GERD/INFECTIOUS ESOPHAGITIS

Question 1

What is the primary cause of esophagitis in patients with gastroesophageal reflux disease (GERD)?

A) Direct caustic injury to the esophageal epithelium
B) Cytokine-mediated inflammatory pathway
C) Infection with Helicobacter pylori
D) Use of nonsteroidal anti-inflammatory drugs (NSAIDs)

Answer 1

Correct Answer: B) Cytokine-mediated inflammatory pathway

Rationale: Experimental evidence suggests that esophagitis in GERD patients is primarily caused by a cytokine-mediated inflammatory pathway, rather than direct caustic injury to the esophageal epithelium from refluxed gastric acid and pepsin.

Question 2

Which of the following is the hallmark feature of esophagitis in GERD patients?

A) Microscopic injury without visible damage
B) Macroscopic erosions and ulcers of the esophageal mucosa
C) Hyperplasia of the esophageal squamous epithelium
D) Development of esophageal adenocarcinoma

Answer 2

Correct Answer: B) Macroscopic erosions and ulcers of the esophageal mucosa

Rationale: Esophagitis in GERD is characterized by macroscopic erosions and ulcers in the esophageal mucosa, which are visible on endoscopic examination. These lesions are the result of the inflammation caused by refluxed gastric contents.

Question 3

In GERD patients, which pathway is most implicated in the development of esophagitis?

A) Direct damage from refluxed acid
B) Bacterial infection of the esophagus
C) Cytokine-mediated inflammatory response
D) T-cell mediated destruction of the esophageal lining

Answer 3

Correct Answer: C) Cytokine-mediated inflammatory response

Rationale: The development of esophagitis in GERD patients is primarily driven by a cytokine-mediated inflammatory pathway, which is supported by experimental evidence, rather than direct caustic injury to the esophageal epithelium.

Question 4

Which of the following is NOT one of the three dominant mechanisms of esophagogastric junction (EGJ) incompetence?

A) Transient lower esophageal sphincter (LES) relaxations
B) LES hypotension
C) Anatomic distortion of the esophagogastric junction
D) Decreased gastric acid production

Answer 4

Correct Answer: D) Decreased gastric acid production

Rationale: The three dominant mechanisms of EGJ incompetence include transient LES relaxations, LES hypotension, and anatomic distortion of the EGJ (such as a hiatal hernia).

Question 5

Which of the following extraesophageal syndromes has an established association with GERD?

A) Pulmonary fibrosis
B) Asthma
C) Sleep apnea
D) Cardiac arrhythmias

Answer 5

Correct Answer: B) Asthma

Rationale: Asthma is one of the extraesophageal syndromes with a well-established association with GERD. Other conditions with established links include chronic cough, laryngitis, and dental erosions.

Question 6

Which condition has only a proposed (not established) association with GERD?

A) Chronic sinusitis
B) Laryngitis
C) Asthma
D) Dental erosions

Answer 6

Correct Answer: A) Chronic sinusitis

Rationale: Chronic sinusitis is among the conditions with a proposed, but not firmly established, association with GERD. Other proposed associations include pharyngitis, pulmonary fibrosis, sleep apnea, and cardiac arrhythmias.

Question 7

What is the endoscopic hallmark of GERD?

A) Barrett’s esophagus
B) Erosive esophagitis at the esophagogastric junction
C) Hiatal hernia
D) Gastric ulcers

Answer 7

Correct Answer: B) Erosive esophagitis at the esophagogastric junction

Rationale: The endoscopic hallmark of GERD is erosive esophagitis at the esophagogastric junction. However, it is identified in only about one-third of GERD patients.

Question 8

Which diagnostic tool can help distinguish among the various etiologies of esophagitis?

A) Barium swallow study
B) Endoscopic appearance and mucosal biopsy
C) CT scan of the abdomen
D) Esophageal manometry

Answer 8

Correct Answer: B) Endoscopic appearance and mucosal biopsy

Rationale: The distinction among etiologies of esophagitis is primarily based on endoscopic appearance. Mucosal biopsies are helpful in evaluating for other causes, such as infectious or eosinophilic esophagitis.

Question 9

Which of the following is the most severe histologic consequence of GERD?

