This document discusses gastroesophageal reflux disease (GERD) and acid peptic disease (APD). It defines GERD and the classifications of erosive esophagitis and nonerosive reflux disease. The pathogenesis of GERD is explained including the roles of the lower esophageal sphincter, transient LES relaxations, hiatal hernias, and irritant effects of the refluxate. Clinical features, diagnosis, and management are outlined along with complications such as Barrett's esophagus. Treatment includes lifestyle modifications, antacids, H2 receptor antagonists, proton pump inhibitors, and surgical procedures.

2. GASTROESOPHAGEAL REFLUX DISEASE (GERD)
&
ACID PEPTIC DISEASE (APD)
By
Dr Muhammad Ubaid
Assistant Professor- Medicine

3. DEFINITIONS
Gastroesophageal Reflux (GER): Escape of gastric
contents into the esophagus which can be Physiologic
or pathologic
Gastroesophageal reflux disease (GERD): is a
condition that develops when the reflux of stomach
contents causes troublesome symptoms
and/or complications

4. CLASSIFICATION
Based on the appearance of the oesophageal mucosa
on Upper Gastrointestinal Endoscopy:
1. Erosive esophagitis — Erosive esophagitis is
characterized by endoscopically visible breaks in
the distal esophageal mucosa with or without
troublesome symptoms of GERD.
2. Nonerosive reflux disease (NERD) — Nonerosive
reflux disease or endoscopy negative reflux disease is
characterized by the presence of troublesome
symptoms of GERD without visible esophageal
mucosal injury.

5. PATHOGENESIS OF GERD
A) Antireflux mechanisms.
B) Gastric Factors.
C) Esophageal Clearance Mechanisms.
D) Esophageal Epithelial Resistance.

6. ANTIREFLUX MECHANISMS
Lower Esophageal Sphincter (LES)
It is a 1-3.5 cm segment of specialized circular muscle
in the wall of distal esophagus. It maintains a resting
pressure of 10-45 mmHg higher than that of the
stomach.

7. TRANSIENT LES RELAXATION (TLESR)
• Normally, the LES relaxes for 3-10 seconds to allow
the swallowed bolus to enter the stomach. TLESR is
not preceded by swallowing & lasts for up to 45
seconds.
• Most reflux episodes occur during transient
relaxations of the LES that are triggered by gastric
distention by a vagovagal reflex.

8. ANTIREFLUX MECHANISMS
• Hiatal hernias are found in one-fourth of patients
with nonerosive GERD, three-fourths of patients
with severe erosive esophagitis, and over 90% of
patients with Barrett esophagus
• Truncal obesity may contribute to GERD,
presumably due to an increased intra-abdominal
pressure, which contributes to dysfunction of the
gastroesophageal junction and increased likelihood
of hiatal hernia.

9. IRRITANT EFFECTS OF REFLUXATE
• Potency of the refluxate and the amount of time it is in
contact with the mucosa.
• Acidic gastric fluid (pH less than 4.0) is extremely
caustic and reflux of bile or alkaline pancreatic
secretions may be contributory.
• Meal-stimulated acid secretion from the proximal
stomach mixes poorly with gastric contents, forming
an unbuffered "acid pocket“. In patients with GERD,
this acid pocket is located near the gastroesophageal
junction and may extend into the LES or hiatal hernia.

10. ABNORMAL ESOPHAGEAL CLEARANCE
• Diminished clearance:
• Due to hypotensive peristaltic contractions (less than
30 mm Hg) or intermittent failed peristalsis after
swallowing.
• Impaired Salivation:
• Scleroderma or Sjögren syndrome
• Anticholinergic medications
• Oral radiation
• Smoking

12. CLINICAL FEATURES
Clinical manifestations —
CLASSIC SYMPTOMS of gastroesophageal reflux disease (GERD) are
heartburn (pyrosis) and regurgitation. When these symptom is
dominant, the diagnosis is established with a high degree of
reliability
Heartburn is typically described as a burning sensation in the
retrosternal area, most commonly experienced in the postprandial
period . Heartburn is considered troublesome if mild symptoms occur
two or more days a week, or moderate to severe symptoms occur
more than one day a week .
Regurgitation is defined as the perception of flow of refluxed
gastric content into the mouth or hypopharynx . Patients typically
regurgitate acidic material mixed with small amounts of undigested
food.

