Problem 1 GIT

Grace Liwanto
405160020
Anatomy of upper GIT
Anatomy of Upper GI
Tract
(Mouth & Esophagus)

Oral
region

Moore Anatomy
Teeth

Moore Anatomy
Palate

Moore Anatomy
Tongue

Moore Anatomy
Muscle of
tongue

Moore Anatomy
ESOPHAGUS
• Muscular tube, continuous w/
laryngopharynx at
pharyngoesophageal junction
• Striated (voluntary) muscle in
upper third, smooth (involuntary)
in lower third, mixture in b/w
• 1st part: cervical esophagus
(voluntary upper third)
• 2nd part: thoracic esophagus
• 3rd part: abdominal esophagus
Kowalczyk M. Anatomy, Physiology and Benign disorders of esophagus.
Available from:
http://www2.tulane.edu/som/departments/medicine/gastroenterology/resid
ent-portal/upload/Kowalczyk-EsophagusPathophys2-revised-091313.pdf
Muscles of Esophagus
• Outer layer
(longitudinal muscles)
• Contraction  shorter
esophagus
• Inner layer (circular
muscles)
• Squeezing motion 
affects peristalsis &
closure of esophageal
sphincters
Physiology of esophageal motility
Hiroshi Mashimo and Raj K. Goyal
GI Motility online (2006)
doi:10.1038/gimo3
Histology of upper GIT
 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 bottom surface of tongue is smooth,

• The back part of tongue surface is covered by some papilla (filiformis,

fungiformis and circumvallate)
• Papilla is epithelial protrusion.
• Papilla filiformis → the most common and the smallest papilla, with
no taste bud, and has stratified squamous epithelium with some
keratin.
• Papilla fungiformis → the “fungi-like” shaped papilla, which has taste
bud.
• Papilla foliate  not developing in human.
• Papilla circumvallate → 7-12 circular papilla, 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
 PHARYNX
• the muscular tubular passage of the vertebrate digestive and
respiratory tracts extending from the back of the nasal cavity and
mouth to the esophagus
• Which has stratified squamous epithelium
• Pharynx  tonsils
 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)
Teeth Blood vessels - carry nutrients to the tooth.
Bone - alveolar bone forms the tooth socket and provides
it with support.
Cementum - the layer of hard bone-like tissue covering
the root of the tooth.
Cemento-enamel junction - the line where the enamel
and cementum meet.
Dentin - the hard yellow tissue underlying the enamel
and cementum, making up the main bulk of the tooth.
Enamel - the hard, white outer layer of the tooth.
Gingiva - the gum tissue surrounding the tooth.
Ligament - the connective tissue that surrounds the tooth
and connects it to bone.
Nerves - relay signals such as pain to and from your brain.

Pulp - located in the center of the tooth, it contains the

arteries, veins and nerves.
Root canal - canal in the root of the tooth where the
nerves and blood vessels travel through.
 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
• 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
Physiology of upper GIT
BASIC DIGESTIVE PROCESSES

MOTILITY

SECRETION

DIGESTION

ABSORPTION

Sherwood Physiology
REGULATION

AUTONOMOUS SMOOTH MUSCLE FUNCTION

INTRINSIC NERVE PLEXUSES

EXTRINSIC NERVES

GASTROINTESTINAL HORMONES

Sherwood Physiology
PATHWAY CONTROLLING DIGESTIVE
SYSTEM ACTIVITIES
GIT
RECEPTORS chemoreceptors

mechanoreceptors
(pressure receptors)

osmoreceptors

Sherwood Physiology
MOUTH

AMILAS
E
• begins digestion of carbohydrate in the mouth
• serves as a solvent for molecules that
stimulate the taste buds
• facilitates swallowing by moistening food
particles, thereby holding them together, and
FUNCTION by providing lubrication through the presence
S OF of mucus
SALIVA
SALIV • exerts some antibacterial action
• aids speech by facilitating movements of the
A lips and tongue
• helping keep the mouth and teeth clean
LYSOZYME, MUCU • rich in bicarbonate buffers
GLYCOPROTEIN, S
LACTOFERRIN

Sherwood Physiology
MOUTH

• SIMPLE SALIVARY REFLEXES

SALIVARY REFLEXES • CONDITIONED SALIVARY
REFLEXES

AUTONOMIC • SYMPATHETIC
INFLUENCE ON • PARASYMPATHETIC
SALIVARY
SECRETION
Sherwood Physiology
PHARYNX AND ESOPHAGUS
Oropharyngeal
Stage of Bolus is voluntarily
Swallowing forced by the tongue Pharyngeal muscles Pharyngoesophageal
to the rear of the contract sphincter opens
mouth

Swallowing center Epiglottis is pressed

Bolus pass into the
inhibits respiratory down over closed
esophagus
center glottis

Tongue against the Pharyngoesophageal

Elevation of uvula
hard palate sphincter closes
Sherwood Physiology
PHARYNX AND ESOPHAGUS
Esophageal
Stage of
Swallowing
Swallowing center The gatroesophageal
triggers a primary sphincter again
peristaltic wave contracts

The peristaltic wave

Bolus enters the
sweeps down the
stomach
esophagus

The bolus ahead of it The gastroesophageal

through the sphincter relaxes so
esophagus to the that the bolus can
stomach pass into the stomach
Sherwood Physiology
Biochemistry of GI
Functions of the Digestive System
• Ingestion – the oral cavity allows food to enter the digestive tract and
have mastication (chewing) occurs , and the resulting food bolus is
swallowed .

