Pemicu BLOK GIT

GIT PROBLEM 1
ANATOMY
MOUTH
Tortora Anatomy
LIPS
• Lips are mobile, musculofibrous
folds surrounding the mouth.
• Extending from nasolabial sulci
and nares laterally and
superiorly to the mentolabial
sulcus inferiorly.
• They contain the orbicularis oris
superior and inferior labial
mucles, vessels, and nerves.
https://elementsofmorphol
ogy.nih.gov/images/anato Moore Anatomy
my-oral1-large.jpg
LIPS
• Upper lip supplied by
• Superior labial branches of the facial and infraorbital arteries
• Superior labial branches of the infraorbital nerves (N V2)
• Lower lip supplied by
• Inferior labial branches of the facial and mental arteries
• Inferior labial branches of the mental nerves (N V3)
• Lymph
• Upper and lateral parts of the lower lip: submandibular lymph nodes
• Medial parts of the lower lip: submental lymph nodes
Moore Anatomy
GINGIVAE
• Composed of fibrous tissue covered with mucous membrane.
• The gingiva proper is attached to the alveolar processes of the
mandible and maxilla and the necks of the teeth.
• The gingiva proper is normally pink, stippled, and keratinizing.
• The alveolar mucosa (unattached gingiva) is normally shiny red and
non-keratinizing.
Moore Anatomy
TEETH
• The crown projects from the gingiva.
• The root is fixed in the tooth socket by the
periodontium.
• The neck is betweem the crown and the
root.
• The crown covered by enamel.
• The root covered by cement.
• The pulp cavity contains connective tissue,
blood vessels, and nerves.
• The root canal transmits the nerves and
vessels through the apical foramen.
Moore Anatomy
TEETH
• Vasculature of teeth
• Superior and inferior alveolar arteries
• Alveolar veins
• Submandibular lymph nodes
• Innervation of teeth
• Superior and inferior alveolar nerves (dental plexuses)
Moore Anatomy
MOUTH
Tortora Anatomy
ESOPHAGUS
Tortora Anatomy
HISTOLOGY
Junqueira Histology
LIPS
Junqueira Histology
TONGUE
Junqueira Histology
PAPILLA
LINGUALIS
Junqueira Histology
TASTE BUDS
Junqueira Histology
TEETH
Junqueira Histology
TEETH
TEETH
Junqueira Histology
TEETH
Junqueira Histology
ESOPHAGUS
Junqueira Histology
PHYSIOLOGY
BASIC DIGESTIVE PROCESSES
MOTILITY
SECRETION
DIGESTION
ABSORPTION
Sherwood Physiology
REGULATION
AUTONOMOUS SMOOTH MUSCLE FUNCTION
INTRINSIC NERVE PLEXUSES
EXTRINSIC NERVES
GASTROINTESTINAL HORMONES
Sherwood Physiology
PATHWAY CONTROLLING DIGESTIVE SYSTEM
ACTIVITIES
GIT
RECEPTORS chemoreceptors
mechanoreceptors
(pressure receptors)
osmoreceptors
Sherwood Physiology
MOUTH
AMILASE
• begins digestion of carbohydrate in the mouth
• serves as a solvent for molecules that
stimulate the taste buds
• facilitates swallowing by moistening food
particles, thereby holding them together, and
FUNCTIONS by providing lubrication through the presence
OF SALIVA of mucus
• exerts some antibacterial action
SALIVA • aids speech by facilitating movements of the
lips and tongue
• helping keep the mouth and teeth clean
LYSOZYME, • rich in bicarbonate buffers
GLYCOPROTEIN,
LACTOFERRIN
MUCUS
Sherwood Physiology
MOUTH
• SIMPLE SALIVARY REFLEXES

SALIVARY REFLEXES • CONDITIONED SALIVARY
REFLEXES
AUTONOMIC • SYMPATHETIC
INFLUENCE ON • PARASYMPATHETIC
SALIVARY SECRETION
Sherwood Physiology
PHARYNX AND ESOPHAGUS
Oropharyngeal
Stage of Bolus is voluntarily
Swallowing forced by the tongue Pharyngeal muscles Pharyngoesophageal
to the rear of the contract sphincter opens
mouth
Swallowing center Epiglottis is pressed

Bolus pass into the
inhibits respiratory down over closed
esophagus
center glottis
Tongue against the Pharyngoesophageal

Elevation of uvula
hard palate sphincter closes
Sherwood Physiology
PHARYNX AND ESOPHAGUS
Esophageal
Stage of
Swallowing
Swallowing center The gatroesophageal
triggers a primary sphincter again
peristaltic wave contracts
The peristaltic wave

