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GIT - Prob 1
GIT - Prob 1
GIT - Prob 1
Anastasia Wibianto
405130125
LO 1
ANATOMY & HISTOLOGY OF CAVITY &
ESOPHAGUS
Mouth Anatomy
• The oral cavity represents the first part of the
digestive tube: entrance of the alimentary tract and
to initiate the digestive process by salivation and
propulsion of the alimentary bolus into the pharynx.
• The oral cavity is oval shaped and is separated into
the oral vestibule and the oral cavity proper.
– Lips anteriorly, the cheeks laterally, the floor of the mouth
inferiorly, the oropharynx posteriorly, and the palate
superiorly.
Mouth Anatomy
Schematic representation of oral cavity and floor of mouth. A: philtrum; B: upper labial
frenulum; C: opening of Stensen's duct; D: labial commissure; E: hard palate; F: soft palate; G:
intermaxillary commissure; H: base of tongue; I: lateral border of tongue, dorsal view;
J: tip of tongue, dorsal view; K: tip of tongue, ventral view; L: lateral border of tongue, ventral
view; M: ventral surface of tongue; N: lingual frenulum; O: floor of mouth;
P: opening of Wharton's duct; Q: vestibular gingiva; R: vestibule.
Mouth Anatomy
• The oropharynx begins superiorly at the
junction between the hard palate and the soft
palate, and inferiorly behind the circumvallate
papillae of the tongue. The bony base of the
oral cavity is represented by the maxillary and
mandibular bones.
Oral Cavity & Pharynx
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2597750/figure/F1/
Development
Sagital section of the head and neck in (A) infant and (B) adult human.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2597750/
Esophagus Anatomy
• A long muscular tube that connects the pharynx to
the stomach. (adult: 25 cm; at birth: 8-10 cm;
adolescent: 19 cm)
• Upper border:
– Adult: lower border of the cricoid cartilage (vert C6)
– Newborn: vert C4-C5
• Lower border
– Adult: cardiac orifice of the stomach (vert T11)
– Newborn: vert T9
http://emedicine.medscape.com/article/1948973-overview
Esophagus Anatomy
• The esophagus has been subdivided into 3 portions,
as follows:
– The cervical portion extends from the cricopharyngeus to
the suprasternal notch
– The thoracic portion extends from the suprasternal notch
to the diaphragm
– The abdominal portion extends from the diaphragm to the
cardiac portion of the stomach.
http://emedicine.medscape.com/article/1948973-overview
Esophagus Anatomy
• 3 constrictions in its vertical course:
– First constriction: 15 cm from the upper incisor teeth,
where the esophagus commences at the cricopharyngeal
sphincter; this is the narrowest portion of the esophagus
and approximately corresponds to the 6th cervical vert.
– Second constriction: 23 cm from the upper incisor teeth,
where it is crossed by the aortic arch and left main
bronchus
– Third constriction: 40 cm from the upper incisor teeth,
where it pierces the diaphragm; the lower esophageal
sphincter (LES) is situated at this level
http://emedicine.medscape.com/article/1948973-overview
Esophagus Anatomy
http://img.webmd.com/dtmcms/live/webmd/consumer_assets/site_images/articles/image_article_collections/anatomy_pages/Esophagus.jpg
Esophagus Blood Supply
• The cervical portion is supplied by the inferior
thyroid artery
• The thoracic portion is supplied by bronchial and
esophageal branches of the thoracic aorta
• The abdominal portion is supplied by ascending
branches of the left phrenic and left gastric arteries.
http://emedicine.medscape.com/article/1948973-overview
Esophagus Nerve Supply
• Recurrent laryngeal branches of the vagus nerve
supply the striated muscle in the upper third of the
esophagus, and cell bodies for these fibers are
situated in the rostral part of the nucleus ambiguus.
