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Truelly J. Chananta
Physiology of Oral Cavity and Esophagus

LO 2
• The gastrointestinal
(GI), or digestive, tract
extends from mouth to
• The GI tract is
conventionally divided
into upper (mouth to
ileum) and lower
(cecum to anus).

• The esophagus is a 25-

cm-long (C6 -T10)
• Esophagus is vertical
muscular tube
• Extent  lower border of
cricoid cartilage (C6) to
cardiac end of stomach
• It is divided into 3 parts:
– Cervicalis (5-8 cm)
– Thoracica(16 cm)
– and Abdominal (1-4 cm)


Infeior thyroid vein

Superior vena cava

Azygos vein

Hemiazygos vein
Microscopic Anatomy of the Esophagus
• The wall of the stomach consists of four coats:
– an outer serous coat;
– a muscular coat, made up of :
• Longitudinal musclefibers,
• Circular musclefibers, thicken the sphincter pylori, forming
M.sphincter pylori
• Oblique musclefibers ;
– submucous coat
• loose connective tissue (contain blood vessel and lymph)
– a mucous coat or membrane forming the inner lining
(plica/rugae gastricae)
• The muscles account for the stomach's ability to expand
when food enters it.

Microscopic Anatomy of the Stomach
• Simple columnar epithelium – contains gastric pits
that secrete gastric juices
• Goblet cells – secrete mucus that coats stomach and
prevents it from being digested itself
• Parietal cells – secrete hydrochloric acid (converts
pepsinogen into pepsin) and intrinsic factor
(necessary for absorption of vitamin B12)
• Chief cells – secrete pepsinogen which is converted
to pepsin to aid in protein digestion
• Enteroendocrine cells – release hormones such as:
– Histamine, Serotonin, Gastrin, Endorphins, and
Microscopic Anatomy of the Digestive
INTESTINUM TENUE (small intestine)
• Duodenum (Retroperitonealis)
– The first part of the small
– The widest and shortest (25
cm) part
– C-shaped or horseshoe-
shaped structure that lies in
the upper abdomen near
the midline
• Jejunum and ileum
– Intraperitonealis
– The jejunum constitutes about 2/5 of the small
intestine and the ileum about 3/5.
– The jejunum has a thicker wall and a wider lumen
than the ileum and mainly occupies the left upper
and central abdomen.
Microscopic Anatomy of Small Intestine
• Villi: fingerlike projections that increase the surface
area of the SI
• Microvilli: tiny projections on the plasma
membranes of columnar cells that appear fuzzy (i.e.
brush border cells)
• Crypts of Lieberkuhn: secrete intestinal juice and
special lysozymes that protect against bacteria
• Peyer’s Patches: aggregated lymphoid tissues
containing lymphocytes
Microscopic Anatomy of the Small
Anatomy of the Liver
• Right and Left Lobes: separated by falciform
• Caudate and Quadrate Lobes: found on posterior
• Blood vessels:
– Hepatic artery/vein and hepatic portal vein
• Gallbladder: found underneath left lobe, stores bile
Gross Anatomy of the Liver
Microscopic Anatomy of the Liver
• Liver Lobules: structural unit of liver
• Hepatocytes: liver cells contained within the lobules
• Hepatic portal vein & Hepatic Artery: the circulation of the
liver, they bring blood into the liver where it is filtered through
the liver sinusoidal capillaries
• Kupffer cells: remove debris
• Filtered blood drains into the central vein, then to the hepatic
vein, and eventually to the inferior vena cava
• Bile (produced by hepatocytes) drains into the bile duct after
passing through portal triad
• Bile then shipped to gallbladder for storage
Microscopic Anatomy of the Liver
• Muscular lips help procure, guide, and contain
the food in the mouth.
• Tounge forms the floor of the oral cavity, is
composed of voluntarily controlled skeletal
muscle. The tounge guides food within the
mouth during chewing and swallowing.
Tounge also has taste buds to taste the food.
• Food  mastication/chewing by the teeth.
• The function of chewing are :
1. Grind and break food into smaller pieces to
facilitate swallowing and to increase the food
surface area on which salivary are can act.
2. To mix food with saliva.
3. To stimulate the taste buds.
• Saliva glands produce saliva that contain 99,5% H2O, and 0,5%
electrolytes and protein (amylase, mucus, lysozyme).
• Function of saliva :
1. Digest starches through action of the enzyme salivary amylase. The
products is maltose (disaccharide consist of two glucose
2. Moistening food particles  holding them together  provide
lubrication by mucus.
3. Antibacteria action :
 Lysozyme is and enzyme that lyses certain bacteria by breaking down
their cell walls.
 By binding glycoprotein that binds IgA antibodies.
 By lactoferrin : binds to the iron needed for bacterial multiplication.
 Rinsing away material that may be a food source for bacteria.
4. Saliva as a solvent for molecules that stimulate the
taste buds. Only molecules in solution can react with
taste bud receptors.
5. Aids speech by facilitating movements of the lips and
6. Keep the mouth and teeth clean. The constant flow of
saliva helps flush away food residues, foreign particles,
and old epithelial cells that have shed from the oral
7. Rich in bicarbonate buffers, which neutralize acids in
food and acids produced by bacteria, thereby helping
prevent dental caries.
Sherwood, 8th ed. Page 621

Both sympathetic and parasympathetic stimulation increase salivary secretion.

