BAHAN PEMICU 3

GASTROINTESTINAL
Ivan Buntara
405120049
Learning Objective 1
Describes the anatomy, histology, physiology and biochemistry of colon until anus
ANATOMY OF THE COLON UNTIL ANUS
Rectum
HISTOLOGY OF THE COLON UNTIL ANUS
 LARGE INTESTINE AND APPENDIX
Layers Large Intestine Components
Mucosa -Simple columnar epithelial with
goblet cells (>> small intestine)
-No intestinal villi
Lamina propria -Crypts/Lieberkuhn glands
-Paneth cells (<< small intestine)
-Solitary lymphonodulus
Muscularis mucosa -Circular (inner layer)
-Longitudinal (outer layer)
Submucosa -Lesser connective tissue
-Plexus Meissner
Appendix Components
-Simple columnar epithelial with
goblet cells
-No intestinal villi
-Lesser and smaller
crypts/Lieberkuhn glands
-Lymphonodulus aggregatii
(surround the lumen; extend to
submucosa)
-Rudimenter
-Lipid, lymph vessels, blood vessels,
nerves
 LARGE INTESTINE AND APPENDIX
Layers Large Intestine Components Appendix Components
Muscularis externa -Circular (inner layer) -Circular (inner layer; >> thick and
-Longitudinal (outer layer) → 3 differentiated)
taenia coli -Longitudinal (outer layer)
Serosa -Lesser connective tissue √
-Mesotel layer
Surface -Plica semilunaris, 3 components :
mucosa, submucosa and
muscularis circularis
 RECTUM
• Upper part :
• Crypts (>> wide and long from colon)
• Simple columnar epithelial with goblet cells
• Lower part :
• Simple columnar epithelial with goblet cells
• Permanent longitudinal fold → rectal column / anal column / column of
Morgagni
• Adventisia (no mesotel)

Separated from anus by linea pectinate / linea anorectalis

 ANUS
Columnar Zone Intermedia Zone Cutanea Zone
Epithelial Multiple layer of Multiple layer of Multiple layer of
columnar or low squamous with no keratin squamous with keratin
columnar (>> thick from cutanea
zone)
++ Dermis : sudorifera
glands, sebacea glands,
hair follicles, circumanal
glands
PHYSIOLOGY OF THE COLON UNTIL ANUS
 LARGE INTESTINE
• Primarily a drying and storage organ
• Consists of
• Colon
• Cecum
• Appendix
• Rectum
• Contents received from small intestine consists of indigestible food
residues, unabsorbed biliary components, and remaining fluid
• Colon
• Extracts more water and salt from contents
• Feces – what remains to be eliminated
Chapter 16 The Digestive System
Human Physiology by Lauralee Sherwood
©2007 Brooks/Cole-Thomson Learning
LARGE INTESTINE

Chapter 16 The Digestive System

Human Physiology by Lauralee Sherwood
©2007 Brooks/Cole-Thomson Learning
 LARGE INTESTINE
• Taeniae coli
• Longitudinal bands of muscle
• Haustra
• Pouches or sacs
• Actively change location as result of contraction of circular smooth muscle
layer
• Haustral contractions
• Main motility
• Initiated by autonomous rhythmicity of colonic smooth muscle cells

Chapter 16 The Digestive System

Human Physiology by Lauralee Sherwood
©2007 Brooks/Cole-Thomson Learning
 LARGE INTESTINE
• Mass movements
• Massive contractions
• Moves colonic contents into distal part of large intestine
• Gastrocolic reflex
• Mediated from stomach to colon by gastrin and by autonomic nerves
• Most evident after first meal of the day
• Often followed by urge to defecate

Chapter 16 The Digestive System

Human Physiology by Lauralee Sherwood
©2007 Brooks/Cole-Thomson Learning
 LARGE INTESTINE
• Defecation reflex
• Initiated when stretch receptors in rectal wall are stimulated by distension
• Causes internal anal sphincter to relax and rectum and sigmoid colon to
contract more vigorously
• If external anal sphincter (skeletal muscle under voluntary control) is also
relaxed, defecation occurs

