GIT- Pemicu 1

Rachelle Betsy- 405140052

Lo 1
 Anatomy (mouth-oesophagus)
• MOUTH (ORAL CAVITY)
• Its boundaries are:
– Anterior : the lips
– Lateral : cheeks
– Superior : palate
– Inferior: tongue
• Its anterior opening is the oral orifice
• Posteriorly, the oral cavity is continuous with the
oropharynx
• The lips (labia) and the cheeks are composed of a
core of skeletal muscle covered externally by skin
• The orbicularis oris muscle forms the fleshly lips
• The cheeks are formed largely by the buccinators
• The recess bounded externally by the lips and cheeks
and internally by the gums and teeth is called the
vestibule
• The area that lies within the teeth and gums is the
oral cavity proper
• The reddened area of the lips  red margin
– Poorly keratinized and translucent
– Lack sweat or sebaceous glands  must be
moistened with saliva periodically
• The labial frenulum is a median fold that joins
the internal aspect of each lip to the gum
• The palate, forming the roof of the mouth
– Hard palate (anterior)
• Underlain by the palatine bones & the palatine
processes of the maxillae
• Forms rigid surface against which the tongue forces
food during chewing
– Soft palate (posterior)
• Mobile fold formed mostly of skeletal muscle  rises
reflexively to close off the nasopharynx when we
swallow
• Anchored to the tongue by the palatoglossal arches &
to the wall of the oropharynx by palatopharyngeal
arches
 Tongue
• Composed of interlacing bundles of skeletal muscle
fibers  grips the food & repositions it between the
teeth
• The tongue mixes food with saliva  bolus 
initiates swallowing
• Root – 1/3 posterior
• Body – ½ anterior
• Apex
• Dorsum
– Foramen cecum : in the midline at the point of the
terminal sulcus
– Terminal sulcus (sulcus terminalis) : divides the anterior
2/3 to the posterior 1/3
– Lingual tonsils : posterior to the terminal sulcus
– Lingual papillae : four types; vallate, foliate, fungiform,
filiform
– Median sulcus
• The intrinsic muscle
– Not attached to bone
– Allow the tongue to change its shape becoming thicker,
thinner, longer or shorter  speech & swallowing
• The extrinsic muscles
– Alter the tongue’s positions  protrude it, retract it &
move it from side to side
• Lingual frenulum secures the tongue to the floor of
the mouth & limits postertior movements of the
tongue
• Tongue’s papillae :
– Filiform Papillae
• The smallest & most numerous type  parallel rows on
the tongue dorsum
• Give the tongue surface a roughness that aids in licking
semisolid foods
• Provide friction for manipulating foods
• Contain keratin  stiffens them & gives the tongue its
whitish appearance
– Fungiform Papillae
• Mushroom-shaped
• Scattered widely over the tongue surface
• Each has a vascular core  gives it a reddish hue
– Circumvallate Papillae
• Located in V-shaped row at the back of the tongue
• Resemble the fungiform papillae but have an additional
surrounding furrow
– Foliate Papillae
• Located on the lateral aspects of the posterior tongue
• The fungiform, circumvallate and foliate papillae
house taste buds
• On the foliate papillae in taste primarily in infancy
and early childhood
• Terminal sulcus (posterior to the circumvallate
papillae), is a groove that distinguishes the portion of
the tongue that lies in the oral cavity (its body) from
its posterior portion in the oropharynx (its root)
 Salivary Glands
• Functions of saliva :
– Cleanses the mouth
– Dissolves food chemicals so that they can be
tasted
– Moistens food and aids in compacting it into a
bolus
– Contains enzyme that begin the chemical
breakdown of starchy foods
 Esophagus
• A muscular tube about 25 cm long from pharynx to
stomach
• Is collapsed when not involved in food propulsion
• It pierces the diaphragm at the esophageal hiatus to
enter the abdomen
• It joins the stomach at the cardiac orifice within the
abdominal cavity
• The cardiac orifice is surrounded by the
gastroesophageal or cardiac sphincter
Lo 2
 Physiology of Swallowing

• Oral stage (voluntary)

• Pharyngeal stage

• Esophageal stage
 Swallowing (Deglution)

Swallowing can be divided into:

Voluntary stage of swallowing
 Bolus  voluntarily squeezed or rolled posteriorly against
the palate
 Swallowing cannot be stopped
Pharyngeal stage of swallowing
 Bolus reaches posterior mouth & pharynx  stimulates
receptors  initiate series of automatic pharyngeal
muscle contraction
 Automatic pharyngeal muscle contraction:

Soft palate is pulled upward and prevents the reflux of

food to nasal cavity
Palatopharyngeal folds are pulled medially to
approximate each other – form a saggital slit
Vocal cords are approximated
Larynx is pulled upward & anterior by neck muscles
Epiglottis swing backward over the opening of larynx

N.B. removal of epiglottis does not cause serious debility

in swallowing.
 Automatic pharyngeal muscle contraction:

Upward movement of larynx & enlargement the

opening of esophagus
Upper 3-4cm of esophagus relaxes
Muscular wall of pharynx contracts to push the food
downward (propulsive contraction)

N.B. pharyngeal stage lasts for < 2 sec

 Swallowing (Deglution)

Esophageal stage of swallowing

 Conducts food rapidly to the stomach
 Two types of peristaltic movements:
1° peristalsis:
– continuation of a peristaltic wave
– begins in pharynx & spreads into esophagus
– passes in 8-10 sec
2° peristaltic waves:
– results from the distention of esophagus
– begins if the 1° wave failed to push the food down
PHYSIOLOGY
PHYSIOLOGY
Oral Cavity and Esophagus
• M : swallowing and chewing.
• S : saliva from salivary gland and lipase.
• D : carbohydrates and minimal for fats.
• A : None
• Swallowing is a reflex respone that is triggered by afferent
impulses in the trigeminal, glossopharyngeal, and vagus
nerves.
The voluntary action of collecting the oral contents on the
tongue and propelling them backward into the pharynx 
Involuntary contraction in the pharyngeal muscles that
pushes the material into the esophagus
 Mouth and Esophagus
• Mastification
• Salivary Glandsaliva (secreted in acinar cells )
Saliva contain: mucins,IgA,lysozyme,lactoferrin, prolinerich
protein.
Enzymes: lingual lipase and salivary α amylase
Ph at about 7help neutralize gastric acid and relieve
heartburn when gastric juice is regurgitated into the
esophagus.
Control: neural control.
Nervus: parasymphatic (>fluid; organic <)and symphatic
(>thick; organic <<)
Lo 3
 Histology (mouth-oesophagus)
• The gastrointestinal tract surrounded by a wall
made up of four principal layers :
– The mucosa
– The submucosa
– The muscularis
– The serosa
The Lips
 The Tongue
• The tongue is a mass of striated muscle covered by a
mucous membrane
• The muscle fibers cross one another in three planes
• The mucous membrane is strongly adherent to the
muscle
• The mucous membrane is smooth on the lower
surface of the tongue
• The tongue’s dorsal surface is irregular, covered
anteriorly by papillae
• Tongue’s papillae :
– Filiform papillae
• Elongated conical shape
• Quite numerous & present over the entire of the tongue
• Their epithelium does not contain taste buds, is frequently
partly keratinized
– Fungiform papillae
• Mushroom shape
• Have a narrow stalk & a smooth surface, dilated upper part
• Contain scattered taste buds
• Irregularly interspersed among the filiform papillae
– Foliate Papillae
• Poorly developed in humans
• Consist of two or more parallel ridges and furrows on the
dorsolateral surface of the tongue
• Ducts from serous glands drain into the bases of the furrows
– Circumvallate papillae
• Large circular papillae
• Distributed in the V-region in the posterior portion of the
tongue
• Numerous serous glands drain their contents into the deep
groove that encircles the periphery of each papilla
• The glands secret a lipase  prevents the formation of a
hydrophobic layer over the taste buds
Foliate papillae
 The Esophagus
• Muscular tube  to transport foodstuffs from the
mouth to the stomach
• Its covered by nonkeratinized stratified squamous
epithelium
• In the submucosa are groups of small mucus-
secreting glands  esophageal glands
• In the lamina propria of the region near the stomach
are groups of glands  esophageal cardiac glands
• At the distal end of the esophagus  smooth muscle
cells
• In the mid portion  mixture of striated & smooth
muscle cells
• At the proximal end  only striated muscle cells
• Only at the portion of the esophagus in the
peritoneal cavity is covered by serosa, the rest is
covered by a layer of loose connective tissue, the
adventitia
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Lo 4
Biochemistry
 Digestive Enzymes
ENZYME SOURCE SUBTRATES PRODUCTS
SALIVA
Salivary amylase Salivary glands. Starches. Maltose, maltotriose, α-
dextrins.
Lingual lipase Lingual glands. Triglycerides (fats & oils) Fatty acids &
and other lipids. diglycerides.
GASTRIC JUICE
Pepsin Stomach chief cells. Proteins. Peptides.
Gastric lipase Stomach chief cells. Triglycerides. Fatty acids &
monoglycerides.
PANCREATIC JUICE
Pancreatic amylase Pancreatic acinar cells. Starches. Maltose, maltotriose, α-
dextrins.
Trypsin Pancreatic acinar cells. Proteins. Peptides.
Chymotrypsin Pancreatic acinar cells. Proteins. Peptides.
Elastase Pancreatic acinar cells. Proteins. Peptides.
 ENZYME SOURCE SUBSTRATES PRODUCTS
Carboxypeptidase. Pancreatic acinar cells. Amino acid at carboxyl Amino acids & peptides.
end peptides.
Pancreatic lipase Pancreatic acinar cells. Triglycerides that have Fatty acids &
been emulsified by bile monoglycerides.
salts.
Ribonuclease Pancreatic acinar cells. RNA. Nucleotides.
Deoxyribonuclease Pancreatic acinar cells. DNA. Nucleotides.
BRUSH BORDERS
α-Dextrinase Small intestine. α-Dextrins. Glucose.
Maltase Small intestine. Maltose. Glucose.
Sucrase Small intestine. Sucrose. Glucose & fructose.
Lactase Small intestine. Lactose. Glucose & galactose.
Enterokinase Small intestine. Trypsinogen. Trypsin.
Aminopeptidase Small intestine. Amino acid at amino end Amino acids & peptides.
of peptides.
Dipeptidase Small intestine. Dipeptidases. Amino acids.
Nucleosidases & Small intestine. Nucleotides. Nitrogenous bases,
phosphatases pentoses & phosphates.
Lo 5
 Dysphagia
• Dysphagia is the medical term for the symptom
of difficulty in swallowing, but not hurting. There
are three most common types of dyphagia:
1. If it is progressive from solids to liquids most
commonly it is due to carcinoma.
2. If it is chronic for many months to years; the
most common cause is Achalasia.
3. and if it is paradoxical (i.e. swallowing of solids
is OK but swallowing liquids elicit difficulty than
it is also due to Achalasia.
LO3

