Problem 1 Group 10 Gastrointestinal

Problem 1
Group 10
Gastrointestinal Track System
26th August 2015
Group 10
Tutor: dr. Juliawati
Leader: Carissa Octaviani (405130090)
Secretary: Sammy Raspati (405130115)
Writer: Febrinavega Wandy (405130099)
Members:
Seri Agustin (405120132)
Putri Ayu (405130019)
Felix Setiawan (405130093)
Nixon Orlando (405130094)
Suni Christina (405130111)
Vica Claudia (405130144)
Jesslyn Rusfardy (405130159)
Almira Nabila (405130193)
Yessica Desbet (405130211)
Unfamiliar Terms
1. Dysphagia: difficulty swallowing
2. Caries dentis: holes in the teeth
Define the Problems

1. Is there any relationship between caries dentis and dysphagia?
2. How smoking and drinking alcohol affects disease?
3. Is there a relationship between the operating history with
complaints?
4. Is there any relationship between the patients complaints with
his grandfather disease?
5. Why dysphagia got worse when swallowing solid food?
6. What examination can be done to confirm the diagnosis?
7. What can cause swelling under the jaw?
8. Is there any relationship between halitosis, dry mouth, cracked
lips with dysphagia and swelling?
9. What causes white patches in the mouth mucosa and tongue
ulcers?
10.Why at birth, patients get surgery?
Brainstorm Possible
Hypothesis
1.
2.
3.
4.
5.
6.
Caries dentis infection swelling dysphagia

Medicine, hormone, alcohol lower esophageal sphincter tonus GERD dysphagia
Yes, surgery scar tissue dysphagia
Caries dentis painful swallowing dysphagia
Examination:
1.
2.
3.
4.
Endoscopy
Video fluoroscopy
Panoramic x-ray
Mouth swab
7. Causes:
1.
2.
3.
4.
Trauma
Tumor
Infection abscess
Swollen lymphatic node
8. Dysphagia difficulty drinking dehydration dry mouth, cracked lips

9. Causes:
1. Less drinking
2. Candidiasis (caused by consuming antibiotic)
3. Chemical burn (caused by aspirin)
10.Congenital disorder: pallatum, esophageal atresia
Review
Caries
dentis
Aspirin
White
patches
Chemical
burn
Oral
thrush
Smoking &
drinking alcohol
Candidiasi
s
Abscess
Congenita
l disorder
Endoscopy
Mouth swab
X-ray
Videofluorosco
py
Teeth
examination
Dysphagi
a
lower
esophageal
sphincter
tonus
GERD
Treatment
Learning Objectives
1. Capable to explain about
digestion system
upper digestion system
digestion system
upper digestion system
digestion system
anatomy of upper
physiology of
histology of upper
biochemistry of
diseases of upper
LO1. ANATOMY OF UPPER

DIGESTION SYSTEM
Anatomy of Upper GI Tract

Upper Gastrointestinal Tract:
Esophagus - Gaster - Duodenum Proximal Jejunum - Treitz ligament
Lower Gastrointestinal Tract:
Treitz ligament - Distal Jejunum
Ileum Colon - Anus
ANATOMY
Oral Cavity (mouth)

Entrance to the GI tract.
Initial site of digestion:
mechanical digestion (via mastication)

chemical digestion (via enzymes in saliva).
Bounded anteriorly by the teeth and lips

Bounded posteriorly by the oropharynx.
Superior boundary is formed by the hard
and soft palates.
Floor, or inferior surface, of the oral cavity
the tongue
the mylohyoid muscle covered with mucosa.
Oral Cavity (mouth)

Two regions of the oral cavity
Vestibule is the space between the cheeks or

lips and the gums.
Oral cavity proper.
The lateral walls are formed by the cheeks.
Contain buccinator muscles