Chapter 16 The Digestive System

Human Physiology by Lauralee Sherwood
©2007 Brooks/Cole-Thomson Learning
BIOCHEMISTRY OF THE COLON UNTIL
ANUS
 LARGE INTESTINE
• Parasympathetic nerve stimulation → goblet cells secretion ↑ →
mucus
• Absorption of water, salts, carboxylic acid and a little bit of nutrients
• Not produce digestive enzyme
 LARGE INTESTINE
• Enteric bacteria
• Normal flora
• Produce enzyme that can ferment food residue, e.g. E. coli
• Convert disaccharides → monosaccharides → carboxylic acid
• Help protein degradation into ammonia
• The growth in the small intestine is inhibited by low pH, foods flow and
peristaltic movement
Learning Objective 2
Describes about gastroenteritis (acute diarrhea and typhoid fever)
 ACUTE DIARRHEA
• Passage of frequent unformed stools less than 14 days
 ETIOLOGY OF ACUTE DIARRHEA-INFECTION
• Virus : astrovirus, calcivirus (norovirus, sapovirus), coronavirus,
cytomegalovirus, echovirus, enteric adenovirus, herpes simplex virus,
rotavirus
Infantile diarrhea : rotavirus, norovirus, astrovirus, adenovirus
 ETIOLOGY OF ACUTE DIARRHEA-INFECTION
• Bacteria : Aeromonas, Bacillus cereus, Bacteroides fragilis,
Campylobacter jejuni, Clostridium difficile, Clostridium perfringens,
Eschericia coli, Klebsiella sp., Plesiomonas shigeloides, Proteus,
Pseudomonas sp., Salmonella sp., Shigella sp., Staphylococcus aureus,
Streptococcus sp., Vibrio cholerae, Vibrio parahaemolyticus, Yersinia
enterocolitica
Infantile diarrhea : enteropathogenic Eschericia coli (EPEC),
enterotoxigenic Eschericia coli (ETEC), enteroinvasive Eschericia coli
(EIEC), Salmonella sp., Shigella sp., Campylobacter jejuni
 ETIOLOGY OF ACUTE DIARRHEA-INFECTION
Parasites :
• Nematodes : Ancylostoma duodenale, Ascaris lumbricoides, Strongyloides
stercoralis, Trichinella spiralis, Trichuris trichiura
• Trematodes : Clonorchis sinensis, Echinostoma, Fasciolopsis buski,
Heterophyidae, Schistosoma haematobium, Schistosoma japonicum,
Schistosoma mansoni
• Cestoda : Diphyllobothrium latum, Hymenolepis nana, Taenia saginata,
Taenia solium
• Protozoa : Balantidium coli, Blastocystis hominis, Cyclospora cayetanensis,
Cryptosporidium parvum, Entamoeba histolytica, Giardia lamblia*,
Isospora belli
* Infantile diarrhea
 ETIOLOGY OF ACUTE DIARRHEA-INFECTION
• Fungal : Candida albicans
 ETIOLOGY OF ACUTE DIARRHEA-
NONINFECTION
• Anatomical defects
• Malabsorption
• Endocrinopathy
• Food-poisoning (metals, insecticides, mushrooms)
• Neoplasma
• Allergy
• Crohn disease
• Immune deficiency
 ETIOLOGY OF ACUTE DIARRHEA-
NONINFECTION
• Bowel motility problem
• Drug side effects (e.g. antibiotics)
• Otitis media
• Meningitis sepsis
Drug Associated Diarrhea
 RISK FACTORS OF ACUTE DIARRHEA
• Food (seafood, chicken, eggs, meat)
• Infectious outbreaks
• Family history (IBD)
• Young age
• Immune deficiency
• Malnutrition
• Measles
• Lack of exclusive or predominant breastfeeding
 CLINICAL ASSESSMENT
• Diagnostic tests to find the cause of diarrhea may include the
following
• Medical history and physical examination
The doctor will ask you about your eating habits and medication use and will
examine you for signs of illness
• Stool culture
A sample of stool is analyzed in a laboratory to check for bacteria, parasites,
or other signs of disease and infection.
