LO 1

ANATOMY AND HISTOLOGY OF MOUTH

- OESOPHAGUS
Anatomy of Abdomen

Upper GI Tract

Lower GI Tract
MOUTH
Salivary gland position
 Saliva
• Glands:
– parotid, sublingual & submandibular
• Minor gland:
– Buccal
• -99.5% H2O, 0.5% protein (amylase, mucus, lysozyme, &
electrolyte)
• Functions:
– Amylase: polisaccharide  dissacharide
– Mucus: lubrication, foodcondensing, as a solvent  stimulate the
tastebud
– articulation
– Hygiene
– HCO3- netralizing acid from foods
– Bacteria  prevent caries
Regulation of saliva
 Esophagus
• The largest part of thorax
• Pars thoracalis (behind trachea)
• Pars abdominalis : enter to the gastric cardia ventriculi
• transition  ostium cardiacum/ cardiac orificium/ junctio gastroesophagei
• It has LES and its function for preventing reflux
• The closing of spincter is controlled by vagal and amplified by gastrin ,and
decreased by secretin response, cholecystokinin, glucacon
• vascularitation:
– a. gastrica sinistra
– Cabang a. phrenica inferior
– V. azygos
– V. gastrica sinistra
• nerves : N. vagus (parasimpatis), N. splanchnici (simpatis)
Esophagus
Histology
 Labium Oris / Lips
• 3 layers:
–Pars cutanea/outer layer:
–Pars Intermedia/Vermillion border: A
–Pars oral mucosa: B
 Pars cutanea
1. Stratified keratinizing squamous cell epithelium
2. Hair follicle with sebaceous and sweat glands
3. Orbicularis oris muscle
 Pars intermedia (A)
Pars oral mucosa (B)
1. Stratified nonkeratinizing squamous cell epithelium
2. Tunica propria
a. Labialis glands
3. Orbicularis oris muscle
4. Labialis artery
5. Small chorium
 Tongue/Lingua
• There are 3 forms of papillae:
–Circumvalata papillae
–Filiform papillae
–Fungiform papillae
 Circumvalata Papillae
A. Circumvalata papillae:
1. Secondary papillae
2. Taste bud
B. Ebneri glands
Filiriform (A) and Fungiform Papillae (B)
 Teeth
1. Dental cement
a. Sharpey’s fiber
2. Tomes granular layer
3. Dentine + dentine canals
ESOPHAGUS
LO 2

PHYSIOLOGY OF SWALLOWING
Swallowing procces
Picture : process of swallowing
Peristalsis
Contraction of circular muscle behind the
bolus

Contraction of longitudinal muscle IN

FRONT of the bolus

Peristalsis: coordinated contraction of both

circular and longitudinal muscle layers of the
G.I. musculature as controlled by the enteric
nervous system
LO 3

BIOCHEMISTRY OF SWALLOWING
Source Enzim Activator Substrat Function or
katalitik product

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

Saliva essence @; produce dextrin
@limit,
maltotriosa, and
maltosa
Lingual gland Lingual lipase Trigliserida Lipid acid plus 1,2
- diasilgliserol

Gaster Pepsin Hcl- Protein and Decompose

(pepsinogen) polipeptida peptida chain
which closer with
aromatic amino
acid
Gaster lipase Trigliserida
Lipid acid and
gliserol
LO 4

DEFINITION AND PATHOPHYSIOLOGY

OF DYSPHAGIA AND ODYNOPHAGIA
 Dysphagia
• Dysphagiadifficulty moving food or liquid
through mouth,pharynx,and esophagus
• Oropharyngeal dysphagiadifficulty initiating
the swallow, foods stick at the level of
suprasternal notch;nasopharyngeal
regurgitation and aspiration only.
• Esophageal dysphagiafood sticks at level of
mid or lower sternal area;can be associated
with regurgitation,aspiration,odynophagia.
 Pathophysiology
Mechanical obstruction Motor dysfunction
• Luminal(e.g.: large food • Defects in initial swallowing
bolus, foreign body) reflex(e.g.:tongue
paralysis,lack of saliva)
• Intrinstic to esophagus(e.g.:
inflammation,strictures,tum • Disorder of pharyngeal
esophageal striated
ors) muscle(e.g.:muscle
• Extrinstic to esophagus(e.g.: disorder,neurologic lesions)
cervical spondylitis,enlarged • Disorder ofesophageal
thyroid) smooth
muscle(e.g.:achalasia,sclrod
erma)
LO 5

