PROBLEM 1B

Group 20

Members of Group 20

Tutor : dr. R. Sugiono Suwandi, MS.

Susan Natalia Isaura Fransiska Anggun Septiyani Reno Prananditya Ashaf Agnes Lasmono Cayadi Sidarta Antonius Theresia Cintia Dewi Julita Suhardi Hans Jaya Sunarto Ariel Nugroho Susanto Fransisca Pekerti

405080-080 405080-103 405080-190 405080-195 405090405090-045 405090-110 405090-126 405090405090-222 405090-225

Mind Mapping

Learning Objectives
1.

2.
3. 4. 5.

Anatomy of the Upper Gastrointestinal Tract Histology the Upper Gastrointestinal Tract Physiology the Upper Gastrointestinal Tract Biochemistry Disorders of the Upper Gastrointestinal Tract
a. b. c.

Vomiting GERD Pyloric Stenosis

Anatomy

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

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

The function of abdominal muscles :

Compression
M.

of abdominal contents

obliquus externus abdominis M. obliquus internus abdominis M. transversus abdominis M. rectus abdominis
Increasing

of intra-abdominal pressure Movements (anteroflexio, lateroflexio, rotatio)

Arteries

Veins

A. epigastrica superior A. epigastrica inferior A. epigastrica superficialis A. lumbalis A. intercostalis A. circumflexa iliaca superficialis A. circumflexa iliaca profunda

V. thoracoepigastrica V. epigastrica superficialis Plexus venosus umbilicalis V. para-umbilicales V. epigastrica inferior V. circumflexa epigastrica superior

Mouth

Esophagus

Gaster

Gaster

Duodenum

Duodenum

Histology

Labium Oris
1.

Pars cutanea / outer layer

a.
b. c.

Stratified keratinizing squamous cell epithelium Hair follicle with sebaceous and sweat glands Orbicularis oris muscle

2.

3.

Pars Intermedia/Vermillion border : A Pars oral mucosa : B

a. b.

Stratified nonkeratinizing squamous cell epithelium Tunica propria

Labialis glands

c. d. e.

Orbicularis oris muscle Labialis artery Small chorium

Labium Oris
2.

Lingua

Stratified keratinized squamous epithelial

2/3 anterior filiform papilla, fungiform papilla, foliate papilla, circumvalatte papilla 1/3 posterior tonsilla lingual

Labium Oris

There are 3 forms of papillae:

Circumvalata

papillae:
Circumvalata

papillae:

Secondary papillae Taste bud

Ebneri

glands

Filiform

papillae (A) Fungiform papillae (B)

Labium Oris

Labium Oris
Lingual Glands :

Parotid glands
1. 2. 3. 4.

Pars terminalis (serous) Secretory duct Intercalaris duct Intelobular tissue Pars terminalis (mucoserous) Secretory duct Excretory duct Pars terminalis (mucoserous) Secretory duct

Submandibular glands
1. 2. 3.

Sublingual glands
1. 2.

Labium Oris
3.

Taste Buds
1. 2. 3.

Receptor cell Sustentacular cell Stem cell (basal cell)

Labium Oris

In general, there are 4 layers that make up the wall of GI tract from the posterior pharynx-anus
1.

The mucosa
Membrane mucosa Lamina propria Muscularis mucosa

2. 3.

The submucosa The muscularis

Outer longitudinal layer Inner circular layer

4.

The serosa

Esophagus
A.

Tunica mucosae
1.

2. 3.
B.

Stratified nonkeratinizing squamous cell epithelium T. propria T. muscularis mucosae

Oesephagus glands Excretory duct T. Musc. Circular T.Musc. Longitudinal

Tunica submucosae
4.

5.
C.

Tunica muscularis
6. 7.

D.

Tunica adventitia

Gaster
1. 2. 3.

Cardiac Corpus Fundus

a.
1.
2. 3. 4. 5.

Tunica mucosa
Columnar surface epithelium Gastric foveolae T.propria+fundus glands Elastic membran T. M. Mucosae

b.

Tunica Submucosa

Gaster
4.

Pyloric
a.
1. 2. 3. 4. 5.

Tunica Mucosa
Columnar surface epithelium Gastric foveolae (wide and deep) T.propria+pyloric glands Elastic membran T. M. Mucosae

b. c.

Tunica Submucosa Tunica Muscularis

Duodenum
A.

