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Charles Ferdinand

405120215
LO 1
• Anatomy of GI tract (mouth – esophagus)
Oral cavity
• 2 parts:
– oral vestibule
• slit-like space between the teeth and buccal gingiva and the lips and
cheeks
– oral cavity proper
• space between the upper and the lower dental arches or arcades
(maxillary and mandibular alveolar arches and the teeth they bear)

• The size of oral fissure (rima oris) controlled by the


circumoral muscles, such as
– the orbicularis oris (the sphincter of the oral fissure),
– the buccinator,
– risorius, and
– depressors and elevators of the lips (dilators of the fissure).
During chewing, the tongue
(centrally), the buccinator
(laterally), and the orbicularis
oris (anteriorly) work together
to retain the bolus of food
between the occlusive surfaces
of the molar teeth
Lips
• Mobile, musculofibrous folds surrounding the mouth,
extending from the nasolabial sulci and nares laterally and
superiorly to the mentolabial sulcus inferiorly
• Labial frenula  free-edged folds of mucous membrane in
the midline, extending from the vestibular gingiva to the
mucosa of the upper and lower lips

– Superior and inferior labial arteries, branches of the facial


arteries, infraorbital arteries / mental arteries, & anastomose
with each other in the lips to form an arterial ring
– upper lip  superior labial branches of the infraorbital nerves
(of CN V2)
– lower lip  inferior labial branches of the mental nerves (of CN
V3
Cheeks (L. Buccae)
• Buccal region
– anteriorly by the oral and mental regions (lips and
chin),
– superiorly by the zygomatic region,
– posteriorly by the parotid region,
– inferiorly by the inferior border of the mandible

• The principal muscles of the cheeks are the


buccinators
• Numerous small buccal glands lie between the
mucous membrane and the buccinators
Gingivae
• composed of fibrous tissue covered with
mucous membrane
• gingiva proper (attached gingiva) is firmly
attached to the alveolar processes of the jaws
and the necks of the teeth
– normally pink, stippled, and keratinizing
• alveolar mucosa (unattached gingiva) is
normally shiny red and non-keratinizing
Teeth
• Types:
– incisors, thin cutting edges
– canines, single prominent cones
– premolars (bicuspids), two cusps
– molars, three or more cusps
• Vasculature of teeth
– superior and inferior alveolar arteries, branches of
the maxillary artery
– Alveolar veins with the same names and
distribution accompany the arteries
• Innervation of teeth
– branches of the superior (CN V2) and inferior (CN
V3) alveolar nerves give rise to dental plexuses that
supply the maxillary and mandibular teeth
Tongue (L. lingua; G. glossa)
• Parts
– root of the tongue is the part of the tongue that rests on
the floor of the mouth (posterior third of the tongue)
– body of the tongue is the anterior two thirds of the tongue
– apex (tip) of the tongue is the anterior end of the body
• Surface
– V-shaped groove, the terminal sulcus or groove (L. sulcus
terminalis),
– lingual papillae
• Vallate papillae, Foliate papillae, Filiform papillae, Fungiform
papillae
Muscles of the tongue
Nerve supply of tongue
Vasculature of tongue
• lingual artery, which arises from the external
carotid artery
Esophagus
• descends into the posterior mediastinum from
the superior mediastinum, passing posterior
and to the right of the arch of the aorta,
passing posterior and to the right of the arch
of the aorta
• compressed by three structures:
– the arch of the aorta
– the left main bronchus
– the diaphragm
LO 2
• Physiology of GI tract (mouth – esophagus)
General aspects
• Primary function of the digestive system
– To transfer nutrients, water, and electrolytes from
the food we eat into the body’s internal
environment
– Ingested food is essential as an energy source, or
fuel, from which the cells can generate ATP to
carry out their particular energy-dependent
activities
4 basic digestive processes
• Motility
– Refers to the muscular contractions that mix and
move forward the contents of the digestive tract
– It also maintains a constant low level of contraction
known as tone (preventing its walls from remaining
permanently stretched following distension)
– 2 basic types of phasic digestive motility
• Propulsive movement
– Push the contents forward through the digestive tract
• Mixing movement
– Mixing food with the digestive juices, these movements promote
digestion of the food
– Facilitate absorption by exposing all parts of the intestinal
contents to the absorbing surfaces of the digestive tract
• Secretion
– Digestive juices are secreted into the digestive tract
lumen by exocrine glands along the route, each with
its own specific secretory product
– Secretion consists of water, electrolytes, spesific
organic constituents  digestive processes (enzyme,
bile salts, mucus)
– On appropriate neural or hormonal stimulation, the
secretions are released into the digestive tract lumen.
– Normally, the digestive secretions are reabsorbed in
one form or another back into the blood after their
participation in digestion
• Digestion
– Biochemical breakdown of the structurally complex
foodstuffs of the diet into smaller, absorbable units
by the enzymes produced within the digestive system
• Most ingested carbohydrate is in the form of
polysaccharides (most common: starch)
• Meat contains glycogen, the polysaccharide storage form of
glucose in muscle
• A lesser source of dietary carbohydrate is in the form of
disaccharides
• The simplest form : glucosa, fructosa, galactosa
• Dietary proteins consist of various combinations of amino
acids held together by peptide bonds
• Most dietary fats are in the form of triglycerides, which are
neutral fats, each consisting of a glycerol with three fatty
acid molecules attached
• Absorption
– The small absorbable units that result from
digestion, along with water, vitamins, and
electrolytes, are transferred from the digestive
tract lumen into the blood or lymph.
Digestive tract & accessory digestive glands

