Professional Documents
Culture Documents
Mescher AL. Junqueira’s basic histology text & atlas.13th Edition. US: McGraw-Hill Education; 2013.
General Structure of The Digestive
Tract
Mescher AL. Junqueira’s basic histology text & atlas.13th Edition. US: McGraw-Hill Education; 2013.
Oral cavity: lip
Mescher AL. Junqueira’s basic histology text & atlas.13th Edition. US: McGraw-Hill Education; 2013.
Mescher AL. Junqueira’s basic histology text & atlas.13th Edition. US: McGraw-Hill Education; 2013.
Tongue, Lingual Pappilae, Taste Buds
Mescher AL. Junqueira’s basic histology text & atlas.13th Edition. US: McGraw-Hill Education; 2013.
Mescher AL. Junqueira’s basic histology text & atlas.13th Edition. US: McGraw-Hill Education; 2013.
Lingual Pappilae
Mescher AL. Junqueira’s basic histology text & atlas.13th Edition. US: McGraw-Hill Education; 2013.
Mescher AL. Junqueira’s basic histology text & atlas.13th Edition. US: McGraw-Hill Education; 2013.
Mescher AL. Junqueira’s basic histology text & atlas.13th Edition. US: McGraw-Hill Education; 2013.
Teeth
Mescher AL. Junqueira’s basic histology text & atlas.13th Edition. US: McGraw-Hill Education; 2013.
Mescher AL. Junqueira’s basic histology text & atlas.13th Edition. US: McGraw-Hill Education; 2013.
Esophagus
Mescher AL. Junqueira’s basic histology text & atlas.13th Edition. US: McGraw-Hill Education; 2013.
Mescher AL. Junqueira’s basic histology text & atlas.13th Edition. US: McGraw-Hill Education; 2013.
Esophagus
Mescher AL. Junqueira’s basic histology text & atlas.13th Edition. US: McGraw-Hill Education; 2013.
Mescher AL. Junqueira’s basic histology text & atlas.13th Edition. US: McGraw-Hill Education; 2013.
Organ Associated with The Digestive
Tract : Salivary Gland
Mescher AL. Junqueira’s basic histology text & atlas.13th Edition. US: McGraw-Hill Education; 2013.
Mescher AL. Junqueira’s basic histology text & atlas.13th Edition. US: McGraw-Hill Education; 2013.
Learning Objective 3
Physiology of Upper GIT
Sherwood L. Human physiology: from cell to systems. 9th Ed.
Control of Saliva Secretion
Tortora GJ, Derrickson B. Principles of anatomy and physiology. 12th Edition. US: John Willey & Sons; 2009.
Digestive Enzymes
Tortora GJ, Derrickson B. Principles of anatomy and physiology. 12th Edition. US: John Willey & Sons; 2009.
Learning Objective 5
Dysphagia & Odynophagia
Dysphagia
Difficulty swallowing
It takes more time and effort to move food or liquid from
mouth to stomach.
Dysphagia can be secondary to defects in any of the 3
phases of swallowing, which are as follows :
Oral phase: Which involves the oral preparatory phase and the
oral transit phase
Pharyngeal phase
Esophageal phase
http://emedicine.medscape.com/article/2212409-overview#a3
Oral Phase
The oral phase of swallowing is divided into the following
2 parts:
Oral preparatory phase: The processing of the bolus to render
it swallowable
Oral propulsive (or transit) phase: The propelling of food from
the oral cavity into the oropharynx
http://emedicine.medscape.com/article/2212409-overview#a4
Oral Preparatory Phase
The process begins with contractions of the tongue and
striated muscles of mastication.
The muscles work in a coordinated fashion to mix the
food bolus with saliva, with the taste, temperature, touch,
and proprioception senses required to form a bolus of
the right size and consistency.
http://emedicine.medscape.com/article/2212409-overview#a4
Oral Propulsive (or Transit) Phase
The swallowing process involves manipulation of the bolus
formed in the preparatory stage in the central portion of the
tongue.
The bolus the pharynx posteriorly with a sequential
anterior-to-posterior tongue elevation in order to trigger the
swallowing reflex as the bolus Enters the pharyngeal phase.
http://emedicine.medscape.com/article/2212409-overview#a4
Pharyngeal Phase
The pharyngeal phase is of particular importance, Because
without intact laryngeal protective mechanisms, aspiration (the
passage of food or liquid through the vocal folds) is most likely
to occur during this phase.
