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GERD
PowerPoint Template
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.
GERD Definition
GERD Definition
GERD Prevalence
โ€ข Worldwide:
Estimated
prevalence of
GERD ranges
from 15% to
25%, with
significant
regional
variations.
GERD Prevalence
โ€ข Western Cultures:
Highest reported
prevalence,
reaching 20% in
adults.
โ€ข North America:
18.1% to 27.8%.
โ€ข Europe: 8.8% to
25.9%.
โ€ข South America:
23.0%.
โ€ข Middle East: 8.7%
to 33.1%.
โ€ข East Asia: Lowest
reported
prevalence, ranging
from 2.5% to 7.8%.
Stomach anatomy
โ€ข J-shaped organ in
the upper left
abdomen.
โ€ข Composed of five
sections: Cardia,
Fundus, Body,
Antrum, and
Pylorus.
โ€ข Three muscle
layers: Outer
longitudinal,
middle circular,
and inner oblique.
โ€ข Highly folded
mucosa with
specialized cells:
Parietal (HCl),
Chief
(pepsinogen),
Mucous
(protection),
Enteroendocrine
(hormones).
GERD
โ€ข Ingestion: Saliva
initiates food
breakdown with
salivary amylase and
lubricates for
swallowing.
โ€ข Esophageal Transit:
Propelled by peristaltic
waves, food reaches
the stomach within 6-8
seconds.
โ€ข Gastric Digestion:
Powerful muscular
contractions mix food
with gastric juices
containing
hydrochloric acid and
pepsinogen. Acid kills
bacteria and pepsin
begins protein
breakdown.
GERD Causes
โ€ข Lower Esophageal
Sphincter (LES)
Dysfunction:
Weakened or
relaxed LES allows
stomach contents to
reflux into the
esophagus.
โ€ข Hiatal Hernia: Upper
part of the stomach
pushes through the
diaphragm,
weakening the LES.
โ€ข Delayed Gastric
Emptying: Slowed
stomach emptying
increases pressure,
leading to reflux.
โ€ข Increased Gastric
Acid Production:
Hypersecretion of
acid can irritate the
esophageal lining.
โ€ข
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
GERD Pathogenesis
โ€ข Loss of Anti-Reflux
Barrier: Impaired
lower esophageal
sphincter function
and/or hiatal hernia
allow gastric contents
to reflux.
โ€ข Esophageal Mucosal
Damage: Refluxate,
particularly acidic
stomach contents,
directly injures the
esophageal lining,
leading to
inflammation and
erosion.
โ€ข Impaired Esophageal
Clearance
Mechanisms:
Reduced esophageal
motility and salivary
bicarbonate buffering
weaken the defense
against refluxate.
โ€ข Visceral
Hypersensitivity:
Increased
sensitivity of
esophageal
sensory nerves
amplifies the
perception of
pain and
discomfort, even
with minimal
reflux.
โ€ข Acid and Non-
Acid Reflux:
Both acidic and
non-acidic
stomach
contents can
trigger reflux
symptoms,
indicating a
complex
interplay beyond
solely acid
exposure.
GERD Symptoms
โ€ขHeartburn: Most
common
symptom, described as a
burning sensation behind
the breastbone, often
worse after meals or
reclining.
โ€ขRegurgitation: Backflow
of stomach contents into
the throat, often
accompanied by a sour
or bitter taste.
โ€ขChest pain: Atypical
chest pain, often
localized to the lower
sternum or epigastric
region, can mimic
angina.
โ€ขDysphagia: Difficulty
swallowing due to
esophageal inflammation
or stricture.
โ€ขRespiratory
symptoms: Cough, whee
zing, and hoarseness can
occur due to aspiration
of refluxate.
โ€ขDental erosions: Long-
standing GERD can lead
to erosion of tooth
enamel due to acid
exposure.
GERD Risk factors
โ€ข Personal History:
o Prior history
of GERD or
esophageal
conditions
(e.g.,
Barrett's
esophagus)
o Obesity or
rapid weight
gain
o Pregnancy
o Smoking
o Hiatal hernia
GERD Risk factors
โ€ข Dietary Habits:
o Fatty, spicy,
and acidic
foods
o Large meals
and late-night
eating
o Carbonated
beverages
o Excessive
alcohol
consumption
โ€ข Lifestyle Factors:
o Stress and
anxiety
o Lack of
physical
activity
o Tight-fitting
clothing
โ€ข Genetic
Predisposition:
o Family history
of GERD
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.
GERD treatment- PPIs
โ€ข Mechanism of
Action: Inhibit H+/K+-
ATPase enzyme in
gastric parietal cells,
leading to significant
and sustained
reduction in acid
production.
โ€ข Indications:
o Erosive
esophagitis
and Barret's
esophagus
o Moderate to
severe GERD
symptoms
o Prophylaxis for
NSAID-
induced ulcers
GERD treatment- H2 blockers
โ€ข Mechanism of Action:
Inhibit histamine at
H2 receptors,
reducing gastric acid
production to a lesser
extent than PPIs.