Lips (labia).
Orbicularis oris muscle

Keratinized stratified squamous ET
Gingivae, or gums.
Dense regular CT
Nonkeratinized ET
Labial frenulum.
Teeth
Collectively known as the dentition.
Responsible for mastication
first part of the mechanical digestion.
A tooth has:
exposed crown
constricted neck
one or more roots
Roots of the teeth fit into dental alveoli
are sockets within the alveolar processes
on both the maxillae and the mandible.
Collectively, the roots, the dental alveoli, and the
periodontal ligament that binds the roots to the
alveolar processes form a gomphosis joint.
LO2. PHYSIOLOGY OF
UPPER DIGESTION
SYSTEM
Physiology
There are four basic digestive
processes:
Motility
Secretion
Digestion
Absorption
Motility
Motility refers to the muscular
contractions that mix and move
forward the contents of the digestive
tract
It also maintains a constant low level
of contraction known ad tone
Two basics type of motility :
Propulsive movement
Mixing movement
Secretion
Each digestive secretion consist of water,
electrolytes, and specific organic constituents
important in digestive process
Secretion of all digestive juices requires energy,
both for active transport of some of the raw
material into the cell and for synthesis of
secretory products by the endoplasmic
reticulum
Normally, the digestive secretions are
reabsorbed in one form or another back into
the blood after their participation in digestion
Digestion
The term digestion refers to the biochemical
breakdown of the structurally complex
foodstuffs of the diet into smaller, absorbable
units by the enzymes produces within the
digestive systems
Carbohydrate : most are in form of
polysacharides which contains of chains of
interconnected glucose molecules
Proteins : amino acids small polypeptides
Fats : triglycerides monoglyceride + free fatty
acid
Digestion
Digestion is accomplished by
enzymatic hydrolysis
Digestive enzymes are specific in the
bonds they can hydrolyze
http://www.chembook.c
o.uk/fig25-4.jpg
Absorption
Digestion completed in the small
intestine and most absorption occurs
Through the process of absorption,
the small absorbable units that
results from digestion are transffered
into the blood or lymph
Control of Salivary Secretion

Thinking of
food
Seeing food
Smelling food
Chapter 16 The
Digestive System
Human Physiology by
Lauralee Sherwood
2007 Brooks/Cole-
Swallowing
Swallowing can be divided into:
1. a voluntary stage, which initiates the
swallowing process.
2. a
pharyngeal
stage,
which
is
involuntary and constitutes passage of
food through the pharynx into the
esophagus.
3. an
esophageal
stage,
another
involuntary phase that transports food
from the pharynx to the stomach.
Matsuo K, Palmer BJ. Anatomy and

physiology of feeding and
swallowing. Phys Med Rehabil Clin
Sherwood L. Introduction to human

physiology. 8th ed. United States:
Brooks/Cole-Cengage Learning;


LO3. HISTOLOGY OF
UPPER DIGESTION
SYSTEM
DIGESTIVE SYSTEM
Two groups of organs compose the
digestive system:
Gastrointenstinal (GI) tract or alimentary
canal mouth, most of pharynx,
esophagus, stomach, small intestine,
and large intestine
Accessory digestive organs teeth,
tongue, salivary glands, liver,
gallbladder, and pancreas
diFiore Atlas of Histology, 247
Histologic organization:
Mucosa:
Epithelium, lamina propria, muscularis mucosa
Submucosa:
connective tissue, vessels, and Meissners plexuses,
some times mucous glands
Muscularis externa: 2-3 layers of smooth muscle (plus
skeletal muscle in esophagus), myenteric (Auerbach)
plexus in between muscle layers
Serosa and adventitia: Outermost layer of loose
connective tissue and blood vessels. Call serosa if
covered my mesothelium; adventitia otherwise
mucosa
submuco
muscula
serosa
ORAL CAVITY
Inner surface of the lips, cheeks, soft
palate, surface of tongue, and floor of the
mouth
Nonkeratinized stratified squamous epithelium
Lamina propria
Submucosa
Gingiva and hard palate

Keratinized stratified squamous epithelium
Lamina propria
Tongue: specialized mucosa with papillae
THE LIP
THE TONGUE
Junquiera, L. C. (2013) Basic Histology text & Atlas, 13rd edn.

