DIGESTIVE SYSTEM

Digestive system consists of:

Digestive tract
Accessory digestive organs

A. DIGESTIVE TRACT
Digestive tract are the organs through which the food
Oral cavitypharyngealoesophagealgastricduodenaljejenumileum
colonrectum anus
1. Oral cavity
Anterior margin: inferior et superior labium
Superior margin : palatum durum and palatum molle
a. Dens :
Table 9. Differences teeth Children and Adults

Children teeth (20) Adult teeth (32)

4medial incisivus, 4 medial incisivus,
4lateral incisivus , 4 lateral incisivus,
4 caninus, 4 caninus,
4 first molar, 4 first premolar,
4 second molar 4second premolar,
4 first molar,
4 second molar,
4 third molar

Important structures in the teeth:

Periodontal ligament
Corona dens
Email
Radix dens
cementum
Dens decidua

b. Lingua
1) Pars of lingua
Apex lingua
Corpus lingua
Radix lingua
2) structures of lingua
Fibrosum mediana septum
Sulcus mediana lingua
Sulcus terminalis lingua
Frenulum lingua
 5) Muscles of lingua
Intrinsic muscles
M. longitudinalis lingua
M. tranversalis lingua
M. vertikalis lingus
Ekstrinsic muscles
M. genioglossus
M. hyoglossus
M. styloglossus
M. palatoglossus

2. Pharynx/pharyngeal
Consists of three parts:
a. Nasopharynx
b. Oropharynx
c. Laryngopharynx

Figure 1. Pharynx

3. Oesophagus
c. Pars :
pars cervicalis
pars thoracalis
pars abdominalis
d. Structure :
superior sphyngter oesophageal
inferior sphyngter oesophageal
oesophageus hiatus

1
0
 4. Gaster / gastric
P
a
pars cardiac, pars fundus, pars corpus, pars phylorus
r and inferior oesofageal sphyngter
sphyngter
incisurasof cardiac and incisura of angularis
I
major curvatura and minor curvatura

Figure 2. Gaster
5. Small intestine (Intestinum Tenue)
a. Duodenum
1) Pars : pars ampulla, pars descende ns, pars horizontalis, pars
ascendens
2) Boils : papilla of major duodeni and papilla of minor duodeni
b. Jejenum
c. Ileum

Table 10. Differences jejunum and ileum

Jejenum Ileum
Long 2,5 m 3,5 m
Wall Thick Thin
Diameter Big Little
Vasa Recta Length/Upright Short
Arcade Loose Bind
Mesentery fat A little Much
Plica circularis Shape feather/brush Tong shape
Structure :
Ileocaecalis sphingter
Valvula ileocecalis/valvula Bauchini

6. Caecum
There is Appendix vermiformis, 6 cm.
Point of Mc. Burney (base of appendix) : 1/3 SIAS dextra with umbilicalis.
Point of V. Lanz (peak appendix that hang down) : 1/3 dextra
between SIAS dextra-sinistra.
7. Colon (Intestinum Crassum)
a. Pars
Colon of ascendens
Colon of descendens
Colon of transversum
Colon of sigmoid
b. Structure
Haustra coli
Taenia coli
Flexura coli dextra
Flexura coli sinistra

8. Rectum - Anus
The rectum is where feces storage prior to release the anal
sphincter.
Anal sphincter : external anal sphincter and internal anal sphingter.
B. DIGESTIVES ACCESSORIUS ORGANS
Digestives accessory organs are organs that do not pass the food but
plays a role in digestion of food.
1. Glandula saliva
Salivary glands are the glands that produce saliva (saliva) containing the
enzyme alpha-amylase or ptialin, salivary gland consists of three pairs :
a. GlandulaParotid
b. Glandula Sublingual
c. Glandula Submandibula