• Motor supply to the nonstriated muscle is
parasympathetic. These fibers reach the esophagus
through the vagus and its recurrent laryngeal
branches. They synapse in the esophagus wall in the
ganglia of submucosal plexus (Meissner) and
myenteric plexus (Auerbach).
http://emedicine.medscape.com/article/1948973-overview
HISTOLOGY
Histology of Lips
http://classconnection.s3.amazonaws.com/340/flashcards/550340/jpg/lip1306729121652.jpg
Tongue: Filiform Papillae
http://www.siumed.edu/~dking2/erg/images/GI053b.jpg
Tongue: Fungiform Papillae
http://www.vetmed.vt.edu/education/curriculum/vm8054/Labs/Lab17/IMAGES/FUNGIFORM%20COMPOSITE.jpg
Tongue: Circumvallate Papillae
http://www.e-histology.or.kr/data/ColorAtlas/0610/610_18_0.jpg
Esopaghus
http://legacy.owensboro.kctcs.edu/gcaplan/anat2/histology/esophagus3.jpg
LO 2
PHYSIOLOGY OF CAVITY & ESOPHAGUS
Physiology of Swallowing
• Swallowing apparatus consists of the pharynx,
cricopharyngeus (upper esophageal
sphincter), body of the esophagus, and lower
esophageal sphincter.
4 Main Stages
1. Oral Preparatory Stage, in which the food is
chewed (masticated), mixed with saliva, and
formed into a cohesive ball (bolus)
2. Oral Stage, in which the food is moved back
through the mouth with a front-to-back
squeezing action, performed primarily by the
tongue
http://calder.med.miami.edu/pointis/tbifam/swal1.html
4 Main Stages
3. Pharyngeal Stage, which begins with the
pharyngeal swallowing response:
– The food enters the upper throat area (above larynx)
– The soft palate elevates
– The epiglottis closes off the trachea, as the tongue moves
backwards and the pharyngeal wall moves forward
– These actions help force the food downward to the
esophagus
http://calder.med.miami.edu/pointis/tbifam/swal1.html
4 Main Stages
4. Esophageal Stage, in which the food bolus
enters the esophagus (the tube that
transports food directly to the stomach). The
bolus is moved to the stomach by a
squeezing action of the throat muscles
(peristaltic).
http://calder.med.miami.edu/pointis/tbifam/swal1.html
LO 3
BIOCHEMISTRY OF CAVITY &
ESOPHAGUS
Digestion
• A natural process of breaking down food into
absorbable forms to our body
• Regulated by mechanical and chemical stimuli,
extrinsic control by the central nervous
system, and local intrinsic control (plexus)
• Occurs with the presence of hydrolase enzyme
along the digestive tract
Mouth
• Mechanical and chemical digestive process by
teeth, saliva, and enzymes:
– α-amylase: secreted by salivary gland, needs Ca2+
to break carbohydrate to mono-/disaccahrides
– lipase: secreted by serous Von Ebner gland to
break short or medium chain triglycerides to 1,2-
diacylglycerol + fatty acid
– mucin: glycosylated protein secreted by
epithelium cells of salivary gland to lubricate food
Mouth
• Mechanical and chemical digestive process by
teeth, saliva, and enzymes:
– Lysozyme: as non-specific antiseptic by
hydrolyzing bacterial cell wall
– IgA: secreted by plasma cells in lamina propria and
is the only antibody which is made in digestive
tract
– Haptocorrin (R-factor): coded by TCN1 gene, a
glycoprotein to protect vit B12 from HCl
Esophagus
• Mechanical process (peristaltic movements)
which started after swallowing process in
oropharynx and ended in the stomach or
gaster
LO 4
SWALLOWING DISORDERS (DYSPHAGIA
& ODYNOPHAGIA)
Swallowing Disorders
• Dysphagia: sense of difficulty with the passage of
food from the pharynx to the stomach.
– Can be divided into oropharyngeal or esophageal
dysphagia
– Further subdivisions: mechanical causes or neuromuscular
causes.
• Globus: a subjective feeling of fullness in the throat
not related to eating.