This phase involves a rapid sequence of overlapping events. The
soft palate rises, the hyoid bone and larynx move upward and
forward, the vocal folds move to the midline, the epiglottis
folds backward to protect the airway, and the tongue pushes
backward and downward into the pharynx to propel the bolus
downward. The tongue is assisted by the pharyngeal walls, the
which move inward with a progressive wave of contraction
from top to bottom.
http://emedicine.medscape.com/article/2212409-overview#a4
Pharyngeal Phase
The upper esophageal sphincter relaxes during the
pharyngeal phase of swallowing and is pulled open by the
forward movement of the hyoid bone and larynx. This
sphincter closes after passage of the food, and the
pharyngeal structures then return to the reference
position.
http://emedicine.medscape.com/article/2212409-overview#a4
Esophageal phase
The bolus is propelled downward by a peristaltic
movement. The lower esophageal sphincter relaxes at initiation
of the swallow, and this relaxation persists until the food bolus
has been propelled into the stomach.
The lower sphincter is not pulled open by extrinsic
musculature. Rather, it closes after the bolus Enters the
stomach, thereby Preventing gastroesophageal reflux
The medulla controls this involuntary swallowing reflex,
voluntary Although swallowing may be initiated by the cerebral
cortex.
http://emedicine.medscape.com/article/2212409-overview#a4
Etiology of Dysphagia
Central nervous system disorders
Muscular disorders
Neuropathic disorders
Endocrine disorders
Pharmacologic causes
Motility disorders
Esophagitis
Structural disorders
http://emedicine.medscape.com/article/2212409-overview#a6
Epidemiology
Stroke is the leading cause of neurologic dysphagia, with
the condition occurring in Approximately 51-73% of
patients with stroke.
According to the US National Medicare database, the
incidence of poststroke dysphagia is higher in Asians and
other minority groups than in whites, suggesting racial
disparities in the development of dysphagia after stroke.
The prevalence of dysphagia increases with age, and
dysphagia is a major health care problem in elderly
patients.
http://emedicine.medscape.com/article/2212409-overview#a7
Pathophysiology
A lesion in the cerebral cortex or the brainstem can
cause swallowing disorders as a result of the following:
Decrease in range of motion (ROM) of muscles of mastication
and bolus propulsion, especially those responsible for buccal,
labial, and lingual strength and the cricopharyngeus
Decreased sensation
Delayed or absent pharyngeal swallowing and reductions in
pharyngeal peristalsis
Delayed or absent laryngeal adduction and elevation
http://emedicine.medscape.com/article/2212409-overview#a5
Oral Phase Disorders
Logemann's Manual for the Videofluorographic Study of
Swallowing cites the following oral-phase swallowing
symptoms and disorders:
Inability to hold food in the mouth anteriorly due to reduced
lip closure
Inability to form a bolus or residue on the floor of the mouth
due to reduced range of tongue motion or coordination
Inability to hold a bolus due to reduced tongue shaping and
coordination
Inability to align teeth due to reduced mandibular movement
Entry of food material into the anterior sulcus or the presence
of residue in the anterior sulcus due to reduced labial tension
or tone
http://emedicine.medscape.com/article/2212409-overview#a5
Entry of food material into the lateral sulcus or the presence
of residue in the lateral sulcus due to reduced buccal tension
or tone
Abnormal hold position or dropping of material to the floor of
the mouth due to tongue thrust or reduced tongue control
Delayed oral onset of swallow due to apraxia of swallow or
reduced oral sensation
Searching motion or inability to organize tongue movements
due to apraxia of swallow
Forward tongue movement to start the swallow due to tongue
thrust
Residue of food on the tongue due to reduced tongue range of
movement or strength
http://emedicine.medscape.com/article/2212409-overview#a5
Disturbed lingual contraction (peristalsis) due to lingual
discoordination
Incomplete tongue-to-palate contact due to reduced tongue
elevation
Inability to mash material due to reduced tongue elevation
Adherence of food to hard palate due to reduced tongue elevation
or reduced lingual strength
Reduced anterior-posterior lingual action due to reduced lingual
coordination
Repetitive lingual rolling in Parkinson disease
Uncontrolled bolus or premature loss of liquid or pudding
consistency into the pharynx due to reduced tongue control or
linguavelar seal
Piecemeal deglutition
Delayed oral transit time
http://emedicine.medscape.com/article/2212409-overview#a5
Pharyngeal Phase Disorders
If pharyngeal clearance is severely impaired, a patient may
be unable to ingest sufficient amounts of food and drink
to sustain life. In people without dysphasia, small amounts
of food commonly are retained in the valleculae or
pyriform sinus after swallowing. If there is weakness in or
a lack of coordination of the pharyngeal muscles or if
there is a poor opening of the upper esophageal
sphincter, patients may retain excessive amounts of food
in the pharynx and experience overflow aspiration after
swallowing.
