GERD

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• 𝐆𝐚𝐬𝐭𝐫𝐨𝐞𝐬𝐨𝐩𝐡𝐚𝐠𝐞𝐚𝐥 𝐫𝐞𝐟𝐥𝐮𝐱 𝐝𝐢𝐬𝐞𝐚𝐬𝐞 (𝐆𝐄𝐑𝐃):

• 𝐃𝐞𝐟𝐢𝐧𝐢𝐭𝐢𝐨𝐧:
A chronic condition characterized by the pathologic reflux of gastric contents into the esophagus.

• 𝐞𝐩𝐢𝐝𝐞𝐦𝐢𝐨𝐥𝐨𝐠𝐲
Global prevalence: 15% to 25%, with significant regional variations.

• 𝐒𝐭𝐨𝐦𝐚𝐜𝐡 𝐚𝐧𝐚𝐭𝐨𝐦𝐲:

o Location: Left upper abdomen, below the diaphragm.
o Shape: J-shaped, with five distinct regions: cardia, fundus, body, antrum, pylorus.
o Musculature: Three layers: outer longitudinal, middle circular, and inner oblique.
o Mucosa: Highly folded lining containing specialized cells for secretion of hydrochloric acid, pepsinogen, mucus, and hormones.

• 𝐜𝐚𝐮𝐬𝐞𝐬:

o Incompetence of the lower esophageal sphincter (LES)
o Hiatal hernia
o Delayed gastric emptying
o Increased gastric acid production
o Lifestyle factors (obesity, smoking, diet, pregnancy, medications)

• 𝐏𝐚𝐭𝐡𝐨𝐩𝐡𝐲𝐬𝐢𝐨𝐥𝐨𝐠𝐲:
o Loss of anti-reflux barrier
o Esophageal mucosal damage
o Impaired esophageal clearance mechanisms
o Visceral hypersensitivity
o Acid and non-acid reflux

• 𝐒𝐲𝐦𝐩𝐭𝐨𝐦𝐬:

o Heartburn
o Regurgitation
o Chest pain
o Dysphagia
o Respiratory symptoms
o Dental erosions

𝐑𝐢𝐬𝐤 𝐅𝐚𝐜𝐭𝐨𝐫𝐬
o Personal history (prior GERD, obesity, pregnancy, smoking, hiatal hernia)
o Medications (aspirin, NSAIDs, calcium channel blockers, nitrates, bisphosphonates)
o Dietary habits (fatty, spicy, acidic foods, large meals, late-night eating, carbonated beverages, alcohol)
o Lifestyle factors (stress, anxiety, lack of physical activity, tight clothing)
o Genetic predisposition

• 𝐃𝐢𝐚𝐠𝐧𝐨𝐬𝐭𝐢𝐜 𝐦𝐞𝐭𝐡𝐨𝐝𝐬:

o Upper endoscopy (EGD)
o Biopsy
o pH monitoring

• 𝐓𝐫𝐞𝐚𝐭𝐦𝐞𝐧𝐭 𝐎𝐩𝐭𝐢𝐨𝐧𝐬:

o Proton pump inhibitors (PPIs) - first-line
o H2 blockers - second-line
o Lifestyle modifications

• 𝐏𝐫𝐨𝐭𝐨𝐧 𝐏𝐮𝐦𝐩 𝐈𝐧𝐡𝐢𝐛𝐢𝐭𝐨𝐫𝐬 (𝐏𝐏𝐈𝐬)
• Mechanism of Action: Inhibit H+/K+-ATPase enzyme in gastric parietal cells, leading to a significant and sustained reduction in acid production.
• Indications:
o Erosive esophagitis and Barret's esophagus
o Moderate to severe GERD symptoms
o Prophylaxis for NSAID-induced ulcers
• Dosage and Duration:
o Varied based on severity and response
o Typically, 4-8 weeks for healing esophagitis
o Long-term maintenance therapy may be necessary

Other information:
• Normal digestion process
• Lower esophageal sphincter (LES) function
• GERD complications (e.g., Barrett's esophagus)
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1. GERD
PowerPoint Template

2. GERD Definition
Gastroesophageal
reflux disease
(GERD) is a
chronic condition
characterized by
the pathologic
reflux of gastric
contents into the
esophagus. This
occurs due to
incompetence of
the lower
esophageal
sphincter (LES),
allowing stomach
acid and other
contents to flow
back up into the
esophagus.

3. GERD Definition

4. GERD Definition

5. GERD Prevalence
•Worldwide:
Estimated
prevalence of
GERD ranges
from 15% to
25%, with
significant
regional
variations.

6. GERD Prevalence
•Western Cultures:
Highest reported
prevalence,
reaching 20% in
adults.
•North America:
18.1% to 27.8%.
•Europe: 8.8% to
25.9%.
•South America:
23.0%.
•Middle East: 8.7%
to 33.1%.
•East Asia: Lowest
reported
prevalence, ranging
from 2.5% to 7.8%.