Bolus enters the
sweeps down the
stomach
esophagus
The bolus ahead of it The gastroesophageal

through the sphincter relaxes so
esophagus to the that the bolus can
stomach pass into the stomach
Sherwood Physiology
BIOCHEMISTRY
SWALLOWING DIFFICULTY
ORAL CANDIDIASIS
DEFINITION
• Oral candidiasis is one of the common fungal infection, affecting the
oral mucosa.
• These lesions are caused by the yeast Candida albicans.
• Candida albicans are one of the components of normal oral
microflora and around 30% to 50% people carry this organism.
• Rate of carriage increases with age of the patient.
• Candida albicans are recovered from 60% of dentate patient's mouth
over the age of 60 years.
https://www.ncbi.nlm.nih.gov
/pmc/articles/PMC4211245/
CLASSIFICATION AND CLINICAL PRESENTATIONS
Keratinized primary
Candida-associated
Acute Chronic lesions superinfected
lesions
with Candida
• Pseudomembranous • Erythematous • Angular cheilits • Leukoplakia
• Erythematous • Pseudomembranous • Denture stomatitis • Lichen planus
• Hyperplastic • Median rhomboid • Lupus erythematous
• Nodular glossitis
• Plaque-like
CLINICAL PRESENTATION
Clinical presentation of the primary forms of
oral candidosis. (a) acute pseudomembranous
candidosis; (b) chronic erythematous candidosis;
(c) acute erythematous candidosis; and (d)
chronic hyperplastic candidosis.
LABORATORY DIAGNOSIS
Histological
Specimen Collection Physiological Tests
Identification
• Smear • PAS stain • Ability to assimilate
• Swabs • Grocott-Gomori's and ferment
• Biopsy methenamine sliver individual carbon and
(GMS) nitrogen source
• Imprint culture
• Impression culture • Gridley stains
• Saliva
• Oral rinse
• Paper points
TREATMENT
TREATMENT
MOUTH ULCER (APHTHOUS)
DEFINITION
• Considered as the most common oral mucosal lesion.
• These present as recurrent, multiple, small, or ovoid ulcers, having
yellow floors and are surrounded by erythematous haloes, present
first in childhood or adolescence.
• Aphthous ulcers affect up to 25% of the general population, and 3-
month recurrence rates are as high as 50%.
• It is more common in female.
• Aphthous ulcers increase by increasing age and minor aphthous
ulcers are 80% of suffered patient.
• The cause of aphthous ulcers is unknown
Major Aphthous Ulceration
Minor Aphthous Ulceration
• 10-15% of all
• The most common form (85%)
• Similar in appearance to
• Involve the non-keratinized
minor
mucosa of the oral cavity
• Larger than 10 mm in
• Usually 4-5 mm in diameter
diameter, deeper, often
• Usually concentrated in the
scarred, last for weeks to
anterior part of the mouth
months
Herpetiform Ulceration • Have a predilcetion for lips,
• Can be small (1-2 mm), tongue, soft palate, and the
multiple (5-100), or be present palatal fauces and cause
at the same time pain and dysphagia
• The affected sites are the • Frequently found in patients
lateral margins and ventral infected with HIV
surface of tongue and the
floor of the mouth
• Cause pain; eating and https://www.ncbi.nlm.nih.gov
speaking difficult /pmc/articles/PMC4441245/
PREDISPOSISING FACTORS
• Hormonal changes
• Trauma
• Drugs
• Food hypersensitivity
• Nutritional deficiency states
• Stress
• Tobacco
• Hereditary predisposition
• Immunological features of RAS
• Systemic disorders https://www.ncbi.nlm.nih.gov
DIAGNOSIS AND INVESTIGATION TESTS
TREATMENT
• The aim of the treatment of RAS is to decrease symptoms; reduce
ulcer number and size; increase disease-free periods
• Predisposing factors should be identified and corrected.
• Chlorhexidine mouthwashes may help.
• Symptoms can often be controlled with hydrocortisone hemisuccinate
pellets or triamcinolone acetonide in carboxymethyl cellulose paste
four times daily, but more potent topical corticosteroids may be
required.
• Systemic corticosteroids are best given by a specialist.
• Thalidomide is also effective but is rarely indicated.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4441245/;
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1118165/
GLOSSITIS
ACHALASIA
DEFINITION
• Achalasia is a primary esophageal motor disorder of unknown
etiology characterized manometrically by insufficient relaxation of the
lower esophageal sphincter (LES) and loss of esophageal
peristalsis; radiographically by aperistalsis, esophageal dilation, with
minimal LES opening, “bird-beak” appearance, poor emptying of
barium; and endoscopically by dilated esophagus with retained saliva,
liquid, and undigested food particles in the absence of mucosal
stricturing or tumor.
EPIDEMIOLOGY
• Achalasia occurs equally in men and women with an incidence of 1 in
100,000 individuals annually and prevalence of 10 in 100,000 ((2,3)). There