13. CLINICAL FEATURES
Clinical manifestations —
ATYPICAL SYMPTOMS
Dysphagia: common in the setting of longstanding heartburn,
often attributable to reflux esophagitis, can be indicative of an
esophageal stricture.
Odynophagia: an unusual symptom of GERD usually indicates
an esophageal ulcer.
GERD-related chest pain: can mimic angina resolve either
spontaneously or with antacids.,usually occurs after meals,
awakens patients from sleep, and may be exacerbated by
emotional stress . Patients may also have typical reflux
symptoms.)

14. CLINICAL FEATURES
Clinical manifestations —
ATYPICAL SYMPTOMS
Water brash or hypersalivation: relatively unusual symptom in which
patients can foam at the mouth, secreting as much as 10 mL of saliva
per minute in response to reflux.
Globus sensation: Almost constant perception of a lump in the throat
(irrespective of swallowing),
Nausea: Diagnosis of GERD should be considered in patients with
otherwise unexplained nausea
Extraesophageal symptoms: chronic cough, hoarseness, wheezing

15. DIAGNOSIS & EVALUATION
• Often be based on clinical symptoms alone
• Response to anti secretory therapy is NOT a diagnostic
criterion for GERD
• Further investigation is required in patients with symptoms
that persist despite empiric acid inhibitory therapy to:
• Identify complications of reflux disease
• diagnose in patients with “alarm features”
• ALARM FEATURES:
• Troublesome dysphagia
• Odynophagia
• Weight loss
• Iron deficiency anemia.

16. DIAGNOSIS & EVALUATION
• UPPER GASTROINTESTINAL ENDOSCOPY &
HISTOPATHOLOGY
• BARIUM ESOPHAGOGRAPHY (DOUBLE
CONTRAST BARIUM SWALLOW EXAMINATION)
• ESOPHAGEAL MANOMETRY
• ESOPHAGEAL PH OR COMBINED ESOPHAGEAL PH-
IMPEDANCE TESTING

18. UPPER GASTROINTESTINAL
ENDOSCOPY & HISTOPATHOLOGY

20. UPPER GASTROINTESTINAL ENDOSCOPY
Indications:
• To Evaluate Alarm Features
• Abnormal Imaging
• Detect Esophageal Manifestations Of GERD (Eg,
Barrett’s Metaplasia, Erosive Esophagitis)
• Rule Out An Upper Gastrointestinal Tract Malignancy.
• Upper Endoscopy Can Also Rule Out Other Etiologies
In Patients With Refractory GERD

21. ALARM FEATURES
Suggestive of a gastrointestinal malignancy include:
●New onset of dyspepsia in patient ≥60 years
●Evidence of gastrointestinal bleeding
●Iron deficiency anemia
●Anorexia
●Unexplained weight loss
●Dysphagia
●Odynophagia
●Persistent vomiting
●Gastrointestinal cancer in a first-degree relative

22. The Los Angeles Classification System
Grade Description
A One or more mucosal breaks no longer than 5 mm, none
of which extends between the tops of the mucosal folds.
B One or more mucosal breaks more than 5 mm long, none
of which extends between the tops of two mucosal folds.
C Mucosal breaks that extend between the tops of two or
more mucosal folds, but which involve less than 75% of
the esophageal circumference.
D Mucosal breaks which involve at least 75% of the
esophageal circumference.