A) Erosive esophagitis
B) Peptic strictures
C) Barrett’s metaplasia
D) Chronic esophagitis

Answer 9

Correct Answer: C) Barrett’s metaplasia

Rationale: Barrett’s metaplasia is the most severe histologic consequence of GERD due to its association with a significantly increased risk of esophageal adenocarcinoma.

Question 10

What is the endoscopic hallmark of Barrett’s esophagus?

A) Salmon-colored mucosa extending proximally from the gastroesophageal junction
B) Ulceration and strictures at the esophagogastric junction
C) White plaques on the esophageal mucosa
D) Nodular masses in the lower esophagus

Answer 10

Correct Answer: A) Salmon-colored mucosa extending proximally from the gastroesophageal junction

Rationale: Barrett’s esophagus is recognized endoscopically by the presence of salmon-colored mucosa extending proximally from the gastroesophageal junction.

Question 11

Barrett’s metaplasia increases the risk of developing which type of cancer?

A) Squamous cell carcinoma of the esophagus
B) Gastric adenocarcinoma
C) Esophageal adenocarcinoma
D) Small cell carcinoma

Answer 11

Correct Answer: C) Esophageal adenocarcinoma

Rationale: Barrett’s metaplasia is associated with a significantly increased risk of esophageal adenocarcinoma, which progresses through intermediate stages of low- and high-grade dysplasia.

Question 12

Which of the following has become less common in the era of potent acid suppression therapy?

A) Barrett’s metaplasia
B) Erosive esophagitis
C) Esophageal adenocarcinoma
D) Low-grade dysplasia

Answer 12

Correct Answer: B) Erosive esophagitis

Rationale: Potent antisecretory medications have made erosive esophagitis and peptic strictures increasingly rare, although the incidence of Barrett’s esophagus and esophageal adenocarcinoma has increased.

Question 13

What is the current recommended treatment for high-grade dysplasia in Barrett’s esophagus?

A) Esophagectomy
B) Endoscopic mucosal ablation therapy
C) Proton pump inhibitors (PPIs) alone
D) Chemotherapy

Answer 13

Correct Answer: B) Endoscopic mucosal ablation therapy

Rationale: Current guidelines recommend endoscopic mucosal ablation therapy as the standard treatment for high-grade dysplasia in Barrett’s esophagus, as it is effective and associated with less morbidity and mortality compared to esophagectomy.

Question 14

What is the typical progression of Barrett’s metaplasia to esophageal adenocarcinoma?

A) Barrett’s metaplasia → Ulceration → Adenocarcinoma
B) Barrett’s metaplasia → Low-grade dysplasia → High-grade dysplasia → Adenocarcinoma
C) Barrett’s metaplasia → Stricture formation → Adenocarcinoma
D) Barrett’s metaplasia → Chronic esophagitis → Adenocarcinoma

Answer 14

Correct Answer: B) Barrett’s metaplasia → Low-grade dysplasia → High-grade dysplasia → Adenocarcinoma

Rationale: Barrett’s metaplasia progresses to esophageal adenocarcinoma through intermediate stages of low- and high-grade dysplasia. Early identification and management of dysplasia are critical to prevent cancer progression.

Question 15

Which of the following foods should be avoided in GERD management because they reduce lower esophageal sphincter (LES) pressure?

A) Citrus fruits
B) Tomato-based foods
C) Fatty foods
D) Spicy foods

Answer 15

Correct Answer: C) Fatty foods

Rationale: Fatty foods reduce LES pressure, making them “refluxogenic.” Other foods in this category include alcohol, spearmint, peppermint, and possibly coffee and tea.

Question 16

Which class of medications is the most effective in managing GERD symptoms?

A) Antacids
B) Histamine-2 receptor antagonists (H2RAs)
C) Proton pump inhibitors (PPIs)
D) Prokinetic agents

Answer 16

Correct Answer: C) Proton pump inhibitors (PPIs)

Rationale: PPIs are the most effective class of medications for GERD management, providing superior symptom relief and esophagitis healing compared to H2RAs and placebo.

Question 17

What is a surgical alternative to PPI therapy in the management of chronic GERD?