• The accessory digestive organs include the


salivary glands, the exocrine pancreas, and the
biliary system, which is composed of the liver and
gallbladder
• The digestive tract is essentially a tube about 4.5
m (15 feet) in length in its normal contractile
state
– mouth; pharynx (throat); esophagus; stomach; small
intestine (consisting of the duodenum, jejunum, and
ileum); large intestine (the cecum, appendix, colon,
and rectum); and anus
Wall of the digestive system
• Mucosa
– Mucous membrane, an inner epithelial layer that
serves as a protective surface
• exocrine gland cells  digestive juices,
• endocrine gland cells  blood-borne gastrointestinal
hormones, and
• epithelial cells  digested nutrients
– lamina propria is a thin middle layer of connective
tissue on which the epithelium rests, houses the gut-
associated lymphoid tissue (GALT)
– Muscularis mucosa, a sparse layer of smooth
muscle, is the outermost mucosal layer that lies
adjacent to the submucosa
• Submucosa
– Thick layer of connective tissue distensibility & elasticity
– Larger blood & lymph vessels, submucosal plexus
• Muscularis externa
– Inner circular layer ( decrease diameters of lumen) &
outer longitudinal layer ( shortens the tube)
– Myenteric plexus
• Serosa
– Secretes a watery, slippery fluid (serous fluid) that
lubricates and prevents friction between the digestive
organs and surrounding viscera
– continuous with the mesentery
Regulation of digestive system
1. Autonomous smooth muscle function
–  pacemaker cells : rhytmic, spontaneous variations
in membrane potential (cell of Cajal)
• lie in the boundary between the longitudinal & circular
smooth muscle layers
– Prominent type of self induced electrical activity 
slow wave potential (digestive tract’s basic electrical
rhythm)
– Threshold reached depends on the effect of various
mechanical, neural, & hormonal
• Rate of self induced rhythmic digestive contractile activity
 rate established by the pacemaker
• Strength of contractions  number of action potentials that
occur when the slow wave potential reached threshold;
how long threshold is sustained
2. Intrinsic nerve plexus
– The submucosal & myenteric plexus (enteric nerveous
system)  lie entirely within the digestive tract
– Affect digestive tract motility, secretion of digestive
juice, secretion of GI hormones
– Some of output neurons are excitatory, some are
inhibitory
• Neuron that release acetylcholine as a neurotransmitter 
contraction; vasoactive intestinal peptidevasoactive
intestinal peptide  relaxation
– Influenced by a vast array of endocrine, paracrine,
extrinsic nerve signals
3. Extrinsic nerve
– Nerve fibers from both branches of the autonomic
nervous system that originate outside the digestive
tract & innervate the various digestive organs
– Modifying ongoing activity in the intrinsic plexus,
altering the level of GI hormone secetion, acting
directly to smooth muscle & glands  digestive tract
motility & secretion
• Sympathetic system  inhibit or slow down digestive tract
contraction & secretion
• Parasympathetic system  increase smooth muscle motility
& promote secretion of digestive enzyme & hormone
4. Gastrointestinal hormones
– Endocrine gland cells  release hormones into
the blood
– These GI hormones carried through the blood to
other areas of digestive tract  exert excitatory or
inhibitory influences on smooth muscle &
exocrine gland cells
– Many of these same hormones are released from
neurons in the brain, they act as neurotransmitter
& neuromodulators
Receptors activation alters digestive
activity
• Chemoreceptors
– Sensitive to chemical components within the lumen
• Mechanoreceptors
– Sensitive to stretch or tension within the wall
• Osmoreceptors
– Sensitive to the osmolarity of the luminal contents