24. SAVARY-MILLER CLASSIFICATION
most widely referenced grading of esophagitis
Grade I – One or more non-confluent reddish spots, with or
without exudate
Grade II – Erosive and exudative lesions in the distal esophagus
that may be confluent, but not circumferential
Grade III – Circumferential erosions in the distal esophagus,
covered by hemorrhagic and pseudomembranous exudate
Grade IV – Chronic complications such as deep ulcers, stenosis,
scarring, or Barrett's metaplasia

25. MANAGEMENT OF GERD
• Lifestyle and dietary modification
• Antacids
• Surface agents and alginates
• Histamine 2 receptor antagonist
• Proton pump inhibitors
• Surgical procedures

26. LIFESTYLE AND DIETARY MODIFICATION
• Weight loss
• Elevation of the head of the bed in individuals with nocturnal or laryngeal
symptoms
• Dietary modification.
• Fatty foods, caffeine, chocolate, spicy foods, food with high fat content,
carbonated beverages, and peppermint
• Avoidance of tight-fitting garments
• Promotion of salivation through oral lozenges/chewing gum
• Avoidance of tobacco and alcohol,
• Abdominal breathing exercises to strengthen the antireflux barrier of the
lower esophageal sphincter.

27. ANTACIDS
• Do not prevent GERD
• Limited to intermittent use for relief of symptoms that
occur less than once a week
• Antacids usually contain a combination of magnesium
trisilicate, aluminum hydroxide, or calcium carbonate,
which neutralize gastric pH
• Provide relief within five minutes, but effect of 30 to
60 minutes.

29. Surface Agents And Alginates
• Sucralfate (aluminum sucrose sulfate), a surface agent,
adheres to the mucosal surface, promotes healing, and
protects from peptic injury
• Short duration of action and limited efficacy as
compared with PPIs
• Limited to the management of GERD in pregnancy
• Sodium alginate is a polysaccharide derived from
seaweed that forms a viscous gum that floats within
the stomach and neutralizes the postprandial acid
pocket in the proximal stomach

31. HISTAMINE 2 RECEPTOR ANTAGONIST
• Decrease the secretion of acid by inhibiting the
histamine 2 receptor on the gastric parietal cell.
• H2RAs have a slower onset of action,but a
significantly longer duration of action of 4 to 10
hours
• Limited efficacy in patients with erosive
esophagitis.

33. PROTON PUMP INHIBITORS
Should be used in patients who fail twice-daily H2RA therapy
and in patients with erosive esophagitis and/or frequent or
severe symptoms of GERD that impair quality of life.
PPIs are the most potent inhibitors of gastric acid secretion
PPIs are most effective when taken 30 minutes before the first
meal of the day because the amount of H-K-ATPase present in
the parietal cell is greatest after a prolonged fast.
PPIs should be administered daily rather than on-demand
PPIs are also more effective than H2RAs in healing erosive
esophagitis, regardless of the severity of esophagitis and the
dose and duration of treatment

36. SURGICAL PROCEDURES
• Nissen fundoplication
• Laparoscopic Nissen fundoplication
• Nissen modifications
• Belsey Mark IV
• Hill gastropexy
• Gastric bypass
• Angelchik prosthesis
• LINX prosthesis
• Endoscopic methods
-

38. COMPLICATIONS OF GERD
Can arise even in patients who lack typical oesophageal symptoms.
These complications may be:
• Oesophageal:
• Barrett’s esophagus
• Stricture
• 0esophageal adenocarcinoma
• Extra-esophageal
• Chronic laryngitis
• Exacerbation of asthma

39. Barrett’s Esophagus
• A condition in which a metaplastic columnar epithelium replaces
squamous epithelium in the distal esophagus.
• Barrett’s esophagus is a strong risk factor for adenocarcinoma of the
esophagus & gastroesophageal junction.

40. ACID PEPTIC DISEASE (APD)
Or
PEPTIC ULCER DISEASE (PUD)

41. DEFINITION
Peptic ulcers are defects in the gastric or duodenal
mucosa that extend through the muscularis mucosa.
By definition, ulcers extend through the muscularis
mucosae and are usually over 5 mm in diameter.
Arises when the normal mucosal defensive factors are
impaired or are overwhelmed by aggressive luminal
factors

42. Ulcers occur either:
In the duodenum, (95% are in the bulb or pyloric channel)
in the stomach, (60% in or or at the junction of the antrum,
25% at body on the lesser curvature)
Duodenal sites are 4x as common as gastric sites