- Parasympathetic has dominant role in salivary secretion  produces a prompt and
abundant flow of watery saliva that is rich in enzymes.
- Sympathetic  produces smaller volume of thick saliva that is rich in mucus.
Pharynx and Esophagus
4 stages of swallowing process :
1. Oral preparatory stage
- Voluntary
- Food  bolus
- During this phase, palatum molle is actively getting lower by the contraction of
M.palatoglossus to prevent bolus/liquid leaking into the pharynx.
2. Oral stage
- Voluntary
- During oral stage, the tongue tip rises, touching the alveolar ridge of the hard
palate just behind the upper teeth, while the posterior tongue drops to open the
back of the oral cavity. This stage makes bolus has contact sequentially from
palatum durum  palatum molle  pharynx.
- Elevation of palatum molle cause bolus get into pharynx.
- The same time as the bolus to leave the mouth, nasopharynx is closed to prevent
reflux of nasopharyngeal
3. Pharyngeal stage
- The soft palate elevates, closing the nasopharynx at about
the same time that the bolus head comes into the pharynx.
- The purpose of pharyngeal stage is to transport bolus
perfectly through pharynx, cricopharynx, and upper
esophageal sphincter.
4. Esophageal stage
- Once the food bolus enters the esophagus passing the UES,
a peristalsis wave carries the bolus down to stomach
through the LES. The peristaltic wave consists of two main
parts, an initial wave of relaxation that accommodates the
bolus, followed by a wave of contraction that propels it.
- Gravity assists peristalsis in upright position
Diagram of swallowing
Biochemical of GI Track
• Mouth  saliva
– Amylase: maltose
– Lysozyme: breaking down bacterial cell,
– Mucus: wrap the food
– Haptocorrin (R-factor): helping absorption vit. B12
– Ig A: anti bacterial
General Structure of Digestive Tract
Common Characteristics:
– Hollow tube composed of a lumen whose diameter varies.
– Surrounded by a wall made up of 4 principal layers:
• Mucosa
– Epithelial lining; A lamina propria of loose connective
tissues rich in blood, lymph vessels and smooth muscle
cells; Muscularis mucosae.
• Submucosa
– Dense connective tissues with many blood and lymph
• Muscularis
– Contains smooth muscle cells, divide into 2 layers;
internal (circular); external (longitudinal)
• Serosa
– Thin layer of loose connective tissue rich in blood and
lymph vessels and adipose and single squamous
covering epithelium (mesothelium)
Oral Cavity
Stratified Squamous Epithelium

Keratinized Non Keratinized

Protects Oral Mucosa

Covers soft palate, lips,
from damage during
cheeks and floor of mouth
masticatory function.

In Gingiva and Hard Lamina Propria has

Palate Papillae, similar to those
in dermis of skin and
continuous with
Lamina Propria has submucosa containing
several papillae and rest diffuse small salivary
directly on bony tissue gland
Oral Cavity
• Tongue
– Papillae
• Filiform
• Fungiform
• Foliate
• Circumvallate
• Pharynx
• Teeth and Associate Structures
– Dentin
– Enamel
– Pulp
– Periodontium
• Mass of striated muscle covered by a mucous
• Muscle fibers cross on another in 3 planes, they
are grouped in bundles, usually separated by
connective tissue.
• Dorsal Surface  Irregular; Thicker epithelium;
Covered anteriorly by a great number of small
eminences papillae; Separated from anterior two
thirds by a V-shaped boundary.
• Ventral Surface  Epithelium on this surface is
Papillae of Tongue
Papillae of Tongue
• Filiform Papillae
– Conical Shape
– Numerous and present over entire surface of tongue
– Their epithelium does not contain taste bud and is Keratinized.
• Fungiform Papillae
– Resemble mushrooms (narrow stalk and smooth surface, dilated
upper part)
– Contain scattered taste buds on upper surfaces
– Irregularly interspersed among filiform papillae.
• Foliate Papillae
– Poorly developed in humans
– 2 or more parallel ridges and furrows on the dorsolateral surface
of tongue
– Contain many taste buds
Papillae of Tongue
• Circumvallate Papillae
– 7 – 12 extremely large circular papillae whose flattened surface extend
above other papillae (Papillae surrounded by deep circular furrows).
– Distribute in the V region at the junction of the anterior 2/3rd and
posterior 1/3rd of tongue.
– The epithelium is smooth on the lateral surface of papillae
– Great number of taste buds present along sides of these papillae.
• Taste Buds
– Onion shaped structures containing 50 – 100 cells.
– Rests in Basal Lamina
– Apical portion project microvilli that poke through an opening called
taste pore.
– 2types of cells are distinguished in relation to taste buds
• Supporting or sustentacular cells
• Neuroepithelial or gustatory cells
Taste Bud
– Arranged peripherally, curved course, narrow at each end and
broader in the centre appearing spindle shaped.
– At both ends the cells surround small openings known as
external and internal pores.


