowing), odynophagia (painful swallowing), unintentional weight loss, and GI bleeding/anemia.
Uncomplicated GERD (typical heartburn, regurgitation without alarm features) may be managed with an
8-week empiric PPI trial. Mild, infrequent symptoms do not require endoscopy. Chronic cough is an
atypical GERD symptom but alone does not mandate endoscopy.
4. Why is self-directed OTC GERD therapy limited to 2 weeks?
A. PPIs lose effectiveness after 2 weeks of continuous use
B. To avoid masking ALARM symptoms such as cancer, erosive disease, bleeding, and strictures
C. Antacids cause irreversible kidney damage after 14 days
D. GERD always resolves spontaneously within 2 weeks
CORRECT ANSWER B — To avoid masking ALARM symptoms such as cancer, erosive disease, bleeding, and strictures
RATIONALE OTC GERD therapy is limited to 2 weeks to prevent patients from self-medicating for prolonged periods
without appropriate diagnostic evaluation. Persistent symptoms beyond 2 weeks may indicate more
serious underlying pathology (malignancy, erosive esophagitis, stricture, bleeding) that requires
endoscopy. PPIs do not lose effectiveness at 2 weeks. Antacids do not cause irreversible kidney damage
with short-term use. GERD is typically a chronic condition that does not resolve spontaneously.
,5. Which PPI is preferred for patients taking clopidogrel due to fewer drug interactions?
A. Omeprazole
B. Pantoprazole
C. Esomeprazole
D. Lansoprazole
CORRECT ANSWER B — Pantoprazole
RATIONALE Pantoprazole is the preferred PPI for patients on clopidogrel because it has the fewest CYP450 drug
interactions, particularly minimal CYP2C19 inhibition. Omeprazole and esomeprazole significantly inhibit
CYP2C19, which decreases clopidogrel activation and may reduce its antiplatelet efficacy — this is an FDA-
warned interaction. Lansoprazole also has CYP2C19 inhibition. For any patient on clopidogrel requiring a
PPI, pantoprazole is the safest choice to maintain clopidogrel's therapeutic effect.
6. What are the long-term risks of PPI therapy?
A. Only mild headache and transient nausea
B. Increased risk of fractures, pneumonia, C. difficile infection, hypomagnesemia, B12/iron malabsorption, atrophic
gastritis, and kidney disease
C. PPIs have no long-term risks — they are safe indefinitely
D. Only increased risk of weight gain and diabetes
CORRECT ANSWER B — Increased risk of fractures, pneumonia, C. diff, hypomagnesemia, B12/iron malabsorption,
atrophic gastritis, and kidney disease
RATIONALE Long-term PPI use is associated with multiple risks — mnemonic "Bad Bones & Bugs": fractures
(especially postmenopausal women from calcium malabsorption), pneumonia (reduced gastric acid
barrier), C. difficile infection (altered gut microbiome), hypomagnesemia, vitamin B12 and iron
malabsorption (acid required for absorption), atrophic gastritis, and chronic kidney disease. These risks
are why PPIs should be used at the lowest effective dose for the shortest duration necessary. They are not
risk-free indefinitely.
7. What are the two most common causes of peptic ulcer disease (PUD)?
A. Stress and spicy foods
B. H. pylori infection and NSAIDs
C. Alcohol and caffeine
D. Genetic factors and autoimmune disease
CORRECT ANSWER B — H. pylori infection and NSAIDs
RATIONALE The two most common causes of PUD are Helicobacter pylori infection (chronic, recurrent ulcers) and
NSAID use (often silent until bleeding occurs). Other causes include stress-related mucosal damage (ICU
patients), Zollinger-Ellison syndrome (gastrinoma), and smoking (mucosal injury, decreased protective
prostaglandins, increased pepsin). Stress and spicy foods are not primary causes of PUD. Alcohol, caffeine,
and genetics play lesser roles compared to H. pylori and NSAIDs.