43. GASTROPROTECTIVE MECHANISMS
The epithelial cells of the stomach and duodenum secrete mucus in response to
irritation of the epithelial lining and as a result of cholinergic stimulation.
The superficial portion of the gastric and duodenal mucosa exists in the form of a gel
layer, which is impermeable to acid and pepsin.
Other gastric and duodenal cells secrete bicarbonate, which aids in buffering acid that
lies near the mucosa.
Prostaglandins of the E type (PGE) have an important protective role, because PGE
increases the production of both bicarbonate and the mucous layer.
In the event of acid and pepsin entering the epithelial cells, additional mechanisms are
in place to reduce injury. Within the epithelial cells, ion pumps in the basolateral cell
membrane help to regulate intracellular pH by removing excess hydrogen ions.
Through the process of restitution, healthy cells migrate to the site of injury. Mucosal
blood flow removes acid that diffuses through the injured mucosa and provides
bicarbonate to the surface epithelial cells.

44. GASTROPROTECTIVE MECHANISMS
• Physiologic balance exists between gastric acid secretion and
gastroduodenal mucosal defense.
• Mucosal injury and, thus, peptic ulcer occur when the
balance between the aggressive factors and the defensive
mechanisms is disrupted.
• Aggressive factors:
• Nonsteroidal anti-inflammatory drugs (NSAIDs)
• H pylori infection
• Alcohol
• Bile salts, acid, and pepsin

45. ETIOLOGY
Peptic ulcer disease (PUD) may be due to any of the following:
• H pylori infection
• Drugs
• Lifestyle factors
• Severe physiologic stress
• Hypersecretory states (uncommon)
• Genetic factors
The incidence of duodenal ulcer disease has been declining
dramatically for the past 30 years (due to the eradication of H
pylori), but the incidence of gastric ulcers has not been declining
(due to the widespread use of NSAIDs and low-dose aspirin)

46. Peptic Ulcers

47. CLINICAL PRESENTATION
Epigastric pain is the most common symptom of both gastric and duodenal ulcers.
• It is characterized by a gnawing or burning sensation and occurs after meals—
classically, shortly after meals with gastric ulcer and 2-3 hours afterward with
duodenal ulcer.
• Food or antacids relieve the pain of duodenal ulcers but provide minimal relief of
gastric ulcer pain.
• Duodenal ulcer pain often awakens the patient at night. About 50-80% of patients
with duodenal ulcers experience nightly pain, as opposed to only 30-40% of
patients with gastric
• Pain with radiation to the back is suggestive of a posterior penetrating gastric
ulcer complicated by pancreatitis.
• Patients who develop gastric outlet obstruction as a result of a chronic, untreated
duodenal ulcer usually report a history of fullness and bloating associated with
nausea and emesis that occurs several hours after food intake.

48. CLINICAL PRESENTATION
• Dyspepsia, including belching, bloating, distention, and fatty food intolerance
• Heartburn
• Chest discomfort
• Hematemesis or melena resulting from gastrointestinal bleeding. Melena may be
intermittent over several days or multiple episodes in a single day.
• Rarely, a briskly bleeding ulcer can present as hematochezia.
• Symptoms consistent with anemia (eg, fatigue, dyspnea) may be present
• Sudden onset of symptoms may indicate perforation.
• NSAID-induced gastritis or ulcers may be silent, especially in elderly patients.
• Only 20-25% of patients with symptoms suggestive of peptic ulceration are found
on investigation to have a peptic ulcer.

49. CLINICAL PRESENTATION
Alarm features that warrant prompt gastroenterology
referralinclude:
• Bleeding or anemia
• Early satiety
• Unexplained weight loss
• Progressive dysphagia or odynophagia
• Recurrent vomiting
• Family history of gastrointestinal cancer

50. PHYSICAL EXAMINATION
In uncomplicated peptic ulcer disease (PUD), the clinical findings
are few and nonspecific and include the following:
• Epigastric tenderness (usually mild)
• Right upper quadrant tenderness may suggest a biliary
etiology or, less frequently, PUD.
• Guaiac-positive stool resulting from occult blood loss
• Melena resulting from acute or subacute gastrointestinal
bleeding
• Succussion splash resulting from partial or complete gastric
outlet obstruction