โ€ข Indications:
o Mild GERD
symptoms
o Short-term
therapy (e.g., 4-
8 weeks)
o Alternative to
PPIs in patients
with concerns
regarding long-
term PPI use
โ€ข Dosage and Duration:
o Varied based
on individual
needs
o Typically, twice
daily
o Shorter
duration
compared to
PPIs
GERD Icons

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GERD

  • 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.
  • 5. GERD Prevalence โ€ข Worldwide: Estimated prevalence of GERD ranges from 15% to 25%, with significant regional variations.
  • 6. GERD Prevalence โ€ข Western Cultures: Highest reported prevalence, reaching 20% in adults. โ€ข North America: 18.1% to 27.8%. โ€ข Europe: 8.8% to 25.9%. โ€ข South America: 23.0%. โ€ข Middle East: 8.7% to 33.1%. โ€ข East Asia: Lowest reported prevalence, ranging from 2.5% to 7.8%.
  • 7. Stomach anatomy โ€ข J-shaped organ in the upper left abdomen. โ€ข Composed of five sections: Cardia, Fundus, Body, Antrum, and Pylorus. โ€ข Three muscle layers: Outer longitudinal, middle circular, and inner oblique. โ€ข Highly folded mucosa with specialized cells: Parietal (HCl), Chief (pepsinogen), Mucous (protection), Enteroendocrine (hormones).
  • 8. GERD โ€ข Ingestion: Saliva initiates food breakdown with salivary amylase and lubricates for swallowing. โ€ข Esophageal Transit: Propelled by peristaltic waves, food reaches the stomach within 6-8 seconds. โ€ข 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 โ€ข Lower Esophageal Sphincter (LES) Dysfunction: Weakened or relaxed LES allows stomach contents to reflux into the esophagus. โ€ข Hiatal Hernia: Upper part of the stomach pushes through the diaphragm, weakening the LES. โ€ข Delayed Gastric Emptying: Slowed stomach emptying increases pressure, leading to reflux. โ€ข Increased Gastric Acid Production: Hypersecretion of acid can irritate the esophageal lining. โ€ข 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 โ€ข Loss of Anti-Reflux Barrier: Impaired lower esophageal sphincter function and/or hiatal hernia allow gastric contents to reflux. โ€ข Esophageal Mucosal Damage: Refluxate, particularly acidic stomach contents, directly injures the esophageal lining, leading to inflammation and erosion. โ€ข Impaired Esophageal Clearance Mechanisms: Reduced esophageal motility and salivary bicarbonate buffering weaken the defense against refluxate. โ€ข Visceral Hypersensitivity: Increased sensitivity of esophageal sensory nerves amplifies the perception of pain and discomfort, even with minimal reflux. โ€ข 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 โ€ขHeartburn: Most common symptom, described as a burning sensation behind the breastbone, often worse after meals or reclining. โ€ขRegurgitation: Backflow of stomach contents into the throat, often accompanied by a sour or bitter taste. โ€ขChest pain: Atypical chest pain, often localized to the lower sternum or epigastric region, can mimic angina. โ€ขDysphagia: Difficulty swallowing due to esophageal inflammation or stricture. โ€ขRespiratory symptoms: Cough, whee zing, and hoarseness can occur due to aspiration of refluxate. โ€ขDental erosions: Long- standing GERD can lead to erosion of tooth enamel due to acid exposure.
  • 12. GERD Risk factors โ€ข Personal History: o Prior history of GERD or esophageal conditions (e.g., Barrett's esophagus) o Obesity or rapid weight gain o Pregnancy o Smoking o Hiatal hernia
  • 13. GERD Risk factors โ€ข Dietary Habits: o Fatty, spicy, and acidic foods o Large meals and late-night eating o Carbonated beverages o Excessive alcohol consumption โ€ข Lifestyle Factors: o Stress and anxiety o Lack of physical activity o Tight-fitting clothing โ€ข Genetic Predisposition: o Family 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 โ€ข Mechanism of Action: Inhibit H+/K+- ATPase enzyme in gastric parietal cells, leading to significant and sustained reduction in acid production. โ€ข Indications: o Erosive esophagitis and Barret's esophagus o Moderate to severe GERD symptoms o Prophylaxis for NSAID- induced ulcers
  • 16. GERD treatment- H2 blockers โ€ข Mechanism of Action: Inhibit histamine at H2 receptors, reducing gastric acid production to a lesser extent than PPIs. โ€ข Indications: o Mild GERD symptoms o Short-term therapy (e.g., 4- 8 weeks) o Alternative to PPIs in patients with concerns regarding long- term PPI use โ€ข Dosage and Duration: o Varied based on individual needs o Typically, twice daily o Shorter duration compared to PPIs