• Digestion:
• Mechanical digestion – muscular movement of the digestive tract (mainly
in the oral cavity and stomach) physically break down food into smaller
particles .
• Chemical digestion – hydrolysis reactions aided by enzymes (mainly in
the stomach and small intestine) chemically break down food particles
into nutrient molecules , small enough to be absorbed .
• Secretion – enzymes and digestive fluids secreted by the digestive tract
and its accessory organs facilitate chemical digestion .

• Absorption – passage of the end – products (nutrients) of chemical

digestion from the digestive tract into blood or lymph for distribution to
tissue cells .

• Elimination – undigested material will be released through the rectum

and anus by defecation .
Regulation of GI Tract Activities
• Autonomic nervous system
• parasympathetic nerves stimulate GI tract activities .
• sympathetic nerves inhibit GI tract activities .
• Hormonal control - hormones from endocrine gland and from GI tract
itself help regulate GI tract activities .
• Reflex mechanism - regions of the GI tract (especially the stomach
and small intestine) use reflexes to stimulate or inhibit one another .
Mouth & Oral Cavity
• Food enters the GI tract by ingestion .
• Food is broken down by mechanical digestion , using mastication .
• One chemical digestive process occur where amylase enzyme in saliva
breaks down polysaccharide into disaccharides .
• The tongue , made of skeletal muscle, manipulates the food during
mastication . it also contains taste buds to detect taste
sensations(intrinsic) .
• Food particles are mixed with saliva during mastication , resulting in a
moist lump called bolus for easier passage into or pharynx .
Ptyalin (α- amylase)

• It is secreted mainly by the parotid glands.

• Ptyalin starts the digestion of carbohydrates such as plant starch and muscle
glycogen.
• Starch is our main source of energy.
• Salivary amylase can hydrolyze starch into the disaccharide maltose and other small
polymers of glucose such as maltotriose and α limit dextrins that originate from the
branch points of the starch molecule.
• However, because ptyalin can only act on the food for a short period, oral digestion
has limited significance. Carbohydrate digestion continues in stomach for a while.
• The optimal pH of salivary amylase is 6.7.
• Starch digestion by ptyalin continues in the corpus and fundus of the stomach for
as long as an hour, and, therefore, as much as 30 to 40% of the starch may be
hydrolyzed mainly to maltose before the food becomes mixed with the acidic
gastric juice
Teeth
• Adapted for mechanical digestion (mastication) in the oral cavity .
• 20 deciduous or primary teeth before the age of 6.
• By age 7, 32 permanent or secondary teeth are developed & are divided
into 4 types: incisors (for cutting) , Canines (for tearing) , Premolars (for
crushing), and Molars (for grinding). these teeth follow the human dental
formula of 2-1-2-3.
Salivary Glands
• 3 pairs of salivary glands called parotid , submandibular , and sublingual
gland secrete most of the saliva in the oral cavity , using salivary ducts .
• Saliva helps moisten the food during mastication , dissolve the food in
forming the bolus , and help cleanse the teeth.
• Saliva consists of 99.5% water , the remaining 0.5% is dissolved
substances including amylase enzyme (for chemically digesting
carbohydrate ), bicarbonate ion (HCO3 - ; maintains pH of saliva at 6.5-
7.5) , and many electrolytes.
• The digestive hormones are secreted in response to specific stimuli (triggers).
• This ensures that the entire process of digestion is coordinated in response to
the changes within the gut and in the bloodstream.

Gastrin
• Source
• G cells in the stomach.
• Trigger
• Protein and amino acids stimulate gastrin secretion but somatostatin and acid
suppresses gastrin secretion.
• Action
• Increases gastric acid secretion.
Grehlin
• Source
• Stomach
• Trigger
• Secretion stimulated by fasting or starvation and suppressed by eating food.
• Action
• Stimulates appetite.