Glandula parotid

Glandula sublingua

Sub~dftAar
duct Glandula submandibula

Figure 3. Saliva Gland

2. Hepar
It is the largest organ in the abdomen
Located in the region of hypochondrium dextra and regions epigastrica
It consists of lobes, namely:
a) Lobus hepatis dextra
b) Lobus hepatis sinistra

c) Lobus quadrates
d) Lobus caudatus
Ligamentum
a) Ligamentum falciforme
b) Ligamentum teres hepatis

c) Ligamentum coronarium
d) Ligamentum triangulare dextra

e) Ligamentum triangulare sinistra

f) Ligamentum venosum
Functions production and secretion of bile, detoxification, protein
production, etc. A - Clinical applications: hepatitis, cirrhosis, liver rupture

3. Vesica biliaris / Vesica fellea (gall bladder)

Consists of
a. Fundus
b. Corpus
c. Collum
Functions concentrate and temporarily store the bile coming
from the liver and eventually be released into the duodenum
Clinical Applications: cystitis

Figure 4. Secretion of biles track

Ducts that play a role in the process of spending the bile

a. Ductus hepaticus dextra et sinistra
a. Ductus hepaticus communis
b. Ductus cycticus
c. Ductus choledocus
4. Pancreas
a. Endocrine organ (hormone-producing insulin, glucagon, somatostatin)
b. Exocrine organ (producing enzymes amylase, lipase, trypsin)
Consists of 4 parts:
1) Caput pancreatis
2) Collura pancreatis
3) Corpus pancreatis
4) Cauda pancreatis
d. There are two ductus namely:
ductus pancreaticus wirsungi which will lead to the papilla duodeni major
ductus pancreaticus sartorini which will lead to the papilla dudeni minor.
Clinical applications: pancreatitis, diabetes mellitus

Figure 5. Pancreas

C. PERITONEUM
The peritoneum is the lining / membranes covering the organs contained in the abdominal cavity,
of which are:
1. Mesenterium
2. Omentum Majus
3. Omentum Minus
CLINICAL APPLICATIONS
 LOCATION DISORDER

Oral Cavity Caries Dentes

Ginggivitis

Oesophagus Striktur Oesophagus

Gastro Oesophageal Refluks

Disease

Atresia Oesophagus

Tracheo oesophageal fistule

Gaster Gastritis

Duodeni Ulcer

Vesica Fellea Colelithiasis

Colecystitis

Hepar Hepatitis

Hepatomegali

Spleen Spleenomegali

Intestinum Tenue Invagination

Irritable Bowel Syndrome

Colon Colitis

Ca colon

Congenital Omphalocele

Diseases Hernia umbilical

Hernia femoralis

Hernia inguinalis

Hirschprung Disease

ESOPHAGEAL ATRESIA AND TRACHEOESOPHAGEAL FISTULA (TEF)

A. Definition
 Esophageal atresia is when the upper part of the esophagus does not connect with the
lower esophagus and stomach. Tracheoesophageal fistula (TEF) is a connection between
the esophagus and the trachea or windpipe.
B. Etiology
Congenital TEF can arise due to failed fusion of the tracheoesophageal ridgesduring the
third week of embryological development.A fistula, from the Latin meaning a pipe, is
an abnormal connection running either between two tubes or between a tube and a
surface. In tracheo-esophageal fistula it runs between the trachea and the esophagus. This
connection may or may not have a central cavity; if it does, then food within the
esophagus may pass into the trachea (and on to the lungs) or alternatively, air in the
trachea may cross into the esophagus.TEF can also occur due to pressure necrosis by
a tracheostomy tube in apposition to a nasogastric tube (NGT)
C. Classification
- Pure Esophageal Atresia
- Esophageal Atresia with Proximal Fistula
- Esophageal Atresia with Proximal and DistalFistulas
- H-type Fistula without Esophageal Atresia
Esophageal Atresia with Distal Fistula (EA/TEF). This is the most common subtype,
accounting for about 85% of EA anomalies
D. Clinical manifestation
- Cough
- Chocking
- Cyanosis
- Excessive salivation
- Drooling
- Respiratory distress
- Very round, full abdomen (TEF)
- Unusually flat abdomen (isolated esophageal atresia)
- Inability to pass NGT down the esophagus into the stomach
CHOLECYSTITIS

