group 20 problem 1b
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PROBLEM 1B
Group 20
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Members of Group 20
Tutor : dr. R. Sugiono Suwandi, MS. Susan Natalia 405080-080
Isaura Fransiska 405080-103
Anggun Septiyani 405080-190
Reno Prananditya Ashaf 405080-195 Agnes Lasmono 405090-
Cayadi Sidarta Antonius 405090-045
Theresia Cintia Dewi 405090-110
Julita Suhardi 405090-126
Hans Jaya Sunarto 405090- Ariel Nugroho Susanto 405090-222
Fransisca Pekerti 405090-225
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Learning Objectives
1. Anatomy of the Upper Gastrointestinal Tract
2. Histology the Upper Gastrointestinal Tract
3. Physiology the Upper Gastrointestinal Tract
4. Biochemistry
5. Disorders of the Upper Gastrointestinal Tract
a. Vomiting
b. GERD
c. Pyloric Stenosis
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Anatomy
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Fascia Superficial :
Fascia Camperi
Fascia Scarpae
Fascia Superficial stick to the Arcus Pubic
Fascia Collesi
Peritonium :
Parietal
Visceral Small intestine : Mesenterium
Appendix : Mesoappendix
Colon : Mesocolon
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Anterolateral muscles of the abdomen :
M. rectus abdominis
M. pyramidalis
M. obliquus externus abdominis M. obliquus internus abdominis
M. transversus abdominis
Posterior muscles of the abdomen :
M. quadratus lumborum M. iliacus
M. psoas major
M. psoas minor
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The function of abdominal muscles :
Compression of abdominal contents
M. obliquus externus abdominis
M. obliquus internus abdominisM. transversus abdominis
M. rectus abdominis
Increasing of intra-abdominal pressure
Movements (anteroflexio, lateroflexio, rotatio)
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A. epigastrica superior
A. epigastrica inferior A. epigastrica
superficialis
A. lumbalis
A. intercostalis
A. circumflexa iliacasuperficialis
A. circumflexa iliacaprofunda
V. thoracoepigastrica
V. epigastricasuperficialis
Plexus venosusumbilicalis
V. para-umbilicales V. epigastrica inferior
V. circumflexaepigastrica superior
Arteries Veins
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Mouth
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Esophagus
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Gaster
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Gaster
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Duodenum
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Duodenum
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Histology
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Labium Oris
1. Pars cutanea / outer layer
a. Stratified keratinizingsquamous cell epithelium
b. Hair follicle with sebaceousand sweat glands
c. Orbicularis oris muscle
2. Pars Intermedia/Vermillionborder : A
3. Pars oral mucosa : B
a. Stratified nonkeratinizingsquamous cell epithelium
b. Tunica propria Labialis glands
c. Orbicularis oris muscle
d. Labialis artery
e. Small chorium
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Labium Oris
2. Lingua
Stratified
keratinized
squamousepithelial
2/3 anteriorfiliform
papilla, fungiform
papilla, foliatepapilla, circumvalatte
papilla
1/3 posterior
tonsilla lingual
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Labium Oris
There are 3 forms of
papillae:
Circumvalata
papillae:Circumvalata
papillae:
Secondary papillae
Taste bud Ebneri glands
Filiform papillae (A)
Fungiform papillae
(B)
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Labium Oris
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Labium Oris
Lingual Glands : Parotid glands
1. Pars terminalis (serous)2. Secretory duct3. Intercalaris duct
4. Intelobular tissue Submandibular glands
1. Pars terminalis(mucoserous)
2. Secretory duct3. Excretory duct
Sublingual glands1. Pars terminalis
(mucoserous)2. Secretory duct
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Labium Oris
3. Taste Buds
1. Receptor cell
2. Sustentacular cell
3. Stem cell (basalcell)
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Labium Oris
In general, there are 4 layers that make up the wall of GItract from the posterior pharynx-anus
1. The mucosa Membrane mucosa
Lamina propria Muscularis mucosa
2. The submucosa
3. The muscularis
Outer longitudinal layer
Inner circular layer
4. The serosa
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Esophagus
A. Tunica mucosae1. Stratified
nonkeratinizingsquamous cellepithelium
2. T. propria3. T. muscularis
mucosae
B. Tunica submucosae4. Oesephagus glands
5. Excretory duct
C. Tunica muscularis6. T. Musc. Circular
7. T.Musc. Longitudinal
D. Tunica adventitia
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Gaster
4. Pyloric
a. Tunica Mucosa1. Columnar surface
epithelium
2. Gastric foveolae (wideand deep)
3. T.propria+pyloricglands
4. Elastic membran
5. T. M. Mucosaeb. Tunica Submucosa
c. Tunica Muscularis
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Duodenum
A. T. mucosae
1. Vili
2. Columnar surface
epithelium+gobletcell
3. Crypt/of lieberkuhn
4. T.M. Mucosae
B. T. submucosae
C. T.muscularis
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Physiology
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Gaster
Function:
Keep the food until transported to duodenum
Secretion HCl and enzymes ( lipase, renin &
pepsin )
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Biochemistry
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Anatomy & Functions of Components of the
Digestive System
Digestive Organ Motility Secretion Digestion Absorption
Mouth &
Salivary Glands
Chewing Saliva
Amylase
Mucus
Lysozyme
Carbohydrate
digestion begins
No foodstuffs; a
few medications
ex: Nitroglycerin
Pharynx &
Esophagus
Swallowing Mucus - -
Stomach Receptiverelaxation,
peristalsis
Gastric Juice
HCl
Pepsin
Mucus
Intrinsic Factor
Carbohydrate
digestion continues in
body of stomach;
protein digestion
begins in antrum of
stomach
No foodstuffs; a
few lipid-soluble
substance, such
as alcohol &
aspirin
Exocrine
Pankreas
Not
applicable
Pancreatic digestive
enzymes
Trypsin,
Chymotrypsin,
Carboxypeptidase
Amylase
LipasePancreatic a ueous
These pancreatic
enzymes accomplish
digestion in duodenal
lumen
Not applicable
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Synthesis of HCl by parietal
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cellsDiagram showing the main
steps in the synthesis of
hydrochloric acid. Active
transport by ATPase is
indicated by arrows and
diffusion is indicated by dotted
arrows. Under the action ofcarbonic anhydrase, carbonic
acid is produced from CO2.
Carbonic acid dissociates into a
bicarbonate ion and a proton
(H+), which is pumped into the
stomach lumen in exchange for
K+. A high concentration of
intracellular K+is maintained by
the Na+, K+ATPase, whileHCO3
is exchanged for Clby
an antiport. The tubulovesicles
of the cell apex are seen to be
related to hydrochloric acid
secretion, because their number
decreases after parietal cell
stimulation as microvilli
increase. Most of the
bicarbonate ion returns to theblood and is responsible for a
measurable increase in blood
pH during digestion, but some is
taken up by surface mucous
cells and used to raise the pH of
mucus.
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Regulation of gastric acid and pepsin secretion by soluble mediators and neural
input.Gastrin is released from G cells in the antrum and travels through the circulation
to influence the activity of ECL (enterochromaffin-like cells) cells and parietal cells. The
specific agonists of the chief cell are not well understood. Gastrin release is negatively
regulated by luminal acidity via the release of somatostatin from antral D cells.
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Vomiting
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Definition
Abnormal emptying of stomach and upper partof intestine via esophagus through mouth.
This is not the same as regurgitation, whichrefers to emitting already swallowed food, andmust be distinguished correctly.
Vomiting is often related to or preceded bynausea, but both nausea-without-vomiting andvomiting-without-nausea are possible.
Any nausea or vomiting symptom needs promptprofessional medical investigation.
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Etiology
Irritation in GIT Mechanical stimulation of pharynx
Pregnancy
Alcohol Stimulation of labyrinth of ear eg sea
sickeness,mountain sickeness
Acute GI infection
Metabolic disorders Increase Intracranial Pressure
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Mechanism
Receptors are stimulated which contribute impulses to the vomiting center in thebrain
Sensory impulse stream from receptors reach the vomiting center and initiate anumber of motor responses.
The diaphragm and the skeletal muscles of the abdominal wall contract
Increase the intra-abdominal pressure
The cardiac sphincter relaxes and soft palate rise to close off the nasal passage
The stomach (or intestinal) contents are then forced upward through theesophagus, pharynx and out the mouth
Emesis or Vomiting
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Mechanism
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Mechanism
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Predisposition factor
Emesis is early manifestation of somedisease, therefore closer identification its soimportant, there are :
Age and sex
Diet
Nutrient status of child
Vomit contains
There is child disease which attack
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Medical examination
Analysis of urine and blood
Foto polos abdomen with or without contrast
USG
Endoscopy with biopsi / monitoring PH
esofagus
Psychiatry check up
Home Care of Nausea &
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Home Care of Nausea &
Vomiting Monitor for dehydration Signs of mild dehydration include:A slightly dry mouth
Thirst
Children who are mildly dehydrated do not need immediatemedical attention but should be monitored for signs ofworsening dehydration.
Signs of moderate or severe dehydration include: Decreased urination (not going to the bathroom or no wet
diaper in 6 hours)
A lack of tears when cryingA dry mouth
Sunken eyes
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Home Care of Nausea &
Vomiting
Dietary recommendations Infant Continue the breastfeed
Oral rehydration therapy
Older infants and children Monitor for signs of dehydration. Other fluids, including
water, diluted juice, or soda can be given in smallquantities.