Somastatin
• Source
• D cells which are located throughout the gastrointestinal tract (gut).
• Trigger
• Eating fatty foods.
• Actions
• Reduces gastrin and stomach acid secretion.
• Inhibits insulin and pancreatic enzyme secretion.
• Decreases nutrient absorption from the gut.
Cholecystokinin (CCK)
• Source
• First two parts of the small intestine (duodenum, jejunum) – I cells.
• Nerve endings in the last part of the small intestine (ileum) and colon.
• Triggers
• Protein and amino acids.
• Fatty foods.
• Trypsin which is a pancreatic enzyme that assists with the digestion of proteins suppresses
the secretion of CCK.
• Actions
• Feeling of satiety which reduces appetite.
• Reduces gastric acid secretion and gastric emptying (passing of food from the stomach into
the duodenum)
• Stimulates pancreatic enzyme secretion.
• Stimulates gallbladder contraction and bile flow.
• Opens the sphincter of Oddi which allows the pancreatic enzymes and bile to enter the
small intestine.
Secretin
• Source
• First two parts of the small intestine (duodenum, jejunum) – S cells.
• Triggers
• Acid in the duodenum (small intestine) – increase in pH.
• Fatty acids.
• Actions
• Stimulates pancreatic fluid and bicarbonate secretion for the dilution and
neutralization of stomach acid in the small intestine.
• Decreases gastric acid secretion.
• Reduces gastric emptying (passing of food from the stomach into the duodenum).
Motilin
• Source
• Small intestine
• Colon
• Triggers
• Fasting, starvation.
• Fatty foods.
• Actions
• Controls peristalsis by stimulating smooth muscle contraction and relaxation to
coordinate the movement of food through the gut.
• Regulates movement of residual undigested material  through the gut (migrating
motor complexes or MMC) between meals.
Gastric Inihibitory Polypeptide (GIP)
• Source
• Duodenum and jejunum – K cells.
• Triggers
• Glucose.
• Fatty foods.
• Actions
• Reduces gastric acid secretion.
• Decreases gastric emptying.
• Stimulates the release of insulin.
Vasoactive Intestinal Peptide (VIP)
• Source
• Nerve fibers supplying all parts of the gastrointestinal tract.
• Triggers
• Unknown at this point.
• Actions
• May have various effects on many parts of the body, not only the gastrointestinal
tract.
• Vasodilator – increases blood flow to the gut.
• Empties water and electrolytes into pancreatic enzymes and bile.
• May affect water and electrolyte transport between the bloodstream and gut
lumen.
• Relaxes smooth muscle, particularly that of the sphincters.
• May play a role in blood glucose regulation.
Guanylin
• Source
• Small intestine.
• Colon
• Trigger
• Unknown at this point.
• Causes diarrhea which may be in response to certain stimuli (not as yet ascertained).
• Actions
• Secretion of chloride.
• Decreases absorption of water from the gut.
Terminology and
pathophysiology of swallowing
Disfagia - odinofagia
Definition and Terminology
Dysphagia
• Phagein (to swallow) & dys
(difficuly, disordered).
• Sensation of food being hindered
in its passage from the mouth to
the stomach.
• Commonly associated w/
obstructive or motor disorders of
the orophaynx, hypopharynx, or
esophagus.
Odynophagia
• Odyne (pain) & phagein (to
swallow)
• Pain w/ swallowing.
• Usually reflects a severe
inflammatory process hat
involves the esophageal mucosa
or muscle.
Mosby’s medical dictionary. 9th ed. 2009. Elsevier.
 Dysphagia
Definition is when a person finds it difficult to swallow, whereas odynophagia is
when swallowing is painful. Dysphagia may occur alongside
odynophagia, but the two conditions can also occur separately.
Risk - Problem with the neural control or the structures
Factors - Weak tongue or cheek muscles
- A stroke or other nervous system disorder
- After cancer surgery
Etiology - Any condition that weakens or damages the muscles and nerves used
for swallowing
- Stroke or head injury
- People born with abnormalities of the swallowing mechanism
- Cancer of the head, neck, or esophagus
- An infection or irritation
- Disorders of the esophagus

http://www.nidcd.nih.gov/health/voice/pages/dysph.aspx
Diagnosis - Transnasal esophagoscopy
- Cervical auscultation
- Blood tests  including TSH, vit B12, CK
- Imaging studies  videofluoroscopy, CT scan, MRI, chest radiography
- Endoscopic examination
- Esophageal pH monitoring
- Pulmonary function tests

Treatments - Flexible Endoscopic Evaluation of Swallowing with Sensory Testing (FEESST)

- Videofluoroscopic swallow study (VFSS)
- Muscle exercises to strengthen weak facial muscles or to improve
coordination
- Exercise and facilitates technique
• Indirect (eg, exercises to strengthen swallowing muscles)
• Direct (eg, exercises to be performed while swallowing)
- Surgical intervention

Complications - Aspiration pneumonia

- Loss weight

http://www.nidcd.nih.gov/health/voice/pages/dysph.aspx
Common Causes of Dysphagia
Symptoms
Oral Phase Pharyngeal Phase Esophageal Phase
- Drooling - Foamy phlegm, nasal regurgitation - Sticking
- Oral retention - Coughing while eating / drinking - Pain
- Difficulty in - Coughing before / after swallow - Regurgitation
chewing or - Wet / hoarse / breathy voice, weak - Hiccups
inadequately cough, inappropriate breathing - More difficulty with
chewed food - Aspiration, food sticking solids
- Stranded phlegm
- Food sticking

www.entlectures.com
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
Etiology of Leukoplakia
• Smoking: the combustion end-products brought about by
burning tobacco and heat (eg, tobacco tars and resins) are
irritating substances capable of producing leukoplakic alterations
of the oral mucosa.
• Chronic exposure  benign keratosis in the hard palate, called
stomatitis nicotina  pale mucosa due to slight increase in
keratinization  the palatal tissue is keratinized more heavily 
nodules appear (hyperplasia of the underlying glands, retention of
saliva, and fibrosis)

http://emedicine.medscape.com/article/853864-overview
Etiology of Leukoplakia
• Alcohol: May irritate the mucosa.
• Dental problems: Malocclusion; chronic cheek biting; ill-fitting
dentures; and sharp, broken-down teeth that constantly irritate the
mucosa.
• Syphilitic glossitis have a higher prevalence.
• Candida albicans: common oral fungus.
• Deficiency of vitamins A and B: inciting factor.

http://emedicine.medscape.com/article/853864-overview
Epidemiology of Leukoplakia
• International Frequency: <1%
• Mortality/Morbidity: potentially malignant, transformation rate in
various studies and locations ranges from 0.6 to 20%.
• Sex: male-to-female ratio of 2:1.
• Age: fifth to seventh decade of life, ± 80% of patients >40 yo.

