Pemicu 1

Dessy 405150011
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
Four of normal eating
Stage Model and
Process swallowing:
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 disorders Pharmacologic Surgical causes
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. Dermatomyos hypothyroidism f. Aminoglycosides
e. CNS infections itis b. Vitamin B-12 g. Anticholinergic
f. Stroke deficiency: drugs
g. TBI leading to Mucosal injury:
h. Parkinson pseudobulbar h. Potassium
disease palsy secondary chlorice tablets
i. Poliomyelitis to i. NSAIDs
j. Cerebral palsy corticolbulbar j. Antibiotc
k. Multiple tract (doxycline,
sclerosis dysfunction tetracycline,
l. ALS clindamycin)
Xerostomia:
k. Antichlinergics
l. ACE-I
m. 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
Causes
malignant esophagus
 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 • fisiologic : pregnancy, age(very young or •The use of antibiotics will
factor very old), menstruation cycle make the unbalance of
•Non fisiologic : trauma(broken skin because mushroom and bacteria
work, maseration skin on wash worker and •Disease like malnutrition,
broken teeth(pressure from fake teeth), blood disease, malignancy
malnutrition (riboflavin defeciency), •The act or Procedure
endocrine disorder(diabetes melitus), medic and the tool that
ferocity(carcinoma, hematologic ferocity), used
patient in ICU, therapy with antibiotics,
corticosteroid, immunosupresan, other
infectious disease or chronic disease and
immunodeficiency (AIDS), neutropenia and
colonization of mushroom
 Difference candidiasis in adult and
child
Adult
Etology •Infection of the buccal
cavity by candida albicans
•The long use of antibiotics
or steroids
•Immunodeficiency
•Child
•Inadequate sterilization of
teats and bottles
•From mother’s breast of
the attendant’s hand
•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
 Angina Ludwig
Definition A bilateral infection of the submandibular space that consists of
two compartments in the floor of the mouth, the sublingual space
and the submylohyoid / submaxillary space
Etiology - Odontogenic infections
- Mandible fracture, neck trauma, tongue piercing, sialdenitis,
neoplasm, and other parapharyngeal infections
- Polymicrobial infection
- Patients with immunocompromising conditions
Symptoms - Dental pain
- Neck pain and swelling
- Dysphonia
- Dysphagia
- Dysarthria
- Respiratory distress with dyspnea, tachypnea, or stridor

http://www.medscape.com/viewarticle/551650_4
https://www.nlm.nih.gov/medlineplus/ency/article/001047.htm
 Mumps
Etiology Paramyxovirus
Sign and - Fever
Symptoms - Headache
- Muscle aches
- Tiredness
- Loss of appetite
- Swollen and tender salivary glands under the ears on one or both

Diagnosis - PCR
- Culture
- Serology
Complications - Orchitis
- Pancreatitis
- Unilateral deafness
- Death
MMR Vaccine - One dose for children 12 months and older
- Second dose for school-age children and adults

http://www.cdc.gov/vaccines/pubs/pinkbook/downloads/mumps.pdf
http://www.cdc.gov/mumps/about/signs-symptoms.html
 Squamous cell carcinoma
• 90% of oral cancers are of the squamous cell type
• Early carcinoma may clinically appear as leukoplakia or
erythroplasia or as a mixture of both
• Risk factors are smoking and alcohol
• Treatment: surgical excision and possible irradiation.
Chemotherapy is adjunctive at this time.
• Prognosis: overall five year survival rate is abt 50%
• DD: all ulcerations present for more than 2-3weeks with
no apparent cause should be biopsied to rule out
carcinoma
 Caries Dentis
Definition A common problem that occurs when acids in your mouth
dissolve the outer layers of your teeth
Risk Factors - Diet (food and drink high in carbohydrats)
- Poor oral hygiene
- Smoking and alcohol
- Dry mouth
Sign and - Toothache
Symptoms - Tooth sensitivity (tenderness or pain)
- Grey, brown or black spots
- Bad breath
- Unpleasant taste in mouth
Physical - Early sign: chalky white appearance of the enamel surface
Examinations - If the caries progresses: enamel surface becomes dark brown or
black
- Late sign: holes or cavites in the affected tooth
Diagnosis X-ray

http://www.nhs.uk/conditions/Dental-decay/Pages/Introduction.aspx
http://www.cdc.gov/healthywater/hygiene/disease/dental_caries.html
http://www.nhs.uk/Conditions/Dental-decay/Pages/Causes.aspx
http://www.myvmc.com/diseases/dental-caries/
 Mouth Ulcers
Definition Small lesions that develop in your mouth or at the base of your gums
Risk Factors - Woman
- Family history of mouth ulcers
Types - Simple canker sores  may appear three or four times a year and
last up to a week; occur in people between 10 and 20 years of age
- Complex canker sores  occur more often in people who have
previously had them
Etiology - Minor injury to mouth
- Toothpastes and mouth rinses that contain sodium lauryl sulfate
- Food sensitivities to acidic foods
- Lack of essential vitamins like B-12, zinc, folate, and iron
- Allergic response to mouth bacteria
- Hormonal influxes during menstruation
- Emotional stress
- Bacterial, viral, or fungal infections

http://www.healthline.com/symptom/mouth-ulcers
http://www.webmd.com/oral-health/guide/canker-sores
 Halitosis
• Definition
– Bad breath, oral malodor
– The result of microbial metabolism

• Diagnostic procedures
– Organoleptic measurements: the use of one’s nose to smell and rank
the intensity of odors.
• Rosenberg scale
– 0 - Odor cannot be detected
– 1 - Questionable malodor, barely detectable
– 2 - Slight malodor, exceeds the threshold of malodor
recognition
– 3 - Malodor is definitely detected
– 4 - Strong malodor
 Dry Mouth
 Definition
 The feeling that there
is not enough saliva
in the mouth.
 A subjective
complaint-symptom
of dry mouth.
 Lymphadenopathy
• Definition
– Swelling of the lymph nodes.

• Diagnostic Procedures
– For chronic lymphadenopathy (>3 wk):
• CBC count, including a careful evaluation of the peripheral
blood smear
• Lactate dehydrogenase (LDH) and uric acid
• Chest radiography
• B henselae (catscratch) serology if exposed to a cat
• Tuberculosis skin test (TST) and interferon-gamma release
assay (eg, Quantiferon Gold)