, 8. What is the treatment for H. pylori using concomitant therapy?
A. PPI alone for 8 weeks
B. PPI plus 2 antibiotics (from metronidazole, amoxicillin, clarithromycin) for 1-2 weeks — approximately 90% cure
rate
C. H2RA plus antacid as needed
D. Single antibiotic therapy for 3 days
CORRECT ANSWER B — PPI plus 2 antibiotics for 1-2 weeks — approximately 90% cure rate
RATIONALE H. pylori concomitant therapy combines a PPI with 2 of the following antibiotics: metronidazole,
amoxicillin, clarithromycin. One-week treatment achieves approximately 90% cure rate. Bismuth
quadruple therapy (PPI + bismuth + tetracycline + metronidazole for 10-14 days) is effective for
clarithromycin-resistant infections. PPI alone or H2RA alone do not eradicate H. pylori. Single antibiotic
therapy is inadequate and promotes resistance. H. pylori eradication requires combination antibiotic
therapy with acid suppression.
9. What is the mechanism of action of metformin in Type 2 Diabetes?
A. Stimulates insulin release from pancreatic beta cells
B. Decreases hepatic glucose production and increases peripheral insulin sensitivity
C. Blocks renal glucose reabsorption
D. Increases glucagon secretion
CORRECT ANSWER B — Decreases hepatic glucose production and increases peripheral insulin sensitivity
RATIONALE Metformin's primary mechanism is decreasing hepatic gluconeogenesis (major effect) and increasing
peripheral insulin sensitivity, which lowers fasting glucose levels. It treats the root problem of Type 2 DM
(insulin resistance) rather than forcing insulin secretion. It does NOT stimulate insulin release (that is
sulfonylureas), does not block renal glucose reabsorption (that is SGLT2 inhibitors), and does not increase
glucagon. The UKPDS study showed metformin reduced cardiovascular events in T2DM — one of the few
glucose-lowering agents with demonstrated CV benefit.
1 MAXE · 335 GSN
★ ★
Rx College of Nursing — Advanced Practice
PHARM
PHARMACOLOGY · CLINICAL REASONING · SAFE PRESCRIBING
NSG 533 Advanced Pharmacology — Exam 1 Comprehensive Review
G E R D/ P U D , D I A B E T E S , T H Y R O I D , CO N T RAC E PT I O N , M E N O PAUS E , B P H / E D , A N T I D E P R E SS A N TS ,
A N X I O LYT I CS , I N S O M N I A & P R E G N A N CY S A F E TY
INSTITUTION Graduate Nursing Program PROGRAM MSN — Advanced Practice Registered Nurse
COURSE CODE NSG 533 COURSE TITLE Advanced Pharmacology Across the Lifespan
ACADEMIC YEAR EXAM TITLE NSG 533 Advanced Pharm Exam 1 —
Comprehensive Review
TOTAL QUESTIONS 200 Questions FORMAT Multiple Choice — Select the Single Best Answer
EXAMINATION INSTRUCTIONS
▸ Select the single best answer for each question.
▸ Content spans GERD/PUD, diabetes mellitus, thyroid disorders, contraception, menopause/HRT, BPH/ED, antidepressants,
anxiolytics, insomnia, and pregnancy medication safety.
▸ Questions reflect NSG 533 Advanced Pharmacology Exam 1 content and competency expectations.
▸ Correct answers and clinical rationales appear below each question for comprehensive test preparation.
▸ Questions have been randomized to promote active recall and simulate authentic testing conditions.
