Pleno 1 Blok

Gatrointestinal
19 Agustus 2019

Kelompok 3
Kelompok 10
• Tutor : dr. MARCELLA ERWINA RUMAWAS, M.S., Ph.D.
Ketua : Blasius Hugo Auriol (405170023)
Sekretaris : Ignatius Loyola Yudo Kris Yulianto (405170177)
Penulis : Andhini Rajo Pujian (405170066)
Anggota :
1. Andreas Galih Sidharta S (405150002)
2. Luthfi Handayanti (405170010)
3. Claudia Agnes Jap (405170030)
4. Annisa Marinda Syach Rizal (405170058)
5. Steven Junius Chandra (405170061)
6. Florencia Danyalson Phang (405170183)
7. Tri Yunita Alicia (405170193)
8. Ririn Efranisa S. B (405170236)
Problem 1
• A 5-year old girl came to family physician with complaints of cheek
swelling accompanied by fever since 2 days ago. From history
assessment, the patient had a surgery on day 3 after birth du to
continuous vomit. The physical examination revealed temperature
38C, swelling on the right and left cheeks and white patches on the
surface of the tongue and oral mucosa. Dental caries was also noticed
in some upper incisivus. Other physical examination were
unremarkable.
What can you learn from the problem?
REVIEW

Anak Perempuan 5 th Riwayat Operasi, 3 hari

setelah kelahiran

- Pipi Bengkak Bilateral

(Inflamasi Kelenja parotis) Karena Muntah terus
- Bercak Putih (Oral candidiasis,
leukoplakia)
- Karies gigi (Aphtea)
- Demam 38° Curiga :
- Atresisa Esofagus
- Achalasia

Kesuliatan Menelan
(Disfagia) + Nyeri
(Odynofagia)
Learning issues
1. MM anatomi dan histologi mulut dan esofagus
2. MM enzim pencernaan mulut dan kelenjar ludah
3. MM fisiologis menelan
4. MM definisi dan patofisiologi Disfagia dan Odinophagia
5. MM Penyakit mulut (oral candidiasis, leukoplakia,
aphtea, parotitis, atresia esophagus, achalasia,
glossitis, Ludwig’s angina, karies gigi)
Anatomi dan Histologi
(Mouth  Esophagus)
LI 1
• Mouth divided into:
• Vestibule
• Oral cavity proper
Mouth extends
from lips (ant) to
oropharynx (post)

• Oropharyngeal
isthmus =
entrance to
oropharynx
formed by
palatoglossal
folds
PHARYNX
• Posterior to nasal & oral cavities
• Inferior end continuous with esophagus
• 3 parts of pharynx:
• Nasopharynx  posterior to the nose & superior to soft palate
• Oropharynx  Posterior to the mouth
• Laryngopharynx  posterior to larynx
Oropharynx
• Has digestive function
• Bounded by:
• Superior: soft palate
• Inferior: base of tongue
• Lateral: palatoglossal & palatopharyngeal arches
• Palatine tonsils: collection of lymphoid tissue on each side of
oropharynx
• Lies in tonsillar bed (formed by superior constrictor of pharynx &
pharyngobasilar fascia)
Muscles of pharynx

groove
The tongue

Floor of mouth and oral vestibule.