– Distributed between the sustentacular cells long narrow, having
slender red shaped form with a nucleus in the middle.
– On the free surface, these cells gives rise to short hair which
project into the lumen of the pit.
– The substances to be tasted gets dissolved in the saliva,
stimulate the hairs in the neuroepithelial cells and the impulses
is conducted along the nerves (sweet, bitter, sour, salty)
• Lined by Stratified non keratinized squamous
epithelium in region continuous with esophagus.
• Lined by ciliated pseudostratified columnar
epithelium containing goblet cells in region close
to nasal cavity.
• Contains tonsils.
• Mucosa of pharynx also has many small mucous
salivary glands in its lamina propria
• Compose of dense connective tissues.
• Muscular Tube function to transport food stuffs from mouth to
• Covered by non keratinized stratified squamous epithelium.
• In general same layers as rest of digestive tract.
• In submucosa  groups of small mucous secreting glands
(esophageal glands) secretion facilitated transport of food stuff and
protects mucosa.
• Lamina Propria near stomach  groups of gland (esophageal
cardiac gland) secrete mucus
• Distal end muscular layer  Only smooth muscle
• Mid Portion  Mixture of striated a
nd smooth muscle
• Proximal end  Only striated muscle cells
• Portion in peritoneal cavity covered by serosa
• The other portion covered by layer of connective tissue, adventitia
that blends into surrounding tissue.
Lower esophagus Upper esophagus
• Mixed exocrine endocrine gland.
• Divides into 4 regions:
– Cardia
– Fundus
– Body
– Pylorus
• Fundus and body are identical in microscopic
• Mucosa and submucosa of undistended stomach
lie in longitudinally directed folds known as
Gastric Mucosa
• Consists surface epithelium invaginates to various
extend into lamina propria forming gastric pits.
• Lamina propria of stomach composed of loose
connective tissue interspersed with smooth
muscle and lymphoid cells.
• Muscularis mucosae to separate mucosa from
underlying submucosa
• Epithelium lining the pits and covering the
surfaces are simple columnar epithelium & all
cells secrete alkaline mucus.
Gastro-esophageal Junction
Stomach (Cardia)
• Mucosa contains simple or branched tubular
cardiac glands
• Terminal portion of these glands are frequently
coiled, often with large lumens.
• Similar in structure to cardiac glands of the
terminal portion of esophagus.
Stomach (Fundus & Body)
• Simple columnar surface epithelium extends into gastric
pits into which opens into gastric glands.
• Lamina propria consist of fine reticular and collagen fibres
fills the spaces between the packed gastric glands.
• Each gastric gland has 3 distinct region:
– Isthmus
– Neck
– Base
• Isthmus contains differentiating mucous cells and
undifferentiated stem cells and parietal cells.
• Neck consist of stem, mucous neck and parietal cells.
• Base contains parietal and chief (zymogenia) cells.
• The muscularis mucosa composed of inner circular and
outer longitudinal smooth muscle.
Stomach (Pylorus)
• Deep gastric pits into which the branched tubular pyloric
glands open.
• The epithelium of the mucous membrane consist of tall
columnar cells which lines the deep pits and short glands.
• Longer pits and shorter coiled secretory portion compare to
glands in cardiac region.
• The acini of pyloric glands and their ducts are in lamina
• G (Gastrin) cells are enteroendocrine cells intercalated
among mucous cells of pyloric glands.
• D cells secrete Somatostatin
• The muscularis externa is made up of thick circular muscle
to form pyloric sphincter which helps to control emptying of
the stomach.
Small Intestine



Small Intestine
• 4 layers:
1. Mucosa
2. Submucosa
3. Muscularis externa
4. Serosa
• Surface area of small intestine increased by
1. Length of small intestine
2. Valves of Kerkring/ Plica Circularis
3. Villi
4. Microvilli
5. Cypts Of Lieberkuhn
Mucosa of Small Intestine
Valves of Kerkring
• Also known as Plica
• Permanent submucosal
circular folds
• Large, seen with naked eye
• Prominent in duodenum &
• Less marked in ileum
• Significance:
– Increases surface area
– Slow down the passage of
• Central lacteal
(lymphatic vessel)
• Core capillaries
• Core of connective
• Epithelial cells – Tall
columnar with striated
Crypt of Lieberkuhn (Intestinal gland)
• Invaginations of lining
epithelium into lamina
• Wall of crypt is lined by
the following cells:
1. Columnar cells
2. Goblet cells
3. Undifferentiated stem cells
4. Paneth / Zymogen cells
5. Argentaffin cells
Crypt of Lieberkuhn

• Absorptive columnar
cells / Enterocytes
– Microvilli which give it a
striated border appearance
• Goblet cells
– Secretes mucus
• Undifferenciated cells
– Actively multiply, move
upwards give rise to other
Crypt of Lieberkuhn
• Paneth cells / Zymogen cells
– Seen in deeper parts of crypts
– rich in Zinc, secrete lysozyme that destroys bacteria
• Endocrine cells
– Seen near lower ends of crypts
– Argentaffin cells
– Entero-chromaffin cells
– APUD cells – secrete serotonin
Submucosa of Small Intestine
Brunner’s Gland

• In duodenum (Also known as duodenal glands)

• Clusters of ramified, coiled tubular glands that opens
into the intestinal crypts.
• Cells are mucous type.
• Secretions are distinctly alkaline (PH8.1 – 9.3), to
protect duodenal mucous membrane from effects of
acid gastric juice and to brings intestinal contents to
optimum PH for pancreatic enzyme action.
Peyer’s Patches
• Lymphoid Nodules.
• Present in ileum, more
prominent in terminal ileum.
• In lamina propria and
• Dome shaped area devoid of
• Instead of absorptive cells,
its covering epithelium
consist M cells.
Differences between duodenum, jejunum
& ileum
Duodenum Jejunum Ileum

