High-Yield Gastroenterology
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1
What is GERD?
Reflux of gastric contents into the esophagus causing symptoms or complications.
2
What are the two classic symptoms of GERD?
Heartburn and regurgitation.
3
How does GERD-related heartburn present?
Retrosternal burning pain.
4
How does GERD-related regurgitation present?
Bitter or sour taste due to refluxed gastric contents.
5
What is the most common type of hiatal hernia associated with GERD?
Sliding hiatal hernia.
6
How does hiatal hernia contribute to GERD?
Disrupts the antireflux barrier and promotes LES dysfunction.
7
What is the primary physiological abnormality in GERD?
Transient relaxation or decreased tone of the lower esophageal sphincter (LES).
8
How does obesity contribute to GERD?
Increases intra-abdominal pressure.
9
How does pregnancy contribute to GERD?
Progesterone decreases LES tone and the gravid uterus increases gastric pressure.
10
Which medications can decrease LES tone?
Nitrates, calcium channel blockers, and anticholinergics.
11
How does smoking contribute to GERD?
Decreases LES tone.
12
How does alcohol contribute to GERD?
Relaxes the LES.
13
What foods commonly aggravate GERD?
High-fat and fried foods.
14
What are common extraesophageal manifestations of GERD?
Chronic cough, asthma, hoarseness, and chronic laryngitis.
15
What is the initial diagnostic approach for uncomplicated GERD?
Clinical diagnosis based on typical symptoms.
16
Is endoscopy routinely required for uncomplicated GERD?
No.
17
What is the role of an empiric PPI trial in GERD?
Supports the diagnosis through symptom improvement.
18
What are the alarm symptoms of GERD?
Dysphagia, odynophagia, weight loss, anemia, GI bleeding, and recurrent vomiting.
19
When is upper endoscopy indicated in GERD?
Alarm symptoms or refractory symptoms.
20
What does ambulatory pH monitoring measure?
Esophageal acid exposure.
21
What does impedance-pH monitoring detect?
Acid and non-acid reflux.
22
What is the initial treatment for erosive esophagitis?
Standard-dose PPI once daily for 8 weeks.
23
When should PPIs be taken?
30–60 minutes before meals.
24
What is the general principle when prescribing PPIs?
Use the lowest effective dose.
25
What should be done when GERD symptoms persist despite once-daily PPI?
Check adherence and timing, then consider twice-daily dosing or switching PPIs.
26
What is the role of alginate-antacid therapy in GERD?
Provides rapid relief of episodic and postprandial symptoms.
27
When are H2-receptor blockers useful in GERD?
Intermittent symptom control or when PPIs are not tolerated.
28
What is the most common mucosal complication of GERD?
Erosive esophagitis
29
What are complications of erosive esophagitis?
Bleeding and peptic stricture.
30
How does peptic esophageal stricture commonly present?
Progressive dysphagia to solids.
31
What is Barrett's esophagus?
Replacement of distal esophageal squamous epithelium with intestinalized columnar epithelium.
32
What is the characteristic endoscopic appearance of Barrett's esophagus?
Salmon-pink velvety mucosa
33
What is the major complication of Barrett's esophagus?
Esophageal adenocarcinoma.
34
What is the only recognized precursor lesion of esophageal adenocarcinoma?
Barrett's esophagus
35
What histologic finding confirms intestinal metaplasia in Barrett's esophagus?
Goblet cells.
36
What is the strongest clinical predictor of neoplastic progression in Barrett's esophagus?
Longer Barrett's segment.
37
What are important risk factors for Barrett's esophagus?
Chronic GERD, male sex, obesity, advanced age, and central adiposity.
38
What is the progression risk of Barrett's esophagus to adenocarcinoma per year?
Approximately 0.1–0.3%.
39
What defines short-segment Barrett's esophagus?
Length less than 3 cm.
40
What defines long-segment Barrett's esophagus?
Length of at least 3 cm.
41
How is nondysplastic Barrett's esophagus managed?
Endoscopic surveillance.