The
Teeth
The palate
Moore’s Clinical Oriented
Anatomy, 5th Edition
The Salivary
Glands
• Parotid gland
• Largest salivary
gland
• Below external
auditory meatus,
behind ramus of
mandible, in front
of
sternocleidomastoi
d muscle
Submandibular gland
• Lies beneath lower border of mandible
• Divided into: superficial & deep by mylohyoid
muscles
Sublingual glands
• Beneath mucous membrane (sublingual
folds) of mouth floor
• Close to frenulum of tongue
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
Upper Esophageal
Sphincter
• Separates pharynx from
esophagus
• 3 skeletal muscle groups:
Lower Esophageal
Sphincter
• External: skeletal muscles of crural
diaphragm (from lumbar vert)
• Internal: Smooth muscle of distal
esophagus
 Hiatus in
diaphragma
• Esophagus passes from chest
 abdomen through
diaphragmatic hiatus
• Opening in right crus of
diaphragm
• Approx 2 cm of distal
esophagus lie w/in abdomen
Muscles of Esophagus
• Outer layer
(longitudinal muscles)
• Contraction  shorter
esophagus
• Inner layer (circular
muscles)
• Squeezing motion 
affects peristalsis &
closure of esophageal
sphincters Physiology of esophageal motility
Hiroshi Mashimo and Raj K. Goyal
GI Motility online (2006)
doi:10.1038/gimo3
Histology of Mouth and Esophagus
ORAL CAVITY
• Stratified squamous epithelium
• May/partially keratinized or non, depending on location
• Keratinized cell layers protect damage from abrasion (trauma), dev in
masticatory mucosa on gingiva, hard palate
• Non-keratinized in lining mucosa over soft palate, cheeks, floor of
mouth, pharynx, posterior region of oral cavity to esophagus
 Lip
• Well dev core of striated muscles
(labia)
• 3 different surfaces:
• Internal mucous surface
• lining mucosa + thick non
keratinized epithelium
• Minor labial salivary gl
• Red vermillion zone
• Thin keratinized stratified squamous
epithelium
• Transitional b/w oral mucosa & skin
• salivary or sweat gl (keeping moist
w/ saliva of tongue)
• Rich in sensory & capillaries (pink
color)
• Outer surface w/ thick skin +
epidermal & dermal layers, sweat
gl & hair follicles + sebaceous gl.
Tongue
• Mass of striated muscle covered w/ mucosa
• Muscle fibers oriented in all directions ( mobility)
• Connective tissues: small fascicles of muscle
penetrated by lamina propria (strong adherence to
muscular zone)
• Lower surface: smooth w/ typical lining mucosa
• Dorsal surface: irregular (hundreds small papillae 2/3
anterior; lingual tonsils on 1/3 posterior)
• Papillary & tonsillar area are separated by V shaped groove
SULCUS TERMINALIS
 4 types of tongue/lingual papillae
• Filliform
• Numerous
• Elongated conical shape
• Heavily keratinized (gray/whitish appearance)
• Rough surface for movement of food during chewing
• Fungiform
• Less numerous
• Lightly keratinized
• Interspersed among filliform
• Mushroom shaped
• Well vascularized & innervated lamina propria
• Foliate
• Several parallel ridges on sides of tongue
• Anterior to sulcus
• Rudimentary in human
• Vallate (circumvallate)
• Largest (d: 1-3 mm)
Taste buds
• Has 50-100 cells, ½ of are elongated
gustatory/sensory cells
• Others are supportive (immature) cells,
basal stem cells (give rise to other cells),
microvilli (taste pore)
5 broad categories of tastants:
• Na+ ions (salt)
• H+ ions (sour) a bitter taste in the mouth. (n.d.) Mosby's Medical Dictionary,
8th edition. (2009). Retrieved August 18 2016 from
http://medical-

• Sugar (sweet) dictionary.thefreedictionary.com/a+bitter+taste+in+the+mout

h

• Toxins & alkaloids (bitter)

