PEMICU 1 GIT

Mudita Dewi
405150016
Anatomy of the upper gastrointestinal 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
Physiology of the upper gastrointestinal tract (mouth-
esophagus)
• Swallowing apparatus consists of the pharynx, cricopharyngeus
(upper esophageal sphincter), body of the esophagus, and lower
esophageal sphincter.
 Physiology of Swallowing

• Two models are used to describe the physiology of normal eating and
swallowing:
Four Stage Model Process Model of Feeding

 drinking and  eating and swallowing solid

swallowing liquid food
 Oral stage in eating solid
 Oral prepatory stage
food
 Oral propulsive stage  Stage 1 transport
 Pharyngeal stage  Food processing
 Esophageal stage  Stage 2 transpport
 Pharyngeal stage
 Esophageal stage
4 Main Stages

1. Oral Preparatory Stage, in which the food is chewed (masticated),

mixed with saliva, and formed into a cohesive ball (bolus)
2. Oral Stage, in which the food is moved back through the mouth
with a front-to-back squeezing action, performed primarily by the
tongue

http://calder.med.miami.edu/pointis/tbifam/swal1.html
4 Main Stages

3. Pharyngeal Stage, which begins with the

pharyngeal swallowing response:
• The food enters the upper throat area (above larynx)
• The soft palate elevates
• The epiglottis closes off the trachea, as the tongue
moves backwards and the pharyngeal wall moves
forward
• These actions help force the food downward to the
esophagus

http://calder.med.miami.edu/pointis/tbifam/swal1.html
4 Main Stages

4. Esophageal Stage, in which the food bolus enters the esophagus

(the tube that transports food directly to the stomach). The bolus
is moved to the stomach by a squeezing action of the throat
muscles (peristaltic).

http://calder.med.miami.edu/pointis/tbifam/swal1.html
Sherwood L. Introduction to human physiology. 8th ed. United States:
Brooks/Cole-Cengage Learning; 2013.
Sherwood L. Introduction to human physiology. 8th ed. United States:
Brooks/Cole-Cengage Learning; 2013.
Sherwood L. Introduction to human physiology. 8th ed. United States:
Brooks/Cole-Cengage Learning; 2013.
Histology of the upper gastrointestinal tract (mouth-
esophagus)
 ORAL CAVITY

• Covered by stratified squamous epithelium for protection

 LIPS (LABIA)

• Covered by thin skin, which has stratified squamous epithelium with

keratin
• The blood vessels near the surface caused the red color of the lips
• There are hairs, glandula sudorifera, glandula sebacea and labialis
gland that produce mucus
• There are orbicularis oris muscle in the middle
THE LIPS
 TONGUE

• Consist of muscle fibres

• The surface is covered by some papilla (filiformis, fungiformis and
circumvallate)
• Papilla filiformis → the most common and the smallest papilla, with
no taste bud
• Papilla fungiformis → the “fungi-like” shaped papilla, which has taste
bud
• Papilla circumvallate → the biggest papilla, on the posterior of the
tongue. It has sulcus, serous gland and taste buds
 TASTE BUDS

• In papilla fungiformis, circumvallate, pharynx, palatum and epiglottis

• It has gustatory pores (porus gustatorius)
• Neuroepithelial cell → connect with afferent axon; receptor for
gustatory
• Sustentacular cell → the supporting cell
• Basal cell → the basic cell
 TONSILS

• Lymphoid aggregation
• Tonsilla palatina and lingualis are covered by stratified squamous
epithelium, and there is a crypt
• There is one tonsilla pharyngeal, which covered by pseudostratified
epithelium with cilia
 TEETH

• Downward growth of the mouth epithelia differentiated into lamina

dentalis → form the ameloblast → produce teeth enamel
• Mesenchymal cell form the papilla dentalis and odontoblast
(odontoblast → produce dentin)
 SALIVARY GLANDS

• Major salivary glands : parotis, submandibularis and sublingualis

• Consists of ductus excretorius and acini secretorius, which flow the
saliva to the oral cavity
• Serous or mucoid cells
• Myoepithel contraction cell surrounds the acini secretorius
• Intercalaris ducts → striated ducts → interlobular ducts →
excretorius ducts
 PRINCIPAL LAYERS OF THE GI LUMEN

• Tunica mucosa → epithelial cell, loosen connective tissue (lamina

propria), smooth muscle layer (muscularis mucosa; circular inner
layer and longitudinal outer layer)
• Tunica submucous → irregular tight connective tissue, with blood
vessels, nerves and lymphoid vessels
• Tunica muscularis externa → thick smooth muscle layer (circular
inner layer and longitudinal outer layer). Between the inner and
outer layer, there are myenteric nerve plexus (Auerbach plexus) →
control the motility of the smooth muscles
 PRINCIPAL LAYERS OF THE GI LUMEN

• Tunica serous or adventisia → thin layer; covered the visceral organs

 ESOPHAGUS

• Canal that connects the pharynx and gaster

• Lumen is covered by stratified squamous epithelial with no keratin
• On the 1/3 proximal area, there is skeletal muscles on the tunica
muscularis externa
• On the 1/3 medial area, there is skeletal and smooth muscles on the
tunica muscularis externa
• On the 1/3 distal area, there is smooth muscles on the tunica
muscularis externa
 ESOPHAGUS

• The mucous glands lies on the lamina propria and tunica submucous
• Tunica adventisia surrounds the esophagus in thorax area
• The muscularis mucous and submucous tunica connects with the
gaster
Biochemistry of the upper gastrointestinal tract (mouth-
esophagus)
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.
Dysphagia
Definition

• A condition in which disruption of the swallowing process interferes

with a patient’s ability to eat.
• It can result in aspiration pneumonia, malnutrition, dehydration,
weight loss, and airway abstruction.