Epithelium Columnar Columnar Columnar

Striated border Striated border goblet cells++
Few goblet cells goblet cells+

Villi Broad Tongue-shaped Few thin finger-

Spatula Shaped Different heights shaped
Closely packed
Lamina Propria Crypts+ Crypts+ Crypts+
No Peyer’s Diffuse infiltration Peyer’s patches
patches of lymphocytes extend into
No Peyer’s submucosa
Submucosa Mucus secreting Only connective Peyer’s patches
Brunner’s glands tissues and blood
Large Intestine

• Consists mucosal membrane with no folds except in its

distal (rectal) portion.
• No vili are present
• Long intestinal glands
• Great abundance of goblet and absorptive cells
• Small number of enteroendocrine cells.
• Fibers of outer longitudinal layer congregates in 3 thick
longitudinal band (Teniae coli).
• Serous layer characterized by small, pendulous
protuberances composed adipose tissues (appendices
• Mucous membrane forms a series of longitudinal folds
(rectal columns of morgagni)

• Evagination of cecum
• Small, narrow and irregular lumen caused by
presence of abundant lymphoid follicles in its
• Although general structure similar to large
intestine, it contains fewer and shorter intestinal
glands and has no teniae coli.
Small Vs Large Intestine

Small intestine Large intestine

Villi 1. Crypts shallow 1. Absence of villi
2. Goblet cells less 2. Crypts deeper,
More Goblet

Longitudinal 1. Uniformly thick 1. Three bands of

muscle coat of Taenia coli
Histology of Accessory Organs of
Salivary Gland
3 pairs of salivary glands:

• Purely serous (few mucous acini maybe present)

• Mixed, Predominantly serous

• Mixed, Predominantly mucous
General Features
• Serous cells
– Pyramidal in shape
– Broad base resting on basal lamina
– Narrow apical surface with short irregular microvilli facing
– Secretory cells are joined together by junctional complex and
usually form spherical mass of cells called acinus
• Mucous Cells
– Usually cuboidal to columnar
– Oval nuclei pressed towards bases of the cells
– Most often organized as tubules, consisting of cylindrical arrays
of secretory cells surrounding a lumen.
General Features
• Duct System
– Intralobular ducts
• Intercalated Ducts
– Lined by Cuboidal Epithelial Cells
– Ability to differentiate into secretory or ductal cells
• Striate Ducts
– Radial striations seen to consist infoldings of basal
plasma membrane with numerous elongated
– Drains into Interlobular Ducts
– Interlobular Ducts (Excretory Ducts)
• Initially lined with pseudo stratified or stratified cuboidal
• Distal parts lined with stratified columnar epithelium
consisting few mucus secreting cells
• Ultimately empties into oral cavity and lined by
nonkeratinized-stratified squamous epithelium.
• Parotid Gland
– Branched acinar glands
– Surrounded by a capsule from which arise numerous
interlobular connective tissue septa that subdivides the gland
into many lobes and lobules.
– Located in the connective tissue septa between the lobules are
arteriole, venule and interlobular excretory ducts.
• Submandibular Gland
– Presence of both serous and mucous acini.
– Mucous acinus are larger than the serous.
– Between the mucous cells and basement membrane are half
moon shaped granules known as demilunes of Gianuzzi.
• Sublingual Gland
– Similar as Sub mandibular
– Intralobular ducts are not as well developed as in other major
salivary gland
• Repeating hepatic lobules (Hexagonal Unit).
• Central Vein in the centre of each hepatic lobule.
• Portal canals (Portal Traids) in periphery the surrounding
connective tissue [Branches of the hepatic artery, hepatic
portal vein, bile duct, and lymph vessels seen.]
• Hepatic sinusoids (dilated blood channels) contains
epithelial cells and macrophages called “Kupffer cells”
• The hepatic sinusoids separated from the underlying
hepatocytes by subendothelial perisinusoidal space of
• The major exocrine functions of hepatocytes is synthesis
and release about 500-1200ml of bile per day which is
delivered to the gallbladder via the bile canaliculli.
Gall Bladder

• It consist of mucosa composed of Simple columnar

epithelium and lamina propria; a layer of smooth
muscle; a perimuscular connective tissue layer and a
serous membrane.
• Mucosa has abundant folds that are particularly
evident when gall bladder is empty.
• Epithelial cells are rich in mitochondria
• Surrounding the bundle of smooth muscle fibres is a
thick dense connective tissue containing large blood
vessels  artery & vein, lymphatic and nerves.
• Serosa covers entire unattached gallbladder surface

• Mixed endocrine and exocrine gland

• Exocrine  compound acinar gland, similar in
structure to parotid gland.
• Distinction between 2 glands can be made based
on absence of striated ducts and presence of
islets of Langerhans.
• Initial portions of intercalated ducts penetrate
lumens of acini.
• Centroacinar cells constitude interacinar portion
of intercalated duct.
Medical Application
• Gastroesophageal Reflux Disease associated with
incompetent barriers at gastroesophageal junction
caused by decrease in lower esophageal sphincter tone
or hiatus hernia. Reflux esophagitis develops when
mucosal defenses are not sufficient to protect
esophageal mucosa from acid, pepsin and bile.
• Stress, ingested aspirin, NSAID or ethanol can disrupt
epithelial layer in stomach lead to ulceration. Ulcer is
disruption of mucosal integrity leading to an excavation
due to active inflammation. Apirin and ethanol irritates
mucosa partly by reducing blood flow.
 Most frequent potentially ETIOLOGY
malignant disorder of oral
mucosa. • Multifactorial
• Leuko : white; Plakia : patch • Most common among
• Male 40th >> smokers
• Usually asymptomatic
CLINICAL APPEARANCE • Detect and prevent malignant
• Homogenous type : appears as transformation
a flat white lesion (uniform) • Decreasing risk activities
• Non-homogenous : speckled (smoking)
(white and red), nodular and • Surgical treatment/ laser
verrucous (elevated, ablation


progressing polymicrobial
cellulitis of the sublingual / • Dental infections by :
submandibular spaces. – α – hemolytic streptococci
• Usually occur in adults with – Staphylococci
dental infections Infected lower molars (3) or from
• May obstruct airways (untreated) pericoronitis


