PROBLEM 3

GROUP 13
GROUP 13
• Tutor : dr. Ayda Rahmat,MS, Sp.Park
• Leader : Adhitia Mahardika (405100124)
• Secretary : Mieliani (405080191)
• Scriber : Rahma Marini Sulwana (405100200)
• Members :
– Renata C.F. Tjieputri (405080137)
– Feny Chandra Dewi (405090208)
– Charlie (405100005)
– Felicia Faustine Faraday (405100070)
– I Putu Mana Nitia (405100103)
– Boe, Obet Agung Sanjaya (405100125)
– Eva Fauziah (405100132)
– Andy Halim (405100193)
– Khairunnisa Nugrahenni (405100210)
 PROBLEM 3
• A 38-year-old-man presents to the emergency room with
2 days of watery diarrhea about five to six times a day,
accompanied with crampy abdominal pain, nausea, and
vomiting. He also has sustained fever and severe
headache since a week ago. The fever usually rises in
afternoon. He has not had any blood in his stool. He
denies contact with anyone with similar symptoms
recently. He has not eaten any raw or unprocessed food
recently. On examination, he is tired appearing, his
temperature is 39°C, and his heart rate is 60 beats per
minute. Mouth examination : mucous membrans appear
dry ; coated tongue. Abdominal exam is notable for
diffuse tenderness. The spleen and liver are enlarged.
• What can you learn from the problem?
 UNFAMILIAR TERMS
• Crampy abdominal pain : contraction
of abdominal muscle continiously
• Coated tongue : The
presence of a whitish layer on the upper
surface of the tongue, composed of
epithelial debris, food particles, and
bacteria.
 LEARNING OBJECTIVE
1. ANATOMY OF LOWER GIT
2. HISTOLOGY OF LOWER GIT
3. PHYSIOLOGY OF LOWER GIT
4. BIOCHEMISTRY OF LOWER GIT
5. EXPLAIN ABOUT GASTROENTERITIS
6. EXPLAIN ABOUT THYPOID FEVER
LO 1. ANATOMY LOWER GIT
Anatomy of GI Tract
 SMALL INTESTINAL
• 6-7 m : - 2 / 5 Jejunum
- 3 / 5 ileum
from the duodeno flexura jejunalis -
estuary of cecum

• Location: intra-peritoneal
 DIFFERENCE BETWEEN
JEJUNUM AND ILEUM

JEJUNUM ILEUM

Diameter > <

Wall thicker thinner
Arcaden one/ two multiple
stacking
Folliculi Folliculi lymphatici
lymph nodes lymphatici aggregati/ Peyer patch
solitarii
 VASCULARITATION
Of intestine
• ARTERY : Aa. Jejunales et ileii
(branch of A.mesenterica superior )

• VEIN : V.mesenterica sup.

Large intestine
LO2. HISTOLOGY LOWER GIT
HISTOLOGY OF LOWER GI
TRACT

Structures of the Alimentary Canal

Duodenum
a. Lieberkhun gland
b. Tunica mucosa
c. Brunner gland
d. Tunica submucosa
e. Tunica muscularis
Jejunum
a. Villi
b. Plica kerckringi
c. Tunica muscularis
mucosa
d. Tunica submucosa
e. Tunica muscularis
Panneth cells
Ileum
a. Villi
b. Lymphonodus aggregati
c. Tunica muscularis
mucosa
d. Tunica submucosa
e. Tunica muscularis
 Appendix

• Lymphatic nodules
with germinal centers
are numerous and highly
characteristic of the
appendix
• Intestinal glands are
less developed