• Stimulation of the receptors  neural reflexes / secretion


of hormones 
– Alter the level of activity in the digestive system’s effector cells
(modifying motility),
– Exocrine gland cells (controlling secretion of digestive juice),
– Endocrine gland cells (for varying secretion of GI hormones)
Saliva
• 99.5% H2O, 0,5% electrolytes, & proteins (amylase,
mucus, lysozyme)
• Functions:
– Action of salivary amylase (breaks polisaccharides 
(maltose)
– Moistioning food particles, holding them together,
lubrication (mucus)
– Antibacterial action (lysozyme  breaking down bacterial
cells wall, IgA antibodies, lactoferrin  binds iron, rinsing
away material (food for bacteria))
– Solvent for the molecules  stimulate taste buds
– Aids speech
– Oral hygiene  keeps mouth & teeth clean
– Rich in bicarbonate buffers  neutralize acids in food
Salivary secretion
• 1-2 liters of saliva are secreted / day
(continuous spontaneous basal rate  0,5
ml/min; maximum flow rate  5 ml/min

Simple & Conditioned


Salivary Reflex
– Autonomic influence on salivary secretion
• Parasympathetic stimulation  dominant role in
salivary secretion, produce a prompt, abudant flow of
saliva that rich in enzymes
• Sympathetic stimulation  produces a much smaller
volume of thick saliva that thick in mucus
– Stress situation  mouth feels dry
– Nerveous about giving a speech  mouth feels dry
Pharynx & esophagus
• Motility associated with pharynx & esophagus is
swallowing  moving food out of the mouth into
the esophagus
• Swallowing  all or none reflex
• During swallowing, food is prevented from
entering the wrong track :
Bolus from mouth  pharinx  esophagus
In esophagus, bolus is controlled by:
- Position of the tounge pressing the palatum
- Uvula
- No respiration
- Elevation of the larynx
- Contraction of the muscles of pharynx
Esophagus is controlled by 2 sphincter:
- Pharyngo-esophageal
- Gastro-esophageal
Swallowing  all or none reflex
• Initiated when a bolus voluntarily forced by
tongue to the rear of the mouth into the
pharynx  stimulates pharyngeal pressure
receptor  afferent impulses  swallowing
center (medula oblongata)  reflexly
activates the muscles involved of swallowing
• Swallowing initiated voluntarily but once
begun it cannot be stopped
Oropharyngeal stage of swallowing
• Last about 1 second  moving the bolus from the mouth
through the pharynx & into the esophagus
• Esophagus  fairly straight muscular tube,
extends between the pharynx and stomach
– Guarded at both ends by sphincters
(pharyngoesophageal & gastroesophageal sphincter)