McGraw Hill, New York.
TONGUE PAPILLAE
There are four types:
fungiform
filliform
foliate
circumvall
ate
TASTE BUD
TEETH
ESOPHAGUS
Mucosa: non-keratinizing stratified
squamous
Submucosa: contains mucous glands
Increased mucous glands at lower esophagus
(GE junction) to protect esophagus from
gastric juices
Muscularis externa: inner circular and

outer longitudinal
Contains skeletal muscle fibers
Esophagus
Squamous
mucosa
Submuco
sa
Musculari
s Externa
Mucosa
Adventitia /
Serosa
Muscularis
mucosa
Lower esophagus
Upper esophagus
LO4. BIOCHEMISTRY OF
UPPER DIGESTION
SYSTEM
The mouth
Digestion of starch
begins in the mouth
Salivary gland releases
a-amylase converts
starch to smaller
polysaccharides (adextrins)
Salivary a-amylase is
inactivated by the
acidity of stomach(HCL)
Marks Basic Medical Biochemistry A Clinical Approach, 2nd Edition
Pancreas
Pancreatic a-amylase and
bicarbonate are secreted by the
exocrine pancreas into the
lumen of the small intestine
Bicarbonate neutralize the
gastric secretions
Pancreatic a-amylase continues
the digestion of a-dextrins
converting them to
disaccharides (maltose),
trischarrides (maltotriose), and
oligosaccharides (limit dextrins)
Intestine
Digestion of the
disaccharides lactose dan
sucrose, maltose,
maltotriose dan limit
dextrins, occurs through
the membrane surface of
the brush border
(microvilli) of intestinal
epithelial cells
converted to
monosaccharides by
glycosidases
LO5. ABNORMALITIES OF
UPPER DIGESTION
SYSTEM
Cleft lip and palate

Cleft lip and cleft palate are birth
defects that occur when a babys lip
or mouth do not form properly during
pregnancy. Together, these birth
defects commonly are called
orofacial clefts. These birth defects
happen early during pregnancy. A
baby can have a cleft lip, a cleft
palate, or both a cleft lip and cleft
http://www.cdc.gov/ncbddd/birthdefects/cleftlip.html
palate.
http://www.cdc.gov/ncbdd
d/birthdefects/cleftlip.html
Cleft lip
The lip forms between the fourth and seventh
weeks of pregnancy. A cleft lip happens if the
tissue that makes up the lip does not join
completely before birth. This results in an
opening in the upper lip. The opening in the
lip can be a small slit or it can be a large
opening that goes through the lip into the
nose. A cleft lip can be on one or both sides
of the lip or in the middle of the lip, which
occurs very rarely. Children with a cleft lip
also can have a cleft palate.
Cleft palate
The roof of the mouth (palate) is
formed between the sixth and ninth
weeks of pregnancy. A cleft palate
happens if the tissue that makes up
the roof of the mouth does not join
together completely during
pregnancy. For some babies, both
the front and back parts of the palate
are open. For other babies, only part
of the palate is open.
The causes of orofacial clefts among most