Cholecystitis is the inflammation (or swelling) of the gallbladder. The gallbladder is located
towards the upper right abdominal. It stores bile, which is responsible for breaking down the
bodys fats. Cholecystitis is caused by gallstones blocking the entrance of the gallbladder. This
causes the bile to build up and the gallbladder to inflame. Cholecystitis can cause serious
abdominal pain.
 Figure 6. Cholecystitis

Symptoms:
Persistent pain in the upper right abdominal region
Abdominal pain that extends to the right shoulder and back

Symptoms that are not better when over-the-counter pain relievers are taken, when body
positioning is changed, or gas is released

Nausea

Vomiting

Fever

Chills

Bloating

Jaundice (yellowing of the skin and eyes)

High Risk of Cholecystitis

Women over 50
 People over 60

People who have a family history of gallstones

People whose diet is high in fat and cholesterol

People who are overweight or obese

People who have diabetes

Management
Cholecystectomy: If the condition worsens the doctor may suggest getting a
cholecystectomy. A cholecystectomy is a low-risk surgical procedure that removes the
gallbladder from the body. The surgery usually only lasts about one hour and the patient is
given general anesthesia. One does not need a gallbladder in order to digest food properly.

Complications
Enlarged gallbladder: If left untreated, the gallbladder may swell to a size that is very
uncomfortable. Swelling also increases the risk of the gallbladder tearing, which could
lead to infection or tissue death.
Infection within the gallbladder: If too much bile builds up within the gallbladder, the bile
may become infected. The infected bile can then leak to the lining of the abdomen and
other organs to cause more complications.

Death of gallbladder tissue: If tearing occurs and the blood flow comes to a stop, the
tissue can die and the gallbladder can burs

CHOLELITHS

Gallstones, or choleliths, are solid masses formed from bile precipitates. These stones
may occur in the gallbladder or the biliary tract (ducts leading from the liver to the small
intestine).There are two types of gallstones: cholesterol and pigment stones. Cholesterolstones
are yellow-green and are primarily made of hardened cholesterol. Cholesterol stones,
predominantly found in women and obese people, are associated withbile supersaturated with
cholesterol. They account for 80% of gallstones and are more commonly involved in obstruction
and inflammatory.
Pigment stones may beblack or brown stones. Black pigment stones are made of pure
calcium bilirubinate or complexes of calcium, copper, and mucin glycoproteins. These
gallstonestypically form in conditions of stasis (e.g., parenteral nutrition) or excess unconjugated
bilirubin (e.g., hemolysis or cirrhosis). Black pigment stones are more likely toremain in the
gallbladder. Brown pigment stones are composed of calcium salts of unconjugated bilirubin with
small amounts of cholesterol and protein. These stonesare often located in bile ducts causing
obstruction and are usually found in conditions where there is infected bile. Brown pigment
stones are prevalent in Asiancountries and are rarely seen in patients in the United States.

Symptoms and Clinical Features

Most people with gallstones do not have symptoms, however those who do have symptoms
are much more likely to develop complications.Seventy to 80% of symptomatic patients
complain of biliary colic. Biliary colic is a visceral pain, thought to be caused by functional
spasm, resulting from transientobstruction of the cystic duct by a stone.
The pain is characterized as episodic and severe epigastric pain; less commonly, it is
located in the right upper quadrant, leftupper quadrant, precordium, or lower abdomen. The pain
generally has a sudden onset, rising in intensity, and lasting from 15 minutes to several hours.
Pain may beaccompanied by radiation to the interscapular region or the right shoulder often with
vomiting and diaphoresis.
Biliary colic may also present with symptoms ofnonspecific dyspepsia such as intolerance
of fatty foods, pyrosis, flatulence, aerophagia sweating, yellowish color of skin or sclera of the
eye, and clay-colored stoolsare symptoms that suggest complications such as cholangitis and
choledocholithiasis and warrant immediate medical attention. The interval between attacks
isunpredictable and may range from days to months or years (Reshetnyak, 2012)
Figure 7. Illustrations of cholesterol and pigments stones (Reshetnyak, 2012)