42
How is Barrett's esophagus with high-grade dysplasia managed?
Endoscopic eradication therapy, usually ablation.
43
How is indefinite-for-dysplasia Barrett's esophagus initially managed?
Optimize acid suppression and repeat endoscopy.
44
What is non-erosive reflux disease (NERD)?
Typical GERD symptoms without visible esophageal mucosal injury on endoscopy.
45
What is the usual treatment for NERD?
PPI therapy.
46
What is refractory GERD?
Persistent symptoms despite compliant twice-daily PPI therapy for at least 8 weeks.
47
What should be checked before diagnosing refractory GERD?
Medication adherence, correct timing, and adequate dosing.
48
What test is useful when endoscopy is normal in refractory GERD?
Ambulatory reflux monitoring.
49
What is the mechanism of baclofen in refractory GERD?
Reduces transient LES relaxations.
50
What is fundoplication?
Wrapping the proximal stomach around the distal esophagus to reinforce the antireflux barrier.
51
What are complications of fundoplication?
Dysphagia, bloating, and gas-bloat syndrome.
52
What tests should be performed before fundoplication?
Esophageal manometry and ambulatory reflux testing.
53
How long should patients avoid lying down after meals to reduce GERD?
At least 3 hours.
54
What lifestyle modification helps nocturnal GERD?
Elevating the head of the bed.
55
What is peptic ulcer disease (PUD)?
A mucosal defect in the stomach or duodenum caused by acid-pepsin injury.
56
What is the endoscopic definition of an ulcer?
A mucosal break greater than 5 mm.
57
What is the endoscopic definition of an erosion?
A mucosal break smaller than 5 mm.
58
What are the two major causes of PUD?
H. pylori infection and NSAID use
59
What is the most common infectious cause of PUD?
Helicobacter pylori
60
How is H. pylori transmitted?
Oral-oral and fecal-oral routes.
61
What are the major risk factors for H. pylori infection?
Crowding, poor sanitation, and low socioeconomic status.
62
How do NSAIDs cause peptic ulcers?
Inhibit prostaglandin synthesis and cause direct mucosal injury.
63
What happens when gastric prostaglandins decrease?
Reduced mucus and bicarbonate secretion, impaired mucosal blood flow, and decreased epithelial repair.
64
How does smoking affect PUD?
Increases acid secretion, impairs mucosal defenses, and delays ulcer healing.
65
Does alcohol commonly cause PUD by itself?
No; it can aggravate mucosal injury.
66
What is Zollinger-Ellison syndrome?
A gastrin-secreting tumor causing excessive gastric acid secretion.
67
What is the characteristic ulcer pattern in Zollinger-Ellison syndrome?
Multiple or refractory peptic ulcers.
68
What additional symptom commonly occurs in Zollinger-Ellison syndrome?
Diarrhea.
69
What is the most frequent physical examination finding in PUD?
Epigastric tenderness
70
What does a board-like abdomen suggest in a patient with PUD?
Perforation.
71
What does a succussion splash suggest in PUD?
Gastric outlet obstruction.
72
How does gastric ulcer pain relate to meals?
Often worsens after eating.
73
How does duodenal ulcer pain relate to meals?
Improves with food and returns 90 minutes to 3 hours later.
74
Which ulcer is more associated with nocturnal pain?
Duodenal ulcer.
75
Which ulcer is more associated with early satiety and weight loss?
Gastric ulcer.
76
Which ulcer has a greater concern for malignancy?
Gastric ulcer.
77
Why must gastric ulcers be biopsied?
To exclude gastric malignancy.
78
Where are most duodenal ulcers located?
First portion of the duodenum (D1).
79
What is the usual acid output in gastric ulcer disease?
Normal or decreased.
80
What is the usual acid output in duodenal ulcer disease?
Increased basal and nocturnal acid secretion.
81
What is the primary pathophysiologic problem in gastric ulcers?
Impaired mucosal defenses.
82
What is the most common complication of PUD?
Gastrointestinal bleeding
83
What is the second most common complication of PUD?
Perforation.
