NSG 533 ADVANCED PHARMACOLOGY EXAM 1 | COMPLETE QUESTIONS WITH
EXPERT SOLUTIONS|2026-2027 LATEST UPDATED| | GET A+
1. GERD physiology: Lower esophageal sphincter dysfunction (LES)- transient relaxtions, low tone Hiatal
hernia=promotes reflux
Delayed gastric emptying/increased intra ab pressure: obesity, pregnancy
Injury is from acid+pepsin exposure to esophageal mucosa-severity relates to exposure time +clearance
2. What worsens GERD: ETOH, smoking, obesity, late meals, large/fatty meals
caffeine, chocolate/peppermint may reduce LES tone- Peppermint may worsen reflux by relaxing LES
MEDS that worsen: anticholinergics, CCB, nitrates, theophylline, progesterone
3. symptoms of GERD: typical: heartburn, regurgitation atypical: chronic cough, hoarseness, asthma like
symptoms
ALARM: dysphagia, odynophagia, wt loss, GI bleed anemia alarm=
endoscopy, not OTC trial
4. when to test vs tx GERD: uncomplicated GERD-> empiric PPI trial 8 wk
Alarm or refractory GERD--> EGD
Persistent symptoms despite PPI--> pH monitioring, manometry
5. PPI risks: Increased risk of fractures (postmenopausal women) pneumonia, C diff, hypomagnesemia, B12
and iron malabsorption, atrophic gastritis, kidney disease
,6. Non-pharm interventions for all GI conditions: Diet+trigger: greasy/spicy foods, ETOH, caffeine;
lactose/FODMAPS is IBS type symptoms hydration tobacco cessation wt mgmt
meds reveiw: remove/replace offending meds when possible- NSAIDs, iron, opiods, anticholinergics.
When to refer/escalate: alarm symptoms (GI bleed, wt loss, progressive dysphagia, severe dehydration, persistent
vomiting, severe ab pain
7. GERD pharmacology: Antacids-PRN fastest relief neutralize acid: short duration
counseling: separate from other meds (chelation/absorption issues)
TUMS (calcium carbonate): highest acid neutralizing, rapid
Risks: hypercalcemia, constipation (Al), kidney stones (Ca), diarrhea (Mg)
H2 receptor antagonist (H2RAs)
good for mild/intermittent symptoms, nocturnal symptoms less
potent that PPIs for healing/maintenance of erosive disease
PEPCID (famotidine): most potent, +Nocturnal, fewer interactions than cimetidine (CYP), longer duration of action,
min CNS effects
PPIs
MOST effective acid suppression + best for esophagitis healing and maintenance
Take before meals (30-60 min before breakfast)
PANTOPRAZOLE (safest): preferred when on clopidogrel, fewer interactions
OMEPRAZOLE/ESOMEPRAZOLE: most potent, part of H.pylori regimen--decreases clopidogrel activation
-long term PPI-Bad bones & bugs (fractures, cdiff, low mg/b12)
Mild intermittent symptoms? Antacid or H2RA’
Erosive GERD or ulcers? PPI’
,On clopidogrel? Pantoprazole’
Needs rapid relief? Antacid’
Needs healing? PPI’
8. Why is self directed GERD therapy (OTC) limited to 2 weeks: avoid masking ALarm symptoms: cancer,
erosive disease, bleeding, strictures
prevent inappropriate, prolonged used without diagnosis/monitoring
9. PUD causes: MOST COMMON
H. pylori (chronic, recurrent)
NSAIDs (often silent--> bleed)
Stress-related mucosal damage (SRMD) (ICU patients)
Other:
Zollinger-Ellison (gastrinoma)
smoking-mucosal injury, decreases protective prostaglandins, increases pepsin)
10. Zollinger-Ellison Syndrome (ZES): ZES --> Peptic Ulcer Disease
Pathophys = gastrin-secreting tumors (gastrinomas) within GI tract --> hypersecretion of gastric acid
FOILS:
(1) Pheochromocytoma --> HTN
(2) Carcinoid Syndrome --> tricuspid and pulmonary valve abnormalities, flushing, bronchoconstriction, severe
diarrhea
11. Risk factors for NSAID ulcer: >65 yo anticoagulants
coagulopathy steroids prior PUD/bleed comormid disease
, multiple NSAIDs (including
ASA) long duration high dose
12. Prevention of NSAID ulcer if NSAID must continue: PPI
prophylaxis (standard dose 4-8 wks): reduces risk and better tolerated
than misoprostol
Misoprostol: 200mcg QID prevents complications but has lots of GI side effects and CONTRAINDICATED
PREGNANCY
H2RAs: less effective
13. NSAID induced ulcer treatment: * test for H pylori * dc the
NSAID
* PPI, H2RA, or sucralfate should be initiated
SUE COATS ULCERS (binds everything->separate meds)
if NSAID cant be stopped= NSAID+PPI
14. What is H. pylori?: common cause of gastric and duodenal ulcers. PUD
15. H. pylori treatment concomitant therapy: PPI + 2 of the following antibiotics Metronidazole Amoxicillin
Clarithromycin
One week treatment: 90% cure rate
Two weeks of PPI + 1 antibiotic (typically clarithromycin): 10-20% lower cure rate
MHD notes:
--Tetracycline can be 1 of the 2 antibiotics
--Bismuth salts, doxycycline, and metronidazole for 14 days is cheap and effective