DYSPHAGIA AND ODYNOPHAGIA

The symptoms of dysphagia include:
• coughing or choking when eating or drinking
• not being able to swallow
• pain when swallowing
• bringing food back up, sometimes through the
nose
• a sensation that food is stuck in the throat or
chest
Longer-term symptoms may include:
• unexplained weight loss
• developing repeated and frequent chest
infections
 Causes of dysphagia
Neurological causes
• The word neurological refers to the nervous system. This is made up
of the brain, nerves and spinal cord.
• Damage to the nervous system can interfere with the nerves
responsible for starting and controlling swallowing. This can lead to
dysphagia.
• Some neurological causes of dysphagia include:
• a stroke
• neurological conditions that cause damage to the brain and nervous
system over time, including Parkinson’s disease, multiple sclerosis, a
head injury or dementia
• Brain tumors
• Myasthenia gravis - a rare condition that causes your muscles to
become weak
Congenital and developmental conditions
Congenital means something you are born
with. Developmental conditions affect the way you
develop.
Congenital or developmental conditions that may cause
dysphagia in children include:
• learning disabilities - where your child finds learning,
understanding and communicating difficult
• Cerebral palsy - a group of neurological conditions that
affect a child's movement and co-ordination
 Odynophagia
• Odynophagia is the medical term for painfull swallowing; it
comes form the Greek words odyno- meaning pain and -
phagia meaning swallowing. Mostly the patients with
odynophagia have linear ulcerations on the surface of
mucosa on endoscopy.
• Most commonly odynophagia is found among immuno
suppressive patients.
1. The No. 1 cause among them is Candida albicans,
2. the No. 2 cause is Cytomegalovirus and
3. last but not the least; it is Herpes Simplex Virus (HSV).
4. If the patient is not immunocompromised and otherwise
healthy but still complaints of odynophagia; check out
the drugs , if found anyone causing discountinue them.
Lo 6
 Mouth Ulcer (Oral Herpes)-Definition
• Oral herpes is an infection of the lips, mouth,
or gums due to the herpes simplex virus
• It causes small, painful blisters commonly
called cold sores or fever blisters
• Oral herpes is also called herpes labialis
 Etiology
• Herpes viruses spread easily
– Have intimate or personal contact with someone
who is infected
– Touch something that is infected with the herpes
virus, such as infected razors, towels, dishes, and
other shared items
• Parents may spread the virus to their children
during regular daily activities
 Pathophysiology
• Oral herpes is a common infection of the mouth
area. It is caused by the herpes simplex virus type
1 (HSV-1)
• After the first infection, the virus goes to sleep
(becomes dormant) in the nerve tissues in the
face. Sometimes, the virus later "wakes up"
(reactivates), causing cold sores
• Herpes virus type 2 (HSV-2) usually causes genital
herpes. However, sometimes HSV-2 is spread to
the mouth during oral sex, causing oral herpes
 Signs and Symptoms
• They usually appear within 1-3 weeks after you come into contact with the
virus. They may last up to 3 weeks
• Warning symptoms
– Itching of the lips or skin around mouth
– Burning near the lips or mouth area
– Tingling near the lips or mouth area
• Before blisters appear
– Sore throat
– Fever
– Swollen glands
– Painful swallowing
• Blisters or a rash may form on
– Gums
– Lips
– Mouth
– Throat
• Many blisters are called an "outbreak"
– Red blisters that break open and leak
– Small blisters filled with clear yellowish fluid
– Several smaller blisters may grow together into a large
blister
– As the blister heals, it gets yellow and crusty,
eventually turning into pink skin
• Symptoms may be triggered by
– Menstruation or hormone changes
– Being out in the sun
– Fever
– Stress
 Treatment
• Symptoms may go away on their own without
treatment in 1 to 2 weeks
• Antiviral medicine  help reduce pain and make
your symptoms go away sooner. Medicines used
to treat mouth sores include
– Acyclovir
– Famciclovir
– Valacyclovir
• These medicines work best if you take them
when you have warning signs of a mouth sore,
before any blisters develop
 Complication
• Return of mouth sores and blisters
• Spread of the virus to other skin areas
• Bacterial skin infection
• Widespread body infection, which may be life
threatening in people who have a weakened
immune system due to atopic dermatitis,
cancer, or HIV infection
 Prognosis
• Oral herpes usually goes away by itself in 1 to
2 weeks. However, it may come back
 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
 Pencegahan
• Pencegahan karies botol susu bayi  hindari
penggunaan botol susu secara tidak benar dan
makann manis yg berlebihan
• Higiene oral memberikan sedikit perlindungan,
namun pada anak usia <8 tahun belum dapat
menyikat gigi mereka dgn baik; sikat gigi dilakukan
oleh orangtua.
• Suplementasi fluorida dari suplai air mas. Hingga
konsentrasi 1 ppm sangat efektif dalam mengurangi
karies gigi. Tapi jika berlebihan fluorosis,
gangguan berupa noda putih seperti kapur dan
noda coklat pada gigi.
 Parotitis
• Definisi
• suatu infeksi virus menular yang menyebabkan pembengkakan
unilateral (satu sisi) ataubilateral (kedua sisi) pada kelenjar liur
disertai nyeri.

Etiologi
• paramyxovirusVirus ini ditularkan melalui percikan ludah yang
berasal dari bersin atau batuk penderita ataukarena
bersentuhan langsung dg benda-benda yg terkontaminasi oleh
ludah penderita.
• Masa inkubasi 14-24hari
• Masa tular/infektiviti:2-4 hari sebelum pembengkakan parotis
& 9 hari sesudah pembengkakannya mulai.
 Epidemiologi
• >>anak usia 2-15tahun
• Jika seseorang pernah terkena gondongan, ia
memiliki kekebalan seumur hidup
• Yg terkena biasanya kelenjar parotis ,yaitu kel
ludah yg terletak diantara telinga dan rahang
• Namun, pd dewasa parotitis menyerang testis
(buah zakar), SSP, pankreas, prostat, payudara
dll
Patogenesis
 Gambaran Klinis
• Stadium Prodrom: 1-2 hari
• Febris sedang, anorexia, nyeri otot umum
• Nyeri didalam atau dibelakang telinga kalau mengunyah atau menelan
• Terkadang diserta nyeri kepala, mual/muntah & kaku kutuk

• Stadium Pembengkakan: (7-9 hari)