• Amino acids (glutamate & aspartate)
(umami/savory)
 TEETH
• Each tooth has a crown exposed above gingiva
• Covered by very hard, acellular
enamel
• Roots by bony-like tissue,
cementum
Both coverings meet at the neck of
tooth
• Constricted neck at the gum
• Bulk of tooth composed of calcified
material, dentin surrounding pulp
cavity
• Roots fit firmly into bony sockets dental alveoli
• Dental pulp, highly vascular, well
innervated, consist of largely loose
Dentin
• Calcified tissue harder than bone
• 70% hydroxyapatite
• Type I collagen + proteoglycans secreted from apical ends of odontoblasts
• Tall cells derived from cranial neural crest lining pulp cavity
• Secretes predentin matrix
• Odontoblast processes extends within dentinal tubules penetrate dentin  longer as
dentin gets thicker
• Processes extends fine branches to smaller lateral branches of tubules
Processes important for: maintenance of dentin matrix
Enamel
• Hardest component of human body
• 69% calcium hydroxyapatite, 2-3% organic material: prots, no collagen
• Resistant to acidic dissolution by microorganisms
• Uniform, interlocking columns, enamel rods (prisms) surrounded by
thin layer of other enamel
• Ameloblasts: secretes matrix for enamel in dev tooth bud, a part of
specialized epithelium called enamel organ
• Apical extension: ameloblast process (tomes)
• Contain secretory granules: prots of enamel matrix
Periodontium
• Maintaining teeth in maxillary & mandibular bones, includes:
• Cementum
• Covers dentin of root
• Resembles bone but avascular
• Thickest around root tip: cementocytes inside lacunae + processes in canaliculi
• Periodontal ligament
• Fibrous connective tissue w/ bundled collagen fibers (Sharpey fibers) binds
cementum & alv bone
• Rich BV & nerves  sensory & nutritive functions
• Permit limited movement of tooth w/in alv
• Protects alv from pressure during mastication
• Alveolar bone
• Has osteoblasts & osteocytes (lacks lamellar pattern)
• Surrounded by periodontal ligament (serves as its periosteum)
• Collagen fiber bundles of periodontal lig penetrate the bone binding it to
cementum
• Associated gingiva
• Keratinized oral mucosa firmly bound to periosteum of maxillary & mandibular
bones
4 LAYERS OF THE GI
TRACT
All regions of GI tract have common structural features: hollow
tube w/ a lumen, walls made up of 4 layers.
1. Mucosa
• Epithelial lining, an underlying lamina propria (loose connective tissue rich in BV,
lymphatics, lymphocytes, SMC, small glands)
• Freq called mucous membrane
Thin layer of smooth muscles called MUSCULARIS MUCOSAE, separates mucosa &
submucosa (allows local movements of mucosa)
2. Submucosa
• Dense connective tissue
• Larger BV & LV
• Submucosal (meissner) plexus of autonomic nerve
• Glands & Significant lymphoid tissues
3. Thick Muscularis
• SMC, 2 or more sublayers
• Internal (closer to lumen): fiber orientation CIRCULAR
• External: LONGITUDINAL
ESOPHAGUS
• Muscular tube (~25 cm in adults)
• 4 layers of GI tract become well-established & clear in esophagus
• Non-keratinized stratified squamous epithelium + mucosa
• Submucosa: small mucus secreting gl (esophageal gl)  lubricate &
protect mucosa
• Near stomach, mucosa contains ESOPHAGEAL CARDIAC GL  secretes
additional mucus
• Swallowing begins w/ voluntary muscle, finishes w/ involuntary
peristalsis
• 1/3 proximal: skeletal muscle
• 1/3 middle: skeletal + smooth muscle
• 1/3 distal: smooth muscle
• At distal 1-2 cm esophagus in peritoneal cavity is covered by serosa.
The rest is closed by adventitia (loose connective tissue, blends into
surrounding tissue)
Enzim Pencernaan Mulut
dan Kelenjar Ludah
LI 2
The digestive enzymes
Digestive enzymes are enzymes which help break down food substances
into forms that can be absorbed and assimilated by the body.
Digestive enzymes are normally secreted :
1) in the mouth (as part of the saliva),
2) by the stomach
3) released into the small intestines from the liver and pancreas.
The major enzymes are:
• Amylase, also called ptyalin, is an enzyme that aids the breakdown of
starches. It is secreted in the saliva and the pancreatic juices.
• Mycozyme is an enzyme that also digests starches.
• Lipase, secreted by the pancreas, refers to any of several enzymes that
increase the breakdown of fats (lipids).
Source Enzim Activator Substrat Function or katalitik
product

Saliva gland @-Amilase Cl- Flour essence Hidrolisis bond 1:4

Saliva @; produce dextrin
@limit, maltotriosa,
and maltosa

Lingual gland Lingual lipase Trigliserida Lipid acid plus 1,2 -

diasilgliserol

Gaster Pepsin Hcl- Protein and Decompose peptida

(pepsinogen) polipeptida chain which closer
with aromatic
amino acid

Gaster lipase Trigliserida Lipid acid and

gliserol
• Function of chewing:
• Grind & break food to smaller pieces (surface area,
facilitate swallowing)
• Mix food w/ saliva
• Stimulate taste buds, salivary, gastric, pancreatic, bile
secretion (prepare arrival of food)
• Chewing: voluntary; while meal: rhythmic reflex
• Activation of skeletal muscles of jaw, lips, cheeks, tongue in
response to pressure of foods against oral tissue
Saliva
• Beginning of carbohydrate digestions & oral hygiene
• Produced by 3 major pairs of glands outside oral cavity: parotid,
sublingual, submandibular
• 99.5% H2O, 0.5% electrolytes & proteins, 1/7 NaCl plasma (salty taste)
• Important proteins:
• Amylase
• Mucus
• Lysozymes
• Function of saliva:
• Begins digestion of carbohydrates (amylase)
• Moistening food particles, holding them together
• Provide lubrication (mucus)
• Antibacterial actions:
• Lysozyme: lyses/destroy by breaking cell walls
• Binding glycoprot. to IgA Ab
• Lactoferrin: binds iron used for bacterial multiplication
• Rinsing food sources for bacteria
• Solvent for mol. that stimulates taste buds
• Only mol.in solution can react w/ taste bud
• Oral hygiene
• Flush away food residues, foreign particles, old epithelial cells from mucosa
• Neutralize acids in foods or bacterial production (prevent dental
caries), rich in HCO3- buffers
• Resting pH: <7.0; active: 8.0
• Digestive enzymes in saliva:
• Lingual lipase
• Salivary α-amylase
• ~1-2 L of saliva secreted/day
• Basal rate: 0.5 mL/min
• Max flow rate: 5 mL/min
• Based on response to stimulus, e.g: sucking lemon
• Continuous basal secretion (stimuli): low lvl
stimulation by parasympathetic nerve ending
terminates in salivary glands
• 2 types of salivary
reflexes (
secretion)
• Simple reflex (w/ Brain stem

