Alterations in Gastrointestinal
Function
Dr. Gerrard Uy
Dysphagia
• a sensation of "sticking" or obstruction of the
passage of food through the mouth, pharynx,
or esophagus
• often used as an umbrella term to include
other symptoms related to swallowing
difficulty
Definition of terms
• Aphagia
– signifies complete esophageal obstruction
• Odynophagia
– painful swallowing
• Globus pharyngeus
– is the sensation of a lump lodged in the throat
• Phagophobia
– meaning fear of swallowing
Physiology of Swallowing
Pathophysiology of Dysphagia
• oral, pharyngeal, and esophageal
• mechanical dysphagia - caused by a large
bolus or a narrow lumen
• motor dysphagia - due to weakness of
peristaltic contractions or to impaired
deglutitive inhibition causing nonperistaltic
contractions and impaired sphincter relaxation
Oral phase dysphagia
• associated with poor bolus formation and
control
• food may either drool out of the mouth or
overstay in the mouth
• patient may experience difficulty in initiating
the swallowing reflex
• premature spillage of food into the pharynx
and aspiration into the unguarded larynx
and/or nasal cavity
Pharyngeal phase Dysphagia
• associated with stasis of food in the pharynx
due to poor pharyngeal propulsion and
obstruction at the UES
• leads to nasal regurgitation and laryngeal
aspiration during or after a swallow
• Nasal regurgitation and laryngeal aspiration
during the process of swallowing are
hallmarks
Esophageal Dysphagia
• the esophageal lumen can distend up to 4 cm
– When the esophagus cannot dilate beyond 2.5 cm
in diameter, dysphagia to normal solid food can
occur
– when the esophagus can’t distend beyond 1.3 cm,
dysphagia ALWAYS occurs
History
• can provide a presumptive diagnosis in >80% of
patients
• Nasal regurgitation and tracheobronchial
aspiration with swallowing are hallmarks of
pharyngeal paralysis or a tracheoesophageal
fistula
• Hoarseness
– precedes dysphagia, the primary lesion is usually in
the larynx
– following dysphagia may suggest involvement of the
recurrent laryngeal nerve
History
• Type of food
– Difficulty only with solids implies mechanical
dysphagia with a lumen that is not severely
narrowed
– dysphagia occurs with liquids as well as solids in
advanced obstruction
• Duration
– Transient dysphagia may be due to an
inflammatory process
– Progressive, lasting days to weeks - carcinoma
Physical Examination
• Careful inspection of the mouth and pharynx
• Neck should be examined for thyromegaly or
spinal abnormality
• Physical examination is often unrevealing in
esophageal dysphagia
Diagnostic Procedures
• Video endoscopy is the diagnostic procedure
of choice
Heartburn
• Pyrosis
• Characterized by burning retrosternal discomfort
that may move up and down the chest
• Characteristic symptom of reflux esophagitis
• Aggravated by bending forward, straining, or lying
recumbent
• Worse after meals
• Relieved by upright posture, swallowing saliva or
water, and antacids
Odynophagia
• Painful swallowing
• characteristic of non reflux esophagitis,
herpes, and pill induced esophagitis
• May occur with peptic ulcer of the esophagus,
carcinoma, and caustic damage
Regurgitation
• Effortless appearance of gastric or esophageal
contents in the mouth
• Associated with incompetence of both UES
and LES
• May result in chronic coughm, laryngitis, and
laryngeal aspiration
• Water Brash – reflex salivary hypersecretion
that occurs in response to peptic esophagitis
Peptic Ulcer Disease
Dr. Gerrard Uy
Peptic Ulcer Disease
• Characterized by burning epigastric pain
exacerbated by fasting and improved with
meals
• Ulcer – disruption of the mucosal integrity of
the stomach and/or duodenum leading to a
local defect or excavation due to active
inflammation