• Difficulties in transferring the food bolus from the oropharynx to the

upper esophagus (oropharyngeal dysphagia) or from impaired
transport of the bolus through the body of the esophagus
(esophageal dysphagia).
 Etiology
CNS Muscular Endocrine Pharmacologic Surgical causes
disorders disorders causes
a. Alzheimer a. Muscular a. Secondary a. CNS depressants a. Laryngectomy
disease dystrophies myopathies in b. Antipsychotics b. Pharyngectomy
b. Brain tumors b. Spinal Cushing c. Corticosteroids c. Esophagectomy
c. Guillain-Barre muscular syndrome, d. Lipid-lowering d. Oral cavity
syndrome atrophy hyperthyroidis agents cancer
d. Huntington c. Polymyositis m, and e. Colchicine
disease d. Dermatomyo hypothyroidism f. Aminoglycosides
e. CNS infections sitis b. Vitamin B-12 g. Anticholinergic
f. Stroke deficiency: drugs
g. TBI leading to Mucosal injury:
h. Parkinson pseudobulbar a. Potassium
disease palsy secondary chlorice tablets
i. Poliomyelitis to b. NSAIDs
j. Cerebral palsy corticolbulbar c. Antibiotc
k. Multiple tract (doxycline,
sclerosis dysfunction tetracycline,
l. ALS clindamycin)
Xerostomia:
a. Antichlinergics
b. ACE-I
c. Antihistamines
Signs and symptoms
Oral or pharyngeal dysphagia:
• Coughing or chocking with
swallowing
• Difficulty initiating swallowing
• Food sticking in the throat
• Sialorrhea (drooling)
• Unexplained weight loss
• Change in dietary habits
• Recurrent pneumonia
• Change in voice or speech
• Nasal regurgitation
Esophageal dysphagia:
• Sensation of food sticking in the
chest or throat
• Change in dietary habits
• Recurrent pneumonia
• Symptoms of gastroesophageal
reflux disease (GERD), including
heartburn, belching, sour
regurgitation, and water brash
Oropharyngeal dysphagia

• Problems with the oral phase of swallowing cause drooling or spillage

of food from the mouth, inability to chew or initiate swallowing, or
dry mouth.
• Pharyngeal dysphagia is characterized by an immediate sense of the
bolus catching in the neck, the need to swallow repeatedly to clear
food from the pharynx, or coughing or choking during meals.
Esophageal dysphagia

• Esophageal dysphagia may be caused by mechanical lesions

obstructing the esophagus or by motility disorders.
• Patients with mechanical obstruction experience dysphagia, primarily
for solids. This is recurrent, predictable, and, if the lesion progresses,
will worsen as the lumen narrows.
• Patients with motility disorders have dysphagia for both solids and
liquids. It is episodic, unpredictable, and can be progressive.
Diagnostic studies
Diagnostic studies

• Non-invasive screening
• Dry swallowing
• Repetitive saliva swallowing test
• Water swallow test
• Colored water test
• Cervical auscultation of swallowing
• Swallowing provocation test
Diagnosis

• Transnasal esophagoscopy
• Cervical auscultation
• Blood test: including thyroid-stimulating hormone, vitamin
B-12, and creatine kinase; may be useful, especially in
neurogenic dysphagia
• Imaging studies: May include videofluoroscopy/modified
barium swallow, CT-scanning, MRI, and chest radiography
• Endoscopic examination
• Esophageal pH monitoring: The criterion standard for
diagnosing reflux disease
• Pulmonary function tests
Endoscopy

• Esophagogastroduodenoscopy (EGD) affords an excellent view of

mucosal surfaces of the esophagus, stomach, and proximal
duodenum.
• Standard diagnostic functions include inspection, biopsy,
photography, and videorecording.
• GI endoscopy is generally indicated:
1. If a change in management is probable based on results of endoscopy.
2. After an empirical trial of therapy for a suspected benign digestive disorder
has been unsuccessful.
3. As the initial method of evaluation as an alternative to radiographic studies.
4. When a primary therapeutic procedure is contemplated
Examination

• The bedside physical examination should include examination of the

neck, mouth, oropharynx, and larynx.
• Direct observation of the following is necessary:
• Lip closure
• Jaw closure
• Chewing and mastication
• Tongue mobility and strength
• Palatal and laryngeal elevation
• Salivation
• Oral sensitivity
Examination

• Look for oral-motor and laryngeal mechanisms; testing of cranial

nerves V and VII-XII is essential (oropharyngeal dysphagia).
• Evaluate patient's level of alertness and cognitive status
• Evaluate pharyngeal elevation
• Testing for the gag reflex
• Cervical auscultation
• Direct observation of the act of swallowing, observe the patient for 1
minute or more to see if a delayed cough response is present
Pharmacologic treatment

• Botulinum toxin type A (BoNT-A)

• Diltiazem
• Glucagon
• Cystine-depleting therapy with cysteamine
• Nitrates
Dietary treatment

• Dysphagia diet 1 : Thin liquids (eg: fruit juice, coffee, tea)

• Dysphagia diet 2 : Nectar-thick liquids (eg: cream, soup, tomato juice)
• Dysphagia diet 3 : Honey-thick liquids (eg: liquids that are thickened to
ahoney consistency)
• Dysphagia diet 4: Pudding-thick liquids/foods (eg: mashed bananas,
cooked cereals, purees)
• Dysphagia diet 5 : Mechanical soft foods (eg: meat loaf, baked beans,
casseroles)
• Dysphagia diet 6 : Chewy foods (eg: pizza, cheese, bagels)
• Dysphagia diet 7 : Foods that fall apart (eg: bread, rice, muffins)
• Dysphagia diet 8 : Mixed textures
Exercise and facilitation techniques
Types of exercises:
• Indirect : exercises to strengthen swallowing muscles
• Direct : exercises to be performed while swallowing
Facilitation techniques:
• Somatosensory stimulation: in the form of an electrical
current applied to the pharynx
• Deep Pharyngeal Neuromuscular Stimulation (DPNS)
• Tactile-thermal stimulation (TTS)
Compensatory techniques