• Odynophagia: presence of pain on swallowing that
may or may not accompany dysphagia.
http://www.ualberta.ca/~loewen/Medicine/GIM%20Residents%20Core%20Reading/DYSPHAGIA,%20G
ERD,%20BARRETTS%20ESOPHAGUS/dysphagia,%20heartburn%20Slezinger.pdf
Odynophagia
• This symptom may range from a dull retrosternal ache on
swallowing to a stabbing pain with radiation to the back so
severe that patients cannot eat or even swallow their own
saliva
• Usually reflects a severe inflammatory process that involves
the esophageal mucosa or, in rare instances, the esophageal
muscle.
• Dysphagia also may be present, but pain is the dominant
complaint
• Infrequent complaint with GERD patients; when present
usually is associated with a severe ulcerative esophagitis
http://www.ualberta.ca/~loewen/Medicine/GIM%20Residents%20Core%20Reading/DYSPHAGIA,%20G
ERD,%20BARRETTS%20ESOPHAGUS/dysphagia,%20heartburn%20Slezinger.pdf
Odynophagia
http://www.ualberta.ca/~loewen/Medicine/GIM%20Residents%20Core%20Reading/DYSPHAGIA,%20G
ERD,%20BARRETTS%20ESOPHAGUS/dysphagia,%20heartburn%20Slezinger.pdf
Mechanisms of Dysphagia
• Failed peristaltic contractions due to: nerves disorder, low-
amplitude peristaltic activity that is insufficient for clearing
the esophagus in elderly, motility disorders
• Mechanical narrowing of esophageal lumen; Symptoms also
vary with the degree of luminal obstruction, associated
esophagitis, and type of food ingested
• GERD: difficulty swallowing in this situation usually results
from intermittent acid-induced motility disturbances
sometimes associated with mild to moderate esophageal
inflammation
• Abnormal sensory perception within the esophagus
http://www.ualberta.ca/~loewen/Medicine/GIM%20Residents%20Core%20Reading/DYSPHAGIA,%20G
ERD,%20BARRETTS%20ESOPHAGUS/dysphagia,%20heartburn%20Slezinger.pdf
Diagnostic Alogarithm
http://www.ualberta.ca/~loewen/Medicine/GIM%20Residents%20Core%20Reading/DYSPHAGIA,%20G
ERD,%20BARRETTS%20ESOPHAGUS/dysphagia,%20heartburn%20Slezinger.pdf
Diagnosis: Clinical Presentation
• History:
– Onset
• Progressive difficulty in swallowing solid foods, whereas liquids pass with
ease, indicates mechanical obstructive cause such as malignancy or
benign stricture.
• Dysphagia involving solids and liquids is consistent with esophageal motor
dysfunction, such as achalasia or diffuse esophageal spasm, but can be
seen in advanced obstruction.
• Intermittent dysphagia for solids, usually meat or bread, can result from
mucosal abnormality of the lower esophagus known as Schatzki ring.
• Hoarseness preceding dysphagia usually is of laryngeal origin; however,
when it follows, the onset of dysphagia involvement of the recurrent
laryngeal nerve by cancer should be considered.
http://umm.edu/health/medical/ency/articles/mouth-ulcers
Mouth ulcers
• Signs and tests: Based on its appearance and
location. Blood tests or a biopsy of the ulcer to
confirm the cause.
• Treatment – to relieve symptoms & treat the cause:
– Gentle, thorough oral hygiene.
– Topical (rubbed on) antihistamines, antacids, or
corticosteroids to sooth the ulcers.
– Avoid hot or spicy foods, which often increase the pain of
mouth ulcers.
http://umm.edu/health/medical/ency/articles/mouth-ulcers
Mouth ulcers
• Complications
– Cellulitis of the mouth, from secondary bacterial
infection of ulcers
– Dental infections (tooth abscesses)
– Oral cancer
– Spread of contagious disorders to other people
http://umm.edu/health/medical/ency/articles/mouth-ulcers
CANDIDIASIS
Oral Candidiasis
• Also known as “thrush" or oropharyngeal
candidiasis
• A fungal infection that occurs when there is
overgrowth of a yeast called Candida.