7. Stomach anatomy
•J-shaped organ in
the upper left
abdomen.
•Composed of five
sections: Cardia,
Fundus, Body,
Antrum, and
Pylorus.
•Three muscle
layers: Outer
longitudinal,
middle circular,
and inner oblique.
•Highly folded
mucosa with
specialized cells:
Parietal (HCl),
Chief
(pepsinogen),
Mucous
(protection),
Enteroendocrine
(hormones).

8. GERD
•Ingestion: Saliva
initiates food
breakdown with
salivary amylase and
lubricates for
swallowing.
•Esophageal Transit:
Propelled by peristaltic
waves, food reaches
the stomach within 6-8
seconds.
•Gastric Digestion:
Powerful muscular
contractions mix food
with gastric juices
containing
hydrochloric acid and
pepsinogen. Acid kills
bacteria and pepsin
begins protein
breakdown.

9. GERD Causes
•Lower Esophageal
Sphincter (LES)
Dysfunction:
Weakened or
relaxed LES allows
stomach contents to
reflux into the
esophagus.
•Hiatal Hernia: Upper
part of the stomach
pushes through the
diaphragm,
weakening the LES.
•Delayed Gastric
Emptying: Slowed
stomach emptying
increases pressure,
leading to reflux.
•Increased Gastric
Acid Production:
Hypersecretion of
acid can irritate the
esophageal lining.
•
Lifest
yle Factors:
o
Obes
ity: Excess
abdominal
pressure weakens
the LES.
o
Smok
ing: Reduces LES
tone and increases
acid production.
o
**Die
t:**Fatty, spicy, and
acidic foods trigger
reflux.
o
Pregn
ancy: Progesterone
relaxes the LES and
displaces the
stomach

10. GERD Pathogenesis
•Loss of Anti-Reflux
Barrier: Impaired
lower esophageal
sphincter function
and/or hiatal hernia
allow gastric contents
to reflux.
•Esophageal Mucosal
Damage: Refluxate,
particularly acidic
stomach contents,
directly injures the
esophageal lining,
leading to
inflammation and
erosion.
•Impaired Esophageal
Clearance
Mechanisms:
Reduced esophageal
motility and salivary
bicarbonate buffering
weaken the defense
against refluxate.
•Visceral
Hypersensitivity:
Increased
sensitivity of
esophageal
sensory nerves
amplifies the
perception of
pain and
discomfort, even
with minimal
reflux.
•Acid and Non-
Acid Reflux:
Both acidic and
non-acidic
stomach
contents can
trigger reflux
symptoms,
indicating a
complex
interplay beyond
solely acid
exposure.

11. GERD Symptoms
•Heartburn:Most
common
symptom,described as a
burning sensation behind
the breastbone,often
worse after meals or
reclining.
•Regurgitation:Backflow
of stomach contents into
the throat,often
accompanied by a sour
or bitter taste.
•Chest pain:Atypical
chest pain,often
localized to the lower
sternum or epigastric
region,can mimic
angina.
•Dysphagia:Difficulty
swallowing due to
esophageal inflammation
or stricture.
•Respiratory
symptoms:Cough,whee
zing,and hoarseness can
occur due to aspiration
of refluxate.
•Dental erosions:Long-
standing GERD can lead
to erosion of tooth
enamel due to acid
exposure.

12. GERD Risk factors
•Personal History:
oPrior history
of GERD or
esophageal
conditions
(e.g.,
Barrett's
esophagus)
oObesity or
rapid weight
gain
oPregnancy
oSmoking
oHiatal hernia

13. GERD Risk factors
•Dietary Habits:
oFatty, spicy,
and acidic
foods
oLarge meals
and late-night
eating
oCarbonated
beverages
oExcessive
alcohol
consumption
•Lifestyle Factors:
oStress and
anxiety
oLack of
physical
activity
oTight-fitting
clothing
•Genetic
Predisposition:
oFamily history
of GERD

14. GERD Diagnosis
Upper Endoscopy
(EGD): Visualizes the
esophagus,
stomach, and
duodenum for direct
assessment of:
Esophagitis:
Presence and
severity of
inflammation (LA
classification).
Barrett's esophagus:
Salmon-colored
mucosal change
indicating increased
cancer risk.
Erosions or ulcers:
Confirmation of
tissue damage.
Hiatal hernia:
Protrusion of the
stomach through the
diaphragm.

15. GERD treatment- PPIs
•Mechanism of
Action: Inhibit H+/K+-
ATPase enzyme in
gastric parietal cells,
leading to significant
and sustained
reduction in acid
production.
•Indications:
oErosive
esophagitis
and Barret's
esophagus
oModerate to
severe GERD
symptoms
oProphylaxis for
NSAID-
induced ulcers

16. GERD treatment- H2 blockers
•Mechanism of Action:
Inhibit histamine at
H2 receptors,
reducing gastric acid
production to a lesser
extent than PPIs.
•Indications:
oMild GERD
symptoms
oShort-term
therapy (e.g., 4-
8 weeks)
oAlternative to
PPIs in patients
with concerns
regarding long-
term PPI use
•Dosage and Duration:
oVaried based
on individual
needs
oTypically, twice
daily
oShorter
duration
compared to
PPIs

17. GERD Icons