SWALLOWING DISORDERS (IN ADULT

AND CHILD)
Esophageal Atresia
 Definition of Esophageal atresia

• Esophageal atresia is a disorder of the

digestive system in which the esophagus does
not develop properly.
• Congenital esophageal atresia (EA) represents
a failure of the esophagus to develop as a
continuous passage.
 Causes, incidence, and risk factor
• Esophageal atresia is a congenital defect, which means it occurs
before birth.
• There are several types.
• In most cases, the upper esophagus ends and does not connect with
the lower esophagus and stomach.
• The top end of the lower esophagus connects to the windpipe.
• This connection is called a tracheoesophageal fistula (TEF).
• Some babies with TEF will also have other problems, such as heart or
other digestive tract disorders.
• Other types of esophageal atresia involve narrowing of the
esophagus, and may also be associated with other birth defects.
• Esophageal atresia occurs in about 1 out of 4,000 births.
 Symptom

• Bluish coloration to the skin (cyanosis) with

attempted feedings
• Coughing, gagging, and choking with
attempted feeding
• Drooling
• Poor feeding
 Achalasia
• Motor obstruction caused by hypertensive
LES,incomplete relaxation LES or loss of
peristalis in smooth muscle portion of
esophagus
• Etiologychagas disease,tumor(lymphoma,
carcinoma),ischemia,neurotropic
viruses,drugs,toxins,radiation therapy
• Based on etiology,achalasia divided into 2
things:
– Primary achalasia the etiology is not clear/
known
– Secondary achalasia etiology is clear/known
• From Castell point of view, there are 2
important things that can caused achalasia:
– Obstruction of tract between esophagus and
gaster caused by increased pressure of LES beyond
normal point and failure of LES to relaxation
perfectly
– Abnormal esophagus peristaltik caused by
aperistaltik and dilatation about 2/3 lower region
of esophagus corpus
 Clinical manifestation
• Disphagia(solid food or liquid) 90% cases
• Regurgitation 70% cases
• Loss weight
• Chest pain
Corrosive Lesion of
Esophagus
 Corrosive injury of GIT
• Classified by cause of ingestion
– Accidental
• More popular in developed countries
• Almost all child ingestion accounts to this
reason
• Approximately 80% of caustic ingestions occur
in children younger than 5 years
– Intentional (suicide)
• Most intentional ingestions occur in adults
• Classified by ingested caustic material
– Alkaline material
• liquefactive necrosis (saponification of fats and solubilization of proteins)
• Most common in developed contries
• The most severely injured tissues are the squamous epithelial cells of
the oropharynx, hypopharynx, and esophagus (the most commonly
involved organ)
• The stomach is involved in only 20% of all alkaline ingestions
– Acid material
• coagulation necrosis (desiccation or denaturation of superficial tissue
proteins)
• More common in developing countries
• The squamous epithelium of the pharynx and esophagus are relatively
resistant to this type of injury. The esophagus is involved in 6-20% of acid
ingestions.
• The stomach is the most commonly involved organ in an acid ingestion
 Evaluation of patient of acute
corrosive injury
• Attempt to identify the specific product, concentration of active ingredients, and
estimated volume and amount ingested
• Physical examination
– Monitor peritoneal signs
• Complete blood count (CBC), electrolyte levels, BUN levels, creatinine level, and ABG
levels
• pH testing of product
– A pH less than 2.0 or greater than 12 indicates the potential for severe tissue
damage
• Chest X-ray
– Be cautious of peritoneal free air
• Upper digestive endoscopy
– Performed within 24 hours is safe
– Gold standard  Esophagoscopy should not be performed in patients with
evidence of gastrointestinal perforation, significant airway edema, or necrosis and
in those who are hemodynamically unstable.
• Bronchoscopy
• EUS (endoscopic ultra-sound)
 Emergency department care
• Airway control
– Equipment for endotracheal intubation and cricothyrotomy should be readily
available.
• Gastric emptying and decontamination
– Do not administer emetics
– Gastric lavage by traditional methods using large bore orogastric Ewald tubes are
contraindicated
– Large-volume liquid acid ingestions may benefit from nasogastric tube (NGT)
suction.
– Activated charcoal is relatively contraindicated
• Dilution:
– Dilution may be beneficial for ingestion of solid or granular alkaline material if
performed within 30 minutes postingestion.
• Neutralization:
– Do not administer a weak acid in alkaline ingestions or a weak base in acid
ingestions.
Treatment of acute corrosive injury
• Because controlled, randomized trials with adequate numbers of patients
are lacking, treatment in many respects remains controversial
• Principle
– Admit all small children, symptomatic patients, and those with altered
mental status
– Ensure that all patients take nothing per mouth (NPO) until extent of
injury has been determined
– PPN (partial parenteral nutrition)
– Administer parenteral analgesics as needed for pain
– Antacid agent
– Monitor respiratory pattern and prevent pneumonia
– Early exploratory laparotomy if acute abdomen is suspected
– Obtain a psychiatric evaluation for all patients with intentional ingestion.
 Alternative treatments
• Early discharge, oral intake and out patient follow up in patients minor than grade 2a injury
– Prediction of bleeding and stricture formation after corrosive ingestion by EUS concurrent with
upper endoscopy. Gastrointest Endosc. 2004 Nov;60(5):827-33
– Ingestion of Caustic Substances by Adults, American Journal of Therapeutics 11, 258–261 (2004)
• Methyl prednisolone, 1mg/kg intravenously
– Ingestion of Caustic Substances by Adults, American Journal of Therapeutics 11, 258–261 (2004)
• Short-term intravenous antibiotics
– Ingestion of Caustic Substances by Adults, American Journal of Therapeutics 11, 258–261 (2004)
• Neutralization by weak acid or alkali administration
– Successful in canine models
– Thermal characteristics of neutralization therapy and water dilution for strong acid ingestion: an
in-vivo canine model. Acad Emerg Med 1998; 5:286 –292.
• Modified Intraluminal Stenting
– Management of corrosive esophageal burns in 149 cases. The Journal of Thoracic and
Cardiovascular Surgery. Volume 130, Number 2 449.e1
 The physiopathological caracteristics
of the caustic lesions
• During the first hours
– there is eosinophilic necrosis with edema and intense hemorrhagic congestion
(caustic esophagitis).
• During the first days
– Perforation will occur if ulceration exceeds the muscle plane.
– Mucosal sloughing occurs 4–7 days after the initial injury
– Repair occurs during the first weeks, especially after the 10th day.
– the tensile strength of healing tissue is low during first 3 weeks
– Fibrosis occurs in layers whose depth depends on the severity of the caustic
injury (caustic stenosis).
• During the first month
– epithelialization of the mucosal ulcerations occurs with difficulty due to the
vascular lesions.
• For the rest of their lives
– these patients may present new ulcerations followed by re-epithelialization due
to small traumas provoked by food. These traumas increase the scars, reducing
even more the lumen of the organ.
 Medical/Legal Pitfalls