T. mucosae
1. 2.

3. 4.
B.
C.

Vili Columnar surface epithelium+goblet cell Crypt/of lieberkuhn T.M. Mucosae

T. submucosae T.muscularis

Physiology

Gaster

Function:

Keep the food until transported to duodenum Secretion HCl and enzymes ( lipase, renin & pepsin )

Biochemistry

Anatomy & Functions of Components of the Digestive System

Digestive Organ Mouth & Salivary Glands Motility
Chewing

Secretion
Saliva Amylase Mucus Lysozyme
Mucus Gastric Juice HCl Pepsin Mucus Intrinsic Factor Pancreatic digestive enzymes Trypsin, Chymotrypsin, Carboxypeptidase Amylase Lipase Pancreatic aqueous

Digestion
Carbohydrate digestion begins

Absorption
No foodstuffs; a few medications ex: Nitroglycerin
No foodstuffs; a few lipid-soluble substance, such as alcohol & aspirin Not applicable

Pharynx & Esophagus Stomach

Swallowing Receptive relaxation, peristalsis

Carbohydrate digestion continues in body of stomach; protein digestion begins in antrum of stomach These pancreatic enzymes accomplish digestion in duodenal lumen

Exocrine Pankreas

Not applicable

Anatomy & Functions of Components of the Digestive System

Digestive Organ Liver Motility
Not applicable

Secretion
Bile Bile salts Alkaline secretion Bilirubin Succus entericus Mucus Salt (Small intestine enzymes disaccharidases and aminopeptidases are not secreted but function within brush border membrane) Mucus

Digestion
Bile does not digest anything, but bile salts facilitate fat digestion and absorption in duodenal lumen In lumen, under influence of pancreatic enzymes & bile, carbohydrate & protein digestion continues and fat digestion is completely accomplish; in brush border, carbohydrate & protein digestion completed -

Absorption
Not applicable

Small Intestine

Segmentation; migrating motility complex

All nutrients, most electrolytes and water

Large Intestine

Haustral contractions, mass movements

Salt & water, converting contents to feces

Synthesis of HCl by parietal cells. Diagram 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 of carbonic 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, while HCO3 is exchanged for Cl by 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 the blood 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.

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.

Vomiting

Definition

Abnormal emptying of stomach and upper part of intestine via esophagus through mouth. This is not the same as regurgitation, which refers to emitting already swallowed food, and must be distinguished correctly. Vomiting is often related to or preceded by nausea, but both nausea-without-vomiting and vomiting-without-nausea are possible. Any nausea or vomiting symptom needs prompt professional medical investigation.

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

Mechanism
Receptors are stimulated which contribute impulses to the vomiting center in the brain Sensory impulse stream from receptors reach the vomiting center and initiate a number 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 the esophagus, pharynx and out the mouth Emesis or Vomiting

Mechanism

Mechanism

Predisposition factor

Emesis is early manifestation of some disease, therefore closer identification its so important, there are :
Age Diet Nutrient

and sex

status of child Vomit contains There is child disease which attack

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 & Vomiting

Monitor for dehydration

Signs of mild dehydration include:

A slightly dry mouth Thirst Children who are mildly dehydrated do not need immediate medical attention but should be monitored for signs of worsening 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 crying A dry mouth Sunken eyes

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 small quantities. 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 be avoided.

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

When to Seek Help?

You should call your doctor or nurse immediately if your child has any of the following:

Bile (green) or blood-tinged (red or brown) vomit Any episode of vomiting in a newborn, or vomiting that continues for more than 24 hours in an infant or child If an infant refuses to eat or drink anything for more than a few hours Moderate to severe dehydration (dry mouth, no tears when crying, 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 than 101F (38.4C) for more than three days Behavior changes, including lethargy or decreased responsiveness

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

GER GERD

Classifications

Physiologic (or functional) gastroesophageal reflux:

No underlying predisposing factors or conditions Growth and development are normal, and pharmacologic treatment is typically not necessary

Pathologic gastroesophageal reflux or gastroesophageal reflux disease (GERD):

Patients frequently experience complications noted above, requiring careful evaluation and treatment

Secondary gastroesophageal reflux :

Underlying condition may predispose Ex. Asthma and gastric outlet obstruction

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

Physical

In toddlers and older children, may lead to significant dental problems caused by acid effects on tooth enamel Esophagitis

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 a more effective barrier against gastroesophageal reflux. The presence of a hiatal hernia may displace the lower esophageal sphincter (LES) into the thoracic cavity Resistance to gastric outflow raises intragastric pressure and leads to reflux and vomiting.