Maintaining oral feeding to reduce aspiration or improve pharyngeal

clearance:
• Use of the chin-tuck position
• Rotation of the head to the affected side
• Tilting of the head to the strong side
• Lying on one’s side or back during swallowing
• Supraglottic swallow
• Bolus-clearing maneuvers
Enteral feeding

• Nasogastric Tube (NGT) feeing

• Oroesophageal tube feeding
• Percutaneous Endoscopic Gastrostomy (PEG)
Surgery for chronic aspiration

• Medialization: to restore glottis closure and subglottic

pressure during the swallow
• Laryngeal suspension: the larynx is in a relatively protected
position under the tongue base
• Laryngeal closure: this may be performed to close the glottis
off, in this way protecting the airway at the expense of
phonation
• Laryngotracheal separation-diversion: this procedure may be
done to separate the airway from the alimentary tract
Odynophagia
Odinophagia

• Odynophagia is sharp substernal pain on swallowing that may limit

oral intake. It usually reflects severe erosive disease.
• It is most commonly associated with infectious esophagitis due to
Candida, herpesviruses, or CMV, especially in immunocompromised
patients, corrosive injury due to caustic ingestions and by pill-induced
ulcers.
• Odynophagia may occur as a result of distension of the esophagus by
food bolus, but it is also a marker for esophageal injuries such as
laceration, abrasion or perforation.
Causes

• Swallowing problems may be due to infections, such as:

• Cytomegalovirus
• Gum disease (gingivitis)
• Herpes simplex virus
• Human immunodeficiency virus (HIV)
• Pharyngitis (sore throat)
• Thrush
• Swallowing problems may be due to a problem with the esophagus, such as:
• Achalasia
• Esophageal spasms
• Gastroesophageal reflux disease
• Inflammation of the esophagus
• Nutcracker esophagus
• Ulcer in the espophagus, especially due to the antibiotic doxycycline
• Other causes of swallowing problems include:
• Mouth or throat ulcers
• Something stuck in the throat (for example, fish or chicken bones)
• Tooth infection or abscess
Diagnostic test

• Upper endoscopy
• Barium esophagography
• Esophageal manomatry
• Esophageal pH recording and impedance testing
Treatment

• Odynophagia from pill esophagitis  withdrawal of offending

medication, acid suppression and topical anesthetics
• Odynophagia from infectious esophagitis 
• Antibiotics  bacterial
• Antifungal  fungal (Nystatin or clotrimazole)
• Self limiting if viral
• Odynophagia from ingestion foreign bodies (fish bone)  remove
the foreign bodies
Home care treatment

• To ease swallowing pain:

• Eat slowly and chew food well.
• Eat pureed foods or liquids if solid foods are hard to swallow.
• Avoid very cold or very hot foods if they make your symptoms worse.
• If someone is choking, immediately perform the Heimlich maneuver.
Pathophysiology of feeding
(swallowing) difficulty
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
Oral phase disorder

• Pocketing of food in the mouth, circumoral leakage, and early

pharyngeal spill can occur with weakness and poor coordination of
the lips, cheeks, and tongue. Weak posterior tongue can lead to
abnormal tongue thrusting.
• Aspiration of food or drink, especially during inhalation, can occur
before pharyngeal swallowing due to premature pharyngeal spillage.
• Changes in mental status with cognitive deficits also may affect the
initiation of swallowing, increasing the tendency to pocket food in
the lateral sulci and leading to possible aspiration.
Pharyngeal-phase disorders

• In people without dysphasia, small amounts of food commonly are

retained in the valleculae or pyriform sinus after swallowing. If there
is weakness in or a lack of coordination of the pharyngeal muscles or
if there is a poor opening of the upper esophageal sphincter, patients
may retain excessive amounts of food in the pharynx and experience
overflow aspiration after swallowing.
• Dysfunction or abnormalities of the soft palate and superior pharynx
(eg, cleft palate) can lead to nasopharyngeal reflux following
uvulectomy.
Esophagel-phase disorders

• Impaired esophageal function can result in retention of food and

liquid in the esophagus after swallowing. This retention may result
from a mechanical obstruction, a motility disorder, or an impairment
of the opening of the lower esophageal sphincter.
• Achalasia can lead to reduced gastroesophageal junction relaxation
or absent esophageal peristalsis.
Approach to the patient
Etiology and epidemiology of
feeding (swallowing)difficulty -
Adult
A. Definition of Achalasia

• Achalasia is a primary esophageal motility disorder characterized by

the absence of esophageal peristalsis and impaired relaxation of the
lower esophageal sphincter (LES) in response to swallowing.
Sign and symptoms

• Dysphagia (most common)

• Regurgitation
• Chest pain
• Heartburn
• Weight loss
Pathophysiology

• LES pressure and relaxation are regulated by excitatory (eg,

acetylcholine, substance P) and inhibitory (eg, nitric oxide, vasoactive
intestinal peptide) neurotransmitters.
• Persons with achalasia lack nonadrenergic, noncholinergic, inhibitory
ganglion cells, causing an imbalance in excitatory and inhibitory
neurotransmission.
• The result is a hypertensive nonrelaxed esophageal sphincter.
• Chagas disease may cause a similar disorder.
Diagnosis

• Performing an esophageal motility test on all patients suspected of

having achalasia;
• Using esophagram findings to support a diagnosis;
• Using barium esophagram, as recommended for patients with
equivocal motility testing; and
• Endoscopic assessment of the gastroesophageal junction and gastric
cardia, as recommended, to rule out pseudoachalasia.
Diagnosis