Dysfunction or abnormalities of the soft palate and
superior pharynx (eg, cleft palate) can lead to
nasopharyngeal reflux following uvulectomy
http://emedicine.medscape.com/article/2212409-overview#a5
Pharyngeal Phase Disorders
Logemann's Manual for the Videofluorographic Study of
Swallowing cites the following pharyngeal-phase
swallowing symptoms and disorders :
Delayed pharyngeal swallow
Nasal penetration during swallow due to reduced
velopharyngeal closure
Pseudoepiglottis (after total laryngectomy): Fold of mucosa at
the base of the tongue
Cervical osteophytes
Coating of pharyngeal walls after the swallow due to bilateral
reduction of pharyngeal contraction
http://emedicine.medscape.com/article/2212409-overview#a5
Vallecular residue due to reduced posterior movement of the
tongue base
Coating in a depression on the pharyngeal wall due to scar
tissue or pharyngeal pouch
Residue at top of airway due to reduced laryngeal elevation
Laryngeal penetration and aspiration due to reduced closure of
the airway entrance (arytenoid to base of epiglottis)
Aspiration during swallow due to reduced laryngeal closure
Stasis of residue in pyriform sinuses due to reduced anterior
laryngeal pressure
Delayed pharyngeal transit time
http://emedicine.medscape.com/article/2212409-overview#a5
Esophageal Phase Disorders
Impaired esophageal function can result in retention of food
and liquid in the esophagus after swallowing. This retention
may result from a mechanical obstruction, a motility disorder,
or an impairment of the opening of the lower esophageal
sphincter.
Achalasia can lead to reduced gastroesophageal junction
relaxation or absent esophageal peristalsis
Other defects in the wall of the esophagus or in the external
structures (eg, in the hilar lymph nodes) can lead to
dysfunction in the propulsion of the bolus from the esophagus
to the stomach (eg, esophageal webs, rings, strictures;
intraluminal obstruction from solids) and result in weak
esophagopharyngeal peristalsis due to scleroderma or other
conditions
http://emedicine.medscape.com/article/2212409-overview#a5
Esophageal Phase Disorders
Logemann's Manual for the Videofluorographic Study of
Swallowing cites the following swallowing symptoms and
disorders of the esophageal phase :
Esophageal-to-pharyngeal backflow due to esophageal
abnormality
Tracheoesophageal fistula
Zenker diverticulum
Reflux
http://emedicine.medscape.com/article/2212409-overview#a5
Longo DL, Fauci AS. Harrison’s gastroenterology & hepatology. 2010
Odynophagia
Odynophagia is pain either caused by or exacerbated by
swallowing
Odynophagia is more common with pill or infectious
esophagitis than with reflux esophagitis and should
prompt a search for these entities
When odynophagia does occur in GERD, it is likely
related to an esophageal ulcer or deep erosion
Learning Objective 6
Upper GIT Disorders
Mouth Ulcers
Mouth Ulcers
Mouth ulcers are sores or open lesions in the mouth.
Mouth ulcers are caused by many disorders. These
include:
Canker sores
Gingivostomatitis
Herpes simplex (fever blister)
Leukoplakia
Oral cancer
Oral lichen planus
Oral thrush
A skin sore caused by histoplasmosis may also appear as a
mouth ulcer.
https://medlineplus.gov/ency/article/001448.htm
Symptomps Treatment
https://medlineplus.gov/ency/article/001448.htm
Prognosis Complication
https://medlineplus.gov/ency/article/001448.htm
Prevention
Brush teeth at least twice a day and floss once a day.
Get regular dental cleanings and checkups.
https://medlineplus.gov/ency/article/001448.htm
Candidiasis
Candidiasis
a fungal infection caused by yeasts that belong to the
genus Candida.
There are over 20 species of Candida yeasts that can
cause infection in humans, the most common of which
is Candida albicans.
http://emedicine.medscape.com/article/213853-overview#a8
Pathophysiology
Candida species contain their own set of well-recognized
but not well-characterized virulence factors that may
contribute to their ability to cause infection.