• Kelenjar parotid makin nyeri & mulai bengkak unilateral kemudian sering
menjadibilateral sampai hari 3-4 pembengkakan lalu mulai mereda selama
1 minggu.
• Kulit diatas parotid erithema & mungkin edema
• Pembengkakan parotid di daerah depan telinga, diatas otot maseter & di
cekunganbelakang liang telinga didepan mastoideus.
• Telinga bagian bawah terangkat keatas & ke depan oleh pembengkakan.
 Candidiasis-Definition
• Candidiasis of the mouth and throat
(“thrush“/oropharyngeal candidiasis)  fungal
infection that occurs when there is overgrowth of a
yeast called Candida
• Candida yeasts normally live on the skin or mucous
membranes in small amounts
• If the environment inside the mouth or throat becomes
imbalanced, the yeasts can multiply and cause
symptoms
• Candida overgrowth can also develop in the esophagus
 Candida esophagitis/esophageal candidiasis
 Etiology
• The use of certain medications or a weakening
of the immune system can cause Candida to
multiply, which may cause symptoms of
infection
 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 Factors
• 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
– Broad-spectrum antibiotic use
 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
 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
 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
 Classification
• Atrophic glossitis
– A condition characterized by a smooth glossy tongue that is often
tender/painful
– Caused by complete atrophy of the lingual papillae (depapillation)
• Median rhomboid glossitis
– This condition is characterized by a persistent erythematous, rhomboidal
depapillated lesion in the central area of the dorsum of the tongue, just in
front of the circumvallate papillae
– A type of oral candidiasis, and rarely causes any symptoms. It is treated with
antifungal medication
• Benign migratory glossitis
– Geographic tongue, also termed benign migratory glossitis, is a common
condition which usually affects the dorsal surface of the tongue
– It is characterized by patches of depapillation and erythema bordered by a
whitish peripheral zone
– These patches give the tongue the appearance of a map. The cause is
unknown, and there is no curative treatment
– Geometric glossitis
• The lesion is usually very painful, and there may be
erosions present in the depths of the fissures
• Chronic lesion associated with HSV-1 infection  deep
fissure in the midline of the tongue and gives off
multiple branches
– Strawberry tongue
• Manifests with hyperplastic (enlarged) fungiform
papillae, giving the appearance of a strawberry
 Signs and Symptoms
• Difficulty with chewing, swallowing, or
speaking
• Smooth surface of the tongue
• Sore and tender tongue
• Tongue color changes
– Pale, if caused by pernicious anemia
– Fiery red, if caused by a lack of other B vitamins
• Tongue swelling
 Treatment
• The goal of treatment is to reduce inflammation
• Good oral hygiene is important. Brush teeth thoroughly
at least twice a day and floss at least once a day
• Antibiotics, antifungal medications, or other
antimicrobials may be prescribed if the glossitis is due
to an infection
• Dietary changes and supplements are used to treat
anemia and nutritional deficiencies
• Avoid irritants (such as hot or spicy foods, alcohol, and
tobacco) to reduce any tongue discomfort
 Complications
• Airway blockage
• Difficulties with speaking, chewing, or
swallowing
• Discomfort
 Prognosis
• Glossitis usually responds well to treatment if
the cause of inflammation is removed or
treated
 Prevention
• Good oral hygiene (thorough tooth brushing
and flossing and regular professional cleaning
and examination)
• Avoid irritants
 Angina ludwig
• merupakan infeksi dan peradangan serius
jaringan ikat (selulitis) pada area
submandibula, berupa pembengkakan
submandibula, teraba keras pd perabaan.
Penyakit ini termasuk dalam grup penyakit
infeksi odontogen, di mana infeksi
bakteri berasal dari rongga mulut seperti gigi,
lidah, gusi, tenggorokan, dan leher.
 ETIOLOGI

Sumber infeksi seringkali berasal dari gigi atau dasar mulut

• Gram positif :
Fusobacterium nucleatum, Aerobacter aeruginosa,
spirochetes,Veillonella, Candida, Eubacteria, dan
Clostridium

• Bakteri Gram negatif :