• Barium swallow: Bird’s beak appearance, esophageal dilatation

• Esophageal manometry (the criterion standard): Incomplete LES
relaxation in response to swallowing, high resting LES pressure,
absent esophageal peristalsis
• Prolonged esophageal pH monitoring to rule out gastroesophageal
reflux disease and determine if abnormal reflux is being caused by
treatment
• Esophagogastroduodenoscopy to rule out cancer of the GEJ or
fundus
• Concomitant endoscopic ultrasonography if a tumor is suspected
Management

• Initial therapy should be either graded pneumatic dilation (PD) or

laparoscopic surgical myotomy with a partial fundoplication in
patients fit to undergo surgery;
• Procedures should be performed in high-volume centers of
excellence;
• Initial therapy choice should be based on patient age, sex,
preference, and local institutional expertise;
• Botulinum toxin therapy is recommended for patients not suited to
PD or surgery; and
• Pharmacologic therapy can be used for patients not undergoing PD or
myotomy and who have failed botulinum toxin therapy (nitrates and
calcium channel blockers most common).
Treatment

• Injection with botulinum toxin (Botox). This may help relax the
sphincter muscles. However, the benefit wears off within a few
weeks or months.
• Medications, such as long-acting nitrates or calcium channel blockers.
These drugs can be used to relax the lower esophagus sphincter.
• Surgery (called an esophagomyotomy). This procedure may be
needed to decrease the pressure in the lower sphincter.
• Widening (dilation) of the esophagus at the location of the
narrowing. This is done during esophagogastroduodenoscopy.
Management

• Pharmacologic and other nonsurgical treatments include the

following:
• Administration of calcium channel blockers and nitrates decrease LES
pressure (primarily in elderly patients who cannot undergo pneumatic
dilatation or surgery)
• Endoscopic intrasphincteric injection of botulinum toxin to block
acetylcholine release at the level of the LES (mainly in elderly patients who
are poor candidates for dilatation or surgery)
 B. Malignant

• Esophagus malignant histologically classified into squamosa cell

carcinoma, adenocarcinoma, carcinocarsinoma, and sarchoma
• Squamosa cell carcinoma is the most common malignant esophagus

Causes
 Idiopathic
 Food carcinogenic (nitrosamin, alcohol, tobacco, and
moldy food )
Symptoms

• Symptoms of obstruction
• progressive dysphagia, regurgitation, loss of weight
• Symptoms of neoplasm spread to the mediastinum
• hoarseness, pain in restrosternal, back, servical area and bronchopulmoner
sypmptom
• Symptomps of metastasis to glands lymph
• Palpable Mass in supraclaviculla area
• Early symptom of malignant esophagus can be like bolus stuck
somewhere during swallowing, pain on swallowing, spread to ears,
throat, chest, arm also spasm esophagus in the proximal of neoplasm
• Dysphagia happened if esophagus tube filled mass neoplsm >50%. In
early dysphagia happened if patient swallow the solid food,
increasing degrees obstruction the patient will difficult to swallowing
soft foods and then fluid food
• If neoplasm infiltrate into trachea  coughing, stridor expiration, and
breathless
Diagnosis

• Biopsy of neoplasm mass

• Sitologic

• both two can used oesophagoscopy with oesophagoscop optical fiber

or rigid oesophagoscop
Esophageal cancer staging

• Stage I.
– This cancer occurs only in the top layer of cells lining your esophagus.
• Stage II.
– The cancer has invaded deeper layers of your esophagus lining and may have
spread to nearby lymph nodes.
• Stage III.
– The cancer has spread to the deepest layers of the wall of your esophagus
and to nearby tissues or lymph nodes.
• Stage IV.
– The cancer has spread to other parts of your body.
Radiological Examination

• Rontgen with barium contras (esofagogram)

• Specific : narrow tube and irreguler and also stiffness esophagus wall
• Eksofitic neoplasm with polipoid form appears filling deffect multiple
and irreguler eksofitic
• Esofagogram with multiple contras  show small lession of
neoplasm
• CT-scan and MRI  may helped to proper diagnosis
• CT-scan can also determine size of primary neoplasm and finding
enlargement of lymph glands along esophagus
Examination Oesophagoscopy

• The malignant tumor of the esophagus with eksofitic looks red or

grayish-white, irreguler and easy bleeding
• With oesophagoscopy can be taking by biopsy and sitology
Management

• Determine location, types, and metastasis

• Surgery, radiotherapy, chemotherapy, surgery and radiotherapy,
surgery and chemotherapy and also surgery, radiotherapy and
chemotherapy
• Surgery  to curative and palliative
• Early stage  do surgery Enblock esophagectomy
• Advanced stage  surgery by pass like end esophagogastrotomy or
side to end esophagocolostomy
Lifestyle and home remedies

• Choose easy-to-swallow foods.

– If you have trouble swallowing, choose foods that are soothing and easy to
swallow, such as soups, yogurt or milkshakes.
• Eat smaller meals more frequently.
– Eat several small meals throughout the day instead of two or three larger
ones.
• Keep nourishing snacks within easy reach.
– If snacks are readily available, you're more likely to eat.
• Talk to your doctor about vitamin and mineral supplements.
– If you haven't been eating as much as you normally would or if your usual
foods are restricted, you could be deficient in a variety of nutrients.
C. Thrush

• Infection of the buccal cavity by Candida albicans

• The disease is typically limited to infants and neonates, patients on
antibiotics or steroids, and patients with polyendocrine disorders or
underlying immune dysfunction
 Pathophysiology

www.nature.com
Physical

• Lesions often start as tiny focal areas that enlarge to white patches
on oral mucosa
• When scraped with a tongue blade, lesions are difficult to remove
and leave behind an inflamed base that may be painful and may
bleed
Causes

• Consider an underlying immune deficiency especially in recurrent

cases and in older infants
• Systemic antibiotic use may disrupt the normal flora, promoting
candidal overgrowth
• Use of systemic and inhaled steroids is associated with incidence of
oral thrush
Treatment