infants are unknown.
Some children have a cleft lip or cleft palate
because of changes in theirgenes.
Cleft lip and cleft palate are thought to be
caused by a combination of genes and other
factors, such as things the mother comes in
contact with in her environment, or what
the mother eats or drinks, or certain
medications she uses during pregnancy.
Risk Factor
SmokingWomen who smoke during pregnancy are
more likely to have a baby with an orofacial cleft than
women who do not smoke.
DiabetesWomen with diabetes diagnosed before
pregnancy have an increased risk of having a child with a
cleft lip with or without cleft palate, compared to women
who did not have diabetes.
Use of certain medicinesWomen who used certain
medicines to treat epilepsy, such as topiramate or
valproic acid, during the first trimester (the first 3
months) of pregnancy have an increased risk of having a
baby with cleft lip with or without cleft palate, compared
to women who didnt take these medicines.
Treatment
Surgery to repair a cleft lip usually occurs in the first few
months of life and is recommended within the first 12
months of life.
Surgery to repair a cleft palate is recommended within
the first 18 months of life or earlier if possible.
Many children will need additional surgical procedures
as they get older. (Surgical repair can improve the look
and appearance of a childs face and might also improve
breathing, hearing, and speech and language
development.)
Children born with orofacial clefts might need other
types of treatments and services, such as special dental
or orthodontic care or speech therapy.
Micrognathia
Micrognathia is a term for a lower jaw that
is smaller than normal
Etiology :
Cri du chat
syndrome
Hallerman-Streiff
syndrome
Marfan syndrome
Pierre Robin
syndrome
Progeria
Russell-Silver
Seckel syndrome
Smith-Lemli-Opitz
syndrome
Treacher-Collins
syndrome
Trisomy 13
Trisomy 18
XO syndrome (Turner
syndrome)
Micrognathia
Pathology :
A small mandible occurs secondary to
abnormalities of the first branchial arch which
in turn are caused by deficient or insufficient
migration of neural crest cells
Occur around the 4thweek of gestation
Clinical manifestasions :
The tongue is usually of normal size, but the
floor of the mouth is foreshortened
The air passages can become obstructed,
particularly on inspiration
Treatments
The infant should be maintained in a
prone or partially prone position so
that the tongue falls forward to
relieve respiratory obstruction
Tracheostomy
Mandibular distraction
Glossitis
A problem in
which the tongue
is swollen and
changes color,
often making the
surface of the
tongue appear
smooth
Glossitis
Glossitis is often a symptom of other
conditions, such as:
Allergic reactions to oralcare products, foods, or
medicine
Dry mouth due to Sjogren syndrome
Infection from bacteria, yeast or viruses (including
oral herpes)
Injury (such as from burns, rough teeth, or badfitting dentures0
Skin conditions that affect the mouth
Irritants such as tobacco, alcohol, hot foods, spices,
or other irritants
Hormonal factors
At times, glossitis may be passed down in families.
Glossitis
Symptoms:
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
Blocked airway (rare)
Glossitis
Examinations:
An exam to look for:
Finger-like bumps on the surface of the tongue (called
papillae) that may be missing
Swollen tongue (or patches of swelling)
Blood tests to rule out other medical problems
Treatment:
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
problems.
Avoiding irritants (such as hot or spicy foods,
alcohol, and tobacco) to ease discomfort.
Glossitis
Prognosis:
Glossitis goes away with if the cause of
problem is removed or treated
Prevention:
Good oral care (thorough tooth brushing
and flossing and regular dental
checkups)
Leukoplakia
Leukoplakia is a white or gray
patch that develops on thetongue,
the inside of the cheek, or on the
floor of themouth. It is
themouth's reaction to chronic
irritation of the mucous
membranes of the mouth
Leukoplakia usually isn't
dangerous, but it can sometimes
be serious. Although most
leukoplakia patches are
noncancerous (benign), some
show early signs of cancer
http://www.mayoclinic.org/diseases-conditions/leukoplakia/basics/definition/con-20023
802
http://www.webmd.com/oral-health/guide/dental-health-leukoplakia
Etiology (Leukoplakia)
Irritation from roughteeth, fillings, or
crowns, or ill-fitting dentures that rub
against your cheek or gum
Chronicsmoking,pipe smoking, or
othertobaccouse
Sun exposure to the lips
HIV or AIDS hairy leukoplakia
EBV
Sign and symptoms (Leukoplakia)

Leukoplakia may appear:
White or grayish in patches that can't be wiped
away
Irregular or flat-textured
The patch may have developed slowly over weeks
to months and be thick, slightly raised, and may
eventually take on a hardened and rough texture
Along with raised, red lesions (erythroplakia), which
are more likely to show precancerous changes
Usually is painless, but may be sensitive to touch,
heat, spicy foods, or other irritation
802
Test and diagnosis