– Esophagus is exposed to subatmospheric intrapleural


pressure (respiratory activity), a pressure gradient
exists between the atmosphere & the esophagus
– During a swallow, pharyngoesophageal sphincter
remain closed (neurally induced contraction) 
prevent large volume of air from entering esophagus
– If large volumes of air enters the digestive tract 
eructation
Esophageal stage of swallowing
• Swallowing center  primary peristaltic wave
(sweeps from the beginning to the end of
esophagus, forcing the bolus ahead of it through
the esophagus to the stomach)
– Peristaltis (ringlike contractions of the circular
smooth muscle that progresively forward, pushing
the bolus into a relaxed area ahead of contraction)
– 5-9 s
• Secondary peristaltic waves
– More forceful peristaltic, mediated by the intrinsic
nerve plexuses at the level of distention
Esophageal secretion
• Entirely mucus
– Lubricating the passage of food
– Lessen the likelihood that esophagus will be
damaged by any sharp edges in the newly
entering food
– Protects esophageal wall from acid & enzymes in
gastric juice if gastric reflux occur
LO 3
• Histology of GI tract (mouth – esophagus)
Introduction
• The digestive system
consists
– Oral cavity, esophagus,
stomach, small and large
intestines, rectum, and
anus
– Its associated glands—
salivary glands, liver, and
pancreas
• Function
– Obtain from ingested
food the molecules
necessary for the
maintenance, growth,
and energy needs of the
body
General Structure
• Mucosa
– Epithelial lining, underlying lamina propria (loose connective tissue
rich in blood vessels, lymphatics, lymphocytes and smooth muscle
cells, sometimes also containing glands)
– Thin layer of smooth muscle called the muscularis mucosae usually
separating mucosa from submucosa
• Submucosa
– Denser connective tissue with many blood and lymph vessels and the
submucosal plexus of autonomic nerves
– Also contain glands and lymphoid tissue
• Muscularis
– Smooth muscle cells that are spirally oriented and divided into two
sublayers (internal – circular; external – longitudinal)
– Autonomic myenteric nerve plexus
• Serosa
– Loose connective tissue, rich in blood vessels, lymphatics, and
adipose tissue, with a simple squamous covering epithelium
(mesothelium).
Lips
• Has striated muscle & a transition from oral
non keratinized epithelium to keratinized
epithelium of the skin
Tongue
• Mass of striated muscle covered by a mucous
membrane whose structure varies according to
the region
• Tongue's dorsal surface is irregular, covered
anteriorly by a great number of small eminences
called papillae
• The posterior third of the tongue's dorsal surface
is separated from the anterior two thirds by a V-
shaped groove, the terminal sulcus
• Papillae
– Filiform papillae
• Elongated conical shape, and are heavily keratinized, which
gives their surface a gray or whitish appearance
• Lacks taste buds; mechanical in providing a rough surface
that facilitates food movement during chewing
– Fungiform papillae
• Lightly keratinized, and mushroom-shaped with connective
tissue cores and scattered taste buds on their upper surfaces
– Foliate papillae
– Vallate (or circumvallate) papillae
• Taste Buds
Teeth
• In the adult human there are normally 32
permanent teeth, arranged in two bilaterally
symmetric arches in the maxillary and
mandibular bones
• Each tooth has
– Crown exposed above the gingiva
– Constricted neck at the gum
– One or more roots below the gingiva that hold the
teeth in bony sockets called alveoli, one for each
tooth
• Dentin
– Calcified tissue consisting of 70% calcium
hydroxyapatite, making it harder than bone
– Organic matrix contains type I collagen fibers and
glycosaminoglycans secreted by odontoblasts
– Mineralization of the predentin matrix involves
matrix vesicles in a process similar to that in osteoid
– Slender apical odontoblast processes lie within
dentinal tubules which penetrate the full thickness of
the dentin, gradually becoming longer as the dentin
becomes thicker
• Enamel
– The hardest component of the human body,
consisting of nearly 98% hydroxyapatite and the
rest organic material (amelogenin and enamelin),
but no collagen
– Containing fluorapatite is more resistant to acidic
dissolution caused by microorganisms
– Consists of interlocking rods or columns, enamel
rods (prisms), bound together by other enamel
– In developing teeth enamel matrix is secreted by
a layer of cells called ameloblasts, each of which
produces one enamel prism
• Pulp
– Consists of connective tissue resembling mesenchyme
– Main components are the layer of odontoblasts, many
fibroblasts, thin collagen fibrils, and ground substance
– Highly innervated and vascularized tissue