• Nystatin
• DOC for oral thrush. Changes permeability of fungal cell membrane after binding to cell membrane sterols,
causing cellular contents to leak

• Amphotericin B deoxycholate
• Clotrimazole
• Very effective treatment in immunocompetent host

• Miconazole oral
• Damages fungal cell wall membrane by inhibiting biosynthesis of ergosterol; increases membrane
permeability, causing nutrients to leak out

• Fluconazole
• Synthetic PO antifungal (broad-spectrum bistriazole) that selectively inhibits fungal CYP450 and sterol C-14
alpha-demethylation, which prevents conversion of lanosterol to ergosterol, thereby disrupting cellular
membranes
 Difference candidiasis in adult and child
Adult Child

Risk factor • fisiologic : pregnancy, age(very young or very old), •The use of antibiotics will make the
menstruation cycle unbalance of mushroom and
•Non fisiologic : trauma(broken skin because work, bacteria
maseration skin on wash worker and broken teeth(pressure •Disease like malnutrition, blood
from fake teeth), malnutrition (riboflavin defeciency), disease, malignancy
endocrine disorder(diabetes melitus), ferocity(carcinoma, •The act or Procedure medic and the
hematologic ferocity), patient in ICU, therapy with tool that used
antibiotics, corticosteroid, immunosupresan, other
infectious disease or chronic disease and immunodeficiency
(AIDS), neutropenia and colonization of mushroom
 Difference candidiasis in adult and child
Adult •Child

Etology •Infection of the buccal cavity by •Inadequate sterilization of teats

candida albicans and bottles
•The long use of antibiotics or •From mother’s breast of the
steroids attendant’s hand
•Immunodeficiency •Newborns are infected during
passage in birth canal
•The long use of antibiotic therapy
•Infant’s auto infection when he has
candida diaper dermatitis and he
touch the diaper area then put his
hands into mouth
D. Glossitis

• Glossitis is a problem in which the tongue is swollen and changes

color, often making the surface of the tongue appear smooth.
Causes

• Glossitis is often a symptom of other condition, such as :

• Allergic reactions to oralcare products, foods, or medicine
• Dry mouth due to Sjogren syndrome
• Infection from bacteria, yeast or viruses (including oral herpes)
• Injury
• Skin conditions that affect the mouth
• Irritants such as tobacco, alcohol, hot foods, spices, or other irritants
• Hormonal factors
Symptoms

• Symptoms of glossitis may come on quickly or develop over time.

• They include :
• Problems chewing, swallowing, or speaking
• Smooth surface of the tongue
• Sore, tender, or swollen tongue
• Pale or bright red color to the tongue
• Tongue swelling
• Rare symptoms or problems include :
• Blocked airway
• Problems speaking, chewing, or swallowing
Treatment

• Treatment may include :

• Good oral care. Brush your teeth thoroughly at least twice a day and floss at
least once a day
• Antibiotics or other medicines to treat infection
• Diet changes and supplements to treat nutrition problems
• Avoiding irritants to ease discomfort
E. Mouth ulcers

• Paniful round or oval sores that form in the mouth, most often on the
inside of the cheeks or lips
• Usually white, red, yellow or grey in colour and are inflamed (red and
swollen) around the edge
Aphthous Ulcers

• Recurrent aphthous stomatitis (RAS) is a common condition,

restricted to the mouth, that typically starts in childhood or
adolescence as recurrent small, round, or ovoid ulcers with
circumscribed margins, erythematous haloes, and yellow or
gray floors.
• A positive family history of similar ulcers is common, and the
natural history is typically of resolution in the third decade of
life.
Pathophysiology

• A genetic basis exists in about one third of patients with RAS,

an increased frequency of HLA types A2, A11, B12, and DR2,
and susceptibility to RAS which segregates in families in
association with HLA haplotypes.
• RAS probably involves cell-mediated mechanisms, but the
precise immunopathogenesis remains unclear. Phagocytic
and cytotoxic T cells probably aid in destruction of oral
epithelium that is directed and sustained by local cytokine
release.
Pathophysiology

• Patients with active RAS have an increased proportion of

gamma-delta T cells compared with control subjects and
patients with inactive RAS. Gamma-delta T cells may be
involved in antibody-dependent cell-mediated cytotoxicity
(ADCC).
• Compared with control subjects, individuals with RAS have
raised serum levels of cytokines such as interleukin (IL)–6
and IL-2R, soluble intercellular adhesion modules (ICAM),
vascular cell adhesion modules (VCAM), and E-selectin;
however, some of these do not correlate with disease
activity
Predisposing factors

• Cessation of smoking: This may precipitate or exacerbate RAS in some cases.

• Stress: This underlies RAS in some cases; ulcers appear to exacerbate during
school or university examination times.
• Trauma: Biting of the mucosa and wearing of dental appliances may lead to
some ulcers; RAS is uncommon on keratinized mucosae.
• Endocrine factors in some women: RAS is clearly related to the progestogen level
fall in the luteal phase of the menstrual cycle, and ulcers may then temporarily
regress in pregnancy.
• Allergies to food: Food allergies occasionally underlie RAS; the prevalence of
atopy is high. Patients with aphthae may occasionally have a reaction to cow's
milk, and may have been weaned at an early age.
• Sodium lauryl sulphate (SLS): This is a detergent in some oral healthcare
products that may aggravate or produce oral ulceration.
Causes

• Hypersensitivity reactions to exogenous antigens other than

gluten do not have a significant etiologic role in RAS, and
associations with atopy are inconsistent.
• Local physical trauma may initiate ulcers in susceptible
people, and RAS is uncommon where mucosal keratinization
is present or in patients who smoke tobacco.
• A consistent association between aphthous ulceration and
psychological illness, zinc deficiency, or sex hormone levels is
unlikely.
• Helicobacter pylori has been detected in lesional tissue of ill-
defined oral ulcers,
Diagnosis