(Leukoplakia)
To test for early signs of cancer:
Remove a tissue sample (biopsy) for
analysis.This involves removing cells from
the surface of the lesion with a small,
spinning brush (oral brush biopsy) or
surgically removing the entire leukoplakia
patch (excisional biopsy) if the patch is small.
Send the tissue for lab analysis.A highly
specialized imaging system allows a
pathologist to detect abnormal cells.
http://www.mayoclinic.org/diseases-conditions/leukoplakia/basics/testsdiagnosis/con-20023802
Treatment (Leukoplakia)
Treatment for leukoplakia, if needed, involves removing the
source of irritation. For example, if leukoplakia is caused by
a rough toothor an irregular surface on a denture or a
filling, thetooth will be smoothed and dental appliances
repaired
For most people, stopping tobacco or alcohol use clears
the condition. When this isn't effective or if the lesions
show early signs of cancer, your dentist may refer you for
treatment, which involves:
Removal of leukoplakia patches.Patches may be
removed using a scalpel, a laser or an extremely cold
probe that freezes and destroys cancer cells.
Follow-up visits.Recurrences are common.
http://www.webmd.com/oral-health/guide/dental-health-leukoplakia?page=2
http://www.mayoclinic.org/diseases-conditions/leukoplakia/basics/treatment/con-20023802
Treatment (Hairy
Leukoplakia)
antiviral medicine acyclovir
antiretroviral medicine zidovudine
apply directly to the lesions in mouth
(topical medication), such as
podophyllum.
http://www.mayoclinic.org/diseases-conditions/leukoplakia/basics/treatment/con-20023802
Candidiasis
Etiologic agents:
Candida albicans (the
most common cause)
All Candida species
pathogenic for humans
are also encountered as
commensals of humans,
particularly in the
mouth, stool, and vagina
Clinical manifestations
Mucocutaneous candidiasis
Oral thrush white plaques on the oral and
pharyngeal mucosa, particularly in the mouth and
on the tounge
Cutaneous candidiasis
Esophageal candidiasis
Often asymptomatic but can cause substernal pain or a
sense of obstruction on swallowing
Can cause bleeding and impaired alimentation
Most lesions are in the distal third of the esophagus and
appear on endoscopy as areas of redness and edema,
focal white patches, or ulcers
Deeply invasive candidiasis

In the obstructed urinary tract, Candida can
cause cystitis, pyelitis, or renal papillary
necrosis
Examinations
Wet smear pseudohyphae
Scrapings for the smear may be obtained
from skin, nails, and oral and vaginalmucosa
Culture for confirmation

Urine, sputum, existing abdominal drains,
endotracheal aspirates, or the vagina
Histologic section of biopsies