Causes

Others :
Medications (diazepam etc) Smoking Alcohol Food and poor dietary habbit, allergies Motility disorder tLESR Obesity Supine position Decreased gastric emptying and reduced acid clearance from the esophagus: These can cause abnormal reflux

Imaging Studies

Upper GI Imaging Series

Not spesific Evaluation of gastric emptying phase 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) Strictures can be demonstrated by esophagography. Chronic esophageal mucosal injury secondary to gastroesophageal reflux involves a mucosal/submucosal inflammatory cell infiltrate as well as basal cell hyperplasia. In severe cases, this may appear as a ragged mucosal outline on radiography

Gastric Scintiscan

Esophagography

Algorithm

Medications

Changes in diet and lifestyle :

Appropriate

weight management of overweight or obese children is important Avoid the seated or the supine position shortly after 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 or placing a foam wedge under the patient's mattress can accomplish this.

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.

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 the frequency 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.

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.

Treatment & Prognosis

Antireflux surgery (fundoplication) is indicated when GERD is unresponsive to medications, thus leading 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 to 23 months of maximal medical therapy. Fundoplication also may be considered in patients whose response to medication is likely to be poorthose with large hiatal hernia, neurologic handicap, previous TE fistula surgery, or severe esophagitis.

Pyloric Stenosis

Background

Pyloric stenosis (Infantile Hypertrophic Pyloric Stenosis IHPS) The most common intestinal obstruction infancy Occurs secondary to hypertrophy & hyperplasia of the muscular layers of the pylorus gastric outlet obstruction

Facts

Narrowing of the pylorus The muscles in the pylorus become enlarged and narrowing the pyloric channel food is prevented from emptying out of the stomach Fairly common, 3 out of 1000 babies in US Common in Caucasian Most infants who develop symptoms of pyloric stenosis are usually between 3 to 5 weeks Common causes of intestinal obstruction during infancy that requires surgery

Causes

Babies are not born with it Progressive thickening of the pylorus that occurs after birth Symptoms only show when the stomach can no 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

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 or a Mallory-Weiss Tear Decreased frequency, fewer, & smaller (constipation) Or stools with mucus Dehydrated infants are less active than usual, and they may develop a sunken "soft spot" on their heads, sunken eyes, and their skin may appear wrinkled Because less urine is made it may be more than 4 to 6 hours between wet diapers

Changes in stools

Failure to gain weight, dehydrated, & lethargy

Lab Studies

Electrolytes, pH, BUN, and creatinine levels should be obtained at the same time as intravenous access in patiens with pyloric stenosis Hypochloremic, hypokalemic metabolik alkalosis is the classic electrolyte and acidbase imbalance Presistent emesis progressive loss of fluids rich in hydrochloric acid kidney retains hydrogen ions in favor of potassium Dehydration hypernatremia or hyponatremia prerenal renal failure

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

Pre-hospital Care :
Immediate

treatment requires correction of fluid loss, electrolytes, and acid-base imbalance. Once intravenous access is obtained, the dehydrated 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

Surgical correction is considered the standard of care for infantile hypertrophic pyloric stenosis (IHPS)

Prognosis

Surgery is curative with minimal mortality.The prognosis is very good, with complete recovery and catch-up growth if detected in a timely fashion

Conclusion

Base on the clinical history, clinical manifestation, and physical examination, the baby boy is suspected to have a Pyloric Stenosis

Suggestion

Immediate correction of fluid loss, electrolytes & acid-base imbalance Consult to surgeon

References

Netter FH. Atlas of human anatomy. 2nd ed. Canada:Icon Learning System, 1997. Ganong WF. Review of medical physiology. 22nd ed. New York: McGraw-Hill Companies, Inc, 2005. Murray RK, Granner DK, Mayes PA, Rodwell VW, editors. Harpers biochemistry. 26th ed. Calinorfia: Lange Medical Publications, 2003. Bloom, Fawcett. A textbook of histology. 12th ed. New York: Chapman & Hall, 1994. Fauci AS, Braunwald E, Kasper DL, Hauser SL, Longo DL, Jameson DL, et al, editors. Harrisons principle of internal medicine. 17th ed. USA: Mc.Graw Hill medical, 2008.