A) Hiatal hernia repair
B) Laparoscopic Nissen fundoplication
C) Esophagectomy
D) Endoscopic mucosal resection

Answer 17

Correct Answer: B) Laparoscopic Nissen fundoplication

Rationale: Laparoscopic Nissen fundoplication is a surgical option for chronic GERD. It involves wrapping the proximal stomach around the distal esophagus to create an antireflux barrier.

Question 18

Which of the following pathogens is the most common cause of infectious esophagitis in immunocompromised patients?

A) Escherichia coli
B) Candida species
C) Mycobacterium tuberculosis
D) Streptococcus pneumoniae

Answer 18

Correct Answer: B) Candida species

Rationale: Candida species are one of the most common pathogens causing infectious esophagitis, particularly in immunocompromised patients. Other common pathogens include herpesvirus and cytomegalovirus (CMV).

Question 19

In patients with AIDS, infectious esophagitis is rare when the CD4 count is above which threshold?

A) 50 cells/μL
B) 100 cells/μL
C) 200 cells/μL
D) 500 cells/μL

Answer 19

Correct Answer: C) 200 cells/μL

Rationale: Infectious esophagitis is rare in AIDS patients with CD4 counts above 200 cells/μL but becomes more common as the CD4 count declines, particularly when it falls below 100 cells/μL.

Question 20

Which symptom is most characteristic of infectious esophagitis, differentiating it from reflux esophagitis?

A) Heartburn
B) Dysphagia
C) Odynophagia
D) Chest pain

Answer 20

Correct Answer: C) Odynophagia

Rationale: Odynophagia (painful swallowing) is a hallmark symptom of infectious esophagitis. It is uncommon in reflux esophagitis, making it an important distinguishing feature.

Question 21

Which organism is the most common cause of Candida esophagitis?

A) Candida glabrata
B) Candida tropicalis
C) Candida albicans
D) Candida krusei

Answer 21

Correct Answer: C) Candida albicans

Rationale: Candida albicans is the most common cause of Candida esophagitis, particularly in immunocompromised or compromised hosts.

Question 22

What clinical symptoms are most characteristic of Candida esophagitis?

A) Chest pain and hematemesis
B) Odynophagia and dysphagia
C) Persistent heartburn and regurgitation
D) Fever and weight loss

Answer 22

Correct Answer: B) Odynophagia and dysphagia

Rationale: Patients with Candida esophagitis typically present with odynophagia (painful swallowing) and dysphagia (difficulty swallowing).

Question 23

What is the preferred initial diagnostic step if oral thrush is present and Candida esophagitis is suspected?

A) Empirical therapy with antifungal medication
B) CT scan of the esophagus
C) Endoscopy with biopsy
D) Esophageal manometry

Answer 23

Correct Answer: A) Empirical therapy with antifungal medication

Rationale: If oral thrush is present, empirical antifungal therapy is appropriate. However, persistent symptoms or a lack of response to treatment should prompt endoscopy with biopsy.

Question 24

What is the characteristic endoscopic finding in Candida esophagitis?

A) Salmon-colored mucosa
B) Deep ulcers with irregular margins
C) White plaques or exudate with friability
D) Cobblestone appearance of the mucosa

Answer 24

Correct Answer: C) White plaques or exudate with friability

Rationale: Candida esophagitis has a characteristic endoscopic appearance of white plaques or exudate with mucosal friability.

Question 25

What is the preferred treatment for Candida esophagitis?

A) Voriconazole 400 mg daily for 14–21 days
B) Oral fluconazole 400 mg on the first day, followed by 200 mg daily for 14–21 days
C) Intravenous amphotericin B for 7 days
D) Posaconazole 300 mg daily for 7 days

Answer 25

Correct Answer: B) Oral fluconazole 400 mg on the first day, followed by 200 mg daily for 14–21 days

Rationale: Oral fluconazole is the preferred treatment for Candida esophagitis, typically prescribed as 400 mg on the first day, followed by 200 mg daily for 14–21 days.

Question 26

Which treatment option is appropriate for patients with Candida esophagitis refractory to fluconazole?

A) Increase the fluconazole dose
B) Voriconazole or posaconazole
C) Empirical treatment with antibiotics
D) Proton pump inhibitors

Answer 26

Correct Answer: B) Voriconazole or posaconazole

Rationale: Patients refractory to fluconazole may respond to voriconazole or posaconazole as alternative antifungal agents.