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 Leukoplakia
• 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
Oral candidiasis
Definition A condition in which Candida albicans accumulates on the lining of your mouth

Symptoms - white lesions on your tounge, inner cheeks, and sometimes on

the roof of your mouth, gums, and tonsils
- A cottage cheese-like appearance
- Redness or soreness
- Slight bleeding
- Cracking and redness at the corner of your mouth
- A cottony feeling in your mouth
- Loss of taste

Risk Factors - Some health conditions  HIV/AIDS, cancer, DM, vaginal yeast
infections
- Undergoing chemotherapy or radiation treatment for cancer
- Wearing dentures
- Taking antibiotics or oral or inhaled corticosteroids
- malnutrition

http://www.mayoclinic.org/diseases-conditions/oral-thrush/basics/definition/con-20022381
http://www.mayoclinic.org/diseases-conditions/oral-thrush/basics/symptoms/con-20022381
http://www.mayoclinic.org/diseases-conditions/oral-thrush/basics/risk-factors/con-20022381
Diagnosis Limited to your mouth  looking at the lesions
In your esophagus  throat culture (swabbed with sterile cotton), endoscopic exam

Treatment - Antifungal (clotimazole, miconazole, nystatin, fluconazole) 7-14 hari

- Practice good oral hygiene
- Try warm saltwater rinses

Prevention - Rinse your mouth

- Brush your teeth at least twice a day and floss daily
- Clean your dentures
- See your dentist regularly
- Watch what you eat
- Maintain good blood sugar control if you have DM
- Treat any vaginal yeast infections
Achalasia
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 symtoms
• Dysphagia (most common)
• Regurgitation
• Chest pain
• Heartburn
• Weight loss
Etiology
• Esophagus divided into 3 parts : upper esophageal sphincter, corpus,
lower esophageal sphincter
• Based on etiology, achalasia divided into :
• Primary achalasia : unknown; lesion dorsal vagus nuclei in brain stem and
misenteric ganglia in esophagus
• Secondary achalasia : cardiac tumour, infection, anticholonergic drug
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
Malignancy
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
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 esophagus and to
nearby tissues or lymph nodes.
• Stage IV.
– The cancer has spread to other parts of your body.
 Radiological Examination
• Chest x-ray: This noninvasive medical test uses a very small dose of ionizing radiation to
produce pictures of the inside of the chest, including the lungs, heart and chest wall.

• Computed Tomography (CT) - Chest

• X-ray (Radiography) - Upper GI Tract: Upper gastrointestinal tract radiography or upper GI uses a
form of real-time x-ray called fluoroscopy and a barium-based contrast material to produce
images of the esophagus, stomach and small intestine. The patient drinks a contrast material
which coats the esophagus and stomach, and x-rays are taken. This procedure is also called an
upper GI series. An upper GI examination that focuses on the esophagus is called a 
barium swallow or an esophagram.
• Esophagoscopy: This procedure allows the physician to view the esophagus directly through an esophagoscope, a thin, tube-

like instrument with a light and a lens. The esophagoscope is inserted through the mouth or nose and down the throat into

the esophagus. Some esophagoscopes are equipped with tools to remove tissue samples for inspection under a microscope

for signs of cancer.

• Endoscopic ultrasound (EUS): In this procedure, an endoscope, a thin, tube-like instrument with a light and a lens for viewing,

is inserted through the mouth. A probe at the end of the endoscope is used to bounce high-energy sound waves (ultrasound)

off internal tissues or organs to create echoes. The echoes form a picture of body tissues called a sonogram. This procedure is

also called endosonography.

• Positron Emission Tomography/Computed Tomography (PET/CT): PET uses small amounts of radioactive materials called

radiotracers, a special camera and a computer to help evaluate your organ and tissue functions. By identifying body changes at

the cellular level, PET may detect the early onset of disease before it is evident on other imaging tests. PET/CT can detect

esophageal cancer, determine if it has spread, assess the effectiveness of a treatment plan and determine if the cancer has

returned after treatment.

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.
Esophageal atresia
 Esophageal Atresia
• Esophageal atresia  esophagus does not develop properly. The esophagus is the tube that
normally carries food from the mouth to the stomach.