food stimulation)
• Conditioned reflex
(w/out food
stimulation 
thinking, smelling,
hearing)
Sympathetic & Parasympathetic
Responses
• Both  salivation, not antagonistic
• Diff quantity, characteristics, mechanism
• Parasympathetic:
• Dominant role
• Prompt & abundant flow of watery saliva rich in enzymes
• Sympathetic: (e.g. during stress)
• Smaller vol.
• Thick saliva rich in mucus

Absorption of foodstuffs in mouth, except for some drugs: Nitroglycerin, vasodilators

Acid inactivates amylases
Fisiologi Menelan
LI 3
Physiology of Swallowing / Deglutition
3 phases:
• Voluntary
• Pharyngeal
• Esophageal

Tate SS., Anatomy and Physiology. Eighth edition. 2008

 Voluntary Phase
• a bolus of food is formed in mouth 
pushed by the tongue against the hard
palate  posterior part of the mouth 
oropharynx

Tate SS., Anatomy and Physiology. Eighth edition. 2008

Pharyngeal Phase
• reflex initiated by stimulation of tactile receptors in oropharynx.
Afferent action potentials travel through trigeminal (V) &
glossopharyngeal (IX) nerves  swallowing center (in medulla
oblongata)  initiate action potentials in motor neurons 
trigeminal (V), glossopharyngeal (IX), vagus (X), accessory (XI) nerves
 soft palate & pharynx

Tate SS., Anatomy and Physiology. Eighth edition. 2008

 Pharyngeal Phase
• Begins w/ elevation of soft palate
(closes the passage between
nasopharynx & oropharynx)  to
receive bolus of food from mouth 
moves bolus down the pharynx 
esophagus

Tate SS., Anatomy and Physiology. Eighth edition. 2008

 Pharyngeal Phase
• During the pharyngeal phase, the vestibular folds & vocal cords close and the
epiglottis is tipped posteriorly so that the epiglottic cartilage covers the opening
into the larynx, and the larynx is elevated (to prevent food from passing through
the opening into the larynx)

Tate SS., Anatomy and Physiology. Eighth edition. 2008

 Pharyngeal Phase
• The superior, middle, inferior pharyngeal
constrictor muscles contract  forcing the
food through the pharynx & the upper
esophageal sphincter relaxes  elevated
pharynx opens the esophagus, food is pushed
into esophagus
• Pharyngeal phase lasts about 1–2 sec.

Tate SS., Anatomy and Physiology. Eighth edition. 2008

 Esophageal Phase
• Esophageal phase takes about 5–8 sec,
responsible for moving food from pharynx 
stomach
• Muscular contractions in the wall of esophagus
occur in peristaltic waves
• Peristaltic waves associated with swallowing
cause relaxation of the lower esophageal
sphincter in the esophagus bolus of food 
approach the stomach

Tate SS., Anatomy and Physiology. Eighth edition. 2008

 Esophageal Phase
• The presence of food in esophagus stimulates
• enteric plexus: controls the peristaltic waves
• tactile receptors: send afferent impulses to medulla oblongata through the
vagus nerves
• Motor impulses, in turn, pass along the vagal efferent fibers to the
striated & smooth muscles within the esophagus stimulating
contractions & reinforcing the peristaltic contractions

Tate SS., Anatomy and Physiology. Eighth edition. 2008

Definisi dan Patofisiologi Dysphagia
and Odyhnophagia
LI 4
Odynophagia
• Refers to painful swallowing, typically resulting from mucosal
ulceration within the oropharynx or esophagus
• Commonly is accompanied by dysphagia, but the converse is not true
• Pain either caused by or exacerbated by swallowing
• More common with pill or infectious esophagitis than with reflux
esophagitis and should prompt a search for these entities
• When odynophagia does occur in GERD, it is likely related to an
esophageal ulcer or deep erosion
Dysphagia
• Difficulty with swallowing
• Refers to problems with the transit of food or liquid from the mouth to the
hypopharynx or through the esophagus
• Severe dysphagia can compromise nutrition, cause aspiration, and reduce quality of
life
• Additional terminology pertaining to swallowing dysfunction is as follows a feeling of
food “sticking” or even lodging in the chest
• Important distinctions are between uniquely solid food dysphagia as opposed to liquid
and solid, episodic versus constant dysphagia, and progressive versus static dysphagia
• If the dysphagia is for liquids as well as solid food, it suggests a motility disorder such
as achalasia
Dysphagia
• Dysphagia can be subclassified by location : oral, pharyngeal, or
esophageal dysphagia
• Dysphagia caused by an oversized bolus or a narrow lumen is called
structural dysphagia
• whereas dysphagia due to abnormalities of peristalsis or impaired
sphincter relaxation after swallowing is called propulsive or motor
dysphagia
Penyakit Mulut
LI 5
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
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
Candidiasis