Neisseria, Escherichia coli, Pseudomonas,Haemophillus
influenza dan Klebsiella
 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
 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
 Signs and Symptoms
• Backflow (regurgitation) of food
• Chest pain, which may increase after eating or
may be felt in the back, neck, and arms
• Cough
• Difficulty swallowing liquids and solids
• Heartburn
• Unintentional weight loss
 Differential Diagnosis
• Cancer of the esophagus or upper stomach
• Parasite infection that causes Chagas disease
 Exams 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
• 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
– Confirms increased lower oesophageal sphincter pressure
 Treatment
• The approach to treatment is to reduce the pressure at the
lower esophageal sphincter
• Injection with botulinum toxin (Botox)  this may help
relax the sphincter muscles, but any benefit wears off
within a matter of weeks or months
• Medications, such as long-acting nitrates or calcium
channel blockers  relax the lower esophagus sphincter
• Surgery (esophagomyotomy)  decrease the pressure in
the lower sphincter
• Widening (dilation) of the esophagus at the location of the
narrowing (done during esophagogastroduodenoscopy)
 Complication
• Backflow (regurgitation) of acid or food from
the stomach into the esophagus (reflux)
• Breathing food contents into the lungs, which
can cause pneumonia
• Tearing (perforation) of the esophagus
 Prognosis
• The outcomes of surgery and nonsurgical
treatments are similar. Sometimes more than
one treatment is necessary
 Prevention
• Many of the causes of achalasia are not
preventable. However, treatment of the
disorder may help to prevent complications
 Malignancies-Definition
• The commonest site : in the distal
• Risk factors :
– Tobacco & alcohol
• Squamous carcinoma
– Being linked to achalasia & celiac disease
• Adenocarcinoma
– Occur in association with Barret’s esophagus as a
consequence of metaplastic change at the
gastroesophageal junction
 Pathophysiology
• The tumour commences as a nodule, which
then develops into either an ulcer, a
papilliferous mass or annular constriction
• Adenocarcinomas arising at the lower end of
the esophagus, either arising in gastric
metaplasia
• Tumours of the upper two-thirds are usually
squamous carcinomas
• Local
– Into the mediastinal structure (trachea, aorta,
mediastinal pleura and lung)
• Lymphatic
– To para-esophageal, tracheobronchial, supraclavicular
& sub-diaphragmatic nodes
• Blood stream
– To liver and lungs
 Signs and Symptoms
• Local symptoms : dysphagia
• Secondary deposit : enlarged neck nodes,
occasionally jaundice or hepatomegaly
• General manifestations of malignant disease :
loss of weight, anorexia, anemia
 Exams and Tests
• Barium swallow
– Shows an irregular filling defect
• Oesophagoscopy
– Enables the tumour to be inspected and a biopsy
taken
• Endoscopic ultrasound
– Enables assesment of the tumour’s depth of
invansion and detection of local and lymphatic
spread
• CT of thorax and abdomen
– To asses the primary growth, local invasion &
secondary spread to the liver and lymph nodes
• Thoracoscopy
– To asses tumour spread prior to resection
• Chest X-ray
– Together with bronchoscopy  exclude a primary
tumour of the lung invading the esophagus
• Liver ultrasound
– Screens for hepatic deposits, useful in staging the
tumour
 Treatment
• To cure the cancer when possible
• To palliate the dysphagia
• Palliation
– Intubation : with a stent may relieve dysphagia if the tumour is inoperable
– Endoscopic laser therapy : may vaporize the growth and restore the lumen
– Radiotherapy : for squamous tumours
– Chemotherapy
• Curative resection
– The growth is removed & the defect is usually bridged by mobilizing the
stomach up into the chest, with anastomosis to residual esophagus or to the
pharynx in the neck
 Leukoplakia
• Leukoplakia merupakan lesi oral precancer dengan
resiko dapat menyebabkan kondisi malignansi
(keganasan). Leukoplakia merupakan suatu istilah
yang digunakan pada lesi/ plak putih yang tidak
normal yang terdapat pada membran
mukosa.Etiologi dari leukoplakia dapat dibagi
menjadi faktor lokal dan faktor sistemik.
-Faktor lokal biasanya berhubungan dengan iritasi kronis,
antara lain: trauma, kemikal atau termal, sertafaktor lokal
yang lain, seperti infeksi bakteri, penyakit periodontal, dan
higiene yang kurang baik.
-Faktor sistemik yang mampu mempengaruhi terbentuknya
leukoplakia meliputi,
• Penyakit sistemik
• sifilis tersier
• anemia hidrofenik
• Xerostomia
yang diakibatkan oleh penyakit kelenjar saliva, bahan
& bahan yang diberikan secara sistemik, misalnya alkohol, o
bat&obat anti metabolit serta kondisi defisiensi Vitamin.
 Tatalaksana
• Dalam penatalaksanaan leukoplakia yang terpenting adalah mengelimin
asi faktor predisposisi yang meliputi:
• penggunaan tembakau
• alkohol
• memperbaiki hiegine mulut
• memperbaiki maloklusi
• memperbaiki status gigi tiruan yang letaknya kurang baik.