• Failure to evaluate and aggressively manage the

airway in patients with respiratory distress or
significant laryngeal involvement
• Attempting to neutralize the ingested caustic
agent with a weak acid or alkaline agent
• Inducing emesis
• Assuming that the absence of oropharyngeal
burns precludes the presence of significant distal
injuries
• Failing to consult a gastroenterologist or surgeon
for evaluation of all symptomatic patients
Esophageal Rupture
 Overview
• Esophageal rupture is rare
– Roughly 300 cases reported per year
– The diagnosis is commonly missed/delayed
• Mortality is high
– Most lethal GI perforation
– Mortality falls with early dx/intervention
• Survival depends on rapid dx and surgery
– Within 24 hours of rupture: 70-75% survival
– Within 25-48 hours: 35-50% survival
– Beyond 48 hours: 10% survival
 Etiology of Esophageal Rupture

• Traumatic Causes (MORE COMMON):

– Endoscopy or dilation procedures
• Stent placement most common cause (up to 25%
cases)
– Vomiting or severe straining
– Stab wounds / penetrating trauma
– Blunt chest trauma (rarely)
• Non-Traumatic Causes (LESS COMMON):
– Neoplasm / Ulceration of esophageal wall
– Ingestion of caustic materials
 Pathophysiology

• Air, Saliva, and Gastric contents released

– mediastinitis
– pneumomediastinum
– empyema
– can progress to sepsis, shock, resp failure
 Presentation
Typical symptoms include the following:
• Pain of variable location, commonly in the lower
anterior chest or upper abdomen
• Vomiting
• Subcutaneous emphysema
• Neck pain
• Dysphagia
• Dyspnea
• Hematemesis
• Melena
• Back pain
Physical signs include the following:
• Fever
• Crepitus
• Tachycardia
• Tachypnea
• Cyanosis
• Dyspnea
• Upper abdominal rigidity
• Shock
• Local tenderness
 Work Up

• Complete blood count (CBC): Evidence of

leukocytosis is common place for almost all
esophageal perforations.
• pH level: Esophageal perforations with
penetrance into the pleural cavity have pH
levels less than 7.2.
 Complications