22
Colon Jejunum

Ileum Rectum
 Rectum

The longitudinal
folds in the upper
rectum and colon
are temporary

25
Rectum and Anal canal

26
LO3. PHYSIOLOGY OF LOWER
GIT
 Colon
• The movements of the colon :
– Segmentation contractions
– Peristaltic waves
– Mass action contraction
• Transit time in the small intestine and colon :
– The 1st part of a test meal reaches cecum in about 4 hours
and all of the undigested portions have entered the colon
in 8-9 hours.
– On average, the 1st remnants of the meal reach the
hepatic flexure in 6 hours, the splenic flexure in 9 hours
and the pelvic colon in 12 hours
– From the pelvic colon to the anus, transport is much
slower
 Colon
• Absorption in the colon :
– The absorptive capacity of the mucosa of the large
intestine is great
– The absorptive capacity of the colon makes rectal
instillation a practical route for drug administration,
especially in children.
• Feces, stools contain :
– Inorganic material
– Undigested plant fibers
– Bacteria
– water
 Defecation
• Distention of the rectum with feces initiates reflex
contractions of its musculature and the desire to
defecate.
• In human, the sympathetic nerve supply to the
internal (involuntary) anal sphincter is excitatory,
where as the parasympathetic supply is inhibitory.
• When rectal pressure increased to about 18 mmHg
 urge to defecate first occur.
• When rectal pressure reaches 55 mmHg  the
external as well as the internal expulsion of the
contents of the rectum.
• The waves start at the stomach and migrate
down the intestine; that is, each new
peristaltic wave is initiated at a site a little
farther down the small intestine.
• After the end of the small intestine is
reached, the cycle begins again and
continues to repeat itself until the next meal
• The migrating motility complex is regulated
between meals by the hormone motilin,
which is secreted during the unfed state by
endocrine cells of the small-intestine mucosa.
LO4. BIOCHEMISTRY OF LOWER
GIT
• Biochemical balance among the stomach,
pancreas, and small intestine is normally
maintained
• HCl + NaHCO3  NaCl + H2CO3
• The resultant H2CO3 decomposes into CO2 +
H2O:
• H2CO3  CO2 + H2O
• Th e end products of these reactions—Na, Cl,
CO2, and
• H2O—are all absorbed by the intestinal
epithelium into the blood.
LO5. EXPLAIN ABOUT
GASTROENTERITIS
 Definition
 An increase in the frequency of bowel
movements (3x per day or more) and a
decrease in the form of stool (greater
looseness of stool) with or without blood.
• Caused by increased secretion of fluid into
the intestine, reduced absorption of fluid from
the intestine / rapid passage of stool through
the intestine

• Adults + typical western diet: stool weight

>200g/d  considered diarrheal
 ETIOLOGY
Viruses : Enterovirus, adenovirus, rotavirus
Enteral Infection
Bacteria : Vibrio, E. coli, Shigella,
Salmonella, Campylobacter,
Yersinia, Aeromonas
Infection Protozoa : G. Lamblia, E.
Histolitica, Isospora belli
Helmin : Ascaris,
Parasites
Trichuris, Oxyyuris,
Caused Strongyloides
of diare
Fungal : Candida albicans

Parenteral Infections : Tonsilofaringitis,

Bronkopneumonia, Morbilli
Malabsorption : Carbohydrate, Lipid, Protein
Food : out-of-date, poisonous
Allergic
Immunodeficiency
Phsycology : afraid, worried
Vibrio cholera Salmonella

Shigella

Campylobacter jejuni E. coli

 Time
• Acute Diarrhea:
Diarrhea who initially suddenly & lasted a
short within a few hours up to 1-2 weeks.
• Chronic diarrhea:
A state of increased stool frequency and
liquidity that can last for weeks (more than 2
weeks) or months either continuously or
repeatedly, can be either functional or
symptom resulting from a severe illness.
Pathophysiological
 Secretory diarrhea:
– Secretion of water and electrolytes into the small
intestine
– This occurs when the absorption of sodium by the
villi failed while chloride secretion in epithelial cells
continue or increase.
– The end result is the secretion of fluid resulting in
loss of water and electrolytes from the body as a
liquid stools -> dehydration.
– Example: E. coli and Vibrio Cholera toxin or
rotavirus
 Osmotic diarrhea:
– Because there was an increase of osmotic contents
of the lumen of the intestine.
Based on the existance of infectious or
not:

– Infective diarrhea is when the cause is infection.