• Blood tests
Blood tests can be helpful in ruling out certain diseases
• Fasting tests
To find out if a food intolerance or allergy is causing the
diarrhea, the doctor may ask you to avoid lactose,
carbohydrates, wheat, or other foods to see whether the
diarrhea responds to a change in diet
• Sigmoidoscopy
For this test, the doctor uses a special instrument to look at
the inside of the rectum and lower part of the colon
• Colonoscopy
This test is similar to a sigmoidoscopy, but it allows the
doctor to view the entire colon
• Imaging tests
These tests can rule out structural abnormalities as the
cause of diarrhea.
• Stool examination :
• Microscopic examination of stool and cultures
• First : examine for mucus, blood and leukocytes
• Culture if there is blood or leukocytes in the stool; or if the patients is
immunosuppressed
 TREATMENT
• Fluid and electrolyte replacement orally in most cases, intravenous if
severe extremes of age/coma
• Anti-diarrheals
• Antimotility agents: diphenoxylate, loperamide (Imodium®); contraindicated
in mucosal inflammation
• Absorbants: kaolin/pectin (Kaopectate®), methylcellulose, activated
attapulgite → act by absorbing intestinal toxins/micro-organisms, or by
coating intestinal mucosa; much less effective than antimotility agents
• Modifiers of fluid transport: bismuth subsalicylate (Pepto-Bismol®) may be
helpful
 TREATMENT
• Antibiotics: rarely indicated; indications for antimicrobial agents in
acute diarrhea:
• Septicemia
• Prolonged fever with fecal blood or leukocytes
• Clearly indicated: Shigella, V. cholerae, C. difficile, traveller’s diarrhea
[enterotoxigenic E. coli (ETEC)], Giardia, Entamoeba histolytica, Cyclospora
• Salmonella: always treat Salmonella typhi (typhoid or enteric fever)
 PREVENTION
• Use of safe water
• Handwashing
• Food safety
• Use of latrines and safe disposal of stools
 PREVENTION IN CHILDREN
• Promotion of exclusive breastfeeding
• Improved feeding practices
• Rotavirus immunization (until 6 months of age)
• After 6 months → side effects; cannot be administered
• Improved water and sanitary facilities
• Promotion of personal and domestic hygiene
TYPHOID FEVER
Definition
• A systemic disease characterized by fever and abdominal pain and
caused by dissemination of S. typhii or S. paratyphii
Epidemiology
• In worldwide, there are an estimated 22 million cases of typhoid
fever, with 200,000 deaths annually
• The incidence is highest (>100 cases per 100,000 population per year)
in south central and southeast Asia
Risk Factors
• Contaminated water or ice
• Flooding
• Food and drinks purchased from street vendors
• Raw fruits and vegetables grown in fields fertilized with sewage
• Ill household contacts
• Lack of hand washing and toilet access
Transmissions
• Oral transmission via food or beverages handled by an individual who
chronically sheds the bacteria through stool or, less commonly, urine
• Hand-to-mouth transmission after using a contaminated toilet and
neglecting hand hygiene
• Oral transmission via sewage-contaminated water or shellfish
(especially in the developing world)
 Time frame
• Occurs gradually over a few weeks after exposure to the bacteria. Sometimes children
suddenly become sick.
• The condition may last for weeks or even a month or longer without treatment.