Figure 8. Normal anatomy of the ballary system (Reshetnyak, 2012)

 Figure 9. Ultrasonography of gallstones; A.ultrasound probe positioning; B.gallstone-filled
gallblader; C.ultrasound image showing gallstones (Reshetnyak, 2012)

Figure 10. It shows a diagram of gallstone formation by taking into account the above impaired
bile production and excretion processes (Reshetnyak, 2012)
OMPHALOCELE

Omphalocele is a congenital midline abdominal defect allowing hearniation of the liver

and gut into the base of umbilicus. There is always a covering over the defect, or at least
remnants of a cover, and the liver is evodent within the larger defects. The sac covering the
omphalocele is thin and allows significanr fluid, electrolyte, and thermal loss. Differentiation of
omphalocele from other abdominal wall defects is dobne by determining the location of the
fascial defect, and the nature of any covering over the bowel. These features are distict for
omphalocele because of the events during embryogenesis that bring out this entity (Bendavid,
2012).

Figure 11. Omphalocele

HIRSCHSPRUNG DISEASE

Hirschsprung disease is a developmental disorder characterized by absence of ganglia in

the distal colon, resulting in a functional obstruction.Most cases of Hirschsprung disease are
diagnosed in the newborn period. Hirschsprung disease should be considered in any newborn
that fails to pass meconium within 24-48 hours of birth. Although contrast enema is useful in
establishing the diagnosis, full-thickness rectal biopsy remains the criterion standard. Once the
diagnosis is confirmed, the definitive treatment is to remove aganglionic bowel and to restore
continuity of the healthy bowel with the distal rectum, with or without an initial intestinal
diversion (Wagner, 2015).

Figure 12. Hirschsprung disease. Barium enema technique shows slow contrast-material infusion
(Neville, 2014).

Figure 13. Intraoperative finding in total colonic aganglionosis. Note the decompressed bowel
adjacent to the distended colon (Yoshida, 2015)

HEPATOMEGALI

Normal size The liver is wedge-shaped and is present in the right upper quadrant of the
abdomen. The liver typically extends from the fifth intercostal space to the right costal margin in
the midclavicular line. The size of the liver increases with age, from an average span of 5 cm at
the age of five years, to 15 cm in adulthood [1]. The size of the normal liver also varies with sex
and body size. The normal liver weighs 1.4 to 1.5 kg in men and 1.2 to 1.4 kg in women.
Relative to body size, the liver is larger in the fetus(1/18 of total body weight) than in the
adult (1/36 of total body weight).

By ultrasound, a normal liver is less than 16 cm in the midclavicular line. In a study of 2080
patients who underwent transabdominal ultrasonography, the average liver span in the
midclavicular line was 14.0 +/- 1.7 cm, with 74 percent having a liver span of 15 cm or less.
Fourteen percent had a liver span of 15 to 16 cm, and 12 percent had a liver span of >16 cm. On
multivariable analysis, liver span correlated directly with height and body mass index and was
greater in men.

Normal anatomy Classically, the liver is divided into right and left lobes. In the normal liver,
the right lobe is larger than the left lobe and occupies the right hypochondrium. The smaller left
lobe is flatter and is situated in the epigastrium and left hypochondrium.

Hepatomegaly is enlargement of the liver beyond its normal size and occurs mainly as a
consequence of pathologic conditions. It can be happens because of liver failure, alcoholism, and
neoplasma.