– Non-infective diarrhea: when not found any
infection
Based on the existance of an organic
cause or not:

– Diarrhoea is when discovered the cause of

organic anatomic, bacteriological, hormonal or
toksikologik.
– Functional diarrhea: when no organic cause
found.
 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.
• It can be caused by bacterial infections, viral infections,
parasitic infections, or autoimmune problems such as
inflammatory bowel diseases.
• It can also be caused by tuberculosis, colon cancer, and
enteritis.
Exudative diarrhea
Exudative diarrhea occurs with the presence of blood and pus in
the stool. This occurs with inflammatory bowel diseases, such as
Crohn's disease or ulcerative colitis, and other severe infections
 Steathorrea
• Fat malabsorption 
– greasy,
– foul-smelling,
– difficult-to-flush diarrhea
– often associated with weight loss and
– nutritional deficiencies due to concomitant
malabsorption of amino acids and vitamins
• Steatorrhea is defined as stool fat
exceeding the normal 7 g/d
• e/  Intraluminal maldigestion, mucosal
malabsorption, or lymphatic obstruction
 Gastroenteritis
Causative Agents of Gastroenteritis
• BACTERIA
– Aeromonas
– Bacillus cereus
– Campylobacter jejuni
– Clostridium perfringens
– Clostridium difficile
– Escherichia coli
– Plesiomonas shigelloides
– Salmonella
– Shigella
– Staphylococcus aureus
– Vibrio cholerae 01 and 0139
– Vibrio parahaemolyticus
– Yersinia enterocolitica
** Norwalk-like viruses
* Generally associated with disease only among immuno compromised persons.
• VIRUSES
– Astroviruses
– Caliciviruses
– Norovirus*
– Enteric adenoviruses
– Rotavirus
– Cytomegalovirus*
– Herpes simplex viruses*
• PARASITES
– Balantidium coli
– Blastocystis hominis
– Cryptosporidium parvum
– Cyclospora cayetanensis
– Encephalitozoon intestinalis*
– Entamoeba histolytica
– Enterocytozoon bieneusi*
– Giardia lamblia
– Isospora belli
– Strongyloides stercoralis
– Trichuris trichiura
Bacteria can also responsible for
diarrhea.accompanied by
cramps,blood in his stool and
fever.
 Salmonella, Shigella and
Campylobacter
• Salmonella is contracted by ingesting the bacteria
in contaminated food or water, and by handling
poultry or reptiles such as turtles that carry the
germs.
• Campylobacter occurs by the consumption of raw
or undercooked poultry meat and cross-
contamination with other foods. Infants may
acquire the infection by contact with poultry
packages in shopping carts. Campylobacter is
also associated with unpasteurized milk or
contaminated water. The infection can be spread
to humans by contact with infected stool of an ill
pet (for example, cats or dogs). It is generally not
passed from human to human.
• Shigella bacteria generally spreads from an
infected person to another person. Shigella
are present in diarrheal stools of infected
individuals while they are ill, and for up to one
to two weeks after contracting the infection.
Shigella infection also may be contracted by
eating contaminated food, drinking
contaminated water, or swimming or playing
in contaminated water (for example, wading
pools, shallow play fountains). Shigella can
also spread among men who have sex with
men.
 Clostridium difficile
• Clostridium difficile (C difficile) bacteria may overgrow in the
large intestine after a person has been on antibiotics for an
infection. The most common antibiotics that pose a potential
risk for C difficile include:
– clindamycin (for example, Cleocin),
– Fluoroquinolones (for example, levofloxacin [Levaquin],
ciprofloxacin [Cipro, Cirpo XR, Proquin XR]),
– penicillins, and
– cephalosporins.