First-Stage Typhoid Fever

The beginning stage is characterized by high fever,fatigue, weakness, headache, sore
throat, diarrhea, constipation, stomach pain and a skin rash on the chest and
abdominal area. According to the Mayo Clinic, adults are most likely to experience
constipation, while children usually experience diarrhea.
 Second stage
Second-stage typhoid fever is characterized by weight loss, high fever, severe
diarrhea and severe constipation. Also, the abdominal region may appear severely
distended.

Typhoid State
When typhoid fever continues untreated for more than two or three weeks, the effected
individual may be delirious or unable to stand and move, and the eyes may be partially
open during this time. At this point fatal complications may emerge.
Jana B. Essentials of practice of medicine. New Delhi: B. Jain
Publishers (P) Ltd.; 2002.
Signs and Symptoms
• Symptoms
• Prolonged Fever (38.8°–40.5°C)
• Headache (80%)
• Chills (35–45%)
• Cough (30%)
• Sweating (20–25%)
• Myalgias (20%)
• Malaise (10%)
• Gastrointestinal symptoms
• Anorexia (55%)
• Abdominal pain (30–40%)
• Nausea (18–24%)
• Vomiting (18%)
• Diarrhea (22–28%)

• Physical findings
• Coated tongue (51–56%)
• Splenomegaly (5–6%)
• Abdominal tenderness (4–5%)
• Early physical findings : rash ("rose spots"; 30%),
hepatosplenomegaly (3–6%), epistaxis, and relative
bradycardia
Clinical Assesment
• Microbiological procedures
• Blood culture
• Gold standard
• A typical blood culture bottle contains 45 ml of tryptic soy broth or brain heart infusion
broth.
• The best agar is blood agar (horse or sheep blood) as this allows the growth of most
bacterial pathogen
• For suspected tyhoid fever, subculture plates should be incubated at 37°C for 18-24
hours in an aerobic incubator
• Stool or rectal swab culture
• This involves inoculating 1 g of stool into 10 ml of selenite F broth and incubating at 37°C
for 18-48 hours
Clinical Assesment
• Microbiological procedures
• Bone marrow culture
• Gold standard
• Colony characteristic
• Blood agar
• On blood agar, S. typhii and S. paratyphii usually produce non-
haemolytic smooth white colonies
• MacConkey agar
• On MacConkey agar, salmonellae produce lactose non-fermenting
smooth colonies
• SS agar
• On SS agar, salmonellae usually produce lactose non-fermenting
colonies with black centres (except S. paratyphi A, whose colonies do
not have black centres)
• Desoxycholate agar
• On desoxycholate agar, salmonellae produce lactose non-fermenting
colonies with black centres (except S. paratyphi A, whose colonies do
not have black centres)
• Widal Test
• This test measures agglutinating antibody levels against O
and H antigens
• The levels are measured by using doubling dilutions of sera
in large test tubes
• Usually, O antibodies appear on days 6-8 and H antibodies
on days 10-12 after the onset of the disease
• The test has only moderate sensitivity and specificity
 TUBEX TEST
• Fast semi-quantitative colorimetric test for typhoid fever
• Detect anti-S. typhi O9 (IgM) antibody on patient’s serum → these
antibodies can inhibit the binding between an indicator-binding
bound particle + magnetic-antigen bound particle
• High sensitivity and specificity (75 – 90%)
• Simple, easy to use
• Has already done in Indonesia

Sudoyo AW, Setiyohadi B, Alwi I, Simadibrata M, Setiadi S, editor. Buku ajar ilmu penyakit dalam. Edisi 5. Jilid I. Jakarta: Pusat Penerbitan Ilmu Penyakit Dalam FKUI;
2008.
Tam FCH, Ling TKW, Wong KT, Leung DTM, Chan RCY, Lim PL. The TUBEX test detects not only typhoid-specific antibodies but also soluble antigens and whole
bacteria. J Med Microbiol March 2008;57(3):316-23.
Choerunisa N, Tjiptaningrum A, Basuki W. Proporsi pemeriksaan IgM anti salmonella typhi 09 positif TUBEX dengan pemeriksaan WIDAL positif pada pasien klinis
demam tifoid akut di RSUD Dr. H. Abdul Moeloek Bandar Lampung; 2014.
 TUBEX TEST
• (+) result : Salmonellae serogroup D infection, Salmonella typhi,
Salmonella enteritidis
• (-) result : Salmonella paratyphi, Salmonella typhimurium, Eschericia
coli, Salmonella enterica serotype enteridis