• Anxious, confused • Angioneuretic edema
• Cellulitis
• Breathing difficulties • Lingual carcinoma
• Neck swelling/pain • Lymphadenitis
• Peritonsillar abscess
• Odenophagia • Salivary gland abscess
• Hot potato sound • Sublingual hematoma


• Bilateral involvement of more • surgical drainage : when there is
than a single deep-tissue space suppurative inf., radiologic evidence
of fluid collection or soft-tissue air,
• Gangrene with serosanguinous
and when there is no clinical
• Involvement of connective tissue, improvement after antibiotic therapy
fasciae, and muscles but not • Removal of infected teeth
glandular structures • Tracheostomy : securing the airway
• Spread via fascial space • Antibiotic :
continuity rather than by – Ampicillin/sulbactam
lymphatic system. – Cefoxitin
• Plain radiographs of the neck – Clindamycin
often show soft-tissue swelling, – Penicillin G plus metronidazole
the presence of gas, and the – Gentamycin
exten of airway narrowing


 Oral thrush; oral mucosal CLASSIFICATION
infection seen in persons with • Pseudomembranous :
human immunodeficiency
– Thrush
virus (HIV/AIDS)
– a coating/individual patches of
• Caused by Candida albicans pseudomembranous white
slough  easily wiped away to
ETIOLOGY reveal erythematous &
sometimes bleed the mucose
• HIV/AIDS beneath.
• Topical/systemic corticosteroids – Curdled milk/cottage cheese
• Chemotherapy/radiotherapy • Atrophic :
• Poor denture hygiene – Red, raw looking lesion
• Malnutrition • Hyperplastic:
• Broad-spectrum antibiotics – Cnadidal leukoplakia
(tetracycline) – Can’t be wiped away


• Whitish patches appear on • By the clinical appearance
the tongue, inside cheecks, • Take a swab & check it w/
or palate.
• Occurs in people TREATMENT
w/abnormal immune • Topical anti-fungal drugs:
system – Nystatin
• Painless ; but burning – Miconazole
sensation may occur – Gential violet
– Amphotericin B
• Difficulty in swallowing
• Increasing the oral hygene
• Hoarseness of the voice (
involved trachea and larynx)


 Referred as repeated episodes ETIOLOGY
of parotid gland inflammation • Remain uncertained
that is non-obstructive and • Believed to have multifactorial
non-suppurative. caused such as congenital
malformation of the parotid
glands  retrograde infection,
DIAGNOSIS alergy, & association
w/autoimmune disease.
• Based on history taking and
physical examination TREATMENT
• Confirmed by imangings: • Analgesics and antibiotics
– Sialography • Radiotherapy
– Ultrasonography • Parotid duct ligation
• parotidectomy