• Can also grow in esophagus and develop
esophageal candidiasis
http://www.cdc.gov/fungal/diseases/candidiasis/thrush/definition.html
Symptoms of Oral Candidiasis
• White patches or plaques on the tongue and
other oral mucous membranes (most
common)
• Redness or soreness in the affected areas
• Difficulty swallowing
• Cracking at the corners of the mouth (angular
cheilitis)
http://www.cdc.gov/fungal/diseases/candidiasis/thrush/definition.html
http://www.cdc.gov/fungal/diseases/candidiasis/thrush/definition.html
People at Risk
• Age: <1 month, elderly
• Groups of people with weakened immune
systems: HIV/AIDS, Cancer treatments, Organ
transplantation
• Diabetes
• Corticosteroid use
• Dentures
• Broad-spectrum antibiotic use
http://www.cdc.gov/fungal/diseases/candidiasis/thrush/definition.html
Treatment
• Topical: clotrimazole troches and nystatin suspension
• Systemic: 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.
http://www.cdc.gov/fungal/diseases/candidiasis/thrush/definition.html
LEUKOPLAKIA
Leukoplakia
• White patch or plaque that cannot be rubbed off, cannot be
characterized clinically or histologically as any other condition,
and is not associated with any physical or chemical causative
agent except tobacco.
http://emedicine.medscape.com/article/853864-overview
Etiology of Leukoplakia
• Most cases = idiopathic.
• In other cases, may depend on extrinsic local
factors and/or intrinsic predisposing factors.
• Factors most frequently blamed: tobacco use,
alcohol consumption, chronic irritation,
candidiasis, vitamin deficiency, endocrine
disturbances, and possibly a virus.
http://emedicine.medscape.com/article/853864-overview
Etiology of Leukoplakia
• Smoking: the combustion end-products brought
about by burning tobacco and heat (eg, tobacco
tars and resins) are irritating substances capable
of producing leukoplakic alterations of the oral
mucosa.
– Chronic exposure benign keratosis in the hard
palate, called stomatitis nicotina pale mucosa due
to slight increase in keratinization the palatal tissue
is keratinized more heavily nodules appear
(hyperplasia of the underlying glands, retention of
saliva, and fibrosis)
http://emedicine.medscape.com/article/853864-overview
Etiology of Leukoplakia
• Alcohol: May irritate the mucosa.
• Dental problems: Malocclusion; chronic cheek
biting; ill-fitting dentures; and sharp, broken-
down teeth that constantly irritate the
mucosa.
• Syphilitic glossitis have a higher prevalence.
• Candida albicans: common oral fungus.
• Deficiency of vitamins A and B: inciting factor.
http://emedicine.medscape.com/article/853864-overview
Epidemiology of Leukoplakia
• International Frequency: <1%
• Mortality/Morbidity: potentially malignant,
transformation rate in various studies and
locations ranges from 0.6 to 20%.
• Sex: male-to-female ratio of 2:1.
• Age: fifth to seventh decade of life, ± 80% of
patients >40 yo.
http://emedicine.medscape.com/article/853864-overview
3 Stages of Leukoplakia
• Earliest lesion: nonpalpable, faintly translucent,
white discoloration.
• Next: localized or diffuse, opaque white, fine
granular, and slightly elevated plaques with an
irregular outline develop.
• Late: lesions progress to thickened, white lesions,
showing induration, fissuring, and ulcer formation.
http://emedicine.medscape.com/article/853864-overview
2 Main Groups of Leukoplakia
• Most common: uniformly white plaques (homogenous)
prevalent in the buccal mucosa, which usually have low
premalignant potential.
• Far more serious: speckled or verrucous leukoplakia, stronger
malignant potential, consists of white flecks or fine nodules
on an atrophic erythematous base. A combination of or a
transition between leukoplakia and erythroplasia, which is flat
or depressed below the level of the surrounding mucosal red
patch, is uncommon in the mouth, and carries the highest risk
of malignant transformation.
http://emedicine.medscape.com/article/853864-overview
Diagnosis of Leukoplakia
• Biopsy:
– The plaque may show hyperorthokeratosis
(granular cell layer, nuclei lost in the keratin layer)
or hyperparakeratosis (No granular cell layer,
nuclei retained in the keratin layer).