Sudoyo AW, Setiyohadi B, Alwi I, Simadibrata M, Setiadi S, editor. Buku ajar ilmu penyakit dalam. Edisi 5. Jilid I. Jakarta: Pusat Penerbitan Ilmu
Penyakit Dalam FKUI; 2008.
Tam FCH, Ling TKW, Wong KT, Leung DTM, Chan RCY, Lim PL. The TUBEX test detects not only typhoid-specific antibodies but also soluble
antigens and whole bacteria. J Med Microbiol March 2008;57(3):316-23.
Choerunisa N, Tjiptaningrum A, Basuki W. Proporsi pemeriksaan IgM anti salmonella typhi 09 positif TUBEX dengan pemeriksaan WIDAL positif
pada pasien klinis demam tifoid akut di RSUD Dr. H. Abdul Moeloek Bandar Lampung; 2014.
 TUBEX TEST
• Antigen O9 → immunodominant
→ initiate immune response quickly → earlier detection (day 4 - 5 for primary
infection; day 2 – 3 for secondary infection)

Sudoyo AW, Setiyohadi B, Alwi I, Simadibrata M, Setiadi S, editor. Buku ajar ilmu penyakit dalam. Edisi 5. Jilid I. Jakarta: Pusat
Penerbitan Ilmu Penyakit Dalam FKUI; 2008.
 TUBEX TEST
• 3 components :
• V cylinder → enhance sensitivity
• Magnetic particle that coated with S. typhi O9 antigen (reagent A)
• Blue-colored latex particle that coated with specific monoclonal antibody for
O9 antigen (reagent B)

Sudoyo AW, Setiyohadi B, Alwi I, Simadibrata M, Setiadi S, editor. Buku ajar ilmu penyakit dalam. Edisi 5. Jilid I. Jakarta: Pusat
Penerbitan Ilmu Penyakit Dalam FKUI; 2008.
 TUBEX TEST
1. 1 drop of serum inserted into a tube that has 1 drop of reagent A
2. 2 drops of reagent B is inserted into the tube
3. The tube is placed on a magnetic rotary and rotated about 2
minutes with 250 rpm velocity
4. Interpretation from the color of the mixture (reddish – bluish)

Sudoyo AW, Setiyohadi B, Alwi I, Simadibrata M, Setiadi S, editor. Buku ajar ilmu penyakit dalam. Edisi 5. Jilid I. Jakarta: Pusat
Penerbitan Ilmu Penyakit Dalam FKUI; 2008.
 TUBEX TEST
Score (Based on the Color Scale) Interpretation Meaning
<2 Negative (red color) No active typhoid infection
3 Borderline Cannot be interpreted. Repeat the
test (on the same day / the next
few days)
4-5 Positive Active typhoid infection
>6 Positive (blue color) Strong indication for typhoid
infection

Sudoyo AW, Setiyohadi B, Alwi I, Simadibrata M, Setiadi S, editor. Buku ajar ilmu penyakit dalam. Edisi 5. Jilid I. Jakarta: Pusat
Penerbitan Ilmu Penyakit Dalam FKUI; 2008.
 TUBEX TEST

Tam FCH, Ling TKW, Wong KT, Leung DTM, Chan RCY, Lim PL. The TUBEX test detects not only typhoid-specific antibodies but
also soluble antigens and whole bacteria. J Med Microbiol March 2008;57(3):316-23.
 TUBEX TEST WEAKNESSES
• Sometimes hard to interpret
• False positive result in :
• Non-typhoid Salmonella infection, e.g. Salmonella enterica serotype enteridis
• Other bacteria species
• Malaria
• Immunology disturbance
• Chronic liver disease
• Incorrect antibiotic regiment

