INTERNAL DISEASES PART II EXAMINATION SYLLABUS
GASTROENTEROLOGY
1. Gastro-esophageal reflux disease
GERD = a chronic condition in which stomach contents flow back into the esophagus → irritation
to the mucosa.
• Gastroesophageal reflux = regurgitation of stomach contents into the esophagus
• GERD = condition in which reflux causes troublesome symptoms typically heartburn or
regurgitation and/or esophageal injury or complications.
o The most common endoscopic finding associated with mucosal injury is reflux
esophagitis.
• NERD = non-erosive reflux disease:
o Characteristic symptoms of esophageal reflux disease, in the absence of
esophageal injury e.g. reflux esophagitis on endoscopy, occurring in 50-75% of
GERD patients.
• ERD = erosive reflux disease: gastroesophageal reflux with evidence of erosive injury such
as reflux esophagitis on endoscopy (30-50%)
Etiology
GERD develops when reflux promoting factors such as corrosiveness of gastric juice, overcome
the protective mechanisms such as the gastroesophageal junction and esophageal acid
clearance. Mechanisms include:
• Gastroesophageal junction dysfunction can occur due to:
o Increased frequency of transient lower esophageal sphincter relaxations (TLESRs)
o Imbalance between intragastric and lower esophageal sphincter pressures
o Anatomic abnormalities of the gastroesophageal junction e.g. hiatal hernia, tumor
o Impaired esophageal acid clearance
Risk factors and associations:
• Smoking, caffeine and alcohol consumption
• Stress
• Obesity, pregnancy
• Angle of his enlargement >40 degrees
• Iatrogenic
• Inadequate esophageal protective factors e.g. saliva, peristalsis
• Gastrointestinal malformations
• Scleroderma
• Sliding hiatal hernia >90% of patients with severe GERD
• Asthma
,Clinical Features
Typical symptoms of GERD include:
• Retrosternal burning pain (heartburn)
• Regurgitation
Atypical symptoms:
• Pressure sensation in the chest/non-cardiac chest pain
• Belching, bloating
• Dyspepsia, epigastric pain
• Nausea
• Halitosis (bad smelling breath)
Extraesophageal symptoms:
• Chronic non productive cough and nightime cough
• Hoarseness
• Dental erosions
Aggravating factors include lying down after meals and specific foods and beverages
Pathology
The histopathological findings may vary depending on the extent and severity of mucosal
damage and include:
• Superficial coagulative necrosis in the nonkeratinized squamous epithelium
• Thickening of basal cell layer
• Elongation of the papillae in the lamina propria and dilation of the vascular channels at
the tip of the papillae → hyperemia
• Inflammatory cells (granulocytes, lymphocytes, macrophages)
• Transformation of the squamous epithelium → columnar leading to barrets esophagus
Differential diagnosis
• Esophagitis, barett esophagus, esophageal cancer, esophageal motility disorders
• Acute gastritis, PUD, gastroparesis, gastric outlet obstruction
• Biliary colic, chronic pancreatitis
• Functional dyspepsia, heartburn, IBS, rumination syndrome
• Celiac disease, crohns disease, Zollinger Ellison syndrome
Other types of esophagitis:
• Infectious esophagitis – usually in IC patients
o Esophageal candidiasis
o Herpes esophagitis
o CMV esophagitis
• Drug induced esophagitis
o Antibitoics – clindamycin, doxycycline, tetracycline
o Anti-inflammatory drugs
o Bisphosphonates
• Eosinophilic esophagitis
o Associated with atopy
,Diagnosis
• When presenting with typical symptoms – presume GERD as diagnosis and start empiric
PPI trial, if good response confirm diagnosis, if symptoms persist, then EGD is indicated
• When presenting with atypical or alarming features, consider endoscopic evaluation and
start treatment based on the findings.
Treatment:
• Lifestyle changes and acid suppression therapy – usually with PPI’s
• PPI standard dose for 8 weeks:
o Patients with symptoms
• H2 therapy can be considered as alternative
• Modifications to lifestyle include:
o Smaller portions, weight loss in the obese, avoid caffeine, alcohol etc.
Surgical treatment in severe cases – includes fundoplication – gastric fundus is wrapped around
the lower esophagus and secured with stitches → a cuff that prevents reflux.
2. Achalasia. Esophageal motility disorders
Achalasia is a failure of the lower esophageal sphincter to relax (LES) it is caused by the
degeneration of inhibitory neurons within the esophageal wall.
• Primary/idiopathic
• Secondary (in the context of another disease)
• It is a rare disorder and most commonly occurs in middle aged individuals
Definition: Esophageal motility disorder characterized by inadequate relaxation of the LES and
nonperistaltic contractions in the distal 2/3 of the esophagus due to degeneration of inhibitory
neurons.