• Mediastinitis
• Intrathoracic abscess
• Sepsis
• Respiratory failure
• Shock
Reflux Esophagitis
 Overview
• A person with reflux esophagitis has
inflammation of the esophagus, caused by
stomach acid that splashes into the
esophagus.
• Reflux esophagitis usually causes symptoms of
severe heartburn.
• About 30 percent of adults with heartburn
have reflux esophagitis
 Underlying Cause
• The lower esophageal sphincter is a ring of muscle
that surrounds the esophagus, where it empties
into the stomach.
• Normally, the lower esophageal sphincter closes
after food passes into the stomach.
• If the lower esophageal sphincter relaxes, or
remains open, stomach acid splashes into the
esophagus.
• The stomach acid irritates the esophagus,
resulting in reflux esophagitis.
 Risk Factors
• Alcohol
• Eating large meals in the evening
• Foods that irritate the esophagus
• Hiatal hernia
• Infection with Helicobacter pylori bacteria
• Obesity
• Smoking
 Symptoms
• belching
• heartburn
• indigestion
• upper abdominal pain
• vomiting
• difficulty swallowing
• sore throat
• coughing
• hoarse voice
 Warning Signs
Warning Signs
• Blood in the stool:
– Black stool
– Rectal bleeding
– Red stools
• Repeated vomiting
• Vomiting blood
• Vomiting dark material that looks like coffee grounds
• Worsening abdominal pain
• Worsening chest pain
• Difficulty breathing
• Difficulty swallowing
• Fainting
 Evaluation
Physical findings in someone with reflux esophagitis may include:
• Tenderness in the upper abdomen
Tests that may be used to evaluate reflux esophagitis include:
• Esophageal manometry
– Measures the pressure inside the esophagus during resting and swallowing
• Complete blood count
• Serum gastrin levels
• Tests for Helicobacter pylori infection:
– Helicobacter pylori breath test
– Helicobacter pylori blood test
– Helicobacter pylori biopsy test
– Helicobacter pylori stool test
• Stool guaiac test
• Chest x-ray
• Upper GI series
• Upper GI endoscopy
• Esophageal biopsy
 Treatment
• Antacids:
– Should be taken after each meal and at bedtime
– Maalox
– Mylanta
• H2 receptor antagonists:
– Ranitidine
– Cimetidine
– Famotidine
– Nizatidine
• Proton pump inhibitors:
– Omeprazole
– Lansoprazole
– Rabeprazole
– Esomeprazole
• Gastric motility agents:
– Metoclopramide
– Can reduce acid reflux by tightening the lower esophageal sphincter muscle.
• Surgery for reflux esophagitis
– For those who fail to respond to medications
 Diet

General dietary measures to reduce acid reflux

include:
• Eating small, frequent meals
• Waiting at least several hours before reclining
after you eat a meal
• Avoiding spicy foods and other foods that
trigger acid reflux
 Complications
• Barrett's esophagus
• Esophageal cancer
• Esophageal stricture
• Gastrointestinal bleeding
• Iron deficient anemia
• Aspiration pneumonia
 REFERENCES
REFERENCES
• Marschall S Runge, M Andrew Greganti. Netter’s Internal Medicine. Edisi 2. China: Saunders, 2009.
• Bannister, L. H. 1995. Gray’s Anatomy, 38th Edition.
• Churchill Livingstone, New York.
• Cahill, D. R. 1997. Lachman’s Case Studies in Anatomy.
• Oxford Univ. Press, New York.
• Netter, F. H. 1997. Atlas of Human Anatomy. CIBA-Geigy,
• Summit.
• Arthur C Guyton, John E Hall. Buku Ajar Fisiologi Kedokteran. Edisi 11. Jakarta: EGC, 2007.
• Frederic H Martini, Edwin F Bartholomew. Essential of Anatomy & Physiology. Edisi 5. Amerika Serikat:
Pearson, 2010.
• Sulaiman H. Ali, Daldiyono, Akbar H. Nurul, Rani A. Aziz. 1997. Gastroenterologi Hepatologi. Jakarta:
Sagung Seto
• Sudoyo, Aru W. Buku Ajar Ilmu Penyakit Dalam. FKUI. Jakarta : 2006.
• Davey, Patrick. At a Glance Medicine. EMS. 2003.
• Robbins, Kumar. Patologi edisi 4. EGC. Jakarta: 1995.
• http://www.umm.edu
• http://emedicine.medscape.com
• Buku Ajar Parasitologi Kedokteran Edisi ke-4