Culture of cerebrospinal fluid, blood,
joint fluid, CT-guided needle aspirates,
or surgical specimens
Treatment
Prophylaxis
Fluconazole the incidence of deeply
invasive candidiasis in recipients of
allogeneic bone marrow transplants
(400 mg, given daily)
Caries Dentis
Etiology :
Frequent ingestion of
sugar, either in the
bottle or in solid foods
Colonization with
cariogenic bacteria
Clinical manifestasions
:
Darkened or cavitated
lesions on the tooth
surfaces
Caries Dentis
Pathophysiology :
Bacterial
fermentation
of
dietary
carbohydrates (Streptococcus mutans)
produce organic acids reduce the pH of
dental plaque adjacent to the tooth
demineralization occurs opaque white
spot lesion on the enamel progressive
loss of tooth mineral cavitation of the
tooth occurs
Complication
Dental caries destroy
most of the tooth and
invade the dental
pulp pulpitis
pulp necrosis
dental abcess
Disrupt normal
development of the
successor permanent
tooth
Sepsis and infection
of the facial space
Caries Dentis
Treatment
Silver amalgam
Plastic composite
Stainless steel crowns
Pulpotomy
Pulpectomy
Oral antibiotics (fever,
cellulitis, and facial
swelling) penicillin
Oral analgesics
ibuprofen
Prevention
Oral hygiene
Diet
Dental sealant
Gingivitis
Gingivitis is a form ofperiodontal disease. Periodontal
disease is inflammation and infection that destroys the
tissues that support the teeth. This caninclude the gums,
the periodontal ligaments, and the tooth sockets (alveolar
bone).
Gingivitis is due to the long-term effects of plaque deposits
on your teeth. Plaque is a sticky material made of bacteria,
mucus, and food debris thatbuilds upon the exposed parts
of the teeth. It is also a major cause oftooth decay.
If you do not remove plaque, it turns into a hard deposit
called tartar (or calculus) that becomes trapped at the base
of the tooth. Plaque and tartar irritate and inflame the
gums. Bacteria and thetoxinsthey produce cause the gums
to become infected, swollen, and tender.
Risk Factor
Certain infections and body-wide (systemic)
diseases
Poordental hygiene
Pregnancy (hormonal changes increase the
sensitivity of the gums)
Uncontrolled diabetes
Misaligned teeth, rough edges of fillings, and illfitting or unclean mouth appliances (such as
braces, dentures, bridges, and crowns)
Use of certain medications, including phenytoin,
bismuth, and some birth control pills
Symptoms
Bleeding gums(blood on toothbrush
even with gentle brushing of the
teeth)
Bright red or red-purple appearance
to gums
Gums that are tender when touched,
but otherwise painless
Mouth sores
Swollen gums
Shiny appearance to gums
Treatment
The goal is to reduce inflammation.
The dentist or dental hygienist will
clean your teeth. The may use
different tools to loosen and remove
deposits from the teeth.
Careful oral hygiene is necessary
after professional tooth cleaning. The
dentist or hygienist will show you
how to brush and floss.
Ludwigs Angina
An infection of
the floor of the
mouth under the
tongue
Causes: infection
of the roots of
the teeth (such
as tooth
abscess) or a
mouth injury
Ludwigs Angina
Symptoms:
Breathing difficulty
Confusion or other mental changes
Fever
Neck pain
Neck swelling
Redness of the neck
Weakness, fatigue, excess tiredness
Difficulty swallowing
Drooling
Earache
Speech that is unusual and sounds like the
person has a "hot potato" in the mouth
Ludwigs Angina
Examinations:
Physical examination (to look for
redness and swelling of the upper neck
and under the chin)
CT scan of the neck
A sample of the fluid from the tissue
may be sent to the lab to test for
bacteria
Ludwigs Angina
Treatment:
If the swelling blocks the airway
breathing tube through mouth or nose
and into the lungs, tracheostomy
(creates an opening through the neck
into the windpipe)
Infection antibiotics
Tooth infections dental treatment
Surgery to drain fluids that are causing
the swelling
Ludwigs Angina
Prognosis
Can be life threatening
Can be cured with getting treatment to keep
the airways open and taking antibiotic
medicine
Possible complications
Airway blockage
Generalized infection (sepsis)
Septic shock
Prevention
Visit the dentist for regular checkups.
Treat symptoms of mouth or tooth infection
right away.
Parotitis
Parotid gland is located in each
cheek over the jaw in front of
the ears. Inflammation of one or
more of these glands is called
parotitis, or parotiditis.
Etiology :
Viral infections such asmumps
often affect the salivary glands
Bacterial infections are most often
the result of a:
Blockage fromsalivary duct stones
Poor cleanliness in the mouth (oral
hygiene)
Low amounts of water in the body,
most often while in the hospital.
Smoking
Chronic illness
Symptoms
Abnormal tastes, foul tastes
Decreased ability to open the mouth
Dry mouth
Fever
Mouth orfacial pain, especially when eating
Redness over the side of the face or the upper neck
Swelling of the face
Exams : A CT scan, MRI scanor ultrasound
Treatment
Antibiotics if you have a fever or pus drainage,
or if the infection is caused by bacteria
Surgery oraspiration to drain an abscess if
you have one.
Outlook (Prognosis)
Most salivary gland infections go away on
their own or are cured with treatment. Some
infections will return. Complications are not
common
Achalasia
Etiology :
loss of ganglion cells within the
esophageal myenteric plexus that
caused by autoimmune process
attributable to a latent infection with
human herpes simplex virus 1
combined with genetic susceptibility
Sign : progressive dilatation and
sigmoid deformity of the esophagus
with hypertrophy of the LES
Symptoms : dysphagia, regurgitation,
chest pain, weight loss, and solid and
liquid food dysphagia
Achalasia
Pathophysiology :
Excitatory (cholinergic) ganglionic neurons
are variably affected and inhibitory (nitric
oxide) ganglionic neurons are necessarily
involved.
Inhibitory neurons mediate deglutitive LES
relaxation and the sequential propagation
of peristalsis.
Their absence leads to impaired deglutitive
LES relaxation and absent peristalsis.
Achalasia
Examinations : endoscopy, CT scanning or
endoscopic ultrasonography, barium swallow xray and/or esophageal manometry
Dx : barium swallow x-ray dilated esophagus
with poor emptying, an air-fluid level, and
tapering at the LES giving it a beak-like
appearance
Complications : bronchitis, pneumonia, or lung
abscess from chronic regurgitation and aspiration
DD : DES, Chagas' disease, and pseudoachalasia
Achalasia
Pharmaco :
Botulinum toxin injected into the LES
Sildenafil, or alternative
phosphodiesterase inhibitors
Nonpharmaco :
Pneumatic dilatation
Heller myotomy
Esophageal Atresia
Failure of fusion between the proximal and distal
esophagus associated with a tracheoesophageal
fistula
Symptoms : frothing and bubbling at the mouth
and nose after birth as well as episodes of
coughing, cyanosis, and respiratory distress
Complication :
Feeding exacerbates these symptoms, causes
regurgitation, and can precipitate aspiration
H-type fistula : chronic respiratory problems, including
refractory bronchospasm and recurrent pneumonias.
Esophageal Atresia
Dx :
The inability to pass a nasogastric or
orogastric tube in the newborn
Plain radiography : a coiled feeding tube
in the esophageal pouch and/or an airdistended stomach EA + TEF
Airless scaphoid abdomen EA
Treatment
Esophageal suctioning minimizes aspiration
Prone positioning minimizes movement of gastric
secretions into a distal fistula
Surgical ligation of the TEF and primary end-to-end
anastomosis of the esophagus
In the premature or complicated infant, a primary
closure may be delayed by temporizing with fistula
ligation and gastrostomy tube placement
If the gap between the atretic ends of the esophagus
is >3-4 cm, primary repair cannot be done; options
include using gastric, jejunal, or colonic segments
interposed as a neo-esophagus
Prognosis
Complications of surgery during the first
5 yr of life
Anastomotic leak
Refistulization
Anastomotic stricture
Gastroesophageal reflux disease (GERD)
Resulting from intrinsic abnormalities of
esophageal function, often combined w/
delayed gastric emptying
Daftar Pustaka
Moore - Clinically Oriented Anatomy 7th Ed