Choerunisa N, Tjiptaningrum A, Basuki W. Proporsi pemeriksaan IgM anti salmonella typhi 09 positif TUBEX dengan
pemeriksaan WIDAL positif pada pasien klinis demam tifoid akut di RSUD Dr. H. Abdul Moeloek Bandar Lampung; 2014.
 TYPHIDOT TEST
• Detect IgM and IgG antibody on the outer protein membrane of
Salmonella typhi
• Done on day 2 – 3 after infection
• Sensitivity : 79 – 98%; specificity : 76,6 – 89%

Sudoyo AW, Setiyohadi B, Alwi I, Simadibrata M, Setiadi S, editor. Buku ajar ilmu penyakit dalam. Edisi 5. Jilid I. Jakarta: Pusat
Penerbitan Ilmu Penyakit Dalam FKUI; 2008.
 TYPHIDOT TEST
• Reinfection case → IgG is over activated → hard to detect IgM
• IgG can exists until 2 years → hard to differentiate between
reinfection case or convalescent stage in primary infection

• Typhidot-M test (modification of typhidot test) → totally inactivates

IgG on sample serum; antigen binds to specific IgM

Sudoyo AW, Setiyohadi B, Alwi I, Simadibrata M, Setiadi S, editor. Buku ajar ilmu penyakit dalam. Edisi 5. Jilid I. Jakarta: Pusat
Penerbitan Ilmu Penyakit Dalam FKUI; 2008.
Treatment
• General management
• Oral or intravenous hydration
• The use of antipyretics
• Appropriate nutrition
• Blood transfusions if indicated
Complication
• Gastrointestinal bleeding (10–20%) and intestinal perforation (1–3%)
• Most commonly occur in the third and fourth weeks of illness
• Result from hyperplasia, ulceration, and necrosis of the ileocecal Peyer's
patches at the initial site of Salmonella infiltration
• Neurologic manifestations (2–40%)
• Meningitis, Guillain-Barré syndrome, neuritis, and neuropsychiatric symptoms
Learning Objective 3
Describes about diarrhea classification
• Based on the onset : acute, persistent or chronic
• Based on the volume : small volume (typical of colonic disease) or
large volume (typical of small bowel disease)
• Based on the type of the secretions : watery or steatorrhea
• Based on the mechanisms : secretory (persists with fasting), osmotic
(stops with fasting), inflammatory or exudative
 BASED ON THE ONSET
• Acute diarrhea  greater number of stools of decreased form from
the normal lasting for less than 14 days
• Persistent diarrhea  if the illness persists for more than 14 days
• Chronic diarrhea  if the duration of symptoms is longer than 1
month
 BASED ON THE MECHANISM
• Secretory Diarrhea
• Due to derangements in fluid and electrolyte transport across the
enterocolonic mucosa
• Characterized clinically by
• Watery, large-volume fecal outputs that are typically painless and persist with fasting
• Because there is no malabsorbed solute, stool osmolality is accounted for by normal
endogenous electrolytes with no fecal osmotic gap
• Osmotic Diarrhea
• Occurs when ingested, poorly absorbable, osmotically
active solutes draw enough fluid into the lumen to exceed
the reabsorptive capacity of the colon
• Fecal water output increases in proportion to such a solute
load
• Characteristically ceases with fasting or with
discontinuation of the causative agent
• Inflammatory Diarrhea
• Damage to the mucosal lining or brush border  passive
loss of protein-rich fluids, and a decreased ability to absorb
these lost fluids
• Features of all three of the other types of diarrhea can be
found in this type of diarrhea
• Exudative Diarrhea
• Occurs with the presence of blood and pus in the stool
• Occurs with inflammatory bowel diseases, such as Crohn‘s
disease or ulcerative colitis, and other severe infections
 BASED ON THE ETIOLOGY