– Acanthosis, which refers to the abnormal
thickening of the prickle cell layer (spinous layer),
may also be observed.
http://emedicine.medscape.com/article/853864-overview
Treatment of Leukoplakia
• Medical care: surgical exicision, cryotherapy ablation and
carbon dioxide laser ablation
• Diet: discontinue the use of alcohol
• Medication:
– High-dose induction followed by low-dose systemic isotretinoin
stabilization of the majority of lesions, preventing malignant changes,
no toxicity.
– Beta-carotene produced sustained remissions of leukoplakia, with a
durable response for at least 1 year.
– Both of these drugs have been used in experimental trials and must be
investigated in more depth.
http://emedicine.medscape.com/article/853864-overview
LUDWIG’S ANGINA
Definition
• Ludwig's angina is an infection of the floor of the mouth
under the tongue. It is due to bacteria.
Alternative name:
• Submandibular space infection
• Sublingual space infection
http://emedicine.medscape.com/article/882461-overview
Etiology of Parotitis
• Varying depending on whether the condition is
chronic or acute:
– Bacterial infection due to staphylococcus, streptococcus, or
haemophilus
– Viral infection due to mumps or AIDS
– A blockage may block saliva flow and lead to a bacterial
infection. Causes include:
• Salivary stone in the parotid gland
• Mucus plug in a salivary duct
• Tumor—usually benign
– Sjogren’s syndrome—an autoimmune disease
http://emedicine.medscape.com/article/882461-overview
Etiology of Parotitis
• Varying depending on whether the condition is
chronic or acute:
– Sarcoidosis
– Malnutrition
– Radiation treatment of head and neck cancer can lead to
parotid gland inflammation
– Other conditions can cause the parotid glands to become
enlarged, but not infected, including:
• Diabetes
• Alcoholism
• Bulimia
Risk Factors of Parotitis
• Factors that increase your chances of getting
parotitis include:
– Dehydration • Malnutrition
• Alcoholism
– Recent surgery
• Bulimia
– Increased age
– Depression
– Medical conditions, such as:
– Use of certain
• HIV-positive or AIDS
medications
• Sjogren’s syndrome
• Diabetes – Poor oral hygiene
http://emedicine.medscape.com/article/882461-overview
Symptoms of Parotitis
• Infectious parotitis
– Acute bacterial parotitis: The patient reports
progressive painful swelling of the gland and
fever; chewing aggravates the pain.
– Acute viral parotitis (mumps): Pain and swelling
of the gland last 5-9 days. Moderate malaise,
anorexia, and fever occur. Bilateral involvement is
present in most instances.
http://emedicine.medscape.com/article/882461-overview
Symptoms of Parotitis
• Infectious parotitis
– HIV parotitis: Nonpainful swelling of the gland
occurs; otherwise, patient is asymptomatic.
– Parotitis in tuberculosis: Chronic nontender
swelling of one parotid gland occurs, or a lump is
noted within the gland. Symptoms of tuberculosis
are found in some cases.
http://emedicine.medscape.com/article/882461-overview
Symptoms of Parotitis
• Chronic punctate (autoimmune) parotitis
– Sjögren syndrome: Recurrent or chronic swelling
of one or both parotid glands with no apparent
cause is noted, frequently associated with
autoimmune disease, discomfort is modest in
most cases and is related to dry mouth and eyes.
http://emedicine.medscape.com/article/882461-overview
Symptoms of Parotitis
• Diseases of uncertain etiology Recurrent
parotitis of childhood:
– Repetitious episodes of unilateral or bilateral
mumps like episodes in a young child are
indicative.
– Sarcoidosis: Chronic nontender swelling of parotid
gland occurs.
http://emedicine.medscape.com/article/882461-overview
Symptoms of Parotitis
• Diseases of uncertain etiology Recurrent
parotitis of childhood:
– Chronic nonspecific parotitis: Most commonly,
patients experience episodes of painful parotid
inflammation that last for hours to weeks with
relative asymptomatic periods between. Pain
varies from mild to incapacitating.
http://emedicine.medscape.com/article/882461-overview
Created by Samuel Freire da Silva, M.D. in homage to The Master And Professor
Delso Bringel Calheiros. Image obtained from Dermatology Atlas
Treatment of Parotitis
• Sialogogues, local heat, gentle massage of the
gland from posterior to anterior, and
hydration provide variable symptomatic relief.