84
What is the classic presentation of perforated PUD?
Sudden severe abdominal pain with tachycardia and abdominal rigidity.
85
What is ulcer penetration?
Extension of an ulcer into an adjacent organ without free perforation.
86
Where do posterior duodenal ulcers commonly penetrate?
Pancreas.
87
What is the least common major complication of PUD?
Gastric outlet obstruction.
88
What causes gastric outlet obstruction in PUD?
Inflammatory edema or scar formation near the pylorus.
89
What are the clinical manifestations of gastric outlet obstruction?
Early satiety, postprandial vomiting, nausea, and weight loss.
90
What is the gold standard diagnostic test for PUD?
Upper gastrointestinal endoscopy (EGD)
91
What is the major advantage of EGD in PUD?
Direct visualization and biopsy of ulcers.
92
What is the most common invasive test for H. pylori?
Rapid urease test.
93
What is the best noninvasive test for active H. pylori infection?
Urea breath test
94
What is the sensitivity of the urea breath test?
Greater than 95%.
95
What does the urea breath test detect?
Active H. pylori infection through urease activity.
96
What isotopes are used in the urea breath test?
$^13C$ or $^14C$ urea.
97
What is another noninvasive test for active H. pylori infection?
Stool antigen test.
98
Can stool antigen testing confirm H. pylori eradication?
Yes.
99
Why is H. pylori antibody testing unsuitable for confirming eradication?
Antibodies may remain positive after the infection has resolved.
100
How long should PPIs generally be withheld before H. pylori testing?
At least 2 weeks before urea breath or stool antigen testing.
101
What are the three main treatment goals of PUD?
Symptom relief, ulcer healing, and prevention of recurrence and complications.
102
What are the components of standard H. pylori triple therapy?
PPI, clarithromycin, and amoxicillin.
103
How long is standard H. pylori triple therapy?
14 days.
104
What replaces amoxicillin in triple therapy for penicillin-allergic patients?
Metronidazole.
105
What does OCA represent in H. pylori treatment?
Omeprazole, clarithromycin, and amoxicillin.
106
What are the components of bismuth quadruple therapy?
PPI, bismuth, metronidazole, and tetracycline.
107
How long is bismuth quadruple therapy?
10–14 days.
108
What does TOMB represent in H. pylori treatment?
Tetracycline, omeprazole, metronidazole, and bismuth.
109
When should H. pylori eradication be confirmed?
At least 4 weeks after antibiotic therapy.
110
Which tests are recommended for confirming H. pylori eradication?
Urea breath test or stool antigen test.
111
Is serology appropriate for confirming H. pylori eradication?
No.
112
What is the first step in managing NSAID-induced ulcers?
Discontinue NSAIDs if possible.
113
What is the preferred treatment for NSAID-induced ulcers?
Proton pump inhibitors.
114
What is the most effective medication for preventing NSAID-induced ulcers?
Proton pump inhibitors
115
What is misoprostol?
A prostaglandin analog that protects gastric mucosa.
116
What is a common adverse effect of misoprostol?
Diarrhea.
117
What is an advantage of selective COX-2 inhibitors?
Lower gastrointestinal injury than nonselective NSAIDs.
118
What is an example of a selective COX-2 inhibitor?
Celecoxib.
119
What is a major cardiovascular risk of COX-2 inhibitors?
Increased risk of myocardial infarction and stroke.
120
When should repeat EGD be performed for gastric ulcers?
After 8–12 weeks to confirm healing.
121
When is a gastric ulcer considered refractory?
Failure to heal after 12 weeks.
122
When is a duodenal ulcer considered refractory?
Failure to heal after 8 weeks.
123
What should be excluded in refractory PUD?
Persistent H. pylori, NSAID use, poor adherence, malignancy, and Zollinger-Ellison syndrome.
124
What is spontaneous bacterial peritonitis (SBP)?
Infection of ascitic fluid without an identifiable intra-abdominal source.
125
In which patients does SBP most commonly occur?
Patients with cirrhosis and ascites.