Question 27

Which viruses are most commonly associated with herpetic esophagitis?

A) Epstein-Barr virus and cytomegalovirus
B) Herpes simplex virus (HSV) types 1 and 2, and varicella-zoster virus
C) Human papillomavirus and cytomegalovirus
D) HIV and hepatitis B virus

Answer 27

Correct Answer: B) Herpes simplex virus (HSV) types 1 and 2, and varicella-zoster virus

Rationale: HSV-1 and HSV-2 are common causes of herpetic esophagitis, with varicella-zoster virus (VZV) occasionally causing esophagitis in children with chickenpox or adults with zoster.

Question 28

What is the characteristic endoscopic finding in herpetic esophagitis?

A) Large, deep ulcers with irregular borders
B) Vesicles and small, superficial ulcerations
C) White plaques with friability
D) Cobblestone appearance of the esophageal mucosa

Answer 28

Correct Answer: B) Vesicles and small, superficial ulcerations

Rationale: Endoscopic findings in herpetic esophagitis typically include vesicles and small, superficial ulcerations limited to the squamous epithelium.

Question 29

Which histological finding is characteristic of HSV esophagitis?

A) Eosinophilic Cowdry’s type A inclusion bodies and multinucleated giant cells
B) Large, hyperchromatic nuclei with nuclear molding
C) Columnar metaplasia of the epithelium
D) Neutrophilic infiltration of the lamina propria

Answer 29

Correct Answer: A) Eosinophilic Cowdry’s type A inclusion bodies and multinucleated giant cells

Rationale: HSV esophagitis shows histological findings such as eosinophilic Cowdry’s type A inclusion bodies, ground-glass nuclei, and multinucleated giant cells on biopsy, especially from ulcer margins.

Question 30

What is the recommended initial treatment for HSV esophagitis in patients with severe odynophagia?

A) Oral acyclovir, 200 mg five times daily
B) Oral fluconazole, 200 mg daily
C) Intravenous acyclovir, 5 mg/kg every 8 hours for 7–14 days
D) Topical antiviral ointment

Answer 30

Correct Answer: C) Intravenous acyclovir, 5 mg/kg every 8 hours for 7–14 days

Rationale: For patients with severe odynophagia, intravenous acyclovir is recommended to reduce morbidity associated with HSV esophagitis.

Question 31

What is the typical endoscopic finding in CMV esophagitis?

A) Vesicles and small ulcerations
B) Cobblestone mucosa
C) Large serpiginous ulcers in normal mucosa, especially in the distal esophagus
D) White plaques or exudates with friability

Answer 31

Correct Answer: C) Large serpiginous ulcers in normal mucosa, especially in the distal esophagus

Rationale: CMV esophagitis is characterized by large serpiginous ulcers in otherwise normal mucosa, predominantly in the distal esophagus.

Question 32

What is the pathognomonic histological finding in CMV esophagitis?

A) Eosinophilic Cowdry’s type A inclusion bodies
B) Multinucleated giant cells
C) Large nuclear or cytoplasmic inclusion bodies
D) Dense lymphocytic infiltration

Answer 32

Correct Answer: C) Large nuclear or cytoplasmic inclusion bodies

Rationale: CMV esophagitis is identified histologically by the presence of large nuclear or cytoplasmic inclusion bodies in biopsy specimens.

Question 33

Which medications are effective in the treatment of CMV esophagitis?

A) Acyclovir and valacyclovir
B) Fluconazole and itraconazole
C) Ganciclovir and valganciclovir
D) Amphotericin B and voriconazole

Answer 33

Correct Answer: C) Ganciclovir and valganciclovir

Rationale: Ganciclovir (5 mg/kg IV every 12 hours) and valganciclovir (900 mg orally every 12 hours) are effective treatments for CMV esophagitis.

Question 34

How long is therapy for CMV esophagitis typically continued?

A) 7–10 days
B) 2–3 weeks
C) 3–6 weeks
D) 1 year

Answer 34

Correct Answer: C) 3–6 weeks

Rationale: Therapy for CMV esophagitis is typically continued for 3–6 weeks, depending on the healing of the esophageal ulcers.