SECTION I — NSG 533 ADVANCED PHARMACOLOGY COMPREHENSIVE
Questions 1 – 200
EXAMINATION
1. What is the underlying pathophysiology of GERD?
A. Overproduction of gastric acid with normal LES function
B. Lower esophageal sphincter dysfunction including transient relaxations and low tone, often with hiatal hernia,
delayed gastric emptying, or increased intra-abdominal pressure
C. Autoimmune destruction of esophageal mucosa
D. Bacterial infection of the lower esophagus
CORRECT ANSWER B — Lower esophageal sphincter dysfunction including transient relaxations and low tone
RATIONALE GERD results from dysfunction of the lower esophageal sphincter (LES) — including transient relaxations
and low basal tone — that allows gastric contents to reflux into the esophagus. Contributing factors
include hiatal hernia (promotes reflux), delayed gastric emptying, and increased intra-abdominal pressure
(obesity, pregnancy). The injury to esophageal mucosa is caused by acid and pepsin exposure; severity
relates to exposure time and clearance. GERD is not primarily caused by acid overproduction,
autoimmune disease, or infection.
,2. Which of the following worsens GERD by reducing LES tone?
A. Fiber supplements
B. Chocolate, peppermint, caffeine, and fatty meals
C. Proton pump inhibitors
D. H2 receptor antagonists
CORRECT ANSWER B — Chocolate, peppermint, caffeine, and fatty meals
RATIONALE Multiple dietary and lifestyle factors reduce LES tone and worsen GERD: chocolate, peppermint (relaxes
LES), caffeine, alcohol, smoking, obesity, late meals, and large/fatty meals. Medications that worsen GERD
include anticholinergics, calcium channel blockers, nitrates, theophylline, and progesterone. PPIs and
H2RAs are treatments for GERD — they do not worsen it. Fiber supplements are generally neutral or
beneficial for GI health.
3. What are ALARM symptoms in GERD that warrant endoscopy rather than an empiric PPI trial?
A. Mild heartburn occurring less than once weekly
B. Dysphagia, odynophagia, weight loss, and GI bleed/anemia
C. Occasional regurgitation after large meals
D. Chronic cough that improves with antacids
CORRECT ANSWER B — Dysphagia, odynophagia, weight loss, and GI bleed/anemia
RATIONALE ALARM symptoms in GERD indicate potential complications (malignancy, stricture, erosive disease,
bleeding) and require prompt endoscopy, NOT an empiric OTC trial. These include: dysphagia (difficulty
swallowing), odynophagia (painful swallowing), unintentional weight loss, and GI bleeding/anemia.
Uncomplicated GERD (typical heartburn, regurgitation without alarm features) may be managed with an
8-week empiric PPI trial. Mild, infrequent symptoms do not require endoscopy. Chronic cough is an
atypical GERD symptom but alone does not mandate endoscopy.
4. Why is self-directed OTC GERD therapy limited to 2 weeks?
A. PPIs lose effectiveness after 2 weeks of continuous use
B. To avoid masking ALARM symptoms such as cancer, erosive disease, bleeding, and strictures
C. Antacids cause irreversible kidney damage after 14 days
D. GERD always resolves spontaneously within 2 weeks
CORRECT ANSWER B — To avoid masking ALARM symptoms such as cancer, erosive disease, bleeding, and strictures
RATIONALE OTC GERD therapy is limited to 2 weeks to prevent patients from self-medicating for prolonged periods
without appropriate diagnostic evaluation. Persistent symptoms beyond 2 weeks may indicate more
serious underlying pathology (malignancy, erosive esophagitis, stricture, bleeding) that requires
endoscopy. PPIs do not lose effectiveness at 2 weeks. Antacids do not cause irreversible kidney damage
with short-term use. GERD is typically a chronic condition that does not resolve spontaneously.
,5. Which PPI is preferred for patients taking clopidogrel due to fewer drug interactions?
A. Omeprazole
B. Pantoprazole
C. Esomeprazole
D. Lansoprazole
CORRECT ANSWER B — Pantoprazole
RATIONALE Pantoprazole is the preferred PPI for patients on clopidogrel because it has the fewest CYP450 drug
interactions, particularly minimal CYP2C19 inhibition. Omeprazole and esomeprazole significantly inhibit
CYP2C19, which decreases clopidogrel activation and may reduce its antiplatelet efficacy — this is an FDA-
warned interaction. Lansoprazole also has CYP2C19 inhibition. For any patient on clopidogrel requiring a
PPI, pantoprazole is the safest choice to maintain clopidogrel's therapeutic effect.