Apple, pear, and cherry juice, and other beverages with
high sugar content, should be avoided. Recommended foods include a combination of complex
carbohydrates, lean meats, yogurt, fruits, and vegetables.High fat foods are more difficult to digest, and should beavoided.
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Home Care of Nausea &
Vomiting
Oral rehydration therapy
Liquid solution that contains glucose (a sugar) and
electrolytes (sodium, potassium, chloride), which are
lost with vomiting and diarrhea.
Antiemetics
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When to Seek Help?
You should call your doctor or nurse immediatelyifyour child has any of the following: Bile (green) or blood-tinged (red or brown) vomit
Any episode of vomiting in a newborn, or vomiting thatcontinues for more than 24 hours in an infant or child
If an infant refuses to eat or drink anything for more than afew hours
Moderate to severe dehydration (dry mouth, no tears whencrying, not urinating or having a wet diaper in six hours)
Abdominal pain that is severe, even if it comes and goes
Fever higher than 102F (39C) once or fever higher than101F (38.4C) for more than three days
Behavior changes, including lethargy or decreasedresponsiveness
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Complication
Loosing fluid and electrolit
Aspiration of gaster contents
Malnutrition and failed to growing up
Sindrom Mallory-Weiss (rupture at epitel of
gastroesopageal junction because of repeated
vomit )
Sindrom Boerhave (rupture esofagus) Esofagitis peptikum
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GERGERD
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Classifications
Physiologic (or functional) gastroesophagealreflux:
No underlying predisposing factors or conditions
Growth and development are normal, and
pharmacologic treatment is typically not necessary
Pathologicgastroesophageal reflux orgastroesophageal reflux disease (GERD):
Patients frequently experience complications noted
above, requiring careful evaluation and treatment Secondarygastroesophageal reflux :
Underlying condition may predispose
Ex. Asthma and gastric outlet obstruction
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Sign & Symptoms (infants)
Typical or atypical crying and/or irritability Apnea and/or bradycardia
Poor appetite
Apparent life-threatening event (ALTE)
Vomiting
Wheezing
Abdominal and/or chest pain
Stridor
Failure to thrive
Recurrent pneumonitis
Sore throat
Chronic cough
Waterbrash
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Physical
In toddlers and older children, may lead to
significant dental problems caused by acid
effects on tooth enamel
Esophagitis
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Causes
Anatomic Factors
The angle of His (made by the esophagus and
the axis of the stomach) is obtuse in newborns
but decreases as infants develop. This ensures amore effective barrier against gastroesophageal
reflux.
The presence of a hiatal hernia may displace the
lower esophageal sphincter (LES) into thethoracic cavity
Resistance to gastric outflow raises intragastric
pressure and leads to reflux and vomiting.
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Causes
Others : Medications (diazepam etc)
Smoking
Alcohol
Food and poor dietary habbit, allergies
Motility disorder
tLESR
Obesity
Supine position
Decreased gastric emptying and reduced acidclearance from the esophagus: These can causeabnormal reflux
S
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Imaging Studies
Upper GI Imaging Series Not spesific
Evaluation of gastric emptying phase
Gastric Scintiscan using milk or formula that contains a small amount of technetium
sulfur colloid, can assess gastric emptying and can reveal reflux(although not the degree or severity)
Esophagography Strictures can be demonstrated by esophagography.
Chronic esophageal mucosal injury secondary to
gastroesophageal reflux involves a mucosal/submucosalinflammatory cell infiltrate as well as basal cell hyperplasia. Insevere cases, this may appear as a ragged mucosal outline onradiography
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M di ti
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Medications
Changes in diet and lifestyle :
Appropriate weight management of overweight or
obese children is important
Avoid the seated or the supine position shortlyafter meals. In addition, sleeping in the prone
position has been demonstrated to decrease the
frequency of gastroesophageal reflux
Placing blocks under the head of the bed orplacing a foam wedge under the patient's
mattress can accomplish this.
T t t & P i
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Treatment & Prognosis
GE reflux resolves spontaneously in 85% of
affected infants by 12 months of age,
coincident with assumption of erect posture
and initiation of solid feedings. Until then, regurgitation volume may be
reduced by offering small feedings at frequent
intervals and
by thickening feedings with rice cereal (23
tsp/oz of formula).
Prethickened "anti-reflux" formulas are
available.
T t t & P i
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Treatment & Prognosis
Histamine-2 (H2)receptor antagonists
(ranitidine, 5 mg/kg/d in two doses) or
proton pump inhibitors (omeprazole, 0.51.0
mg/kg/d in one dose) do not reduce thefrequency of reflux but may reduce pain
behavior.
Prokinetic agents such as metoclopramide
hasten gastric emptying and improve
esophageal motor function, but studies have
not shown efficacy in controlling symptoms.