Figure 14. Hepatomegaly

INTUSSUSCEPTION

Intussusception is a condition that usually occurs in children , and is very rare in adults,
intussusception is the entry segment of bowel proximal (towards oral) kerongga intestinal lumen
more distal (towards anal) , causing symptoms of obstruction continues strangulated bowel
Another definition invagination or intususcepti the entry segment of intestine (Intesusceptum)
into the intestine segment nearby (intususcipient) . In general, the proximal part of the intestine
that experienced invaginasi (intussuceptum) enters the distal intestine (intussucipient) , but rarely
there is also the opposite , or retrograde. Most often the entry of the terminal ileum to the colon
.Intussusceptumie incoming intestinal segments and that segment of the intestine intususipien
enter other segments.

Pathophysiology
The wide variety of etiologies that causes intussusception in adults is essentially a disturbance in
intestinal motility consists of two components : one part of the intestine that move freely and one
part of the intestine others are Fixed / or less free than any other part, because the direction of
peristalsis is of oral keanal so that part kelumen entering the intestine is the oral or proximal
direction , other circumstances as a disritmik intestinal peristalsis, in special circumstances may
be otherwise called retrograde intussusception in patients with post gastrojejunostomy. Due to
the intestinal segment that goes kesegmen other intestinal will cause the intestinal wall is
sandwiched so will result in decreased blood flow and the final state is going to cause necrosis of
the bowel wall.
According to high-low split : bowel obstruction high location , small bowel obstruction lies low
and large bowel obstruction .
TRIAS invaginasi :
1. Children sudden episodic pain , crying and pick- foot ( Craping pain) , if further
continuous pain
2. Vomiting green ( gastric fluid )
3. Mucus mixed stool defecation ( mucosal damage ) or blood (inner lining ) currant jelly
stool
 Figure 15. Intussusception
Radiological Examination :
Photo abdomen 3 positions
Obstruction sign ( + ) : Distension, Air fluid level, Hering bone ( picture circularis cords gut )

Figure 16. Intussusception

INGUINAL HERNIA

The pinchcock action of the internal ring musculature during abdominal muscular straining
prohibits protrusion of the intestine into a patent processus. Muscle paralysis or injury can
disable the shutter effect. In addition, the transversus abdominis aponeurosis flattens during
tensing, thus reinforcing the inguinal floor. A congenitally high position of the aponeurotic arch
may preclude the buttressing effect. Neurapraxic or neurolytic sequelae of appendectomy or
femoral vascular procedures may increase the incidence of hernia in these patients.

Clinical presentations suggest repetitive stress as a factor in hernia development. Increased intra-
abdominal pressure is seen in a variety of disease states and seems to contribute to hernia
formation in these populations. Elevated intra-abdominal pressure is associated with chronic
cough, ascites, increased peritoneal fluid from biliary atresia, peritoneal dialysis or
ventriculoperitoneal shunts, intraperitoneal masses or organomegaly, and obstipation (Matthews,
2008).

FEMORAL HERNIA

A femoral hernia follows the tract below the inguinal ligament through the femoral canal. The
canal lies medial to the femoral vein and lateral to the lacunar (Gimbernat) ligament. Because
femoral hernias protrude through such a small defined space, they frequently become
incarcerated or strangulated. Perihernial fasciae or muscles may be malformed (Katz, 2001).

UMBILICAL HERNIA

An umbilical hernia occurs through the umbilical fibromuscular ring, which is usually obliterated
by age 2 years. They are congenital in origin and are repaired if they persist in children older
than 2-4 years. Although umbilical hernias in children arise from failed closure of the umbilical
ring, only 1 in 10 adults with umbilical hernias had this defect as a child. Adult umbilical hernias
occur through a canal bordered anteriorly by the linea alba, posteriorly by the umbilical fascia,
and laterally by the rectus sheath. Proof that umbilical hernias persist from childhood to present
in adulthood is only hinted at by an increased incidence among black Americans. Multiparity,
increased abdominal pressure, and a single midline decussation are associated with umbilical
hernias.