The main virulence factors include the following:
Surface molecules that permit adherence of the organism to
other structures (eg, human cells, extracellular matrix,
prosthetic devices)
Acid proteases and phospholipases that involve penetration
and damage of cell envelopes
Ability to convert to a hyphal form (phenotypic switching)
http://emedicine.medscape.com/article/213853-overview#showall
Host defense mechanisms against Candida infection and their
associated defects that allow infection are as follows:
Intact mucocutaneous barriers - Wounds, intravenous catheters,
burns, ulcerations
Phagocytic cells -Granulocytopenia
Polymorphonuclear leukocytes - Chronic granulomatous disease
Monocytic cells -Myeloperoxidase deficiency
Complement -Hypocomplementemia
Immunoglobulins -Hypogammaglobulinemia
Cell-mediated immunity - Chronic mucocutaneous candidiasis,
diabetes mellitus, cyclosporin A, corticosteroids, HIV infection
Mucocutaneous protective bacterial flora - Broad-spectrum
antibiotics
http://emedicine.medscape.com/article/213853-overview#showall
Risk Factors
Granulocytopenia Recent chemotherapy or
Bone marrow radiation therapy
transplantation Corticosteroids
Solid organ Broad-spectrum
transplantation (liver, antibiotics
kidney) Burns
Parenteral Prolonged hospitalization
hyperalimentation Severe trauma
Hematologic malignancies Recent bacterial infection
Foley catheters Recent surgery
Solid neoplasms
http://emedicine.medscape.com/article/213853-overview#showall
Risk Factors
Gastrointestinal tract
surgery
Central intravascular
access devices
Premature birth
Hemodialysis
Acute and chronic renal
failure
Mechanical ventilation for
longer than 3 days
http://emedicine.medscape.com/article/213853-overview#showall
Signs & Symptoms
Chronic mucocutaneous candidiasis
Findings reveal disfiguring lesions of the face, scalp, hands, and
nails. Chronic mucocutaneous candidiasis is occasionally
associated with oral thrush and vitiligo.
http://emedicine.medscape.com/article/213853-overview#showall
Signs & Symptoms
Oropharyngeal candidiasis
Individuals with oropharyngeal candidiasis (OPC) usually have
a history of HIV infection, wear dentures, have diabetes
mellitus, or have been exposed to broad-spectrum antibiotics
or inhaled steroids. Although patients are frequently
asymptomatic, when symptoms do occur, they can include the
following:
Sore and painful mouth
Burning mouth or tongue
Dysphagia
Thick, whitish patches on the oral mucosa
http://emedicine.medscape.com/article/213853-overview#showall
Signs & Symptoms
The following are the 5 types of OPC:
Membranous candidiasis - One of the most common types;
characterized by creamy-white, curdlike patches on the
mucosal surfaces
Chronic atrophic candidiasis (denture stomatitis) - Also
thought to be one of the most common forms of the disease;
presenting signs and symptoms include chronic erythema and
edema of the portion of the palate that comes into contact
with dentures
Erythematous candidiasis - Associated with an erythematous
patch on the hard and soft palates
Angular cheilitis - Inflammatory reaction characterized by
soreness, erythema, and fissuring at the corners of the mouth
Mixed - A combination of any of the above types is possible
http://emedicine.medscape.com/article/213853-overview#showall
Signs & Symptoms
Nonesophageal
Esophageal Candidiasis
Gastrointestinal Candidiasis
Patients with esophageal
candidiasis may be Epigastric pain
asymptomatic or may have 1 or
more of the following Nausea and vomiting
symptoms: Abdominal pain
Normal oral mucosa (>50% of
patients) Fever and chills
Dysphagia
Odynophagia Abdominal mass (in some
Retrosternal pain cases)
Epigastric pain
Nausea and vomiting
Physical examination almost
always reveals oral candidiasis
http://emedicine.medscape.com/article/213853-overview#showall
Signs & Symptoms
Genitourinary tract candidiasis
The types of genitourinary tract candidiasis are as follows:
Vulvovaginal candidiasis (VVC) - Erythematous vagina and labia; a
thick, curdlike discharge; and a normal cervix upon speculum
examination
Candida balanitis - Penile pruritus and whitish patches on the penis
Candida cystitis - Many patients are asymptomatic, but bladder
invasion may result in frequency, urgency, dysuria, hematuria, and
suprapubic pain
Asymptomatic candiduria - Most catheterized patients with
persistent candiduria are asymptomatic
Ascending pyelonephritis - Flank pain, abdominal cramps, nausea,
vomiting, fever, chills and hematuria
Fungal balls - Intermittent urinary tract obstruction with subsequent
anuria and ensuing renal insufficiency
http://emedicine.medscape.com/article/213853-overview#showall