Gastroesophageal Reflux Disease
• GERD happen when the lower esophageal sphincter becomes weak
or relaxes when it shouldn’t due to certain things, such as
– overweight, obese, or pregnant  increased pressure on your
– calcium channel blockers—medicines that treat high blood pressure
– Antihistamines
– Painkillers
– Sedatives
– Antidepressants
– Smoking, or inhaling secondhand smoke
– A hiatal hernia can also cause GERD. Hiatal hernia is a condition in
which the opening in your diaphragm lets the upper part of the
stomach move up into your chest, which lowers the pressure in
the esophageal sphincter.
Sign & Symptom
• Heart burnt (feel a burning in the chest or throat)
• taste food or stomach acid in the oropharyngeal
• bad breath
• nausea
• pain in your chest or the upper part of abdomen
• problems swallowing or painful swallowing
• respiratory problems (dry coughing or asthma
• vomiting
• the wearing away of teeth
• Gastroesophageal reflux disease (GERD)
happens when a muscle at the end of the
esophagus does not close properly. This allows
stomach contents to leak back, or reflux, into
the esophagus and irritate it.
• Upper gastrointestinal (GI) endoscopy and biopsy
– the procedure only diagnoses GERD if you have moderate to severe
• Upper GI series
– taking several x-rays as the barium moves through your GI tract.
– To diagnose hiatal hernias, esophageal strictures, ulcers
• Antacid
• Proton pump inhibitor (lower the amount of
– Esomeprazole, Lansoprazole, Omeprazole,
Pantoprazole, rabeprazole
• H2 blockers (decrease acid production)
– cimetidine, famotidine, nizatidine, ranitidine
• Prokinetics (emptying stomach faster)
– Bethanechol and metoclopramide
• not eating or drinking items that may cause GER,
such as greasy or spicy foods and alcoholic drinks
• not overeating
• not eating 2 to 3 hours before bedtime
• losing weight if the patient
is overweight or obese
• quitting smoking and avoiding secondhand smoke
• wear loose-fitting clothing around your abdomen.
• Fundoplication
– is a type of surgery wrapping the upper portion of
the stomach (fundus) around the lower portion of
the esophagus to tightens the lower esophagus so
that food and fluid can go down into the stomach
but can not return up to the esophagus.
• Endoscopic techniques
– Endoscopic sewing uses small stitches to tighten
the sphincter muscle.
Esophageal Atresia
• A disorder of the digestive system in which the
esophagus does not develop properly. The
esophagus is the tube that normally carries
food from the mouth to the stomach.
• It is a congenital defect. Esophageal atresia
occurs in about 1 out of 4,000 births.
Sign & Symptom
• Bluish coloration to the skin (cyanosis) with
attempted feedings
• Coughing, gagging, and choking with
attempted feeding
• Drooling
• Poor feeding
• Before birth, an ultrasound performed on the pregnant
mother may show too much amniotic fluid, which can be a
sign of esophageal atresia or other blockage of the
digestive tract.
• The disorder is usually detected shortly after birth when
feeding is attempted and the infant coughs, chokes, and
turns blue. As soon as the diagnosis is suspected, an
attempt to pass a small feeding tube through the mouth or
nose into the stomach should be made by a health care
professional. The feeding tube will not be able to pass all
the way to the stomach in a baby with esophageal atresia.
• An x-ray of the esophagus shows an air-filled pouch and air
in the stomach and intestine. If a feeding tube has been
inserted, it will appear coiled up in the upper esophagus.
• Esophageal atresia is considered a surgical
emergency. Surgery to repair the esophagus
should be done quickly after the baby is
stabilized so that the lungs are not damaged
and the baby can be fed.
• Before the surgery, the baby is not fed by
mouth. Care is taken to prevent the baby from
breathing secretions into the lungs.
• An early diagnosis gives a better chance of a
good outcome.
• 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.
• Achalasia is a disorder of the esophagus, the tube that
carries food from the mouth to the stomach. This condition
affects the ability of the esophagus to move food into the
• Normally, the lower esophageal sphincter relaxes when you
swallow. In people with achalasia, it does not relax as well.
In addition, the normal muscle activity of the esophagus
(peristalsis) is reduced.
• This problem is caused by damage to the nerves of the
esophagus (n.vagus).
• Achalasia is rare. It may occur at any age, but is most
common in middle-aged or older adults. The problem may
be inherited in some people.
Sign & Symptoms
• Dysphagia (most common)
• Regurgitation
• Chest pain
• Heartburn
• Weight loss
• Barium swallow: Bird’s beak appearance, esophageal
• 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
Barium swallow demonstrating the bird-beak appearance of the lower
esophagus, dilatation of the esophagus, and stasis of barium in the
Differential Diagnose
• Other problems can cause similar symptoms,
such as cancer of the esophagus or upper
stomach, and a parasite infection that
causes Chagas disease.
• Administration of calcium channel blockers
and nitrates decrease LES pressure (primarily
in elderly patients who cannot undergo
pneumatic dilatation or surgery)
• Endoscopic intrasphincteric injection of
botulinum toxin to block acetylcholine release
at the level of the LES (mainly in elderly
patients who are poor candidates for
dilatation or surgery)
• Laparoscopic Heller myotomy, preferably with
anterior (Dor; more common) or posterior
(Toupet) partial fundoplication
• Peroral endoscopic myotomy (POEM)
Swallowing Disorders