• Complete blood cell count

• Hemoglobin test
• White blood cell count with differential
• Red blood cell indices
• Iron studies (usually an assay of serum ferritin levels)
• Red blood cell folate assay
• Serum vitamin B-12 measurements
• Serum antiendomysium antibody and transglutaminase
assay (positive in celiac disease)
Treatment

• Vitamin B12 used orally may have some effect

• Topical corticosteroids (TCs) remain the mainstays of treatment. A
spectrum of different TCs can be used. At best, TCs reduce painful
symptoms but not the rate of ulcer recurrence. The commonly used
preparations are as follows:
- Hydrocortisone hemisuccinate pellets (Corlan), 2.5 mg used 4 times daily
- Triamcinolone acetonide in carboxymethyl cellulose paste (Adcortyl in
orabase [withdrawn in some countries], Kenalog), administered 4 times daily
- Betamethasone sodium phosphate as a 0.5-mg tablet dissolved in 15 mL of
water to make a mouth rinse, used 4 times daily for 4 minutes each time
Corticosteroids

• Triamcinolone topical (Aristocort, Flutex, Kenalog)

• Decreases inflammation by suppressing migration of PMNs and reversing capillary
permeability.
• Betamethasone topical (Alphatrex, Diprolene, Maxivate)
• For inflammatory dermatoses responsive to steroids. Decreases inflammation by
suppressing migration of PMNs and reversing capillary permeability.
• Fluocinolone (Synalar, Fluonid)
• High-potency topical corticosteroid that inhibits cell proliferation and is
immunosuppressive, antiproliferative, and anti-inflammatory.
• Fluocinonide (Fluonex, Lidex)
• High-potency topical corticosteroid that inhibits cell proliferation and is
immunosuppressive and anti-inflammatory.
• Clobetasol (Temovate)
• Class I superpotent topical steroid; suppresses mitosis and increases synthesis of
proteins that decrease inflammation and cause vasoconstriction.
Oral Rinses - Bioadherent oral (Gelclair)
• Adheres to the mucosal surface of mouth and forms a protective
coating that shields exposed and overstimulated nerve endings.
Ingredients:
- Water
- Maltodextrin
- propylene glycol
- polyvinylpyrrolidone (PVP)
- sodium hyaluronate
- potassium sorbate
- sodium benzoate
- hydroxy ethylcellulose
- polyethylene glycol (PEG)–40
- hydrogenated castor oil
- disodium edetate
- benzalkonium chloride
- Flavoring
- saccharin sodium
- glycyrrhetinic acid.
Herpes Oral
Causes

• Herpes Simplex Virus (type 1, herpes-1or HSV-1) causes about 80% of

cases of oral herpes infections.
• Herpes Simplex Viruses (type 2, herpes-2 or HSV-2) causes the other
20% and causes the majority of genital herpes infections.
Symptoms and Signs

• Pain, burning, tingling, or itching occurs at the infection site before

the sores appear.
• These symptoms happen prior to the appearance of sores, bumps, or
blisters
• Clusters of blisters erupt  break down rapidly and appear as tiny,
shallow gray ulcers on a red base.
• A few days later, they become crusted or scabbed and appear drier
and more yellow.
Symptoms and Signs

Oral sores: The most intense pain caused by these sores

occurs at the onset and can make eating and drinking difficult.
• The sores can occur on the lips, gums, throat, the front of the tongue,
the inside of the cheeks, and the roof of the mouth.
• They can also extend down the chin and neck.
• The gums can become mildly swollen, red-colored, and may bleed.
• Neck lymph nodes often swell and become painful.
• People in their teens and 20s can develop a painful throat with
shallow ulcers and a grayish coating on the tonsils.
Risk Factors

• 14-49 years of age, about 60% of the population has been infected
• by age 60, about 85% of the population has been infected with HSV-1
Pathophysiology

• HSV-1 affects only humans (mouth sores most commonly)

Oral inflammation from HSV-1 is also termed herpes
gingivostomatitis.
• People contract HSV-1 by touching infected saliva, mucous
membranes, or skin.
• Because the virus is highly contagious, a majority of the
population is infected by at least one herpes subtype of HSV-
1 before adulthood.
Pathophysiology

• After HSV-1 infects a person, it has a rather unique ability to

proceed through three stages.
• Stage 1 -- Primary infection: The virus enters the skin or mucous
membrane, usually through small cracks or breaks, and then
reproduces. During this stage, oral sores, blisters, and other
symptoms, such as fever, may develop.
• The virus may not cause any sores and symptoms. People may not know
that they have an infection. This is called asymptomatic infection.
• Asymptomatic infection occurs twice as often as the disease with
symptoms.
Pathophysiology

• Stage 2 -- Latency: From the infected site, the virus moves to a mass of
nerve tissue in the spine called the dorsal root ganglion. There the virus
reproduces again, usually without any symptoms, and becomes inactive,
until reactivated by certain body conditions.
• Stage 3 -- Recurrence: When people encounter certain stresses,
emotional or physical, the virus may reactivate and cause new sores and
symptoms. The following factors may contribute to recurrence: stress,
ultraviolet light (including sunshine), fever, fatigue, hormonal changes
(for example, menstruation), immune depression, and trauma to a site
or a nerve region where previous HSV infection occurred.
Diagnosis

• A sample (tissue or fluid) from the sores to identify the virus

as HSV
• A viral culture analysis
• A staining test called the Tzanck smear (shows nonspecific
cell nucleus changes due to HSV)
• Antigen and antibody studies (serologic and PCR tests to
determine if infection is caused by HSV-1 or HSV- 2)
Treatment

• A topical anesthetic such as viscous Lidocaine (Dilocaine,

Nervocaine, Xylocaine, Zilactin-L)  relieve pain associated
with oral blisters and lesions.
• Oral or IV medication does exist for HSV but is not
recommended for people with a normal immune system. It
is used only for people with weakened immune systems,
infants younger than 6 weeks of age, or people with severe
disease
Treatment