• Periodontium
– Maintaining the teeth in the maxillary and mandibular
bones
– consists of the cementum, periodontal ligament, alveolar
bone, and gingiva
• Cementum covers the dentin of the root and is similar in
composition to bone
Esophagus
• A muscular tube whose function is to transport
food from the mouth to the stomach
• Lined by nonkeratinized stratified squamous
epithelium with stem cells scattered throughout
the basal layer
• In the submucosa are groups of small mucus-
secreting glands, the esophageal glands,
secretions of which facilitate the transport of
foodstuffs and protect the mucosa
4th LO
• Explain the biochemstry of GI tract (mouth –
esophagus)

Nath,R.L. A Textbook of Medicinal Biochemistry. New Delhi: New Age International; 2002
The digestive enzymes
Digestive enzymes are enzymes which help
break down food substances into forms that
can be absorbed and assimilated by the body.
Digestive enzymes are normally secreted :
1) in the mouth (as part of the saliva),
2) by the stomach
3) released into the small intestines from the
liver and pancreas.
Mouth (oral cavity)
• Principal functionally active component in
mouth is saliva, a slimy fluid secreted from the
parotid, submandibular and sublingual glands.
• Saliva is stimulated by mechanical chewing,
taste, and even sight, smell, and thought of
food.
• The average daily: more than 1000 ml.
• The main constituents of saliva:
- Water(99.5%)
- Some inorganic substance (e.g. Na, K, Cl,
HCO3, traces of iodide and thiocynate)
- Few organic substances (urea, glucosa, lactic
acid) along with some enzyms like lysozyme(a
proteolytic enzyme) and ptyalin(alpha amylase).
- Mucin (glycoprotein)
• pH of saliva is about: 6,8
• Electrolytes in saliva
Na & Cl < K & HCO3
Function of saliva
• Saliva moistens food & act as a lubricant (mainly due to
mucin) for mastication and swallowing.
• It also facilitates tounge movement
• Some food stuffs are partly dissolved in saliva
• Mastication increased the solubility and surface area
by subviding the food so that it becomes easier for the
enzymes to attack them at later stage.
• Also the vehicle for excretion of some drugs &
inorganic constituents secreted into it.
• Oral hygiene (by washing away bacteria, lysozyme)
• So, the chemical process occuring in the
mouth for digestion is only a little hydrolysis of
starch and glycogen into maltose by
amylase(ptyalin)
• Amylase continues its action until it is
deactivated in the stomach when pH falls
below 4
Esophagus
• The connecting channel between mouth and
stomach secretes only mucus that mainly acts
as a lubricant.
• Mucus also protects the upper esophageal
part from being excoriated by food particles &
the lower esophageal part from being
digested by the gastric juice flowing back from
the stomach.
LO 5
• Dysphagia
Disphagia
• Defintion
Derived from the Greek meaning: the
sensation of distractions during the passage of
food or drink from the mouth, pharynx, and
esophagus into the stomach.
Definiton
• Sensation of “sticking” or obstruction of the
passage of food through the mouth, pharynx, or
esophagus ~ swallowing difficulty
– Aphagia  complete esophageal obstruction
– Odynophagia  painful swallowing
– Globus pharyngeus  sensation of a lump lodged in
the throat
– Misdirection of food  nasal regurgitation and
laryngeal and pulmonary aspiration during
swallowing (oropharyngeal dysphagia)
– Phagophobia  fear of swallowing, and refusal to
swallow may occur in hysteria, rabies, tetanus, and
pharyngeal paralysis due to fear of aspiration
• Oropharyngeal dysphagia, loss / decrease in:
- Swallowing ability(oropharyngeal phase)
- Post nasal regurgitation
- Discharge through the nose when swallowing
- Coughing during chewing (aspiration) &
repeated swallowing efforts to push food from
the hypopharynx.
LO 7
• Patophysiology of dysphagia
Pathophysiology
• Based on anatomic site of involvement 
oropharyngeal and esophageal dysphagia
• Normal transport of an ingested bolus depends on the
size of the ingested bolus & size of the lumen, force of
peristaltic contraction, deglutitive inhibition
– Dysphagia caused by a large bolus or narrow lumen 
mechanical dysphagia
– Dysphagia caused by weakness of peristaltic contractions or
to impaired deglutitive inhibition causing non peristaltic
contraction and impaired spincter relaxation  motor
dysphagia
Oropharyngeal dysphagia
Esophageal dysphagia
Approach to the patient
Dysphagia (Child)
• ~ difficulty of swallowing
• Caused by structural defect or motility disorder
– Structural defect : narrowing within the esophagus (stricture,
web, tumor); Extrinsic obstruction (vascular ring)
– Motility abnormalities of the oropharynx or the esophagus