Causes
• congenital defect the upper esophagus ends and does not connect with the lower
esophagus and stomach.
• tracheoesophageal fistula (TEF)abnormal connection between the esophagus and the
windpipe (trachea).
• infants with EA/TEF often have tracheomalacia weakness and floppiness of the walls of the
windpipe, which can cause breathing to sound high-pitched or noisy.
• Some babies with EA/TEF have other defects as well, most commonly heart defects.
 Classification Gross of Boston
• Type A - Esophageal atresia without fistula or so-called pure esophageal atresia
(10%)
• Type B - Esophageal atresia with proximal TEF (< 1%)
• Type C - Esophageal atresia with distal TEF (85%)
• Type D - Esophageal atresia with proximal and distal TEFs (< 1%)
• Type E - TEF without esophageal atresia or so-called H-type fistula (4%)
• Type F - Congenital esophageal stenosis (< 1%)

http://emedicine.medscape.com/article/935858-overview
https://www.nlm.nih.gov/medlineplus/ency/article/000961.htm
Symptoms of EA may include:  The disorder is usually detected shortly
• Bluish coloration to the skin (cyanosis) after birth when the infant tries to feed
with attempted feeding and then coughs, chokes, and turns
blue. If EA is suspected, the health care
• Coughing, gagging, and choking with provider will try to pass a small feeding
attempted feeding tube through the infant’s mouth or nose
• Drooling into the stomach. If the feeding tube
can’t pass all the way to the stomach,
• Poor feeding the infant will likely be diagnosed with
 Before birth, a mother's ultrasound may EA.
show too much amniotic fluid. This can • An x-ray is then done and will show any
be a sign of EA or other blockage of the of the following:
baby's digestive tract. 
• An air-filled pouch in the esophagus.
• Air in the stomach and intestine.
• If a feeding tube has been inserted
before the x-ray, it will appear coiled in
the upper esophagus.
Treatment
• EA is a surgical emergency. Surgery to repair the esophagus is done as
soon as possible after birth so that the lungs are not damaged and the
baby can be fed.
Prognosis
• An early diagnosis gives a better chance of a good outcome.
Complications
• The infant may breathe saliva and other fluids into the lungs, causing
aspiration pneumonia, choking, and possibly death.
Other complications may include:
• Feeding problems
• Reflux (the repeated bringing up of food from the stomach) after surgery
• Narrowing (stricture) of the esophagus due to scarring from surgery
• Prematurity may complicate the condition. As noted above, there may
also be defects in other areas of the body.
Caries
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/
Pathogenesis of Caries Dentis

Mouth full of
bacteria Bacteria in plaque turn
The plaque soften the
the carbohydrates →
enamel, by removing
energy they need +
Consume minerals from the tooth
producing acid
carbohydrats

The plaque and bacteria

Plaque and bacteria will The process of tooth
can reach the dentine
enter the pulp (contains decay speeds up.
nerves and blood
vessels

Toothache

http://www.nhs.uk/Conditions/Dental-decay/Pages/Causes.aspx
Treatments - Flouride : early stage
- Fillings and crowns : if the decay is more extensive → replaces your
missing enamel
- Root canal treatment : if tooth decay has spread to the pulp → may
have to be removed and replaced with an artificial pulp that will keep
the tooth in place
- Tooth extraction : may be removed to prevent the spread of infection
Complications - Gum disease (gingivitis)
- Dental abscesses
Prognosis Depends on the health of the patient, oral health practices and the
extent of dental caries
Prevention - Brush twice a day with a fluoride toothpaste
- Clean the teeth daily with floss or interdental cleaner
- Eat nutritious and balanced meals and limit snacking
- Visit your dentist regularly for professional cleanings and oral
examination
- Check with your dentist about use of supplemental fluoride

http://www.nhs.uk/Conditions/Dental-decay/Pages/Treatment.aspx
http://www.hse.ie/eng/health/az/D/Dental-caries/Complications-of-tooth-decay.html
http://www.myvmc.com/diseases/dental-caries/
http://www.cdc.gov/healthywater/hygiene/disease/dental_caries.html
Parotitis
• Inflammation of the parotid salivary gland
• The etiology of parotitis is assumed to be ascending infection from
the oral cavity.
• Many risk factors are associated with acute parotitis based on patient
population with dehydration being the most significant.
• Staphylococcus aureus is the most common bacterial pathogen;
however anaerobes and mixed infections are increasingly being
identified. Treatment includes antimicrobials, hydration, and
excluding an obstructive process within Stensen’s duct that would
warrant intervention
 Symptoms
Infectious parotitis
• Acute bacterial parotitis: The patient reports
progressive painful swelling of the gland and fever;
chewing aggravates the pain.
• Acute viral parotitis (mumps): Pain and swelling of the
gland last 5-9 days. Moderate malaise, anorexia, and
fever occur. Bilateral involvement is present in most
instances.
• HIV parotitis: Nonpainful swelling of the gland occurs;
otherwise, patient is asymptomatic.
• Parotitis in tuberculosis: Chronic nontender swelling of
one parotid gland occurs, or a lump is noted within the
gland. Symptoms of tuberculosis are found in some
cases.
Chronic punctate parotitis (chronic autoimmune
parotitis)
• Sjögren syndrome: Recurrent or chronic swelling of
one or both parotid glands with no apparent cause is
noted. It is frequently associated with autoimmune
disease. Discomfort is modest in most cases and is
related to dry mouth and eyes.
Diseases of uncertain etiology
• Recurrent parotitis of childhood: Repetitious
episodes of unilateral or bilateral mumps like
episodes in a young child are indicative.
• Sarcoidosis: Chronic nontender swelling of parotid
gland occurs.
• Chronic nonspecific parotitis: Most commonly,
patients experience episodes of painful parotid
inflammation that last for hours to weeks with
relative asymptomatic periods between. Pain varies
from mild to incapacitating.
Prevention:
• Generic deterrence is not available.
• Adequate hydration, oral hygiene, and minimizing
medications with atropine effects are helpful.
• Immunization avoids epidemic parotitis (mumps).