DEFINITION ETIOLOGY

• Candidiasis of the mouth and throat • The use of certain

(“thrush“/oropharyngeal candidiasis) 
fungal infection that occurs when there medications or a weakening
is overgrowth of a yeast called Candida of the immune system can
• Candida yeasts normally live on the skin
or mucous membranes in small amounts
cause Candida to multiply,
• If the environment inside the mouth or which may cause symptoms
throat becomes imbalanced, the yeasts of infection
can multiply and cause symptoms
• Candida overgrowth can also develop in
the esophagus  Candida
esophagitis/esophageal candidiasis
Candidiasis
EPIDEMIOLOGY
• It is estimated that between 5%
and 7% of babies less than one
month old will develop oral
candidiasis
• The prevalence of oral
candidiasis among AIDS patients
is estimated to be between 9%
and 31%, and studies have
documented clinical evidence of
oral candidiasis in nearly 20% of
cancer patient
PREDISPOSING FACTOR
• Oral thrush occurs most frequently among
babies less than one month old, the elderly,
and groups of people with weakened
immune systems
• Other factors associated with oral and
esophageal candidiasis include:
• HIV/AIDS
• Cancer treatments
• Organ transplantation
• Diabetes
• Corticosteroid use
• Dentures
Candidiasis
SIGNS AND SYMPTOMS
• The most common symptom of
oral thrush  white patches or
plaques on the tongue and other
oral mucous membranes
• Redness or soreness in the
affected areas
• Difficulty swallowing
• Cracking at the corners of the
mouth  angular cheilitis
EXAMS AND TESTS
• Complete medical evaluation and history,
with physical exam that focuses on the
area of the body with symptoms
• Diagnosis is made based on signs and
symptoms, and clusters of budding yeast
• Generally, a doctor takes a sample of the
vaginal discharge or swabs an area of oral
or skin lesions, urine, feces, and nail
clippings
• Fungal blood and stool cultures for
detection of Candida should be taken for
patients suspected of having deep organ
candidiasis
• Tissue biopsy may be needed for invasive
systemic disease
 Candidiasis
TREATMENT
• Candida infections of the mouth and throat must be
treated with prescription antifungal medication. The
type and duration of treatment depends on the
severity of the infection and patient-specific factors
such as age and immune status. Untreated infections
can lead to a more serious form of invasive
candidiasis
• Oral candidiasis usually responds to topical
treatments such as clotrimazole troches and nystatin
suspension (nystatin “swish and swallow”)
• Systemic antifungal medication such as fluconazole or
itraconazole may be necessary for oropharyngeal
infections that do not respond to these treatments
• Candida esophagitis is typically treated with oral or
intravenous fluconazole or oral itraconazole
• For severe or azole-resistant esophageal candidiasis,
treatment with amphotericin B may be necessary
PREVENTION
• Good oral hygiene practices may help to
prevent oral thrush in people with
weakened immune systems
• Some studies have shown that
chlorhexidine (CHX) mouthwash can help
to prevent oral candidiasis in people
undergoing cancer treatment
• People who use inhaled corticosteroids
may be able to reduce the risk of
developing thrush by washing out the
mouth with water or mouthwash after
using an inhaler
Mouth Ulcer

DEFINITION ETIOLOGY

• Oral herpes is an infection of the • Herpes viruses spread easily

lips, mouth, or gums due to the • Have intimate or personal contact with
herpes simplex virus someone who is infected
• It causes small, painful blisters • Touch something that is infected with
commonly called cold sores or fever the herpes virus, such as infected razors,
towels, dishes, and other shared items
blisters
• Parents may spread the virus to their
• Oral herpes is also called herpes
children during regular daily activities
labialis
 Mouth Ulcer
PATHOPHYSIOLOGY SIGNS AND SYMPTOMS
• Oral herpes is a common infection of the • They usually appear within 1-3 weeks after you come
mouth area. It is caused by the herpes into contact with the virus. They may last up to 3 weeks
simplex virus type 1 (HSV-1) • Warning symptoms
• Itching of the lips or skin around mouth
• After the first infection, the virus goes to • Burning near the lips or mouth area
sleep (becomes dormant) in the nerve • Tingling near the lips or mouth area
tissues in the face. Sometimes, the virus later • Before blisters appear
"wakes up" (reactivates), causing cold sores • Sore throat
• Fever
• Herpes virus type 2 (HSV-2) usually causes • Swollen glands
genital herpes. However, sometimes HSV-2 is • Painful swallowing
spread to the mouth during oral sex, causing • Blisters or a rash may form on
oral herpes • Gums
• Lips
• Mouth
• Throat
Mouth Ulcer