• Penatalaksanaan lain yang dapat dilakukan adalah dengan melakukan

eksisi secara:
• Chirurgis : pembedahan terhadap lesi yang mempunyai ukuran kecil
atau agak besar. Apabila lesi sudahmeluas dan mengenai dasar mulut
maka pada daerah yang terkena perlu dilakukan.
• stripping : Pemberian Vitamin B kompleks dan Vitamin C dapat
dilakukan sebagai tindakan penunjang umum, terutama apabila pada
pasien tersebut ditemukan malnutrisi $itamin
 Atresia esofagus
kelainan esofagus yang berakhir pada sebuah kantung buntu,
umumnya disertai dengan fistula antara esofagus dan trakea
di sebelah distal . Paling sedikit dengandefek esofagus juga
mempunyai kelainan kongenital lain.
Atresia esofagus mungkin disertai oleh kelainan jantung,
atresia rektum atau anus, kelainan
tulang belakang serta kelahiran prematur,
kelainan ini terjadi karena gangguan perkembangan jaringan
pemisah antara trakea dan esofagus yang dibentuk selama
minggu keempat sampai keenam kehidupan dalam rahim.
Defek terjadi saat perkembangan endodermis. Gangguan
fusi dari dinding lateral foregut berakhir pada kurang
sempurnanya penutupan laryngotracheal tube dan
terbentuknya fistula
 GERD
• condition in which the
esophagus becomes
irritated or inflamed
because of acid backing up
from the stomach.
 Reflux Disease (GERD) Symptoms

Persistent heartburn is the most common symptom of GERD.