• Some people may require hospital admission:

• Those with severe local infection
• People whose infection has spread to other organ systems
• People with weakened immune systems
• Dehydrated individuals who need IV hydration
• Infants younger than 6 weeks of age
Treatment

• Oral antiviral drugs include

• Acyclovir (Zovirax),
• Valacyclovir (Valtrex),
• Famcyclovir (Famvir),
• Topical acyclovir or penciclovir (Denavir) creams may shorten attacks
of recurrent HSV-1 if it is applied early, usually before lesions
develop.
Prevention

• avoid touching saliva, skin, or mucous membranes of people who

have HSV-1 lesions
Complications

• Atopic eczema
• Encephalitis
• Keratoconjunctivitis,
• Pharyngitis,
• Hepatitis,
• Herpes whitlow (HSV blisters or lesions on the finger[s])
Etiology and epidemiology of
feeding (swallowing)difficulty -
Child
A. Reflux esophagitis

• Esophagitis (inflammation of the squamous esophageal epithelium)

may result from various causes, including acid and nonacid
gastroesophageal reflux (GER), food allergies, dysmotility due to
various causes, infections, trauma, and iatrogenic causes.
• Infants with gastroesophageal reflux are at greater risk of aspiration.
Symptoms include weight loss, regurgitation, excessive crying,
backache, respiratory distress, and apnea.
• Diagnosis can be obtain from a thorough history and physical
examination
Sign and symptoms

Specific sign Nonspecific sign (esophageal pain)

• Effortless emesis • Crying
• Regurgitation • Irritability
• Hematemesis
• Sleep or feeding problem
• Hiccoughs last a long time
• Hard swallows • Arching of the back
• Apnea (chronic) • Colic
• Chronic respi illness
• Asthma exacerbation
• Food aversion
• Weight loss
• Failure to thrive
Pathophysiology

• Distal esophageal inflammation results when gastric and duodenal

fluids, including gastric acid, pepsin, trypsin, and bile, are
regurgitated into the esophagus.
• A decrease in the lower esophageal sphincter (LES) tone and altered
motility increase esophageal clearance time and cause GER
• Esophageal inflammation can further induce both mechanisms,
creating a vicious circle.
• Factors that increase esophageal clearance time include posture-
gravity interactions, size and content of a meal, abnormal gastric
emptying, and abnormal esophageal peristalsis.
Pathophysiology

• Mild, early changes may include irritation of the esophageal mucosa

with basal cell hyperplasia and thickening of the papillae.
• This progresses along a spectrum of severity that can lead to
infiltration of inflammatory cells, ulcerations, scarring, and fibrosis
with stenosis.
• Cellular metaplasia to columnar epithelium, known as Barrett
esophagus, can also occur. Barrett esophagus is rare in the pediatric
population; within the pediatric population, this condition is more
frequent in adolescents than in younger children.
Diagnosis

• Esophagogastroduodenoscopy => Biopsy samples are always

obtained to look for histologic confirmation
• Barium studies => vomiting and dysphagia
• Chest radiography
• Computed tomography
• Esophageal pH probe monitoring
• Intraluminal impedance monitoring
• Gastroesophageal scintigraphy
• Esophageal manometry
Treatment

• Prone and elevated head positioning

• Feeding recommendations (eg, thickening formula, providing smaller
and more frequent feedings, fasting for at least 2 h before sleeping in
older children)
• Conservative reflux measures (eg, eliminating tobacco smoke
exposure)
• Proton pump inhibitors (PPIs)
• Surgical referral for Nissen fundoplication
• A gastrostomy or jejunostomy tube may be placed to assist with
feeding.
Complications

• Perforation of the esophagus => bleeding or upper airway

obstruction
• Apnea, chronic respiratory illnesses (including asthma), and failure to
thrive
• Barret esophagus and adenocarcinoma (rare)
• Prolong and severe esophagitis=> stricture
DDx

• Burns, Chemical
• Candidiasis
• Cytomegalovirus Infection
• Gastroesophageal Reflux
• Gastrointestinal Foreign Bodies
• Herpes Simplex Virus Infection
• Peptic Ulcer Disease
• Sandifer Syndrome
• Torticollis
B. Candidiasis orofaring

• Candidiasis pseudomembrane acute/oral trush

• Candidiasis atroficans acute
• Angular cheilitis
Candidiasis pseudomembrane acute/oral
trush
• Most common in baby and child
• Form with white patches which are easily wiped off leaving red,
bleeding, sore surface
• At start, to look membrane mucus red with thick granula
• At next day to look white patch at sewing needle large.
• At 2-3 days will combine to become large patch like membrane
• The more common place on mucosa bukalis, dorsal and lateral
tongue, gums and pharynx.
Candidiasis atroficans acute (glositis)

• Cause by therapy with antibiotics

• Erotion in mouth mucosa and lost of papil tongue in dorsal
• No pseudomembrane, tongue look slippery and red
• Sore at tongue
• This symptom lost at the same time the antibiotics got stop
Angular cheilitis

• Sore cracks and rednesss at angle of mouth

• Cause by pile of liquid and make ideal place for candida
• Can be granula, with erithematous erotion and become
deskuamation epitel surrounded by hyperceratosis
Candidiasis esophagus

• The main symptoms is dysfagia

• The most common place candida live on 1/3 dorsal esophagus
• Endoscopy : like oral thrush
• Esofagogram : mucosa ulceration with draw cobble-stone
• At advance : like tumour with edeme and inflamation, fistula and
esophagus perforation
C. Food Allergy

Food allergy is a group of disorders in which symptoms result from

immunologic responses (histamines and IgE antibodies) to specific
food antigens
Food Allergy Response