• Dysphagia during the oropharyngeal phase of swallowing


(transfer)  neuromuscular disorders
– sensation that something is stuck in the upper esophagus is
globus (GER)
• Dysphagia during the esophageal phase of swallowing
– child may be able to point to the level of the chest where the
delay occurs; a child points to the suprasternal notch
Transfer dysphagia
• Complex sequence of neuromuscular events is
involved in the transfer of foods to the upper
esophagus
• Abnormalities of the muscles involved in the
ingestion process, their innervation, strength, or
coordination that usually cause transfer
dysphagia in infants and children
• Oropharyngeal problem is almost always part of
a more generalized neurologic or muscular
problem (botulism, diphtheria, cerebral palsy);
Painful oral lesions, such as acute viral stomatitis
or trauma
Non transfer dysphagia
• Primary motility disorders causing impaired peristaltic
function and dysphagia are rare in children
• Esophageal web, tracheobronchial remnant, or
vascular ring may cause dysphagia in infancy
• An esophageal stricture secondary to chronic
gastroesophageal reflux and esophagitis occasionally
presents with dysphagia as the first manifestation
• A Schatzki ring is another mechanical cause of
recurrent dysphagia presenting after infancy
• An esophageal foreign body or a stricture secondary
to a caustic ingestion
LO 8
• Classification based on Pathophysiology
A. Impaired inhibitory innervation
Decreasing function
- The corpus of the esophagus (diffuse
esophageal spasm)
- The lower esophageal corpus & lower
esophageal sphincter (LES) -> achalasia
B. Excitatory innervation disorder
Decreasing function: LES hypotension (GERD)
Rising function: hypertensive esophageal
peristaltic contraction
Akalasia
• Definition
Impaired motor segment of the smooth
muscle in the lower 2/3 of the esophagus, as a
result of degeneration of neurons myenterik
intramural plexus. (As a result disruption and
loss of LES relaxation peristaltik-> dysphagia,
chest pain, and regurgitation)
• Akalasia :
- Primer (unknown)
- Sekunder
• Pathogenesis
In achalasia, myenterik neurons in esophageal
plexus myenterikus reduced. Originally inhibitory
neurons containing VIP (vasoactive intestinal
peptide) and NOS (nitric oxide synthase) is
reduced, but at an advanced stage of excitatory
neurons containing acetylcholine are also
reduced. -> inhibitory neurons doesn’t work right
-> cause coordination of relaxation and peristaltic
of LES also doesn’t work right.
Clinical manifestation
• Dysphagia
• Weight loss
• Chest pain
• Regurgitation
• Nocturnal coughing
• Hiccups
• Pulmonary complication
Examination
• Clinical complaints
• Phisical examination not always specific
• Chest radiograph (loss of gastric air)
• Esophageal manometry, esophagogram
barium, esophagoscopy
Complication
• Mega-esophagus with heavy transit disorders,
risk of pneumonia aspiration, esophagus
malignoma, esophagus perforation.
Treatment
• CCB
• NCB
• Phospodiesterase inhibitor
• Bougie dilatation / baloon dilatation
• Botulinum toxin
• Myotomi Heller
Oropharyngeal candidiasis
• Fungal infection of Candida sp especially albicans
in the esophagus mukosas.
• Common in neonates from contact with the
organism in the birth canal
• lesions of oropharyngeal candidiasis (OPC)
appear as white plaques covering all or part of
the oropharyngeal mucosa
– plaques are removable from the underlying surface,
which is characteristically inflamed with pinpoint
hemorrhages
Risk Factor
• Antibiotic uses
• Surgery history
• Burns history
• Bacterial infection at the same time
• IV nutrition only
• Age
• Immune deficiency
• Acoholism
• Etc.
Pathophysiology

www.nature.com
Manifestation
• Dysphagia
• Odynophagia
• Heartburn
• Weight loss
• Fever
• Oral thrush
Diagnosis & Therapy
• confirmed by direct microscopic examination
on potassium hydroxide smears
• culture of scrapings from lesions