• Infectious agents
• Most infectious diarrheas are acquired by:
• fecal-oral transmission
• ingestion of food or water contaminated with pathogens from human or animal feces
• Disturbances of flora by antibiotics can lead to diarrhea by reducing the
digestive function or by allowing the overgrowth of pathogens
• Non-infectious agents
Learning Objective 4
Describes about alarm symptoms of gastroenteritis
Learning Objective 5
Describes about stage of dehydration
DEHYDRATION
 DEFINITION
• Lack of water content in the body
 PATHOPHYSIOLOGY OF DEHYDRATION
BECAUSE OF DIARRHEA
• Diarrhea  excess loss of fluids and essential electrolytes from the
body  fluid lost in the stools is not replaced  dehydration
 TREATMENT OF DEHYDRATION
• Minimal or no dehydration
• Rehydration therapy - Not applicable
• Replacement of losses
• Less than 10 kg body weight - 60-120 mL oral rehydration solution for each diarrhea stool
or vomiting episode
• More than 10 kg body weight - 120-140 mL oral rehydration solution for each diarrhea
stool or vomiting episode
• Mild-to-moderate dehydration
• Rehydration therapy - Oral rehydration solution (50-100 mL/kg
over 3-4 h)
• Replacement of losses
• Less than 10 kg body weight - 60-120 mL oral rehydration solution
for each diarrhea stool or vomiting episode
• More than 10 kg body weight - 120-140 mL oral rehydration
solution for each diarrhea stool or vomiting episode
• Severe dehydration
• Rehydration therapy - Intravenous lactated Ringer solution or
normal saline (20 mL/kg until perfusion and mental status
improve), followed by 100 mL/kg oral rehydration solution over
4 hours or 5% dextrose (half normal saline) intravenously at
twice maintenance fluid rates
• Replacement of losses
• Less than 10 kg body weight - 60-120 mL oral rehydration solution
for each diarrhea stool or vomiting episode
• More than 10 kg body weight - 120-140 mL oral rehydration
solution for each diarrhea stool or vomiting episode
• If unable to drink, administer through nasogastric tube or
intravenously administer 5% dextrose (one fourth normal saline)
with 20 mEq/L potassium chloride
 REHYDRATION
• Oral rehydration with fluids containing glucose, Na+, K+, Cl–, and
bicarbonate or citrate is preferred when feasible
• Fluids should be given at rates of 50–200 mL/kg/24 h depending on the
hydration status
• Intravenous fluids are preferred in patients with severe dehydration
 REFERENCES
• Managing acute gastroenteritis among children. CDC Morbidity and
Mortality Weekly Report; 2003.
• Netter FH. Atlas of human anatomy. 6th ed. Philadelphia: Saunders Elsevier;
2014.
• Eroschenko VP. Atlas histologi diFiore: dengan korelasi fungsional. Ed 11.
Jakarta: EGC; 2008.
• Sherwood L. Introduction to human physiology. 5th ed. United States:
Brooks/Cole-Thomson Learning; 2007.
• Jana B. Essentials of practice of medicine. New Delhi: B. Jain Publishers (P)
Ltd.; 2002.
• Wyllie R. The digestive system. In: Kliegman RM, Behrman RE, Jenson HB,
Stanton BF. Nelson’s textbook of pediatrics. 18th ed. Philadelphia: WB
Saunders Co; 2007: 1521-645.
 REFERENCES
• Tam FCH, Ling TKW, Wong KT, Leung DTM, Chan RCY, Lim PL. The
TUBEX test detects not only typhoid-specific antibodies but also
soluble antigens and whole bacteria. J Med Microbiol March
2008;57(3):316-23.
• Choerunisa N, Tjiptaningrum A, Basuki W. Proporsi pemeriksaan IgM
anti salmonella typhi 09 positif TUBEX dengan pemeriksaan WIDAL
positif pada pasien klinis demam tifoid akut di RSUD Dr. H. Abdul
Moeloek Bandar Lampung; 2014.