Complications: dental infections, caries, lymphomas

Patient education: Patients with chronic parotitis are
instructed to maintain scrupulous dental care. Minor
swelling and discomfort are managed with local heat
and massage.
Angina ludwig
 Ludwig’s Angina
• Ludwig's angina is an infection of the floor of the mouth under
the tongue. It is due to bacteria.

Causes
• Ludwig's angina is a type of skin infection that occurs on the
floor of the mouth, under the tongue. It often develops after an
infection of the roots of the teeth (such as tooth abscess) or a
mouth injury.
• This condition is uncommon in children.
Symptoms
The infected area swells quickly. This may block the airway or prevent you
from swallowing saliva.
Symptoms include:
• Breathing difficulty, difficulty swallowing, drooling, unusual speech
(sounds like the person has a "hot potato" in the mouth), tongue swelling
or protrusion of the tongue out of the mouth, fever, neck pain, neck
swelling, redness of the neck
Other symptoms that may occur with this disease:
• Weakness, fatigue, excess tiredness
• Confusion or other mental changes
• Earache
Treatment
• Tracheostomy.
• Antibiotics are given to fight the infection. They are most often given through a vein
until symptoms go away. Antibiotics taken by mouth may be continued until tests
show that the bacteria have gone away.
• Dental treatment may be needed for tooth infections that cause Ludwig's angina.
• Surgery may be needed to drain fluids that are causing the swelling.
Prognosis
• Ludwig's angina can be life-threatening. It can be cured with getting treatment to
keep the airways open and taking antibiotic medicine.
Complications
• Airway blockage
• Generalized infection (sepsis)
• Septic shock
Herpes
• Herpes is the name of a group of herpesviridae viruses that can infect
humans.
• Herpes virus infection can be characterized by the appearance of
blisters of skin and dry skin.
• The most famous type of herpes virus is the herpes simplex virus or
HSV.
• Herpes simplex can cause infection in the mouth, face and genital
area (genital herpes).
• The division of the herpesviridae virus group is as follows:

Alfa herpesvirus  This group of viruses has a short life cycle to multiply, and has the
potential to be hidden and infection reappears (latent infection) in nerve cells.
Examples of alpha herpesviruses are HSV types 1 and 2, and the varicella-zoster virus.
Beta herpesvirus  This group of viruses has a life cycle to reproduce long and this
viral infection is slow in the human body. Examples of beta herpesvirus are
cytomegalovirus, and herpesvirus 6 and 7.
Gamma herpesvirus  Examples are Epstein-Barr virus and human herpesvirus 8.
stages of herpes infection Primary stadium.

Primary stage  occurs on the second to eighth day after herpes infection. The symptoms that appear
are small, but painful blisters (blisters). Blisters usually contain clear or cloudy liquid, and can rupture
and cause open sores. The area around the blister will be reddish.
Latent stage  At this stage, symptoms of herpes such as blisters and ulceration will subside. But at this
stage, the virus is actually spreading to the nerves near the spinal cord through the skin.
Decay Stadium  At this stage, the virus begins to multiply at the nerve endings of the body's organs. If
the infected nerve endings are located on organs that produce fluid, such as the testicles or vagina, the
herpes virus can be contained in body fluids such as semen and mucus. There are usually no visible
symptoms, but actually there is a proliferation of viruses in the body.
Recurrence stadium (reappears)  At this stage, blisters on the skin that occur in the first stage can
reappear. Usually not as bad as the previous blisters and scabs. Symptoms that generally appear at this
stage of recurrence are itching, tingling, and pain in the area affected by infection in the first stage.
the virus that causes herpes symptoms

• HSV 1

Herpes simplex type 1 virus (HSV 1) is a virus that can spread quickly, and generally causes
oral (oral) herpes. However, HSV 1 can also cause genital herpes if it spreads from the mouth
to the genitals during sexual intercourse by oral.

Symptoms that can be caused by HSV 1 infection or oral herpes are:

• Beginning with fever, muscle aches, and weakness.

• Pain, itching, burning or stabbing occur at the site of infection.
• Then blisters arise, namely skin lesions such as blisters that break and dry out in a few days.
• The ruptured blister causes pain. When it happens in the mouth, it can interfere with eating.
• HSV 2

Herpes simplex type 2 virus (HSV 2) is a cause of genital herpes. This virus is spread
through contact with wounds in herpes sufferers, for example during sexual intercourse.
In addition, HSV 2 can also be transmitted from mother to baby at the time of delivery.