is no racial predilection. The peak incidence occurs between 30 and 60
years of age. The etiology is autoimmune, viral immune, or
neurodegenerative ((2,3)). The pathologic consequence of the disease is
degeneration of ganglion cells in the myenteric plexus of the esophageal
body and the LES. Although the cause for the degenerative processes is
unclear, the end result of the inflammatory process is loss of inhibitory
neurotransmitters nitrous oxide and vasoactive intestinal peptide and
consequently imbalance between the excitatory and inhibitory neurons.
This results in unopposed cholinergic activity that leads to incomplete
relaxation of the LES and aperistalsis due to loss of latency gradient along
the esophageal body.
TREATMENT
ANGINA LUDWIG
MALIGNANCY
LEUKOPLAKIA
DEFINITION
• Oral leukoplakia is the most frequent potentially malignant disorder
of oral mucosa.
• It defined by World Health Organization as a white patch or plaque
which cannot otherwise be characterized clinically or pathologically as
any other disease.
https://www.ncbi.nlm.nih.gov/p
mc/articles/PMC4268300/
EPIDEMIOLOGY
• Between 16% and 62% of oral squamous carcinomas are associated
with oral leukoplakia.
• Is often found among men, and its prevalence increases with age
advancement.
• It has been estimated that it mainly affects men over 40 years.
ETIOLOGY
• Is considered multifactorial, but smoking is appreciated to be a
frequently involved factor.
• Much more common among smokers than among non-smokers.
• Alcohol is thought to be an independent risk factor, but definitive
data are still lacking.
• As ora leukoplakia can mimic a large variety of lesions, in case a
possible causal factor is suspected such as dental restoration,
mechanical irritation.
CLINICAL PRESENTATIONS
TREATMENT
• The ceasing of the risk activities such as smoking is recommended.
• Oral leukoplakia presenting low malignant risk (no dysplasia or simple
displasia) may be either completely removed or not, and the decision
should consider other factors such as location, size and, in the case of
smokers, the patient's engagement in smoking cessation.
• In the presence of moderate or severe epithelial dysplasia, surgical
treatment is recommended The surgical treatment can use conventional
surgery or laser ablation, electrocauterization, or cryosurgery.
• The medical treatment uses local and systemic chemo-preventive agents
such as vitamin A and retinoid, systemic beta carotene, lycopene (a
carotenoid), ketorolac (as mouthwash), local bleomycin.
ESOPHAGEAL ATRESIA
DEFINITION
• EA with or without TEF remains the most common congenital
anomaly of the esophagus. Although EA with or without TEF is a
relative rare condition, this complex anomaly is still a challenging
problem in pediatric surgery.
https://www.ncbi.nlm.nih.gov/
pmc/articles/PMC3406418/
CLASSIFICATION
(A) Esophageal atresia without
tracheoesophageal fistula;
(B) Proximal tracheoesophageal with distal
Esophageal atresia;
(C) Distal tracheoesophageal with proximal
Esophageal atresia;
(D) Proximal and distal tracheoesophageal;
(E) Tracheoesophageal without
Esophageal atresia or “H”-type
DIAGNOSIS
TREATMENT
REFLUX ESOPHAGITIS
DEFINITION
• Gastroesophageal reflux disease (GERD) is defined as symptoms or
mucosal damage produced by the abnormal reflux of gastric contents
into the esophagus or beyond, into the oral cavity (including larynx)
or lung.
• GERD can be classified as non-erosive reflux disease (NERD) or erosive
reflux disease (ERD) based on the presence or absence of esophageal
mucosal damage seen on endoscopy.
EPIDEMIOLOGY
• GERD (defined by at least weekly heartburn and/or acid regurgitation)
to be as high as 10%-20% in the Western world compared to a
prevalence of less than 5% in Asia.
SYMPTOMS
DIAGNOSIS
TREATMENT
TREATMENT
• Lifestyle and diet modification traditionally have included weight
loss, head of bed elevation, avoidance of nighttime meals, and
elimination of trigger foods such as chocolate, caffeine and
alcohol.
• For nighttime reflux symptoms, patients should elevate the head
of the bed and avoid recumbency 3 hours postprandially.
• The authors found that a shorter dinner-to-bedtime interval was
the most significant factor influencing the recurrence of GERD
and patients who usually slept within 3 hours after eating had
higher recurrence.
PAROTITIS
DENTAL CARIES

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GIT PROBLEM 1

AUTONOMOUS SMOOTH MUSCLE FUNCTION

INTRINSIC NERVE PLEXUSES

• SIMPLE SALIVARY REFLEXES

Swallowing center Epiglottis is pressed

Tongue against the Pharyngoesophageal

The peristaltic wave

The bolus ahead of it The gastroesophageal

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