SIGNS AND SYMPTOMS TREATMENT

• Many blisters are called an "outbreak" • Symptoms may go away on their own without
treatment in 1 to 2 weeks
• Red blisters that break open and leak
• Antiviral medicine  help reduce pain and make
• Small blisters filled with clear yellowish fluid your symptoms go away sooner. Medicines used to
• Several smaller blisters may grow together into a large treat mouth sores include
blister • Acyclovir
• Famciclovir
• As the blister heals, it gets yellow and crusty, eventually
• Valacyclovir
turning into pink skin
• These medicines work best if you take them when
• Symptoms may be triggered by you have warning signs of a mouth sore, before any
• Menstruation or hormone changes blisters develop
• Being out in the sun
• Fever
• Stress
Mouth Ulcer

COMPLICATION PROGNOSIS

• Return of mouth sores and blisters • Oral herpes usually goes

• Spread of the virus to other skin areas
away by itself in 1 to 2
• Bacterial skin infection
weeks. However, it may
• Widespread body infection, which may
be life threatening in people who have come back
a weakened immune system due
to atopic dermatitis, cancer, or HIV
infection
Prevention
• Avoid direct contact with herpes sores
• Wash items such as towels and linens in boiling hot water after each
use
• Do not share utensils, straws, glasses, or other items if someone has
oral herpes
• Do not have oral sex if you have oral herpes, especially if you have
blisters
Glossitis
DEFINITION
• Glossitis is a condition in
which the tongue is
swollen and changes color,
often making the surface
of the tongue appear
smooth
ETIOLOGY
• Allergic reaction to toothpaste, mouthwash, breath fresheners, dyes in candy,
plastic in dentures or retainers, or certain blood pressure medications (ACE
inhibitors)
• Dry mouth, when the glands that produce saliva are destroyed  Sjorgen
syndrome)
• Infections with bacteria or viruses (including oral herpes simplex)
• Injury from burns, rough edges of teeth or dental appliances, or other trauma
• Low iron levels (called iron deficiency) or certain B vitamins, such as vitamin
B12
• Skin conditions such as oral lichen planus, erythema multiform, apthous
ulcers, syphilis, and others
• Tobacco, alcohol, hot foods, spices, or other irritants
• Yeast infection in the mouth
• At times, glossitis may be passed down in families and is not due to another
disease or event
 Glossitis

CLASSIFICATION CLASSIFICATION
• Atrophic glossitis • Geometric glossitis
• A condition characterized by a smooth glossy tongue that is often tender/painful • The lesion is usually very painful, and there
• Caused by complete atrophy of the lingual papillae (depapillation)
may be erosions present in the depths of the
• Median rhomboid glossitis fissures
• This condition is characterized by a persistent erythematous, rhomboidal
depapillated lesion in the central area of the dorsum of the tongue, just in front • Chronic lesion associated with HSV-1 infection
of the circumvallate papillae  deep fissure in the midline of the tongue
• A type of oral candidiasis, and rarely causes any symptoms. It is treated with and gives off multiple branches
antifungal medication • Strawberry tongue
• Benign migratory glossitis
• Manifests with hyperplastic (enlarged)
• Geographic tongue, also termed benign migratory glossitis, is a common
condition which usually affects the dorsal surface of the tongue
fungiform papillae, giving the appearance of a
• It is characterized by patches of depapillation and erythema bordered by a strawberry
whitish peripheral zone
• These patches give the tongue the appearance of a map. The cause is unknown,
and there is no curative treatment
Glossitis

SIGNS AND SYMPTOMS TREATMENT

• Difficulty with chewing, swallowing, or • The goal of treatment is to reduce inflammation
speaking • Good oral hygiene is important. Brush teeth
thoroughly at least twice a day and floss at least once
• Smooth surface of the tongue a day
• Sore and tender tongue • Antibiotics, antifungal medications, or other
antimicrobials may be prescribed if the glossitis is
• Tongue color changes due to an infection
• Pale, if caused by pernicious anemia • Dietary changes and supplements are used to treat
• Fiery red, if caused by a lack of other B vitamins anemia and nutritional deficiencies
• Tongue swelling • Avoid irritants (such as hot or spicy foods, alcohol,
and tobacco) to reduce any tongue discomfort
Glossitis