EXPERT SOLUTIONS|2026-2027 LATEST UPDATED| | GET A+
1. GERD physiology: Lower esophageal sphincter dysfunction (LES)- transient relaxtions, low tone Hiatal
hernia=promotes reflux
Delayed gastric emptying/increased intra ab pressure: obesity, pregnancy
Injury is from acid+pepsin exposure to esophageal mucosa-severity relates to exposure time +clearance
2. What worsens GERD: ETOH, smoking, obesity, late meals, large/fatty meals
caffeine, chocolate/peppermint may reduce LES tone- Peppermint may worsen reflux by relaxing LES
MEDS that worsen: anticholinergics, CCB, nitrates, theophylline, progesterone
3. symptoms of GERD: typical: heartburn, regurgitation atypical: chronic cough, hoarseness, asthma like
symptoms
ALARM: dysphagia, odynophagia, wt loss, GI bleed anemia alarm=
endoscopy, not OTC trial
4. when to test vs tx GERD: uncomplicated GERD-> empiric PPI trial 8 wk
Alarm or refractory GERD--> EGD
Persistent symptoms despite PPI--> pH monitioring, manometry
5. PPI risks: Increased risk of fractures (postmenopausal women) pneumonia, C diff, hypomagnesemia, B12
and iron malabsorption, atrophic gastritis, kidney disease
,6. Non-pharm interventions for all GI conditions: Diet+trigger: greasy/spicy foods, ETOH, caffeine;
lactose/FODMAPS is IBS type symptoms hydration tobacco cessation wt mgmt
meds reveiw: remove/replace offending meds when possible- NSAIDs, iron, opiods, anticholinergics.
When to refer/escalate: alarm symptoms (GI bleed, wt loss, progressive dysphagia, severe dehydration, persistent
vomiting, severe ab pain
7. GERD pharmacology: Antacids-PRN fastest relief neutralize acid: short duration
counseling: separate from other meds (chelation/absorption issues)
TUMS (calcium carbonate): highest acid neutralizing, rapid
Risks: hypercalcemia, constipation (Al), kidney stones (Ca), diarrhea (Mg)
H2 receptor antagonist (H2RAs)
good for mild/intermittent symptoms, nocturnal symptoms less
potent that PPIs for healing/maintenance of erosive disease
PEPCID (famotidine): most potent, +Nocturnal, fewer interactions than cimetidine (CYP), longer duration of action,
min CNS effects
PPIs
MOST effective acid suppression + best for esophagitis healing and maintenance
Take before meals (30-60 min before breakfast)
PANTOPRAZOLE (safest): preferred when on clopidogrel, fewer interactions
OMEPRAZOLE/ESOMEPRAZOLE: most potent, part of H.pylori regimen--decreases clopidogrel activation
-long term PPI-Bad bones & bugs (fractures, cdiff, low mg/b12)
Mild intermittent symptoms? Antacid or H2RA’
Erosive GERD or ulcers? PPI’
,On clopidogrel? Pantoprazole’
Needs rapid relief? Antacid’
Needs healing? PPI’
8. Why is self directed GERD therapy (OTC) limited to 2 weeks: avoid masking ALarm symptoms: cancer,
erosive disease, bleeding, strictures
prevent inappropriate, prolonged used without diagnosis/monitoring
9. PUD causes: MOST COMMON
H. pylori (chronic, recurrent)
NSAIDs (often silent--> bleed)
Stress-related mucosal damage (SRMD) (ICU patients)
Other:
Zollinger-Ellison (gastrinoma)
smoking-mucosal injury, decreases protective prostaglandins, increases pepsin)
10. Zollinger-Ellison Syndrome (ZES): ZES --> Peptic Ulcer Disease
Pathophys = gastrin-secreting tumors (gastrinomas) within GI tract --> hypersecretion of gastric acid
FOILS:
(1) Pheochromocytoma --> HTN
(2) Carcinoid Syndrome --> tricuspid and pulmonary valve abnormalities, flushing, bronchoconstriction, severe
diarrhea
11. Risk factors for NSAID ulcer: >65 yo anticoagulants
coagulopathy steroids prior PUD/bleed comormid disease
, multiple NSAIDs (including
ASA) long duration high dose
12. Prevention of NSAID ulcer if NSAID must continue: PPI
prophylaxis (standard dose 4-8 wks): reduces risk and better tolerated
than misoprostol
Misoprostol: 200mcg QID prevents complications but has lots of GI side effects and CONTRAINDICATED
PREGNANCY
H2RAs: less effective
13. NSAID induced ulcer treatment: * test for H pylori * dc the
NSAID
* PPI, H2RA, or sucralfate should be initiated
SUE COATS ULCERS (binds everything->separate meds)
if NSAID cant be stopped= NSAID+PPI
14. What is H. pylori?: common cause of gastric and duodenal ulcers. PUD
15. H. pylori treatment concomitant therapy: PPI + 2 of the following antibiotics Metronidazole Amoxicillin
Clarithromycin
One week treatment: 90% cure rate
Two weeks of PPI + 1 antibiotic (typically clarithromycin): 10-20% lower cure rate
MHD notes:
--Tetracycline can be 1 of the 2 antibiotics
--Bismuth salts, doxycycline, and metronidazole for 14 days is cheap and effective