• Therapy
– nystatin will hasten recovery and reduce the risk
of spreading to other infants
– Persistent infections should be treated with
fluconazole
Schatzki Ring
• A lower esophageal mucosal ring
– thin, weblike constriction located at the
squamocolumnar mucosal junction at or near the
border of the LES
• It may result from GERD or be congenital in origin
• Invariably produces dysphagia (lumen < 1.3 cm)

• Symptom: dysphagia to solids, usually episodic

• Treatment: dilatation
Contractile ring
• A lower esophageal muscular ring
– proximal to the site of mucosal rings
– represent an abnormal uppermost segment of the LES
– they are not constant in size and shape

• Cause dysphagia & should be differentiated from


peptic strictures, achalasia, schiatzki ring,

• Do not respond well to dilatation


Gastroesophageal Reflux Disease
• Most common esophageal disorder in children of
all ages
• ~ retrograde movement of gastric contents across
the lower esophageal sphincter (LES) into the
esophagus

• Although occasional episodes of reflux are


physiologic  the phenomenon becomes
pathologic (GERD) in children who have episodes
that are more frequent or persistent, and thus
produce esophagitis or esophageal symptoms
Epidemiology
• Infant reflux becomes symptomatic during the
first few months of life, peaking at about 4 mo
and resolving in most by 12 mo and nearly all
by 24 mo
• Symptoms in older children tend to be chronic
Pathophysiology
• Transient LES relaxation (TLESR)
– is the major primary mechanism allowing reflux to
occur; independent of swallowing
– reducing LES pressure to 0-2 mm Hg (above gastric),
and last more than 10 s; appear by the 26 wk of
gestation
– Gastric distention (postprandially, or due to abnormal
gastric emptying or air swallowing) is the main
stimulus for TLESR
• increased movement, straining, obesity, large volume or
hyperosmolar meals, and increased respiratory effort (e.g.,
coughing, wheezing)  influence gastric pressure – volume
dynamics
Clinical manifestation
• Regurgitation (especially postprandially),
• Signs of esophagitis (irritability, arching, choking, gagging,
feeding aversion), resulting failure to thrive
• symptoms resolve spontaneously in the majority by 12 to
24 mo

• regurgitation during the preschool years


• complaints of abdominal and chest pain supervene during
later childhood and adolescence
• The respiratory (extraesophageal) presentations (GERD in
infants may manifest as obstructive apnea  stridor or
lower airway disease in which reflux complicates primary
airway disease such as laryngomalacia or
bronchopulmonary dysplasia)
Diagnosis
• history may be facilitated and standardized by
questionnaires (the Infant Gastroesophageal Reflux
Questionnaire, the I-GERQ)