Gastroduodenal Mucosal Defense
• Preepithelial
– Mucus
– Bicarbonate
– Surface actvie phospholipids
• Epithelial
– Cellular resistance
– Restitution
– Growth factors
– Cell proliferation
Gastroduodenal Mucosal Defense
• Subepithelial
– Blood flow
– Leukocyte
Mucus Bicarbonate Layer
• First line of defense
• Serves as a physicochemical barrier to
multiple molecules
• Mucous gel functions as a nonstirred water
layer impeding diffusion of ions and molecules
such as pepsin
• Bicarbonate forms a ph gradient from 1 to 2 at
the gastric luminal surface
Cellular Resistance
• Next line of defense
• Consist of ionic transporters maintaining
intracellular ph
• Intracellular tight junctions
Restitution
• If the preepithelial barrier were breached,
gastric epithelial cells bordering the site of
injury can migrate to restore a damaged
region
• Occurs independent of cell division
Cellular Proliferation
• When larger defects are present that are not
effectively repaired by restitution
• Regulated by prostaglandins and growth
factors
Prostaglandins
• Play a central role in gastric epithelial defense
• Functions:
– Regulate the release of mucosal bicarbonate and
mucus
– Inhibit parietal cell secretion
– Maintains mucosal blood flow and epithelial
restitution
Prostaglandins
• Derived from arachidonic acid, which is
formed from phospholipids
• rate limiting enzyme is cyclooxygenase (COX)
• 2 isoforms – cox1 and cox2
• COX1 – constitutively expressed
– Stomach
– Platelets
– Kidneys
– Endothelial cells
Prostaglandins
• COX2 – inducible by inflammatory stimuli
– Macrophages
– Leukocytes
– Fibroblasts
– Synovial cells
Subepithelial Defense
• Key component is the elaborate microvascular
system providing HCO3
• Neutralizes acid generated by the parietal cells
• Provides adequate supply of micronutrients
and oxygen while removing toxic metabolites
Physiology of Gastric Secretion
• Hydrochloric acid and pepsinogen
– principal gastric secretory products capable of
inducing mucosal injury
• Acid secretion occurs under basal and
stimulated conditions
• Basal secretion is controlled by cholinergic
input via vagus nerve and histaminergic input
from local gastric sources
Physiology of Gastric Secretion
• 3 phases of stimulated gastric acid secretion
– Cephalic
– Gastric
– intestinal
Physiology of Gastric Secretion
• Cephalic
– Sight, smell, and taste of food
– Stimulates gastric secretion via vagus nerve
• Gastric
– Activated once food enters the stomach
– Driven by amino acids and amines that directly
stimulate the G cells to release gastrin
Physiology of Gastric Secretion
• Intestinal
– Mediated by luminal distention and nutrient
assimilation
Pathophysiologic Basis of Peptic
Ulcer Disease
• Encompasses both gastric and duodenal ulcers
• Ulcers are defined as breaks in the mucosal
surface > 5mm in size with depth to the
submucosa
Peptic Ulcer Disease
Gastric Ulcers
• occur later in life
• More common in males
• Can represent a malignancy
• Benign GUs most often
found distal to the junction
of the antrum and mucosa
• H. pylori and NSAID induced
injury
Duodenal Ulcers
• Occur most often in the first
portion of the duodenum
(90% - within 3cm of the
pylorus)
• Usually < 1cm in diameter
• Malignany is rare
• H. pylori and NSAID induced
injury
H. Pylori and Acid Peptic Disease
• Initially named Campylobacter pyloridis
• Gram negative microaerophilic rod
• Most commonly found in the deeper portions
of the mucous gel coating the gastric mucosa
• Under normal conditions, does not invade
cells
• S – shaped and contains multiple sheathed
flagella
H. Pylori and Acid Peptic Disease
• First step in infection is dependent on the
bacteria’s motility and its ability to produce
urease
Epidemiology