• Heartburn is a burning pain in the center of the chest, behind the

breastbone. It often starts in the upper abdomen and spreads up
into the neck.
• The pain can last as long as 2 hours.
• Heartburn is usually worse after eating.
• Lying down or bending over can bring on heartburn or make it
worse.
• The pain usually does not start or get worse with physical activity.
• Heartburn is sometimes referred to as acid indigestion.
• Not everyone with GERD has heartburn.
Typical (esophageal) symptoms include the following:
• Regurgitation is an effortless return of gastric and/or
esophageal contents into the pharynx. Regurgitation
can induce respiratory complications if gastric contents
spill into the tracheobronchial tree.
• Dysphagia occurs in approximately one third of
patients because of a mechanical stricture or a
functional problem (eg, nonobstructive dysphagia
secondary to abnormal esophageal peristalsis).
Patients with dysphagia experience a sensation that
food is stuck, particularly in the retrosternal area.
Atypical (extraesophageal) symptoms include the following:
• Coughing and/or wheezing are respiratory symptoms resulting from
the aspiration of gastric contents into the tracheobronchial tree or
from the vagal reflex arc producing bronchoconstriction.
Approximately 50% of patients who have GERD-induced asthma do
not experience heartburn.
• Hoarseness results from irritation of the vocal cords by gastric
refluxate and is often experienced by patients in the morning.
• Reflux is the most common cause of noncardiac chest pain,
accounting for approximately 50% of cases. Patients can present to
the emergency department with pain resembling a myocardial
infarction.
 Reflux Disease (GERD) Causes
The following are several contributing factors
that weaken or relax the lower esophageal
sphincter, making reflux worse:
•Lifestyle - Use of alcohol or cigarettes, obesity,
poor posture
•Medications - Calcium channel blockers,
theophylline (Tedral, Hydrophed, Marax,
Bronchial, Quibron), nitrates, antihistamines
 Complications
• Esophagitis (esophageal mucosal damage)
occurs in approximately 50% of patients with
gastroesophageal reflux disease (GERD).
• Barrett esophagus is one of the most serious
complications of gastroesophageal reflux
disease (GERD), because it may progress to
cancer
• Diet - Fatty and fried foods, chocolate, garlic
and onions, drinks with caffeine, acid foods
such as citrus fruits and tomatoes, spicy foods,
mint flavorings
• Eating habits - Eating large meals, eating soon
before bedtime
• Other medical conditions - Hiatal hernia,
pregnancy, diabetes, rapid weight gain
 Pathophysiology
The physiologic and anatomic factors that
prevent the reflux of gastric juice from the
stomach into the esophagus include the
following:
• The lower esophageal sphincter (LES) must have a
normal length and pressure and a normal
number of episodes of transient relaxation
(relaxation in the absence of swallowing).
• The gastroesophageal junction must be located in
the abdomen so that the diaphragmatic crura can
assist the action of the LES, thus functioning as an
extrinsic sphincter.
• Esophageal clearance must be able to
neutralize the acid refluxed through the LES.
(Mechanical clearance is achieved with
esophageal peristalsis. Chemical clearance is
achieved with saliva.)
• The stomach must empty properly.
Abnormal gastroesophageal reflux is caused by the
abnormalities of one or more of the following protective
mechanisms:
•A functional (frequent transient LES relaxation) or mechanical
(hypotensive LES) problem of the LES is the most common