LO 4
• The term dysphagia, a Greek word that means disordered eating,
typically refers to difficulty in eating as a result of disruption in the
swallowing process.
• Any disorder that causes no coordination between that 4 phases of
swallowing properly will cause the disorder of swallowing or
dysphagia. It can cause by :
– Anatomy disorder of digestive tract and upper aerodigestive that
connected with the process of swallowing either congenital or
acquired such as agenesis, stenosis, anatomical defects, mechanical
pressure by the tumor mass, stricture due to physical trauma or
– Neuromuscular disorder either central or peripheral of digestive tract
and aerodigestive. Either congenital or acquired such as weakness of
the muscles of the mouth and tongue including lips, cheeks, tongue,
palate, pharynx, and larynx, esophagus, and motility disorders of the
esophagus, stomach, duodenum (weakness of peristaltic contractions)
• The muscles and nerves that help move food through the throat
and esophagus are not working right. This can happen if you have:
– Had a stroke or a brain or spinal cord injury.
– Certain problems with your nervous system, such as post-polio
syndrome, multiple sclerosis, muscular dystrohphy, or Parkinson’s
– Immune system problem that cause swelling (inflammation) and
weakness, such as polymyositis or dermatomyositis.
– Esophageal spasm. This means that the muscles of the esophagus
suddenly squeeze. Sometimes this can prevent food from reaching the
– Scleroderma. In this condition, tissues of the esophagus become hard
and narrow, it can also make the lower esophageal muscle weak,
which may cause food and stomach acid to come back up into your
throat and mouth.
• Something is blocking your throat or esophagus. This may happen if
you have:
– Gastroespohageal reflux disease (GERD). When stomach acid backs up
refulary into yout esophagus, it can cause ulcers in the esophagus,
which can then cause scars to form. These scars can make your
esophagus narrower.
– Esophagitis. This is inflammation of the esophagus. This can be caused
by different problems, such as GERD or having an infection or getting a
pill stuck in the esophagus. It can also be caused by an allergic reaction
to food or things in the air.
– Diverticula. These are small sacs in the walls of the esophagus or the
– Esophageal tumors. These growths in the esophagus may be
cancerous or not cancerous.
– Masses outside the esophagus, such as lymoh nodes, tumors or bone
spurs on the vertebrae that press on your esophagus.
Sign & symptoms
Signs and symptoms of oral or pharyngeal dysphagia include the following:
• Coughing or choking with swallowing
• Difficulty initiating swallowing
• Food sticking in the throat
• Sialorrhea
• Unexplained weight loss
• Change in dietary habits
• Recurrent pneumonia
• Change in voice or speech (wet voice)
• Nasal regurgitation
Signs and symptoms of esophageal dysphagia include the following:
• Sensation of food sticking in the chest or throat
• Change in dietary habits
• Recurrent pneumonia
• Symptoms of gastroesophageal reflux disease (GERD), including heartburn,
belching, sour regurgitation, and water brash
Other associated factors/symptoms of dysphagia include the following:
• General weakness
• Mental status changes
• A videofluoroscopy, or modified barium swallow, is one
of the most effective ways of assessing your swallowing
ability and finding exactly where the problem is.
• An x-ray machine records a continuous moving x-ray on
to video.
• You'll be asked to swallow different types of food and
drink of different consistencies, mixed with a non-toxic
liquid called barium that shows up on X-rays.
• A videofluoroscopy usually takes about 30 minutes.
You constipation.
• Manometry is a procedure to assess the
function of your oesophagus. It involves
passing a small tube (catheter) with pressure
sensors through your nose and into your
oesophagus to monitor its function. The test
measures the pressures within
your oesophagus when you swallow, which
determines how well it's working.
Medications used in the treatment of dysphagia
include the following:
• Botulinum toxin type A (BoNT-A)
• Diltiazem
• Glucagon
• Cystine-depleting therapy with cysteamine
• Nitrates
Dietary modification is the key component in the general treatment program
of dysphagia. Diets for patients with dysphagia include the following:
• Dysphagia diet 1: Thin liquids (eg, fruit juice, coffee, tea)
• Dysphagia diet 2: Nectar-thick liquids (eg, cream soup, tomato juice)
• Dysphagia diet 3: Honey-thick liquids (ie, liquids that are thickened to a
honey consistency)
• Dysphagia diet 4: Pudding-thick liquids/foods (eg, mashed bananas,
cooked cereals, purees)
• Dysphagia diet 5: Mechanical soft foods (eg, meat loaf, baked beans,
• Dysphagia diet 6: Chewy foods (eg, pizza, cheese, bagels)
• Dysphagia diet 7: Foods that fall apart (eg, bread, rice, muffins)
• Dysphagia diet 8: Mixed textures
Enteral feeding
• Nasogastric tube (NGT) feeing
• Oroesophageal tube feeding
• Percutaneous endoscopic gastrostomy (PEG)
• Odynophagia is pain during swallowing.
• The causes of odynophagia are usually associated with
a destruction or irritation of the mucosa. Mucosa is a
moist tissue that lines certain parts of the inside of
your body and release mucus. Damage to the mucosa
could be caused by the habitual consumption of
extremely hot or cold food and beverages
• In immunocompromised patients, infectious etiologies
such as Candida, HSV, CMV must be considered. In
some populations, it causes by chronic reflux,
radiation, and pill-induced damage
• 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.
– Primary achalasia : idiopathic, suspected caused by
neurotropic viruses that cause lesions in the dorsal vagal
nucleus in the brain stem and ganglia misentrikus the
– Secondary achalasia : caused by infection (chagas disease),
tumor intraluminer such as tumor cardia / pancreatic

• LSE pressure increases >

26mmHg or > 30mmHg.
• Relaxation LSE is not
• Aperistaltis corpus
• Intraesofagus pressure
increased (> gastric).
Primary Secondary
Dysphagia (most common) Mild to severe (>1 year) Moderate to severe (<6
Chestpain Mild to moderate Rarely
Weight loss Mild (5 kg) Severe (15 kg)
Regurgitation Moderate to severe Mild
Lung complications Moderate Rarely

Other symptoms :
– Heartburn
– Patient’s may sense a lump in their throat
– Hiccups

• 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
• Important for diagnostic confirmation
• Three classic findings :
– Elevated resting LES pressure (often above 45
– Incomplete LES relaxation
◦ The LES should drop to <8 mmHg
◦ In achalasia LES relaxation in response to a swallow may
be incomplete or absent.
– Aperistalsis of the esophagus
• Medical therapy with
calcium channel blockers or
nitrates (taken 10-30
minutes before meals) 
not recommended as first
line therapy
• Pneumatic dilatation
– The most effective non
surgical treatment of