• Esophageal tests:
– Contrast (usually barium) radiographic study of the
esophagus and upper gastrointestinal tract
– Esophageal pH monitoring of the distal esophagus
– Endoscopy  complications (stricture & Barrett’s
esophagus)
– Radionucleotide scintigraphy  aspiration and delayed
gastric emptying
Management
• Conservative therapy and lifestyle modification
– Dietary measures
• A short trial of a hypoallergenic diet may be used to exclude milk
or soy protein allergy before pharmacotherapy
• Older children  avoid acidic foods (tomatoes, chocolate, mint)
and beverages (juices, carbonated and caffeinated drinks,
alcohol).
• Weight reduction, elimination of smoke exposure
– Positioning measures
• Seated position worsens infant reflux and should be avoided in
infants with GERD
• nonprone positioning during sleep
• prone position and upright carried position may be used to
minimize reflux
• avoid abdominal flexion and compression that might worsen
reflux
• Pharmacotherapy
– Antacids
– H2RAs
• treatment of mild-to-moderate reflux esophagitis
• first-line therapy because of their excellent overall safety profile
– PPIs
• the most potent antireflux effect by blocking the hydrogen-potassium
ATPase channels of the final common pathway in gastric acid
secretion
• superior to H2RAs in the treatment of severe and erosive esophagitis
• Doses of omeprazole for children have been established (0.7-3.3
mg/kg/day)
– Prokinetic agents
• metoclopramide (dopamine-2 and 5HT-3 antagonist), bethanechol
(cholinergic agonist), and erythromycin (motilin receptor agonist)
• increase LES pressure; some improve gastric emptying or esophageal
clearance
– Surgery (fundoplication)
Caustic ingestion
• results in esophagitis, necrosis, perforation, and
stricture formation
• Most cases (70%) are accidental ingestions of liquid
alkali substances that produce severe, deep
liquefaction necrosis
• Acidic agents (20% of cases) are bitter, so less may be
consumed  coagulation necrosis

• Sign & symptoms: vomiting, drooling, refusal to drink,


oral burns, dysphagia, abdominal pain, and stridor.
– Twenty percent of patients develop esophageal strictures
– hematemesis, respiratory distress, or presence of at least
three symptoms predict severe lesions
• Diagnostic & treatment
– An upper endoscopy is recommended as the most
efficient means of rapid identification of tissue
damage and must be undertaken in symptomatic
children

– Dilution by water or milk is recommended as acute


treatment, but neutralization, induced emesis, and
gastric lavage are contraindicated
– Stricture risk is increased by circumferential
ulcerations, white plaques, and sloughing of the
mucosa. They may require treatment with dilation
– Some severe cases surgical resection
Foreign bodies in esophagus
• The majority (80%) of foreign body ingestions occur in
children, most of whom are between 6 mo and 3 yr of
age
• Food impactions are less common in children than in
adults and usually occur in children with an underlying
structural anomaly or motility disorder, such as repair
of esophageal atresia or eosinophilic esophagitis
• Most esophageal foreign bodies lodge at either the
level of the cricopharyngeus (upper esophageal
sphincter [UES]), the aortic arch, or just superior to the
diaphragm at the gastroesophageal junction (lower
esophageal sphincter [LES])
• Sign & symptoms
– 30% of children with esophageal foreign bodies may
be totally asymptomatic
– choking, gagging, and coughing may be followed by
excessive salivation, dysphagia, food refusal, emesis,
or pain in the neck, throat, or sternal notch regions
– Respiratory symptoms
• stridor, wheezing, cyanosis, or dyspnea may be encountered
if the foreign body impinges on the larynx or membranous
posterior tracheal wall
• Diagnostic & treatment
– plain anteroposterior radiographs of the neck,
chest, and abdomen, along with lateral views of
the neck and chest
– endoscopic visualization of the object and
underlying mucosa and removal of the objec

– An alternative technique for removing esophageal


coins impacted for under 24 hr, performed most
safely by experienced radiology personnel,
consists of passage of a Foley catheter beyond the
coin at fluoroscopy, inflating the balloon, and then
pulling the catheter and coin back simultaneously
with the patient in a prone oblique position
References
• Dalley, Arthur F. Keith L Moore. Clinically Oriented
Anatomy. 5th edition. Lippincott Williams & Wilcins; 2006
• Fauci. Braunwald. Dkk. Harrison’s Principles of Internal
Medicine. 17th edition. United State: The McGraw-Hills;
2008
• L. Mescher, Anthony. Junquera’s Basic Histology Text and
Atlas. 20th edition. United State: The McGraw-Hills; 2010
• Nath,R.L. A Textbook of Medicinal Biochemistry. New Delhi:
New Age International; 2002
• Nelson Textbook of Pediatric, 19th edition
• Sherwood,Lauralee. Fisiologi Manusia dari Sel ke Sistem.
Cetakan pertama edisi 2. Jakarta: EGC; 2001

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