Problem 1 GIT

CINDY MARCELLINA
405160063
Learning issues
1. Describe the anatomy of upper GIT
2. Describe histology of upper GIT
3. Describe physiology of upper GIT
4. Describe biochemistry of upper GIT
5. Describe the pathophysiology of swallowing difficulty
6. Describe the terminology of swallowing difficulty
7. Describe the epidemiology of swallowing difficulty
8. Describe the etiology of swallowing difficulty
9. Describe the sign & symptoms, laboratory findings, and imaging studies of swallowing difficulty
10. Describe the therapeutic management of swallowing difficulty (pharmacologic and non
pharmacologic)
11. Describe the complication & prognosis of swallowing difficulty
12. Describe the prevention & education for swallowing difficulty
13. Write a prescription commonly used for this illness
LI 1
• Oral cavity :
- Vestibule / Vestibulum Oris
- Oral Cavity Proper / Cavitas Oris Propria
• Oral cavity consists of :
a. Mouth
b. Tongue
c. Teeth and periodontium
d. Major and minor salivary glands
e. Tonsils

Ross MH, Pawlina W. Histology A Text And Atlas. 6th Edition.

Paulsen F, Waschke J.Sobotta Atlas Anatomi Manusia. Jilid 3. Edisi 23.
Anatomy of Upper GI Tract
(Mouth & Esophagus)

Oral
region

Moore Anatomy
Mouth

Paulsen F, Waschke J.Sobotta Atlas Anatomi Manusia. Jilid 3. Edisi 23.

Paulsen F, Waschke J.Sobotta Atlas Anatomi Manusia. Jilid 3. Edisi 23.
Tongue

Paulsen F, Waschke J.Sobotta Atlas Anatomi Manusia. Jilid 3. Edisi 23.

• Tongue is divided into 3 parts : • Papillae that cover the dorsal
- Apex lingua surface of tongue :
- Dorsum lingua - filiform papillae
- Radix lingua - fungiform papillae
• Function of tongue : - circumvallate papillae (von
- play role in swallowing Ebner’s gland)
- human speech - foliate papillae
- taste

Ross MH, Pawlina W. Histology A Text And Atlas. 6 th Edition.

Paulsen F, Waschke J.Sobotta Atlas Anatomi Manusia. Jilid 3. Edisi 23.
Tongue

Moore Anatomy
Muscle of
tongue

Moore Anatomy
Teeth
• Teeth and their supporting tissues
periodontium are essentials for the beginning
of digestive process.
• Teeth consists of 3 layer of specialized tissues
a. Enamel
- hard, thin, translucent layer of acellular
mineralized tissue
b. Dentin
- most abundant dental tissue
c. Cementum
- thin, pale-yellowish layer of bone like
calcium tissue covering the dentin of the
root of the teeth.

Paulsen F, Waschke J.Sobotta Atlas Anatomi Manusia. Jilid 3. Edisi 23.

Teeth

Moore Anatomy
Teeth

Child
Adult

Paulsen F, Waschke J.Sobotta Atlas Anatomi Manusia. Jilid 3. Edisi 23.

Salivary Gland

Paulsen F, Waschke J.Sobotta Atlas Anatomi Manusia. Jilid 3. Edisi 23.

Salivary Glands
a. Major salivary glands b. Minor salivary glands
- lingual gland
1. Parotid gland - labial gland
- (Stensen’s duct) - buccal gland
- serous acini - molar gland
2. Submandibular gland - palatine gland
- (Wharton’s duct)
- seromucose acini
3. Sublingual gland
- mucoserose acini

Ross MH, Pawlina W. Histology A Text And Atlas. 6 th Edition.

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
ESOPHAGUS
Physiology - Deglutition
LI 2
 Histology
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
Mouth
• Oral cavity is lined by oral
mucosa.
• Oral mucosa is consist of :
- masticatory mucosa
{keratinized (4 layer) and
parakeratinized stratified
squamous epithelium}
- lining mucosa (nonkeratinized,
only got three layers)
- specialized mucosa The Lip

Ross MH, Pawlina W. Histology A Text And Atlas. 6 th Edition.

https://www.studyblue.com/notes/note/n/dr-das-oral-cavity/deck/10890625
Histology of Mouth

Ross MH, Pawlina W. Histology A Text And Atlas. 6 th Edition.