Sherwood L. Introduction to Human Physiology. 8th Ed. USA: Brooks/Cole; 2013.
Junqueira LC, Carneiro J. Basic Histology Text and Atlas. 13th ed. McGraw-Hill; 2013
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Problem 1 Group 10 Gastrointestinal

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Problem 1 Group 10 Gastrointestinal

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Problem 1

Define the Problems

Caries dentis infection swelling dysphagia

8. Dysphagia difficulty drinking dehydration dry mouth, cracked lips

10.Congenital disorder: pallatum, esophageal atresia

LO1. ANATOMY OF UPPER

Anatomy of Upper GI Tract

Oral Cavity (mouth)

mechanical digestion (via mastication)

Bounded anteriorly by the teeth and lips

Oral Cavity (mouth)

Vestibule is the space between the cheeks or

Contain buccinator muscles

Orbicularis oris muscle

Control of Salivary Secretion

Matsuo K, Palmer BJ. Anatomy and

Sherwood L. Introduction to human

Sherwood L. Introduction to human

Sherwood L. Introduction to human

Gingiva and hard palate

Tongue: specialized mucosa with papillae

Junquiera, L. C. (2013) Basic Histology text & Atlas, 13rd edn.

There are four types:

Muscularis externa: inner circular and

Marks Basic Medical Biochemistry A Clinical Approach, 2nd Edition

Marks Basic Medical Biochemistry A Clinical Approach, 2nd Edition

Cleft lip and palate

The causes of orofacial clefts among most

Blood tests to rule out other medical problems

Sign and symptoms (Leukoplakia)

Test and diagnosis

Deeply invasive candidiasis

Culture for confirmation

Histologic section of biopsies

Moore - Clinically Oriented Anatomy 7th Ed

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