• Culture of pus and sensitivity studies guide
antibiotic selection.
• Treatment of the primary disease (eg, HIV,
rheumatoid arthritis) is all that is required.
http://emedicine.medscape.com/article/882461-overview
Treatment of Parotitis
• Intermittent irrigation of the ductal system
with saline, steroid solution, and/or an
antibiotic to treat the infection and
mechanically remove inspissated mucous or
pus from the ducts.
http://emedicine.medscape.com/article/882461-overview
GLOSSITIS
Definition
• Glossitis is a problem in which the tongue is swollen and
changes color, often making the surface of the tongue appear
smooth.
• Geographic tongue is a type of glossitis.
• The health care provider may ask questions about your health
history and lifestyle to help discover the cause of tongue
inflammation.
• It may need blood tests to rule out other medical problems.
• Crowns
Crowns or "caps" are used if tooth decay is extensive and there is limited
tooth structure, which may cause weakened teeth. A crown is fitted over the
remainder of the tooth.
• Root canals
A root canal is recommended if the nerve in a tooth dies from decay or injury.
The center of the tooth, including the nerve and blood vessel tissue (pulp), is
removed along with decayed portions of the tooth. The roots are filled with a
sealing material.
http://reference.medscape.com/article/169974-overview
Pathophysiology of Achalasia
• LES pressure and relaxation are regulated by
excitatory (eg, acetylcholine, substance P) and
inhibitory (eg, nitric oxide, vasoactive intestinal
peptide) neurotransmitters.
• Persons with achalasia lack nonadrenergic,
noncholinergic, inhibitory ganglion cells, causing an
imbalance in excitatory and inhibitory
neurotransmission. The result is a hypertensive
nonrelaxed esophageal sphincter.
http://reference.medscape.com/article/169974-overview
Diagnosis of Achalasia
• Physical examination & laboratory
studies are non-contributory
• Imaging studies:
– Barium swallow: The esophagus appears
dilated, and contrast material passes
slowly into the stomach as the LES opens
intermittently. The distal esophagus is
narrowed and has been described as
resembling a bird's beak.
http://reference.medscape.com/article/169974-overview
https://globalgenes.org/raredaily/september-achalasia-awareness-month-
will-spread-awareness/
Diagnosis of Achalasia
• Other tests:
– Esophageal manometry is the criterion standard in helping
to diagnose the classic findings of achalasia. Findings
include:
• Incomplete relaxation of the LES in response to swallowing
• High resting LES pressure
• Absent esophageal peristalsis
– Prolonged esophageal pH monitoring is important for the
following reasons: To rule out (GERD) and to determine if
abnormal reflux is being caused by treatment
http://reference.medscape.com/article/169974-overview
Treatment of Achalasia
• Goal: relieve symptoms by eliminating the outflow
resistance caused by the hypertensive and
nonrelaxing LES food bolus can travel through the
aperistaltic body of the esophagus by gravity.
• Calcium channel blockers (nifedipine) and nitrates
(isosorbid dinitrate) are used to decrease LES
pressure, used primarily in elderly patients who have
contraindications to either pneumatic dilatation or
surgery.
http://reference.medscape.com/article/169974-overview
Treatment of Achalasia
• Endoscopic treatment includes an intrasphincteric
injection of botulinum toxin to block the release of
acetylcholine at the level of the LES.
• Pneumatic dilatation via fluoroscopic and
endoscopic visualization.
• Laparoscopic Heller myotomy is considered by many
to be the appropriate primary treatment of patients
with achalasia
http://reference.medscape.com/article/169974-overview
ESOPHAGEAL ATRESIA
Definition
• Esophageal atresia is a disorder of the digestive system in
which the esophagus does not develop properly. The
esophagus is the tube that normally carries food from the
mouth to the stomach.