COMPLICATIONS PROGNOSIS

• Airway blockage • Glossitis usually responds well to

treatment if the cause of
• Difficulties with speaking, inflammation is removed or treated
chewing, or swallowing
• Discomfort PREVENTION
• Good oral hygiene (thorough tooth
brushing and flossing and regular
professional cleaning and
examination)
• Avoid irritants
 Leukoplakia
DEFINITION
• Leukoplakia are patches on the tongue, in the
mouth, or on the inside of the cheek
• Leukoplakia affects the mucous membrane of
the mouth. The exact cause is not known. It
may be due to irritation such as:
• Rough teeth
• Rough places on dentures, fillings, and
crowns
• Smoking or other tobacco use (smoker's
keratosis), especially pipes
• Holding chewing tobacco or snuff in the
mouth for a long period of time
• Drinking a lot of alcohol
SYMPTOMS
• Patches in the mouth usually develop
on the tongue (sides of the tongue with
oral hairy leukoplakia) and on the
insides of the cheeks.
• Leukoplakia patches are:
• Most often white or gray
• Uneven in shape
• Fuzzy (oral hairy leukoplakia)
• Slightly raised, with a hard surface
• Unable to be scraped off
• Painful when the mouth patches
come into contact with acidic or
Leukoplakia
DIAGNOSIS TREATMENT

•The goal of treatment is to get rid of the

•A biopsy of the lesion leukoplakia patch. Removing the source of
confirms the diagnosis. irritation may cause the patch to disappear.
•Treat dental causes such as rough teeth, irregular
Examination of the denture surface, or fillings as soon as possible.
biopsy may find changes •Stop smoking or using other tobacco products.
that indicate oral cancer •Do not drink alcohol.
•If removing the source of the irritation does not
work, your health care provider may suggest
applying medicine to the patch or using surgery to
remove it.
•For oral hairy leukoplakia, taking antiviral medicine
usually causes the patch to disappear. Your
provider may also suggest applying medicine to the
patch.
Leukoplakia
COMPLICATION AND PROGNOSIS
• Leukoplakia is usually
harmless. Patches in the
mouth often clear up in a few
weeks or months after the source
of irritation is removed.
• In some cases, the patches may
be an early sign of cancer.
PREVENTION
• Stop smoking or using other
tobacco products
• Do not drink alcohol, or limit
the number of drinks
• Have rough teeth treated and
dental appliances repaired right
away
Parotitis
• Viral (mumps) or bacterial infections (postoperative) of the parotid
glands cause parotid swelling and pain
• Oral antibiotics may help, but surgical drainage is required if there is
abscess formation
• The differential for parotid swelling includes:
• Salivary gland stones
• Sjögren’s syndrome
• Sarcoidosis
• Tumours (mostly benign adenoma, rarely mucoepidermoid tumours or
cancers)
Ludwig’s Angina
DEFINITION SYMPTOMS
• Ludwig's angina is an infection of the floor of • The infected area swells quickly, this may block
the mouth under the tongue due to bacteria the airway or prevent from swallowing saliva

• Ludwig's angina is a type of skin infection that • Symptoms include:

occurs on the floor of the mouth, under the • Breathing difficulty
tongue, develops after an infection of the • Difficulty swallowing
roots of the teeth (such as tooth abscess) or a • Drooling
mouth injury
• Unusual speech (sounds like the person has
• This condition is uncommon in children 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:
Ludwig’s Angina
DIAGNOSIS
• exam the neck and head to look for
redness and swelling of the upper neck,
under the chin
• The swelling may reach to the floor of
the mouth, tongue may be swollen or
out of place
• may need a CT scan
• A sample of the fluid from the tissue
may be sent to the lab to test for
bacteria
TREATMENT
• If the swelling blocks the airway 
emergency medical help right away.
A breathing tube may needed to be
placed through mouth or nose and
into the lungs to restore breathing.
May need to have surgery called
a trachestomy.
• 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.
Ludwig’s Angina
COMPLICATION AND PROGNOSIS PREVENTION