Some of the symptoms that commonly occur in people with genital herpes include:

• Itchy.
• Pain when urinating.
• Fluid discharge from the vagina.
• The appearance of a lump in the groin.
• The appearance of a painful scab on the genitals, buttocks, anus, or thighs.
Diagnosis of Herpes

Herpes can be diagnosed through a physical examination In addition, to help diagnose herpes
to be more accurate, additional checks can be done, such as:
• Culture of the herpes simplex virus  Herpes virus culture aims to diagnose the herpes virus.
Herpes virus culture is done by rubbing the infected skin or genital area, taking genital fluid
or other body fluids that are suspected of having herpes to be examined in the laboratory.
• Antibody test  Specific antibody tests for HSV 1 and HSV 2 viruses can be performed to
detect primary herpes infection, but cannot detect recurrent herpes infection. Antibody tests
are carried out by taking blood samples from the body, then analyzed in the lab to check for
the presence of HSV 1 specific antibodies or HSV 2. Keep in mind that the body takes around
12-16 weeks to form anti HSV 1 or HSV 2 antibodies, after the HSV virus enters into the body
for the first time. HSV 1 and HSV 2 antibody tests are very helpful in diagnosis, especially if
the patient does not experience sores or blisters on the skin.
Treatment of Herpes

• The focus of herpes treatment is to eliminate blisters, as well as to prevent the

spread of herpes

• In addition, the provision of antiviral drugs can also reduce complications due to
herpes. Some antiviral drugs that can be used include:

Acyclovir.
Valacyclovir.
Famciclovir.
Complications of Herpes

• Herpes simplex rarely causes serious complications in patients. Herpes simplex

can cause complications, especially if the patient also has HIV infection.

• Some complications are rare, but serious, what can be caused by herpes
simplex are:

- Spread of infection to other body parts.

- Inflammation of the brain and membranes.
- Pneumonia.
- Hepatitis.
- Esophagitis.
- Death of the retinal tissue of the eye.
Prevention of Herpes
• To prevent the spread of the herpes virus to others, the following steps can be
taken:

- Avoid physical contact with others

- Wash your hands regularly.
- Apply topical antiviral drugs using cotton so that the skin does not touch the
area infected with the herpes virus.
- Don't share items that can spread viruses, such as glasses, cups, towels, clothes,
makeup, and lip balm.
- Do not do oral sex, kissing or other sexual activity, during the appearance of
symptoms of herpes.
Stomatitis
Definition
• Stomatitis is an inflammation of the mucosal lining of any structure in
the mouth; such as cheeks, gums (gingivitis), tongue (glossitis), [2]
lips, and roof or floor of the mouth.
• Inflammation can be caused by the condition of the mouth itself (such
as poor oral hygiene, poor tooth structure), mouth injury due to hot
food or drinks, or by conditions that affect the whole body (such as
drugs, allergic reactions, or infections).
Sign and symptoms
• Inflammation of the mouth can cause pain, fever, fatigue, headaches,
and loss of appetite. Usually, the sufferer has one or more small
wounds on the lips, gums, upper tongue, or the inside of the cheeks.
The wound looks red and can be painful, burning or itchy. Pain when
eating and swallowing. Sometimes, patients also have bad breath
(halitosis).
Etiologi
• Herpes virus is the main cause. In addition, other causes such as:

- Reaction to allergies
- Smoke
- Dental disease
- Vitamin deficiency
- Systemic disease
- Drugs
- Other bacterial infections
Risk factor
• There is a small wound in the mouth, which is usually caused by brushing your
teeth too hard, due to sports activities, or accidentally biting the inside of the
cheek
• Toothpaste or mouthwash containing sodium sulfate (SLS)
Eating foods that cause mouth irritation such as chocolate, coffee,
strawberries, eggs, nuts, cheese, and sour and spicy foods
• Malnutrition, especially vitamin B12, zinc, iron or folic acid
• Menstrual hormone changes during menstruation
• Stress
Treatment
• Stomatitis caused by local irritation can be prevented by good oral
hygiene, regular dental check-ups, and good habits.
• Stomatitis problems caused by systemic diseases can be minimized by
good oral hygiene and carefully following medical therapy for example
by antibiotics
Prognosis
• The prognosis for healing stomatitis depends on the cause of the
problem.
• Many local factors can be modified, treated, or avoided.
• Infectious causes of stomatitis can usually be treated with medication,
or if the problem is caused by certain drugs, by replacing the
causative agent.
Mouth ulcers
(aptus)
MOUTH ULCER (APHTHOUS) -
sariawan
DEFINITION
• Considered as the most common oral mucosal lesion.
• These present as recurrent, multiple, small, or ovoid ulcers, having
yellow floors and are surrounded by erythematous haloes, present
first in childhood or adolescence. 
• Aphthous ulcers affect up to 25% of the general population, and 3-
month recurrence rates are as high as 50%.
• It is more common in female.
• Aphthous ulcers increase by increasing age and minor aphthous ulcers
are 80% of suffered patient.
• The cause of aphthous ulcers is unknown
https://www.ncbi.nlm.nih.gov
/pmc/articles/PMC4441245/
CLASSIFICATION AND CLINICAL
PRESENTATIONS
Major Aphthous Ulceration
Minor Aphthous Ulceration
• 10-15% of all
• The most common form (85%)
• Similar in appearance to
• Involve the non-keratinized
minor
mucosa of the oral cavity
• Larger than 10 mm in
• Usually 4-5 mm in diameter
diameter, deeper, often
• Usually concentrated in the
scarred, last for weeks to
anterior part of the mouth
months
Herpetiform Ulceration • Have a predilcetion for lips,
• Can be small (1-2 mm), tongue, soft palate, and the
multiple (5-100), or be present palatal fauces and cause
at the same time pain and dysphagia
• The affected sites are the • Frequently found in patients
lateral margins and ventral infected with HIV
surface of tongue and the
floor of the mouth
• Cause pain; eating and https://www.ncbi.nlm.nih.gov
speaking difficult /pmc/articles/PMC4441245/
CLASSIFICATION AND CLINICAL
PRESENTATIONS