• In developing countries, 80% maybe infected
by the age of 20
• 20 – 50% in industrialized countries
Epidemiology
• Factors that favor colonization rate
– Poor socioeconomic status
– Less education
– Birth or residence in a developing country
– Domestic crowding
– Unsanitary living conditions
– Unclean food and water
– Exposure to gastric contents of infected
individuals
Pathophysiology
• Virtually always associated with chronic active
gastritis
• Only 10-15% develop frank peptic ulceration
• Bacterial factors:
– Urease
– Chemotactic surface factors
– protease
• Host factors:
– Inflammatory response
Pathogenetic Factors in Acid Peptic
Disease
• Cigarette smoking
– Decrease healing rates
– Impair response to therapy
– Increases ulcer related complications
• Genetic predisposition
– Blood group O
• Psychological stress
Pathogenetic Factors in Acid Peptic
Disease
• Diet
– Highly acidic diet
– Beverages containing alcohol and caffeine
• Chronic Disorders
– Systemic mastocytosis
– Chronic pulmonary disease
– Chronic renal failure
– Cirrhosis
Pathogenetic Factors in Acid Peptic
Disease
• Chronic Disorders
– Nephrolithiasis
– Polycythemia vera
– Coronary artery disease
– Chronic pancreatitis
Clinical Features
• Epigastric pain – burning/gnawing discomfort
• Usually ill defined, aching sensation or as
hunger pain
• DU
– Pain occurs 90 mins to 3 hrs after a meal
– Frequently relieved by antacids or food
– Awakens the patient from sleep (between
midnight and 3am)
Clinical Features
• GU
– Discomfort is usually precipitated by food
– Nausea and weight loss is more common
Modified Johnsons Classification
• Type I: Ulcer along the body of the stomach,
most often along the lesser curve at incisura
angularis along the locus minoris resistantiae
• Type II: Ulcer in the body in combination with
duodenal ulcers. Associated with acid
oversecretion.
• Type III: In the pyloric channel within 3 cm of
pylorus. Associated with acid oversecretion.
Modified Johnsons Classification
• Type IV: Proximal gastroesophageal ulcer
• Type V: Can occur throughout the stomach.
Associated with chronic NSAID use (such as
aspirin)
Physical Examination
• Epigastric tenderness – most frequent finding
• Tachycardia suggests dehydration
• Severe boardlike abdomen suggests
perforation
• Succussion splash indicates retained fluid in
the stomach suggesting gastric outlet
obstruction
PUD related Complications
• Gastrointestinal bleeding
– Most common complication
• Perforation
– 2nd most common
– DUs tend to penetrate posteriorly into the
panceas
– Gus tend to penetrate into the left hepatic lobe
• Gastric Outlet Obstruction
– Least common occurring in 1 – 2% of patients
Differential Diagnosis
• Nonulcer dyspepsia (NUD)
– Functional dyspepsia or essential dyspepsia
– Heterogeneous disorders typified by upper
abdominal pain without ulceration
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•
•
•
Proximal gastrointestinal tumors
GERD
Pancretobiliary disease
Gastroduodenal crohn’s disease
Diagnostic Evaluation
• Endoscopy
– most sensitive and specific approach
– Permits direct visualization of the mucosa
– Tissue biopsy can be done to rule out malignancy
• Serology
• Urea breath test
• Stool antigen
Treatment
• Acid neutralizing/Inhibitory drugs
– Antacids
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•
•
•
Aluminum hydroxide
Magnesium hydroxide
Ca carbonate
Na bicarbonate
– H2 receptor antagonist
• Famotidine
• Cimetidine
• ranitidine
Treatment
• Acid neutralizing/Inhibitory drugs
– Proton pump inhibitors
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•
•
•
Omeprazole
Esomeprazole
Lansoprazole
pantoprazole
Treatment
• Cytoprotective Agents
– Sucralfate
– Bismuth containing preparations
– Prostaglandin analogues