Congenital hypothyroidism, fetal hydantoin syndrome, Freeman-Sheldon syndrome, Beckwith-

Wiedemann syndrome, and disorders of collagen and polysaccharide metabolism (such as
Hunter-Hurler syndrome, osteogenesis imperfecta, and Ehlers-Danlos syndrome), should be
considered as possibilities in children with large umbilical hernias (Scherer, 1993).

Figure 17. Location of Hernia (Matthews, 2008).

HEMORRHOIDS

a. Definition
Hemorrhoids are dilation and inflammation of the veins of the anus region derived from
plexus hemorrhoidalis.
b. Sign and symptoms
Hematochezia
Itching
Perianaldiscomfort
Soiling
The rectal bleeding typically occurswith or immediately after defecation

c. Classification
 Figure
18.
Classification of Hemmorhoids (Jacobs, 2014).

d. Categorized
Internal hemorrhoid
External hemorrhoid
Internal and external hemorrhoid are separated by dentata line.

Figure 19. Internal

Hemorrhoids (Jacobs, 2014).

e. Treatment
Hemorrhoidectomy For patientswho have grade IV disease, complications,or clinically
significant internal and external diseaseor in whom nonoperative treatment hasfailed
(Jacobs, 2014).
 REFFERENCES

Bendavid, Robert et all. 2012. Abdominal Wall Hernias : Principal and Management. New
York : Matrix Publishing Services.

Jacobs, Danny M.D. 2014. Hemorrhoids. Office of the Provost, University of Texas Medical
Branch at Galveston, Massachusetts Medical Society. Available from : nejm.org
(Accessed 30 November 2015).

Katz DA. Evaluation and Management of Inguinal and Umbilical Hernias. Pediatric Ann. 2001
Dec. 30(12) : 729 35.

Matthews RD, Neumayer L. Inguinal Hernia in the 21st Century : An Evidence-Based Review.
Curr Probl Surg. 2008 Apr. 45(4) : 261-312.

Neville, Holly L. 2014. Pediatric Hirschsprung Disease, Medscape Referance, Professor.

Division of Pediatric Surgery, University of Miami, Leonard M Miller School of
Medicine. Available from : http://emedicine.medscape.com/article/929733-
overview#showall (Accessed 30 November 2015).

Reshetnyak, Vasily I. 2012. Concept of the Pathogenesis and Treatment of Cholelithiasis. World
Journal Hepatology 2012 February 27; 4(2):18-34.

Scherer LR 3rd, Grosfeld JL. Inguinal Hernia and Umbilical Anomalies. Pediatric Clinic North
Am. 1993 Dec. 40(6) : 1121-31.

Wagner, Justin P. 2015. Hirschsprung Disease, Medscape Referance, Resident Physician.

Department of Surgery, University of California, Los Angeles, David Geffen School of
Medicine. Available from : http://emedicine.medscape.com/article/178493-
overview#showall (Accessed 30 November 2015).

Yoshida, Ciro. 2015. Hirschsprung Disease Imaging, Medscape Referance, Staff Physician.
Department of Diagnostic Imaging, Federal University of So Paulo (UNIFESP).
Available from : http://emedicine.medscape.com/article/409150-overview#showall
(Accessed 30 November 2015).
Edited by :
Anatomys Assistant Class of 2013
1. Bayu Aji Wicaksono
2. Almira Meida
3. Faradilla Nur Muliana
4. Rosela Alfi Sahara
5. Afra Bryges Tamia
6. Cita Dianita Zealand
7. Nila Munaya
8. Riska Siela Setyawan
9. Zaky Rabbani Mussaad
10. Mukhammad Arifin