• If the swelling blocks the airway  • Visit the dentist for regular checkups
emergency medical help right away.
A breathing tube may needed to be • Treat symptoms of mouth or tooth
placed through mouth or nose and infection right away
into the lungs to restore breathing.
May need to have surgery called
a trachestomy.
• 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
Esophageal Atresia
• The most common congenital esophageal anomaly is esophageal atresia, occurring in
about 1 in 5000 live births
• Atresia can occur in several permutations, the common denominator being
developmental failure of fusion between the proximal and distal esophagus
associated with a tracheoesophageal fistula, most commonly with the distal segment
excluded
• Alternatively, there can be an H-type configuration in which esophageal fusion has
occurred, but with a tracheoesophageal fistula
• Esophageal atresia is usually recognized and corrected surgically within the first few
days of life
• Later life complications include dysphagia from anastomotic strictures or absent
peristalsis and reflux, which can be severe
Achalasia
DEFINITION
• Achalasia is a disorder of the tube that
carries food from the mouth to the
stomach (esophagus), which affects the
ability of the esophagus to move food
toward the stomach
• A primary esophageal motility disorder
characterized by failure of a hypertensive
LES (lower esophageal sphincter) to relax
and the absence of esophageal peristalsis
ETIOLOGY
• Achalasia is caused by damage to
and loss of the nerves in the gullet
wall. The reason for this is unknown,
although it could be due to a viral
infection earlier in life
• There is no evidence to suggest that
achalasia is an inherited illness
Achalasia
EPIDEMIOLOGY
• Achalasia is a rare disorder. It may occur at
any age, but is most common in middle-aged
or older adults. This problem may be
inherited in some people
• Achalasia is an uncommon condition that
affects about 6,000 people in Britain
• In USA the incidence of achalasia is
approximately 1 per 100.000 people per year
• The male-to-female ratio of achalasia is 2:3
• Achalasia typically occurs in adults aged 25-
60 years. Fewer than 5% of cases occur in
children
PATHOPHYSIOLOGY
• A muscular ring at the point where the esophagus
and stomach come together (lower esophageal
sphincter) normally relaxes during swallowing. In
people with achalasia, this muscle ring does not
relax as well. The reason for this problem is
damage to the nerves of the esophagus
• LES pressure and relaxation are regulated by
excitatory and inhibitory neurotransmitters
• Person with achalasia lack nonadrenergic,
noncholinergic, inhibitory ganglion cells, causing an
imbalance in excitatory and inhibitory
neurotransmission
• The result is a hypertensive nonrelaxed esophageal
sphincter
Achalasia
SIGNS AND SYMPTOMS TREATMENTS
• Backflow (regurgitation) of food • The approach to treatment is to reduce
the pressure at the lower esophageal
• Chest pain, which may increase after sphincter
eating or may be felt in the back,
neck, and arms • Injection with botulinum toxin (Botox)
 this may help relax the sphincter
• Cough muscles, but any benefit wears off
• Difficulty swallowing liquids and within a matter of weeks or months
solids • Medications, such as long-acting
• Heartburn nitrates or calcium channel blockers 
relax the lower esophagus sphincter
• Unintentional weight loss
• Surgery (esophagomyotomy) 
decrease the pressure in the lower
sphincter
• Widening (dilation) of the esophagus
at the location of the narrowing (done
during esophagogastroduodenoscopy)
Achalasia
EXAM AND TESTS
• 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
• Endoscopic assessment of the
gastroesophageal junction and
gastric cardia, as recommended, to
rule out pseudoachalasia
EXAM AND TESTS
• Chest X-ray
• May reveal the dilated esophagus as
a mediastinal mass
• Barium swallow
• Shows gross dilatation and
tortuosity of the esophagus leading
to an unrelaxing narrowed segment
at the lower end
• Oesophagoscopy
• Demonstrates an enormous sac of
esophagus containing a pond of
stagnant food & fluid
• Oesophageal manometry
Daftar Pustaka
• Tate SS., Anatomy and Physiology. Eighth edition. 2008
• Sherwood L. Human physiology. 5th ed. Belmont:Thomson Learning,2004.
• Kahrilas PJ, Hirano I. Dysphagia. In: Longo DL, Fauci AS, Kasper DL, Hauser SL, Jameson JL, Loscalzo J, editors.
Harrison’s gastroenterology and hepatology. 2nd ed. San Fransisco: McGraw-Hill Education; 2013. p.27-31.
• http://emedicine.medscape.com/article/1610393-overview
• Inns S, Emmanuel A. Lecture notes gastroenterology and hepatology. 2nd ed. Oxford: Blackwell Publishing; 2011.
• Young, Barbara. Wheater’s Functional Histology A Text and Colour Atlas. United States of America : Elsevier,
2014.
• Medline Plus Medical Ensiclopedia. Glossitis. (Update: 13 February 2015). Available from:
https://medlineplus.gov/ency/article/001053.htm
• Medscape. Parotitis. (Update: 17 January 2017)Available from:
http://emedicine.medscape.com/article/882461-overview#a4
• http://www.nhs.uk/conditions/Dental-decay/Pages/Introduction.aspx