• Botulinum neurotoxin
type A
• Inhibits the release of
acethylcholine by
blocking the release of
Ach from the presynaptic
channels in the ganglia of
Auerbach’s plexus.
• Aphthous ulcers are ulcers that form on the
mucous membranes.
• Recurrent aphthous ulcers usually begin as a
round yellowish elevated spot surrounded by a
red halo. This then breaks down into a punched-
out ulcer, which is covered with a loosely
attached white, yellow or greyish membrane.
Surrounding tissue is healthy and unaffected.
• Sometimes these ulcers can be painful,
particularly if they are irritated by movement or
from eating certain types of food.
There are basically 3 types of aphthous ulcers :
• Recurrent minor aphthous ulcers, which occur in
up to 80% of aphthous ulcer cases. They are
usually less than 5mm in diameter and heal
within 1-2 weeks.
• Major aphthous ulcers, which are large ulcers
(more than 10mm) that take weeks or months to
heal and do so with scarring.
• Herpetiform ulcers, which are multiple pinpoint
ulcers that heal within a month. These are most
commonly on the tongue.
Herpetiform ulcers
• Is not yet clearly defined.
• Current thinking is that the immune system is disturbed by
some external factor and reacts abnormally against a protein
in mucosal tissue.
• Factors that seem to trigger outbreaks of ulcers include:
– Emotional stress and lack of sleep
– Mechanical trauma, for example self-inflicted bite
– Nutritional deficiencies, particularly vitamins B, iron, and
folic acid
– Drugs, especially NSAIDs, alendronate, and nicorandil
– Viral infections
– Sodium lauryl sulphate (SLS): This is a detergent in some
oral healthcare products that may aggravate or produce
oral ulceration.
• Blood tests may include:
- Blood count, iron, B12 and folate studies
- Gluten antibody tests for celiac disease
- Faecal calprotectin test for Crohn disease
- Swabs for microbiology evaluate the
presence of Candida albicans, Herpes simplex
virus and Vincent's organisms.
• The main goal of treatment is to lessen the pain and
discomfort, and promote healing.
• Topical prescription medicines include:
– Tetracycline suspension as mouthwash
– Topical corticosteroids as lotions, creams or paste, often
triamcinolone in dental paste
– Calcineurin inhibitors: topical pimecrolimus or tacrolimus.
• In severe cases, particularly if there are systemic
symptoms, anti-inflammatory oral medications may be
– Tetracycline, e.g. doxycycline 50-100mg daily for 3-6
months or longer
• Dental caries or cavities, more commonly
known as tooth decay, are caused by a
breakdown of the tooth enamel.
• This breakdown is the result of bacteria on
teeth that breakdown foods and produce acid
that destroys tooth enamel and results in
tooth decay.
Tooth decay may not cause any symptoms until it has reached
an advanced stage. As the problem develops, symptoms of
tooth decay can include:
– Toothache
– Tooth sensitivity –feel tenderness or pain when eating or drinking
something hot, cold or sweet
– Grey, brown or black spots appearing on teeth
– Bad breath
– An unpleasant taste in your mouth
If left untreated, tooth decay can lead to further problems such
as a cavities (holes in the teeth) gum disease or dental
abscesses(collections of pus at the end of the teeth or in the
• The dentist may apply a fluoride varnish to the
area to help stop further decay, when the decay is
in the early stages
• Root canal treatment, which involves removing
the nerve and restoring the tooth with a filling or
crown, (If the nerve in the middle tooth is

Root fillings
• Glossitis is a problem in
which the tongue is
swollen and changes
color, often making the
surface of the tongue
appear smooth.
• Caused by complete
atrophy of the lingual
papillae (depapillation)

Möller-Hunter glossitis,
• Atrophic glossitis is a non-specific finding, and has a great
many causes, usually related to various nutritional
deficiencies or other factors such as xerostomia (dry
mouth) or anemia
• Etiology :
– vit B12 deficiency
– Allergic reactions to oral care 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 dentures0
– Skin conditions that affect the mouth
– Irritants such as tobacco, alcohol, hot foods, spices, or other
– Hormonal factors
• 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
• The goal of treatment is to reduce swelling and
soreness. Most people do not need to go to the
hospital unless the tongue is very swollen.
Treatment may include:
– Good oral care. Brush your teeth thoroughly at least
twice a day and floss at least once a day.
– Antibiotics or other medicines to treat infection.
– Diet changes and supplements to treat nutrition
– Avoiding irritants (such as hot or spicy foods, alcohol,
and tobacco) to ease discomfort.
• There are several types of oral cancers, but over 90%
are squamous cell carcinomas.
• Risk factors for developing oral cancer include:
– Smoking: 75% of those diagnosed with oral cancer are
tobacco users. The higher the tar yield the greater the risk.
– Smoking and alcohol consumption: tobacco and heavy
drinking act together to significantly increase the risk
(greater than the sum of 2 effects independently).
– Poor oral health.
– Infective agents, particularly the wart virus human
papillomavirus types 16 and 18, have been implicated in
some oral cancers.
– A white patch (leukoplakia) and/or red patch
(erythroplasia) on the gums, tongue, or lining of the mouth
– A small sore or indurated ulcer that looks like a
common aphthous ulcer that fails to heal
– A lump or mass that can be felt on the lip or in the mouth
or throat
– Unusual bleeding, pain, or numbness in the mouth
– Difficulty or pain with chewing or swallowing
– A persistently sore throat, or a feeling that something is
caught in the throat
– Swelling of the jaw that causes dentures to fit poorly or
become uncomfortable
– A change in the voice or hoarseness that lasts for a long
– Pain in the ear

Inner lip alveolar

– Biopsy of the lession
– Oral cancer squamous cell carcinoma is generally
treated by surgery and/or radiation therapy.
– Chemotherapy may also be used, particularly in
patients with confirmed metastases to other tissues
and organs.
– Oral health needs are addressed prior to cancer
therapy. This is to minimise oral disease and post-
therapeutic complications.