Etiology
• Primary achalasia – most commonly, and the cause is unknown
• Secondary achalasia (pseudoachalasia) presentation and manometric findings of a
mechanical cause of obstruction e.g. a malignancy that mimics achalasia
o Esophageal cancer
o Stomach cancer
o Chagas disease
o Amyloidosis
o Neurofibromatosis type 1
o Sarcoidosis
Pathophysiology
• Swallowing is controlled through excitatory (acetylcholine, substance P) and inhibitory
(NO, VIP) neurohumoral substances
• Atrophy of inhibitory neurons in Auerbach plexus → lack of inhibitory neurotransmitters
→ inability to relax and increased resting pressure of the LES as well as dysfunctional
peristalsis → esophageal dilation proximal to the LES
, Clinical features
• Dysphagia to solids and liquids, can be progressive or paradoxical
• Regurgitation
• Retrosternal pains and cramps
• Weight loss
Diagnostics
• Upper endoscopy and/or esophageal barium swallow
• Esophageal manometry is indicated to establish the diagnosis and is the confirmatory test
of choice, if manometry is inconclusive and an esophageal swallow was not obtained, a
esophagram can be used to confirm.
• Endoscopy should be performed to rule out psuedoachalasia because presentation and
manometric findings of a mechanical cause of obstruction can mimic achalasia
Esophageal barium swallow:
• Bird beak sign – dilation of proximal esophgaus with stenosis of gastroesophageal
junction
• Delayed barium emptying or barium retention
Esophageal manometry:
• Peristalsis is absent or uncoordinated in the lower 2/3 of esophagus
• Incomplete or absent LES relaxation and high LES resting pressure, no evidence of
obstruction
Differential diagnosis:
• Esophageal cancer
• Schatzki ring
• Esophageal stricture
• Chagas disease
• Extrinsic compression
Treatment:
• If low surgical risk – pneumatic dilation
o Endoscopic guided graded dilation of the LES that tears the surrounding muscle
fibres with the help of a balloon LES myotomy
• If high surgical risk – botulinum toxin injection to LES
Complications:
• Pulmonary – e.g. pneumonia, abscess, asthma – due to aspiration
• Megaesophagus
• Increased risk of esophageal cancer
GASTROENTEROLOGY
1. Gastro-esophageal reflux disease
GERD = a chronic condition in which stomach contents flow back into the esophagus → irritation
to the mucosa.
• Gastroesophageal reflux = regurgitation of stomach contents into the esophagus
• GERD = condition in which reflux causes troublesome symptoms typically heartburn or
regurgitation and/or esophageal injury or complications.
o The most common endoscopic finding associated with mucosal injury is reflux
esophagitis.
• NERD = non-erosive reflux disease:
o Characteristic symptoms of esophageal reflux disease, in the absence of
esophageal injury e.g. reflux esophagitis on endoscopy, occurring in 50-75% of
GERD patients.
• ERD = erosive reflux disease: gastroesophageal reflux with evidence of erosive injury such
as reflux esophagitis on endoscopy (30-50%)
Etiology
GERD develops when reflux promoting factors such as corrosiveness of gastric juice, overcome
the protective mechanisms such as the gastroesophageal junction and esophageal acid
clearance. Mechanisms include:
• Gastroesophageal junction dysfunction can occur due to:
o Increased frequency of transient lower esophageal sphincter relaxations (TLESRs)
o Imbalance between intragastric and lower esophageal sphincter pressures
o Anatomic abnormalities of the gastroesophageal junction e.g. hiatal hernia, tumor
o Impaired esophageal acid clearance
Risk factors and associations:
• Smoking, caffeine and alcohol consumption
• Stress
• Obesity, pregnancy
• Angle of his enlargement >40 degrees
• Iatrogenic
• Inadequate esophageal protective factors e.g. saliva, peristalsis
• Gastrointestinal malformations
• Scleroderma
• Sliding hiatal hernia >90% of patients with severe GERD
• Asthma
,Clinical Features
Typical symptoms of GERD include:
• Retrosternal burning pain (heartburn)
• Regurgitation
Atypical symptoms:
• Pressure sensation in the chest/non-cardiac chest pain
• Belching, bloating
• Dyspepsia, epigastric pain
• Nausea
• Halitosis (bad smelling breath)
Extraesophageal symptoms:
• Chronic non productive cough and nightime cough
• Hoarseness
• Dental erosions
Aggravating factors include lying down after meals and specific foods and beverages
Pathology
The histopathological findings may vary depending on the extent and severity of mucosal
damage and include:
• Superficial coagulative necrosis in the nonkeratinized squamous epithelium
• Thickening of basal cell layer
• Elongation of the papillae in the lamina propria and dilation of the vascular channels at
the tip of the papillae → hyperemia
• Inflammatory cells (granulocytes, lymphocytes, macrophages)
• Transformation of the squamous epithelium → columnar leading to barrets esophagus
Differential diagnosis
• Esophagitis, barett esophagus, esophageal cancer, esophageal motility disorders
• Acute gastritis, PUD, gastroparesis, gastric outlet obstruction
• Biliary colic, chronic pancreatitis
• Functional dyspepsia, heartburn, IBS, rumination syndrome
• Celiac disease, crohns disease, Zollinger Ellison syndrome
Other types of esophagitis:
• Infectious esophagitis – usually in IC patients
o Esophageal candidiasis
o Herpes esophagitis
o CMV esophagitis
• Drug induced esophagitis
o Antibitoics – clindamycin, doxycycline, tetracycline
o Anti-inflammatory drugs
o Bisphosphonates
• Eosinophilic esophagitis
o Associated with atopy
,Diagnosis
• When presenting with typical symptoms – presume GERD as diagnosis and start empiric
PPI trial, if good response confirm diagnosis, if symptoms persist, then EGD is indicated
• When presenting with atypical or alarming features, consider endoscopic evaluation and
start treatment based on the findings.
Treatment:
• Lifestyle changes and acid suppression therapy – usually with PPI’s
• PPI standard dose for 8 weeks:
o Patients with symptoms
• H2 therapy can be considered as alternative
• Modifications to lifestyle include:
o Smaller portions, weight loss in the obese, avoid caffeine, alcohol etc.
Surgical treatment in severe cases – includes fundoplication – gastric fundus is wrapped around
the lower esophagus and secured with stitches → a cuff that prevents reflux.
2. Achalasia. Esophageal motility disorders
Achalasia is a failure of the lower esophageal sphincter to relax (LES) it is caused by the
degeneration of inhibitory neurons within the esophageal wall.
• Primary/idiopathic
• Secondary (in the context of another disease)
• It is a rare disorder and most commonly occurs in middle aged individuals
Definition: Esophageal motility disorder characterized by inadequate relaxation of the LES and
nonperistaltic contractions in the distal 2/3 of the esophagus due to degeneration of inhibitory
neurons.
Etiology
• Primary achalasia – most commonly, and the cause is unknown
• Secondary achalasia (pseudoachalasia) presentation and manometric findings of a
mechanical cause of obstruction e.g. a malignancy that mimics achalasia
o Esophageal cancer
o Stomach cancer
o Chagas disease
o Amyloidosis
o Neurofibromatosis type 1
o Sarcoidosis
Pathophysiology
• Swallowing is controlled through excitatory (acetylcholine, substance P) and inhibitory
(NO, VIP) neurohumoral substances
• Atrophy of inhibitory neurons in Auerbach plexus → lack of inhibitory neurotransmitters
→ inability to relax and increased resting pressure of the LES as well as dysfunctional
peristalsis → esophageal dilation proximal to the LES
, Clinical features
• Dysphagia to solids and liquids, can be progressive or paradoxical
• Regurgitation
• Retrosternal pains and cramps
• Weight loss
Diagnostics
• Upper endoscopy and/or esophageal barium swallow
• Esophageal manometry is indicated to establish the diagnosis and is the confirmatory test
of choice, if manometry is inconclusive and an esophageal swallow was not obtained, a
esophagram can be used to confirm.
• Endoscopy should be performed to rule out psuedoachalasia because presentation and
manometric findings of a mechanical cause of obstruction can mimic achalasia
Esophageal barium swallow:
• Bird beak sign – dilation of proximal esophgaus with stenosis of gastroesophageal
junction
• Delayed barium emptying or barium retention
Esophageal manometry:
• Peristalsis is absent or uncoordinated in the lower 2/3 of esophagus
• Incomplete or absent LES relaxation and high LES resting pressure, no evidence of
obstruction
Differential diagnosis:
• Esophageal cancer
• Schatzki ring
• Esophageal stricture
• Chagas disease
• Extrinsic compression
Treatment:
• If low surgical risk – pneumatic dilation
o Endoscopic guided graded dilation of the LES that tears the surrounding muscle
fibres with the help of a balloon LES myotomy
• If high surgical risk – botulinum toxin injection to LES
Complications:
• Pulmonary – e.g. pneumonia, abscess, asthma – due to aspiration
• Megaesophagus
• Increased risk of esophageal cancer