T t t & P i
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Treatment & Prognosis
A 2-week trial of protein hydrolysate formula
(hypoallergenic) sometimes controls emesis
and pain behavior in infants with protein
sensitivity. Special formulas and acid suppression agents
are costly and should be discontinued if
there is no improvement of symptoms in 1
2 weeks.
T t t & P i
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Treatment & Prognosis
Antireflux surgery (fundoplication) is indicatedwhen GERD is unresponsive to medications, thusleading to severe symptoms that include
(1) persistent vomiting with failure to thrive,
(2) esophagitis or esophageal stricture, (3) life-threatening apneic spells, or
(4) chronic pulmonary disease unresponsive to23 months of maximal medical therapy.
Fundoplication also may be considered in patientswhose response to medication is likely to bepoorthose with large hiatal hernia, neurologichandicap, previous TE fistula surgery, or severeesophagitis.
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Pyloric Stenosis
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B k d
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Background
Pyloric stenosis (Infantile Hypertrophic PyloricStenosisIHPS)
The most common intestinal obstruction
infancy Occurs secondary to hypertrophy &
hyperplasia of the muscular layers of the
pylorusgastric outlet obstruction
F t
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Facts
Narrowing of the pylorus The muscles in the pylorus become enlarged and
narrowing the pyloric channelfood is preventedfrom emptying out of the stomach
Fairly common, 3 out of 1000 babies in US
Common in Caucasian
Most infants who develop symptoms of pyloricstenosis are usually between 3 to 5 weeks
Common causes of intestinal obstruction duringinfancy that requires surgery
C
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Causes
Babies are not born with it
Progressive thickening of the pylorus that
occurs after birth
Symptoms only show when the stomach canno longer empty properly
Some factors :
The use of erythromycin in the first 2 weeks of life Same antibiotic at the end of pregnancy or during
breastfeeding
Si & S t
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Signs & Symptoms
Vomiting Early stage : spitting up frequently
Late : projectile vomiting (soon after feeding or delayed)
Does not contain bile secrets
May become brown or coffee color due to blood secondary to gastritis ora Mallory-Weiss Tear
Changes in stools
Decreased frequency, fewer, & smaller (constipation)
Or stools with mucus
Failure to gain weight, dehydrated, & lethargy
Dehydrated infants are less active than usual, and they may develop a
sunken "soft spot" on their heads, sunken eyes, and their skin mayappear wrinkled
Because less urine is made it may be more than 4 to 6 hours betweenwet diapers
Lab St dies
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Lab Studies
Electrolytes, pH, BUN, and creatinine levelsshould be obtained at the same time asintravenous access in patiens with pyloricstenosis
Hypochloremic, hypokalemic metabolikalkalosis is the classic electrolyte and acid-base imbalance
Presistent emesis
progressive loss of fluidsrich in hydrochloric acidkidney retainshydrogen ions in favor of potassium
Dehydrationhypernatremia or
hyponatremiaprerenal renal failure
Imaging
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Imaging
Ultrasonography :
pyloric muscle thickness greater than 4 mm
length of the pyloric canal is variable and may
range from 14 mm to 20 mm pyloric diameter may range from 10-14 mm
Treatments
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Treatments
Pre-hospital Care :
Immediate treatment requires correction of fluid
loss, electrolytes, and acid-base imbalance.
Once intravenous access is obtained, thedehydrated infant should receive an initial bolus
(20 mL/kg) of crystalloid fluid.
The infant should remain nothing by mouth (NPO)
Emergency Department Care
Consultations
Medications
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Medications
Surgical correction is considered the standardof care for infantile hypertrophic pyloric
stenosis (IHPS)
Prognosis
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Prognosis
Surgery is curative with minimal mortality.Theprognosis is very good, with complete
recovery and catch-up growth if detected in a
timely fashion
Conclusion
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Conclusion
Base on the clinical history, clinicalmanifestation, and physical examination, the
baby boy is suspected to have a Pyloric
Stenosis
Suggestion
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Suggestion
Immediate correction of fluid loss, electrolytes& acid-base imbalance
Consult to surgeon
References
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References
Netter FH. Atlas of human anatomy. 2nded.Canada:Icon Learning System, 1997.
Ganong WF. Review of medical physiology. 22nded.New York: McGraw-Hill Companies, Inc, 2005.
Murray RK, Granner DK, Mayes PA, Rodwell VW,editors. Harpers biochemistry. 26thed. Calinorfia:Lange Medical Publications, 2003.
Bloom, Fawcett. A textbook of histology. 12thed. NewYork: Chapman & Hall, 1994.
Fauci AS, Braunwald E, Kasper DL, Hauser SL,Longo DL, Jameson DL, et al, editors. Harrisonsprinciple of internal medicine. 17thed. USA: Mc.GrawHill medical, 2008.