https://www.studyblue.com/notes/note/n/dr-das-oral-cavity/deck/10890625
Papillae

Filiform papilla Fungiform papilla

Ross MH, Pawlina W. Histology A Text And Atlas. 6 th Edition.
http://www.lab.anhb.uwa.edu.au/mb140/corepages/oral/oral.htm
Papillae

Foliate papilla Circumvallate papilla

Ross MH, Pawlina W. Histology A Text And Atlas. 6 th Edition.

https://www.studyblue.com/notes/note/n/dr-das-oral-cavity/deck/10890625
Taste Bud
 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
 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
Salivary Gland
 Salivary ducts :
• Three types of acini :
a. Intercalated duct
a. Serous acini - possess carbonic anhydrase
- protein secreting cells - secrete HCO3-
- zymogen granules - absorb Cl-
b. Mucous acini b. Striated duct
- reabsorption Na+
- secrets mucin
- secretion of K+, HCO3-
- mucinogen granules
c. Excretory ducts
c. Mixed acini (serous demilunes)

Ross MH, Pawlina W. Histology A Text And Atlas. 6 th Edition.

Parotid Gland

SUBMANDIBULA SUBLINGUAL
R GLAND GLAND

Eroschenko VP. diFiore’s Atlas of Histology with Functional Correlations. 10 th Edition.

Parotid Gland

Eroschenko VP. diFiore’s Atlas of Histology with Functional Correlations. 10 th Edition.

Submandibular Gland

Eroschenko VP. diFiore’s Atlas of Histology with Functional Correlations. 10 th Edition.

Sublingual Gland

Eroschenko VP. diFiore’s Atlas of Histology with Functional Correlations. 10 th Edition.

Histology of Salivary Gland
• Saliva : combined secretion of all the major and minor salivary glands
• Function of saliva :
Moistening oral mucosa
Moistening dry food
Dissolved and suspended food materials  stimulates taste buds
Buffering contents of oral cavity

Ross MH, Pawlina W. Histology A Text And Atlas. 6 th Edition.

Histology of Salivary Gland
• Function of saliva :
Digests carbohydrate by a-amylase
Contains lysozyme (muramidase)
Source of calcium and phosphate essentials for normal tooth
development and maintenance
Contains IgA

Ross MH, Pawlina W. Histology A Text And Atlas. 6 th Edition.

 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
 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
 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
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.
Histology of Teeth
• Supporting tissues of the teeth are :
a. Alveolar processes of maxilla
and mandible
b. Periodontal ligaments
- tooth attachment
- tooth support
- bone remodelling
- propioception
- tooth eruption
c. Gingiva
Ross MH, Pawlina W. Histology A Text And Atlas. 6 th Edition.
https://www.studyblue.com/notes/note/n/gi-lecture-1/deck/3719939
 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)
 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
• 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
 Esophagus

(a): Longitudinal section of esophagus shows mucosa consisting of nonkeratinized stratified

squamous epithelium (SS), lamina propria (LP), and smooth muscles of the muscularis mucosae
(MM). Beneath the mucosa is the submucosa containing esophageal mucous glands (GL) which
empty via ducts (D) onto the luminal surface. X40. H&E.
LI 3
 PHYSIOLOGY
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 • begins digestion of
carbohydrate in the mouth
• serves as a solvent for
AMILASE
molecules that stimulate the
taste buds
• facilitates swallowing by
moistening food particles,
thereby holding them together,
FUNCTIONS
SALIVA OF SALIVA
and by providing lubrication
through the presence of mucus
• exerts some antibacterial action
• aids speech by facilitating
movements of the lips and
LYSOZYME, tongue
GLYCOPROTEI • helping keep the mouth and
N, MUCUS
teeth clean
LACTOFERRIN • rich in bicarbonate buffers

Sherwood Physiology
MOUTH

• SIMPLE SALIVARY REFLEXES

SALIVARY REFLEXES • CONDITIONED SALIVARY
REFLEXES

AUTONOMIC • SYMPATHETIC
INFLUENCE ON • PARASYMPATHETIC
SALIVARY
SECRETION
Sherwood Physiology
 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
PHARYNX AND ESOPHAGUS
Esophageal
Stage of
Swallowing center
Swallowing The gatroesophageal
triggers a primary
sphincter again contracts
peristaltic wave