126
What is the diagnostic ascitic fluid PMN threshold for SBP?
At least 250 cells/mm³
127
Can SBP be diagnosed with a negative ascitic fluid culture?
Yes.
128
Is SBP usually monomicrobial or polymicrobial?
Monomicrobial.
129
What are the most common organisms causing SBP?
E. coli and other enteric gram-negative bacilli.
130
What is the preferred empiric antibiotic class for SBP?
Third-generation cephalosporins
131
What is the ceftriaxone dose for SBP?
2 g IV every 24 hours.
132
What is the cefotaxime dose for SBP?
2 g IV every 8 hours.
133
How long is the usual antibiotic treatment for uncomplicated SBP?
At least 5 days.
134
What is the main mechanism of SBP development?
Bacterial translocation from the intestine into ascitic fluid.
135
Which patients qualify for primary SBP prophylaxis?
High-risk cirrhotic patients with low ascitic fluid protein and renal dysfunction or severe liver failure.
136
What ascitic fluid protein level indicates increased SBP risk?
Less than 1.5 g/dL.
137
Who requires secondary SBP prophylaxis?
Patients with a previous episode of SBP.
138
What is the recurrence risk of SBP without secondary prophylaxis?
Up to 70% within 1 year.
139
What antibiotics are used for secondary SBP prophylaxis?
Norfloxacin, ciprofloxacin, or trimethoprim-sulfamethoxazole.
140
How long should cirrhotic patients with GI bleeding receive antibiotic prophylaxis?
7 days.
141
What is secondary peritonitis?
Peritoneal infection caused by an identifiable intra-abdominal source.
142
What are common causes of secondary peritonitis?
Perforated appendicitis, diverticulitis, perforated PUD, bowel ischemia, and anastomotic leakage.
143
Is secondary peritonitis usually monomicrobial or polymicrobial?
Polymicrobial.
144
What organisms commonly cause secondary peritonitis?
Enteric gram-negative bacilli and anaerobes, especially E. coli and Bacteroides.
145
What is the cornerstone of secondary peritonitis management?
Source control
146
What procedures achieve source control in secondary peritonitis?
Surgery, drainage, debridement, or repair of the underlying lesion.
147
Why are antibiotics alone inadequate for secondary peritonitis?
They do not eliminate the source of contamination.
148
What organisms must empiric secondary peritonitis antibiotics cover?
Gram-negative bacilli and anaerobes.
149
What is an empiric antibiotic regimen for community-acquired secondary peritonitis?
Ceftriaxone plus metronidazole.
150
What is the typical antibiotic duration after adequate source control in secondary peritonitis?
4–7 days.
151
What is CAPD-associated peritonitis?
Peritoneal infection occurring as a complication of continuous ambulatory peritoneal dialysis.
152
What dialysate WBC count supports CAPD-associated peritonitis?
Greater than 100 WBCs/µL with more than 50% PMNs.
153
What is the characteristic appearance of dialysate in CAPD peritonitis?
Cloudy dialysate.
154
What organisms commonly cause CAPD-associated peritonitis?
Staphylococcus aureus and coagulase-negative staphylococci.
155
What is the preferred route of antibiotic administration for CAPD peritonitis?
Intraperitoneal administration.
156
What organisms must empiric CAPD peritonitis treatment cover?
Gram-positive and gram-negative bacteria.
157
What antibiotic provides empiric MRSA coverage in CAPD peritonitis?
Vancomycin.
158
What is the recommended treatment for fungal CAPD-associated peritonitis?
Immediate catheter removal plus antifungal therapy
159
When should catheter removal be considered in bacterial CAPD peritonitis?
Refractory or relapsing infection.
160
What is an intra-abdominal abscess?
A localized collection of pus within the abdominal cavity or an abdominal organ.
161
What is the most common anaerobe isolated from intra-abdominal infections?
Bacteroides fragilis
162
What is the preferred imaging modality for intra-abdominal abscesses?
Abdominal CT scan
163
What is the main advantage of CT in abscess diagnosis?
Identifies the location, size, and extent of the abscess and guides drainage.
