Group 20 Problem 1B

8/12/2019 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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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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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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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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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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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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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.

Documents

Group 20 Problem 1B