 Chemical triggers like histamine and IgE antibodies are released in

response to an allergen and can cause allergic reactions with a
variety of symptoms
 Symptoms may vary from person to person and not all reactions
appear the same
Food Allergy

• Epidemiology:
• Males > females; more in infants w/ history of atopy
• 6% of children during 1st 3yr of life
• Reactions: IgE mediated & non IgE mediated
• IgE mediated (Reaction within minutes to two hours) are
caused by inflammatory mediators released when food
antigen binds specific IgE antibody on mast cells and
basophils  rapid development of symtomps
• Non IgE mediated reactions are cell mediated and
develop over hours to days
Most common food allergies

• Children
• Milk, egg, peanuts, wheat, soy, tree nuts
• Most will outgrow eggs, milk, wheat, and soy
• Adults
• Peanuts, tree nuts (almonds, walnuts), fish, shellfish (shrimp, lobster, crab),
mollusks (oysters, clams, scallops)
Diagnosed Food Allergy

• Physician
• Medical history, physical exam
• Skin test
• Lab tests
• Elimination diet
Avoid Food Allergies

• Identify those at risk

• Consult a doctor
• Maternal diet avoiding eggs, cow milk, peanuts, fish
Tips to Prevent Allergies

• Do not consume allergic foods

• If traveling, bring special foods
• When eating out, ask about foods
• Know which children have allergies and what those are
• Know how to recognize symptoms
• Have a plan in cause of allergic response
If a child has a reaction

• Take medication
• Seek medical help
• Keep injectable epinephrine
• Wear Medic-Alert bracelet
D. Atresia esofagus (AE)

• Esophageal atresia (AE) is a disorder of the digestive system in which

the esophagus does not develop properly.

• Tracheoesophageal fistula (TEF) is a condition in which an abnormal

channel(fistula) connect the windpipe (tracea) to the tube that leads
ffrom the mouth to the stomach ( esophagus)
Variasi Atresia Esofagus

Gross of Boston :
Tipe A – atresia esofagus without fistula or pure atresia esofagus (10%)
Tipe B – atresia esofagus withTEF proksimal (<1%)
Tipe C – atresia esofagus with TEF distal (85%)
Tipe D – atresia esofagus with TEF proksimal and distal (<1%)
Tipe E – TEF withoutatresia esofagus or fistula tipe H (4%)
Tipe F – stenosis esofagus kongenital (<1%)
Causes

• the upper esophagus ends blindly and does not connect with the
lower esophagus and stomach

Symptoms
• Breating problem
• Choughing or choking when baby try to swallow
Diagnosed

• Prenatal ultrasound
• chest x-rays and other x-rays
• a special chest x-ray that is done after a nasogastric tube is put
through the nose into the esophagus to the point where the
esophagus stops
 Treatment

• Surgery only

Complication
 Lung infections or pneumonia
E. Leukoplakia

• White patch or plaque that cannot be rubbed off, cannot be

characterized clinically or histologically as any other condition, and is
not associated with any physical or chemical causative agent except
tobacco.

http://emedicine.medscape.com/article/853864-overview
Etiology of Leukoplakia

• Most cases : idiopathic.

• In other cases, may depend on extrinsic local factors and/or intrinsic
predisposing factors.
• Factors most frequently blamed: tobacco use, alcohol consumption,
chronic irritation, candidiasis, vitamin deficiency, endocrine
disturbances, and possibly a virus.

http://emedicine.medscape.com/article/853864-overview
3 Stages of Leukoplakia

• Earliest lesion: nonpalpable, faintly translucent,

white discoloration.
• Next: localized or diffuse, opaque white, fine
granular, and slightly elevated plaques with an
irregular outline develop.
• Late: lesions progress to thickened, white lesions,
showing induration, fissuring, and ulcer formation.

http://emedicine.medscape.com/article/853864-overview
2 Main Groups of Leukoplakia

• Most common: uniformly white plaques (homogenous)

prevalent in the buccal mucosa, which usually have low
premalignant potential.
• Far more serious: speckled or verrucous leukoplakia,
stronger malignant potential, consists of white flecks or fine
nodules on an atrophic erythematous base. A combination
of or a transition between leukoplakia and erythroplasia,
which is flat or depressed below the level of the surrounding
mucosal red patch, is uncommon in the mouth, and carries
the highest risk of malignant transformation.

http://emedicine.medscape.com/article/853864-overview
Diagnosis of Leukoplakia

• Biopsy:
• The plaque may show hyperorthokeratosis (granular cell layer, nuclei lost in
the keratin layer) or hyperparakeratosis (No granular cell layer, nuclei
retained in the keratin layer).
• Acanthosis, which refers to the abnormal thickening of the prickle cell layer
(spinous layer), may also be observed.

http://emedicine.medscape.com/article/853864-overview
Treatment of Laukoplakia

• Medical care: surgical exicision, cryotherapy ablation and

carbon dioxide laser ablation
• Diet: discontinue the use of alcohol
• Medication:
• High-dose induction followed by low-dose systemic isotretinoin 
stabilization of the majority of lesions, preventing malignant changes,
no toxicity.
• Beta-carotene produced sustained remissions of leukoplakia, with a
durable response for at least 1 year.
• Both of these drugs have been used in experimental trials and must
be investigated in more depth.

http://emedicine.medscape.com/article/853864-overview
Symptoms

• Leukoplakia patch appear :

• Usually white or gray
• Uneven in shape
• Fuzzy (hairy leukoplakia)
• Slightly raised with a hard surface
• Unable to be scraped off
• Painful when the mouth patches come into contact with acidic or spicy food
Conclusions and Suggestions

• Low apetite might be caused by oral thrush from candidiasis or

leukoplakia, further examination are needed.
• Complete physical examination of oral, pharyngeal, and esophageal
are needed.
• Diagnostic test such as endoscopic examination and
videofluoroscopy/ modified barium swallow to determine diagnosis.
• Treatment according to the etiologies.