The peristaltic wave

Bolus enters the
sweeps down the
stomach
esophagus

The gastroesophageal
The bolus ahead of it
sphincter relaxes so that
through the esophagus
the bolus can pass into
to the stomach
the stomach Sherwood Physiology
LI 4
 Biochemistry
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.
LI 6
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 People with dysphagia have difficulty swallowing and may even
experience pain while swallowing (odynophagia), may be completely
unable to swallow or may have trouble safely swallowing liquids, foods,
or saliva
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
- The development of a pocket outside the esophagus

http://www.nidcd.nih.gov/health/voice/pages/dysph.aspx
Dysphagia

• Abnormality/difficulty of swallowing
• A sensation of "sticking" or obstruction of the passage of food through the
mouth, pharynx, or esophagus. (Harrison's Internal Medicine)
• Etiology :
• Structural (congenital or acquired)
• Functional (congenital or acquired)
Structural
• Something blocking the way of the
bolus
• Could be:
• GERD ( ulcers  scars  narrowed
esophagus)
• Esophagitis
• Cleft lip and palate
• Cervical osteophytes (eldery)
• Zenker diverticulum (above
cricopharyngeus muscle)
• Infection (candidiasis)
• Tumor
http://www.webmd.com/digestive-disorders/tc/difficulty-swallowing-dysphagia-
FUNCTIONA
L
• Muscle and/or nerve problem
• Could be:
• Stroke / brain / spinal cord injury
• Esophangeal spasm
• Scleroderma
• Problem with the nerves system (post-
polio syndrome, multiple sclerosis,
muscular dystrophy, parkinson’s disease
• Physiology
• Process of swallowing begins with a Voluntary (oral) phase  food
bolus  transfer phase into the end of mouth  pushed into pharynx
 activated oropharyngeal sensory receptors  initiate deglutition
reflex  upper esophageal sphincter opens  bolus moved to
pharynx  peristaltic contraction  bolus moved from pharynx to
esophagus  Lowe esophageal sphincter opens as the food enters the
esophagus and remain open until peristaltic contraction has swept the
bolus into stomach.
• Phatophysiology of Dhysphagia

1. Pharyngeal Dhysphagia

Associated with poor bolus formation and control.

Pharyngeal stasis leads to nasala regurgitation and laryngeal aspiration

during the process of swallowing.

2. Esophageal Dysphagia

Results abnormalites in peristaltis and deglutitive inhibition due to diseases

of the esophageal striated or smooth muscles.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2597750/
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 - Swallowing in-coordination solids
- Stranded phlegm - Aspiration, food sticking
- Food sticking

www.entlectures.com
Odynophagia
• Odynophagia : painful during swallowing.
• Usually there is ulcer at the mucosa of oropharynx or esophagus.
• The most common causes : caustic ingestion, pill induced esophagitis,
radiation injury, and infectious disease (Candida, herpes, and
cytomegalovirus).

Harrison’s Principles of Internal Medicine. 18th Edition. Vol 1.