cause of gastroesophageal reflux disease (GERD).
•Certain foods (eg, coffee, alcohol), medications (eg, calcium
channel blockers, nitrates, beta-blockers), or hormones (eg,
progesterone) can decrease the pressure of the LES.
•Obesity is a contributing factor in gastroesophageal reflux
disease (GERD), probably because of the increased intra-
abdominal pressure.
 Mortality/Morbidity
• In addition to the typical symptoms of
gastroesophageal reflux disease (GERD) (eg,
heartburn, regurgitation, dysphagia), abnormal
reflux can cause atypical symptoms, such as
coughing, chest pain, and wheezing. Additional
atypical symptoms from abnormal reflux include
damage to the lungs (eg, pneumonia, asthma,
idiopathic pulmonary fibrosis), vocal cords (eg,
laryngitis, cancer), ear (eg, otitis media), and
teeth (eg, enamel decay).
• Approximately 50% of patients with gastric
reflux develop esophagitis
Esophagitis is classified into the following 4
grades based on its severity:
• Grade I – Erythema
• Grade II – Linear nonconfluent erosions
• Grade III – Circular confluent erosions
• Grade IV – Stricture or Barrett esophagus.
Barrett esophagus is thought to be caused by
the chronic reflux of gastric juice into the
esophagus. Barrett esophagus occurs when
the squamous epithelium of the esophagus is
replaced by the intestinal columnar
• Barrett esophagus is present in 8-15% of
patients with gastroesophageal reflux disease
(GERD) and may progress to adenocarcinoma
 Epidemiologi
Race
• White males are at a greater risk for Barrett
esophagus and adenocarcinoma than other
populations.
Sex
• No sexual predilection exists. Gastroesophageal
reflux disease (GERD) is as common in men as in
women.
• The male-to-female incidence ratio for
esophagitis is 2:1-3:1. The male-to-female
incidence ratio for Barrett esophagus is 10:1.
Age
• Gastroesophageal reflux disease (GERD)
occurs in all age groups.
• The prevalence of gastroesophageal reflux
disease (GERD) increases in people older than
40 years
 Medical Care

• The goals are to control symptoms, to heal

esophagitis, and to prevent recurrent
esophagitis or other complications. The
treatment is based on lifestyle modification
and control of gastric acid secretion.
Lifestyle modifications include the following:
• Losing weight (if overweight)
• Avoiding alcohol, chocolate, citrus juice, and
tomato-based products
• Avoiding large meals
• Waiting 3 hours after a meal before lying
down
• Elevating the head of the bed 8 inches
 Medications
Proton pump inhibitors (PPIs)
• PPIs include omeprazole (Prilosec), esomeprazole
(Nexium), lansoprazole (Prevacid), rabeprazole
(Aciphex), and pantoprazole (Protonix).

• They block the production of an enzyme needed

to produce stomach acid.

• PPIs stop acid production more completely than

H2-blockers.
Coating agents
• Sucralfate (Carafate) coats mucous
membranes and sores to provide an additional
protective barrier against stomach acid
Promotility agents
• Promotility agents include metoclopramide (Reglan, Clopra,
Maxolon) and bethanechol (Duvoid, Urabeth, Urecholine).

• They help tighten the lower esophageal sphincter and promote

faster emptying of the stomach.

• Health care providers often are reluctant to prescribe these

medications because they have fairly significant side effects.

• Promotility agents also do not work as well as PPIs for most people.
 Surgery

• Not reccomended.
• Changes in lifestyle and habits,
nonprescription antacids, and prescription
medications all must be tried before resorting
to surgery. Only if all else fails is surgery
recommended
• The operation used most often for GERD is
called fundoplication.