https://www.ncbi.nlm.nih.gov
/pmc/articles/PMC4441245/
PREDISPOSISING FACTORS

• Hormonal changes
• Trauma
• Drugs
• Food hypersensitivity
• Nutritional deficiency states
• Stress
• Tobacco
• Hereditary predisposition
• Immunological features of RAS
• Systemic disorders https://www.ncbi.nlm.nih.gov
/pmc/articles/PMC4441245/
DIAGNOSIS AND INVESTIGATION TESTS
TREATMENT

• The aim of the treatment of RAS is to decrease symptoms; reduce ulcer

number and size; increase disease-free periods
• Predisposing factors should be identified and corrected.
• Chlorhexidine mouthwashes may help.
• Symptoms can often be controlled with hydrocortisone hemisuccinate
pellets or triamcinolone acetonide in carboxymethyl cellulose paste four
times daily, but more potent topical corticosteroids may be required.
• Systemic corticosteroids are best given by a specialist.
• Thalidomide is also effective but is rarely indicated.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4441245/;
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1118165/
Glossitis
Definition 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 conditions, 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 (such as from burns, rough teeth, or bad-fitting dentures)
• Skin conditions that affect the mouth
• Irritants such as tobacco, alcohol, hot foods, spices, or other irritants
• Hormonal factors
• Certain vitamin deficiencies
Classification
• Atrophic glossitis
• A condition characterized by a smooth glossy tongue that is often tender/painful
• Caused by complete atrophy of the lingual papillae (depapillation)
• Median rhomboid glossitis
• This condition is characterized by a persistent erythematous, rhomboidal depapillated lesion in the
central area of the dorsum of the tongue, just in front of the circumvallate papillae
• A type of oral candidiasis, and rarely causes any symptoms. It is treated with antifungal medication
• Benign migratory glossitis
• Geographic tongue, also termed benign migratory glossitis, is a common condition which usually
affects the dorsal surface of the tongue
• It is characterized by patches of depapillation and erythema bordered by a whitish peripheral zone
• These patches give the tongue the appearance of a map. The cause is unknown, and there is no
curative treatment
• Geometric glossitis
• The lesion is usually very painful, and there may be erosions present in the depths of
the fissures
• Chronic lesion associated with HSV-1 infection  deep fissure in the midline of the
tongue and gives off multiple branches
• Strawberry tongue
• Manifests with hyperplastic (enlarged) fungiform papillae, giving the appearance of a
strawberry
 Glossitis
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

Diagnosis Your dentist or health care provider will do an exam to look for:
• Finger-like bumps on the surface of the tongue (called papillae)
that may be missing
• Swollen tongue (or patches of swelling)
 Glossitis
Treatment Treatment may include:
(The goal of • Good oral care. Brush your teeth thoroughly at least twice a day
treatment is to and floss at least once a day.
reduce swelling and • Antibiotics or other medicines to treat infection.
soreness) • Diet changes and supplements to treat nutrition problems.
• Avoiding irritants (such as hot or spicy foods, alcohol, and
tobacco) to ease discomfort.

Call your health care provider if:

• Symptoms of glossitis last longer than 10 days.
• Tongue swelling is very bad.
• Breathing, speaking, chewing, or swallowing causes problems.
• Get emergency care right away if tongue swelling blocks the
airway.
 Glossitis
Prognosis Glossitis goes away with if the cause of problem is removed or
treated.
Prevention Good oral care (thorough tooth brushing and flossing and regular
dental checkups) may help prevent glossitis.
References
• Mescher A Junqueira L. Junqueira's basic histology. New York: McGraw-
Hill Medical; 2013.
• Malagelada JR, Bazzoli F, Elewaut A, Fried M, Krabshuis JH, Lindberg G,
et al. Dysphagia. World Gastroenterology Organisation Practice
Guideline; 2007.
• Moore, Keith L, et al. Moore Clinically Oriented Anatomy. 7th ed
• Sobotta, Atlas der Anatomie des Menschen , 23. A. Elsevier GmbH.
Munchen. 2010.
• Sherwood L. Human physiology: from cells to systems. 8th ed.
Belmont:Brooks/Cole cencage Learning; 2013