http://www.ualberta.ca/~loewen/Medicine/GIM%20Residents%20Core%20Reading/DYSPHAGIA,%20GERD,
%20BARRETTS%20ESOPHAGUS/dysphagia,%20heartburn%20Slezinger.pdf
LI 7 - 12
 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
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)
- 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
MOUTH ULCER (APHTHOUS)
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
Minor Aphthous Ulceration
Major Aphthous Ulceration
• The most common form (85%)
• 10-15% of all
• Involve the non-keratinized
• Similar in appearance to minor
mucosa of the oral cavity
• Larger than 10 mm in diameter,
• Usually 4-5 mm in diameter
deeper, often scarred, last for
• Usually concentrated in the
weeks to months
anterior part of the mouth
• Have a predilcetion for lips,
tongue, soft palate, and the palatal
Herpetiform Ulceration fauces and cause pain and
• Can be small (1-2 mm), multiple (5- dysphagia
100), or be present at the same • Frequently found in patients
time infected with HIV
• The affected sites are the lateral
margins and ventral surface of
tongue and the floor of the mouth
• Cause pain; eating and speaking https://www.ncbi.nlm.nih.gov
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/
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
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)
• Mikulicz disease: This is a historical disease only; it should
not be diagnosed today.
• 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.
• Lymphoepithelial lesion of Godwin: This is a historical
category that is not used today.
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.
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 • Geometric glossitis
• Caused by complete atrophy of the lingual papillae (depapillation) • The lesion is usually very
• Median rhomboid glossitis painful, and there may be
erosions present in the depths
• This condition is characterized by a persistent erythematous,
rhomboidal depapillated lesion in the central area of the dorsum of of the fissures
the tongue, just in front of the circumvallate papillae • Chronic lesion associated with
• A type of oral candidiasis, and rarely causes any symptoms. It is HSV-1 infection  deep fissure
treated with antifungal medication in the midline of the tongue
• Benign migratory glossitis and gives off multiple branches
• Geographic tongue, also termed benign migratory glossitis, is a • Strawberry tongue
common condition which usually affects the dorsal surface of the • Manifests with hyperplastic
tongue (enlarged) fungiform papillae,
• It is characterized by patches of depapillation and erythema giving the appearance of a
bordered by a whitish peripheral zone
strawberry
• These patches give the tongue the appearance of a map. The cause
is unknown, and there is no curative treatment
 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.
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
• Complications may include:
• Airway blockage
• Generalized infection (sepsis)
• Septic shock
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.
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 Etiology
• Dysphagia (most common) • Esophagus divided into 3 parts :
• Regurgitation upper esophageal sphincter,
corpus, lower esophageal sphincter
• Chest pain • Based on etiology, achalasia
• Heartburn divided into :
• Primary achalasia : unknown; lesion
• Weight loss 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
REFLUX ESOPHAGITIS
• Reflux esophagitis is an esophageal mucosal injury that occurs
secondary to retrograde flux of gastric contents into the esophagus
• Clinically, this is referred to as gastroesophageal reflux disease (GERD)
• Typically, the reflux disease involves the distal 8-10 cm of the
esophagus and the gastroesophageal junction
• The disease is patchy in distribution
• Affects the gastroesophageal junctional mucosa, and the histologic
features include multilayered epithelium and inflammation of gastric
cardiac mucosa

http://emedicine.medscape.com/article/1610393-
overview#showall
REFLUX ESOPHAGITIS
• The acidic nature of the refluxed gastric contents is predominantly responsible for
the esophageal mucosal damage and subsequent development of reflux esophagitis
• Strong acid (pH < 2), however, can cause mucosal damage independent of the
presence of pepsin
• Occasional reflux of gastric contents into the esophagus is a universal phenomenon,
and the majority of people do not develop reflux disease because of intact antireflux
mechanisms, which clear the refluxed contents back into stomach before damage is
done
• Symptomatic reflux occurs when these antireflux mechanisms become impaired,
such as in the cases of weak lower esophageal sphincter (LES) function, impaired
esophageal clearance due to esophageal dysmotility or the presence of hiatal hernia,
and poor gastric emptying
http://emedicine.medscape.com/article/1610393-
overview#showall
REFLUX ESOPHAGITIS
• The clinical symptoms of gastroesophageal disease (GERD) can be
divided into 2 groups: esophageal and extra-esophageal
• The typical presentation of GERD includes esophageal symptoms such
as heartburn, acid dyspepsia, regurgitation, and chest pain
• The extra-esophageal symptoms are also referred to as “atypical”
symptoms of reflux disease and include, but are not limited to, cough,
asthma, throat pain, aspiration pneumonia, globus sensation, and
hoarseness due to pharyngitis, laryngitis, or sinus problems

http://emedicine.medscape.com/article/1610393-
overview#showall
REFLUX ESOPHAGITIS
• The diagnosis of GERD depends upon the appropriate clinical scenario
• Various modalities have been utilized for diagnosis of GERD, and these
include esophagogastroduodenoscopy (EGD) (or, upper
gastrointestinal [GI] endoscopy) with biopsy, 24-hour pH study,
manometry, barium contrast study, and gastric emptying study
• However, none of these modalities is the “gold standard” for
diagnosis, and each is recommended in specific clinical situations

http://emedicine.medscape.com/article/1610393-
overview#showall
 Reflux Esophagitis
• Mild esophagitis  microscopic changes of mucosal infiltration w/
granulocytes or eosinophils
• Non erosive reflux disease: endoscopic app may be normal or mild erythema
• Erosive esophagitis: apparent mucosal damage, redness, friability, bleeding,
superficial linear ulcers, exudates
• Histology: polymorphic infiltrates & granulation tissue
• Peptic stricture  result from fibrosis  luminal constriction
• Erosive esophagitis heal by intestinal metaplasia (Barrett’s esophagus)
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 oaf 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.
LI 13
Prescription
• R/
Omeprazole 20 mg caps no.V
2 dd caps. I
GERD
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