Diagnosis
Mucocutaneous candidiasis - For a wet mount, scrapings or
smears obtained from skin, nails, or oral or vaginal mucosa are
examined under the microscope; a potassium hydroxide smear,
Gram stain, or methylene blue is useful for direct
demonstration of fungal cells
Cutaneous candidiasis - Using a wet mount, scrapings or
smears obtained from skin or nails can be examined under the
microscope; potassium hydroxide smears are also useful
Genitourinary candidiasis - A urinalysis should be performed;
evidence of white blood cells (WBCs), red blood cells (RBCs),
protein, and yeast cells is common; urine fungal cultures are
useful
Gastrointestinal candidiasis - Endoscopy with or without biops
http://emedicine.medscape.com/article/213853-overview#showall
Management
Cutaneous candidiasis - Most localized cutaneous candidiasis
infections can be treated with any number of topical antifungal
agents (eg, clotrimazole, econazole, ciclopirox, miconazole,
ketoconazole, nystatin)
Chronic mucocutaneous candidiasis - This condition is generally
treated with oral azoles
Oropharyngeal candidiasis - This can be treated with either topical
antifungal agents or systemic oral azoles
Esophageal candidiasis - Treatment requires systemic therapy with
fluconazole
VVC - Topical antifungal agents or oral fluconazole can be used [4]
Candida cystitis - In noncatheterized patients, Candida cystitis should
be treated with fluconazole; in catheterized patients, the Foley
catheter should be removed or replaced; if the candiduria persists
after the catheter change, then patients can be treated with
fluconazole
http://emedicine.medscape.com/article/213853-overview#showall
Achalasia
Achalasia
Achalasia is a primary esophageal motility disorder
characterized by the absence of esophageal peristalsis and
impaired relaxation of the lower esophageal sphincter
(LES) in response to swallowing.
The LES is hypertensive in about 50% of patients.
These abnormalities cause a functional obstruction at the
gastroesophageal junction (GEJ).
http://reference.medscape.com/article/169974-overview
Epidemiology
The incidence of achalasia is approximately 1 per 100,000
people per year.
The incidence of esophageal dysmotility appears to
increased in patients with spinal cord injury (SCI).
The male-to-female ratio of achalasia is 1:1.
Achalasia typically occurs in adults aged 25-60 years. Less
than 5% of cases occur in children.
http://reference.medscape.com/article/169974-overview#a2
Etiology
Achalasia primer : unknown cause. Allegedly caused by
neurotropic viruses that cause lesions in the dorsal vagal
nucleus in the brain stem and ganglia misenterikus
esophagus.
Achalasia sekunder : can be caused by infection (eg cagas
disease), tumor intraluminer like cardia tumors or extra
encouragement luminaire as pancreatic pseudocyst.
Another possibility could be caused by an anticholinergic
drug or post vagotomi.
http://reference.medscape.com/article/169974-overview#a6
Sign & Symptoms
Backflow (regurgitation) of food
Chest pain, which may increase after eating, or may be felt
as pain in the back, neck, and arms
Cough
Difficulty swallowing liquids and solids
Heartburn
Unintentional weight loss
https://medlineplus.gov/ency/article/000267.htm
Diagnosis
Barium swallow: Bird’s beak appearance, esophageal
dilatation
Esophageal manometry (the criterion standard):
Incomplete LES relaxation in response to swallowing, high
resting LES pressure, absent esophageal peristalsis
Prolonged esophageal pH monitoring to rule out
gastroesophageal reflux disease and determine if
abnormal reflux is being caused by treatment
Esophagogastroduodenoscopy to rule out cancer of the
GEJ or fundus
Concomitant endoscopic ultrasonography if a tumor is
suspected
http://reference.medscape.com/article/169974-overview#a1
Diagnosis
http://reference.medscape.com/article/169974-overview#a1
Management
Surgical treatment includes the following:
Laparoscopic Heller myotomy, preferably with anterior (Dor;
more common) or posterior (Toupet) partial fundoplication
Peroral endoscopic myotomy (POEM)
Patients in whom surgery fails may be treated with an
endoscopic dilatation first.
If this fails, a second operation can be attempted once the
cause of failure has been identified with imaging studies.
Esophagectomy is the last resort.
http://reference.medscape.com/article/169974-overview#a1
Prognosis Complication
https://medlineplus.gov/ency/article/000267.htm
Prevention
Many of the causes of achalasia cannot be prevented.
However, treatment may help to prevent complications.
https://medlineplus.gov/ency/article/000267.htm