51. PHYSICAL EXAMINATION
In complicated peptic ulcer disease (PUD), the clinical findings are few and
nonspecific and include the following:
• sudden onset of severe, sharp abdominal pain. slight movement can
tremendously worsen their pain, these patients assume a fetal position.
• Abdominal examination usually discloses generalized tenderness, rebound
tenderness, guarding, and rigidity.
• Influenced by a number of factors, including the size of perforation,
amount of bacterial and gastric contents contaminating the abdominal
cavity, time between perforation and presentation, and spontaneous
sealing of perforation.
• These patients may also demonstrate signs and symptoms of septic shock

52. INVESTIGATIONS FOR DIAGNOSIS
• CBC:
• CBC count and iron studies can help detect anemia, which is
an alarm signal that mandates early endoscopy to rule out
other sources of chronic gastrointestinal (GI) blood loss.
• LFTS, AMYLASE, LIPASE
• A fasting Serum Gastrin Level should be obtained in
certain cases to screen for Zollinger-Ellison syndrome
• Testing for H pylori infection:
• Essential in all patients with peptic ulcers.

53. INVESTIGATIONS FOR DIAGNOSIS
Upper gastrointestinal Endoscopy:
• Upper gastrointestinal (GI) endoscopy is the preferred diagnostic
test
• It is highly sensitive for the diagnosis of gastric and duodenal
ulcers
• Allows for biopsies and cytologic brushings in the setting of a
gastric ulcer to differentiate a benign ulcer from a malignant
lesion
• Allows for the detection of H pylori infection with antral biopsies
for a rapid urease test and/or histopathology in patients with PUD

56. INVESTIGATIONS FOR DIAGNOSIS
• Radiography
• Angiography
• Biopsy
• A single biopsy offers 70% accuracy in diagnosing
gastric cancer, but 7 biopsy samples obtained from the
base and ulcer margins increase the sensitivity to 99%

57. TREATMENT OF PEPTIC ULCERS
Treatment of peptic ulcers varies depending on the
etiology and clinical presentation.
The initial management of a stable patient with
dyspepsia differs from the management of an
unstable patient with upper gastrointestinal (GI)
hemorrhage.

58. TREATMENT OF PEPTIC ULCERS
Bleeding Peptic Ulcers
• Endoscopic therapy is the MODALITY OF CHOICE
• Endoscopic evaluation of the bleeding ulcer can decrease the
duration of the hospital stay by identifying patients at low
risk for rebleeding.
• Moreover, endoscopic therapy reduces the likelihood of
recurrent bleeding
• Patients can be stratified as having high or low risk for
rebleeding depending on the presence or absence of
stigmata

59. TREATMENT OF PEPTIC ULCERS
High-risk stigmata are :
Active hemorrhage (90% risk of rebleeding)
A visible vessel (50% risk of rebleeding)
A fresh overlying clot (30% risk of rebleeding)
• Ulcers with such stigmata require endotherapy, while
ulcers with a clean base need not be treated
endoscopically. In the absence of these stigmata,
patients can be discharged home on medical therapy
within 48 hours.

60. TREATMENT OF PEPTIC ULCERS
Several modalities of endoscopic therapy are available:
• Injection therapy
• Coagulation therapy
• Hemostatic clips
• Argon plasma coagulator
• Combination therapy.
Injection therapy is performed with epinephrine in a 1:10,000
dilution or with absolute alcohol.
Combination therapy with epinephrine injection followed by
thermal coagulation appears to be more effective than
monotherapy for ulcers with a visible vessel, active hemorrhage,
or adherent clot.

61. ACTIVE HELICOBACTER PYLORI–
ASSOCIATED ULCER

62. ACTIVE HELICOBACTER PYLORI–ASSOCIATED ULCER

63. COMPLICATIONS OF PEPTIC ULCER DISEASE
• Obstruction
• Perforation
• Penetration
• Fistula formation
• Patients with gastric ulcers are also at risk of developing
gastric malignancy. (2% in the initial 3 years).
• H pylori is associated with atrophic gastritis, which, in turn,
predisposes to gastric cancer.
• H pylori infection is associated with gastric lymphoma or
mucosa-associated lymphoid tissue (MALT) lymphoma.