164
What is the cornerstone of intra-abdominal abscess treatment?
Drainage and source control.
165
What organisms should empiric intra-abdominal abscess antibiotics cover?
Aerobic gram-negative bacilli and anaerobes.
166
What is a common empiric antibiotic regimen for intra-abdominal abscess?
Piperacillin-tazobactam or ceftriaxone plus metronidazole.
167
What is the most common reason for intra-abdominal abscess treatment failure?
Inadequate drainage or failure to achieve source control.
168
How long are antibiotics generally continued after adequate abscess drainage?
Approximately 4–5 days.
169
What is the most commonly affected visceral organ in intra-abdominal abscesses?
Liver
170
What is the most common source of hepatic abscess?
Biliary tract disease.
171
What is the most common presenting feature of hepatic abscess?
Fever.
172
What is the most reliable diagnostic method for hepatic abscess?
Imaging.
173
What is the preferred imaging modality for hepatic abscess?
Contrast-enhanced abdominal CT.
174
What is the most reliable laboratory abnormality in hepatic abscess?
Elevated alkaline phosphatase.
175
What is the most common organism associated with hepatic abscess in Southeast Asia?
Klebsiella pneumoniae
176
What organism causes amebic liver abscess?
Entamoeba histolytica.
177
What is the mainstay of hepatic abscess treatment?
Drainage plus antimicrobial therapy.
178
What is the first-line drainage method for hepatic abscess?
Image-guided percutaneous drainage.
179
What type of catheter is commonly used for percutaneous hepatic abscess drainage?
Pigtail catheter.
180
When may hepatic abscess be treated with antibiotics alone?
Selected stable patients with small abscesses under 3 cm.
181
When is surgical drainage considered for hepatic abscess?
Large or multiple abscesses, unsuitable percutaneous drainage, associated surgical disease, or failed treatment.
182
What is a splenic abscess?
A localized infection and pus collection within the spleen.
183
What is the most common route of infection in splenic abscess?
Hematogenous spread
184
What infection is commonly associated with splenic abscess?
Infective endocarditis.
185
What is the most common clinical manifestation of splenic abscess?
Fever.
186
What is the most sensitive imaging modality for splenic abscess?
Abdominal CT scan.
187
What is the traditional standard treatment for splenic abscess?
Splenectomy plus antibiotics.
188
When may percutaneous drainage be considered for splenic abscess?
Single small abscesses or patients at high surgical risk.
189
Which vaccines are needed after splenectomy?
Pneumococcal, Haemophilus influenzae type B, and meningococcal vaccines.
190
When should vaccines be administered before elective splenectomy?
At least 2 weeks before surgery.
191
What is a renal abscess?
A localized collection of pus within the renal parenchyma.
192
What is a perinephric abscess?
An abscess located around the kidney within the perirenal space.
193
What is the most common source of renal and perinephric abscesses?
Ascending urinary tract infection.
194
What is the most important risk factor for renal and perinephric abscesses?
Nephrolithiasis with urinary obstruction
195
What is the most common pathogen in renal and perinephric abscesses?
Escherichia coli.
196
Which organism produces urease and promotes struvite stone formation?
Proteus species.
197
Which organism suggests hematogenous renal abscess, particularly with endocarditis?
Staphylococcus aureus.
198
What are the common manifestations of renal or perinephric abscess?
Fever and flank pain.
199
When should renal abscess be suspected in a patient treated for pyelonephritis?
Persistent fever after 4–5 days of appropriate therapy.
200
What is the most useful diagnostic modality for renal or perinephric abscess?
Contrast-enhanced abdominal CT.
201
What is the characteristic CT appearance of a renal abscess?
Hypodense intraparenchymal lesion with an enhancing rim.
202
What is the usual drainage treatment for perinephric abscess?
Percutaneous drainage.
203
What is the usual antibiotic duration for renal or perinephric abscess?
2–4 weeks, depending on clinical response and source control.
204
What underlying problems must be addressed in renal abscess?
Urinary obstruction and nephrolithiasis.
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