6. What are the long-term risks of PPI therapy?
A. Only mild headache and transient nausea
B. Increased risk of fractures, pneumonia, C. difficile infection, hypomagnesemia, B12/iron malabsorption, atrophic
gastritis, and kidney disease
C. PPIs have no long-term risks — they are safe indefinitely
D. Only increased risk of weight gain and diabetes
CORRECT ANSWER B — Increased risk of fractures, pneumonia, C. diff, hypomagnesemia, B12/iron malabsorption,
atrophic gastritis, and kidney disease
RATIONALE Long-term PPI use is associated with multiple risks — mnemonic "Bad Bones & Bugs": fractures
(especially postmenopausal women from calcium malabsorption), pneumonia (reduced gastric acid
barrier), C. difficile infection (altered gut microbiome), hypomagnesemia, vitamin B12 and iron
malabsorption (acid required for absorption), atrophic gastritis, and chronic kidney disease. These risks
are why PPIs should be used at the lowest effective dose for the shortest duration necessary. They are not
risk-free indefinitely.
7. What are the two most common causes of peptic ulcer disease (PUD)?
A. Stress and spicy foods
B. H. pylori infection and NSAIDs
C. Alcohol and caffeine
D. Genetic factors and autoimmune disease
CORRECT ANSWER B — H. pylori infection and NSAIDs
RATIONALE The two most common causes of PUD are Helicobacter pylori infection (chronic, recurrent ulcers) and
NSAID use (often silent until bleeding occurs). Other causes include stress-related mucosal damage (ICU
patients), Zollinger-Ellison syndrome (gastrinoma), and smoking (mucosal injury, decreased protective
prostaglandins, increased pepsin). Stress and spicy foods are not primary causes of PUD. Alcohol, caffeine,
and genetics play lesser roles compared to H. pylori and NSAIDs.
, 8. What is the treatment for H. pylori using concomitant therapy?
A. PPI alone for 8 weeks
B. PPI plus 2 antibiotics (from metronidazole, amoxicillin, clarithromycin) for 1-2 weeks — approximately 90% cure
rate
C. H2RA plus antacid as needed
D. Single antibiotic therapy for 3 days
CORRECT ANSWER B — PPI plus 2 antibiotics for 1-2 weeks — approximately 90% cure rate
RATIONALE H. pylori concomitant therapy combines a PPI with 2 of the following antibiotics: metronidazole,
amoxicillin, clarithromycin. One-week treatment achieves approximately 90% cure rate. Bismuth
quadruple therapy (PPI + bismuth + tetracycline + metronidazole for 10-14 days) is effective for
clarithromycin-resistant infections. PPI alone or H2RA alone do not eradicate H. pylori. Single antibiotic
therapy is inadequate and promotes resistance. H. pylori eradication requires combination antibiotic
therapy with acid suppression.
9. What is the mechanism of action of metformin in Type 2 Diabetes?
A. Stimulates insulin release from pancreatic beta cells
B. Decreases hepatic glucose production and increases peripheral insulin sensitivity
C. Blocks renal glucose reabsorption
D. Increases glucagon secretion
CORRECT ANSWER B — Decreases hepatic glucose production and increases peripheral insulin sensitivity
RATIONALE Metformin's primary mechanism is decreasing hepatic gluconeogenesis (major effect) and increasing
peripheral insulin sensitivity, which lowers fasting glucose levels. It treats the root problem of Type 2 DM
(insulin resistance) rather than forcing insulin secretion. It does NOT stimulate insulin release (that is
sulfonylureas), does not block renal glucose reabsorption (that is SGLT2 inhibitors), and does not increase
glucagon. The UKPDS study showed metformin reduced cardiovascular events in T2DM — one of the few
glucose-lowering agents with demonstrated CV benefit.