• Other risk factors for C difficile infection are hospitalization,
individuals 65 years of age or older, and existing chronic
medical conditions.
• The CDC lists C. Difficile as one of the most common causes
of death due to gastroenteritis and suggest that new strains of
the bacteria have become more aggressive and dangerious.
 Durati
Incubation Associated Laboratory
Etiology Sign and Symptom on of Treatment
Period Foods Testing
Illness
Supportive care for
raw and Routine stool
severe cases,
undercooked, culture;
Watery diarrhea, antibiotics such as
poultry, Campylobacter
Campylobacter cramps, fever and 2-10 erithromycin,
2-5 days unpasturized requires special
jejuni vomiting, diarrhea days quinolones early in
milk, and medium and
may be bloody the diarrhea
contaminated incubation at
disease. GBS can
water 42C to grow
be a sequela.
water or food Supportive care ,
watery diarrhea,
Enterotoxigenic 3 to >7 contaminated antibiotics, include
1-3 days abdominal cramps, stool culture
E. coli ( ETEC ) days with human TNP-smx and
some vomiting
feces quinolones
Supportive care
with aggressive oral
Conaminated and IV rehydration;
Profuse watery
water, fish, tetracyclin,
diarrhea with
shellfish, doxycyclin is
vomiting, wihich can 3-7
Vibrio Cholerae 24-72 hours street-vended Stool culture recommended for
lead to severe days
food typically adult, and TMP-
dehydration and
from latin smx is
death within hours
america recommended for
children ( < 8 years
old )
Unrefrigerate
Normally a
d or
Sudden onset severe clinical
improperly
nausea and diagnosis.
refrigerated
Staphylococcus vomiting. Abdominal 24-48 Stool, vomitus,
1-6 hours meats, Supportive care
aureus cramps, diarrhea, hours and food can be
potato, and
and fever may be tested for toxin
egg salads.
present and culture if
Cream
indicated
pastries.
Gastroenteritis
Gastroenteritis
Gastroenteritis
 Parasitic can also cause
diarrhea.symptoms may include
gas,bloating and greasy stools.
 Entamoeba histolytica
• Although many species of amoeba exist, only E.
histolytica is clearly pathogenic. Transmission occurs by
fecal contamination of food or water. Infection is endemic
throughout the world, especially where poor sanitation
exists.
• Clinical manifestations :
– Diarrhea (with blood & mucus)
– Abdominal pain / acute colitis with abdominal cramps,
• Diagnosis is usually made by identification of trophozoites
in stool. Serology also may be helpful,particularly with
diagnosis of extraintestinal amebiasis and
liverinvolvement.
 Strongyloides stercoralis
• This roundworm,2.5 mm in length, is endemic in southern
U.S. and common in tropicsand Asia.
• Clinical manifestation:
– Skin becomes red and pruritic after penetration by larvae, which
usually occurs on feet.
– Diarrhea,
– Vomiting
– Abdominal pain ( larva penetrate to mucous)
– Cough and pneumonia after migration of larvae through lung
scan
– Peripheral eosinophilia may occur.
– Autoinfection
• Identification of larvae in stool isdiagnostic.
• Complication : hyperinfection
 Ascaris lumbricoides
• Clinical manifestations:
• Can be asymptomatic
• Mild diarrhea
• Intermittent epigastric pain
• Anorexia
• Vomiting
• Syndrome loeflerr
• Obstruction
• Diagnosed: by identifying whitish-brown Ascaris worm,20–
40 cm in length, or finding Ascaris eggs on microscopic
exam of stool is diagnostic.
 Hookworm Infection
• Adult hookworms (N. americanus and A. duodenale)
• Clinical manifestations:
– Red, pruritic lesions on feetor between toes where larvae
penetrate.
– Diarrhea
– Vomiting
– Abdominal pain
– Anemia from GI blood loss
– Peripheral eosinophilia.
– Pneumonia

• Detecting hookworm eggs on stool smear is diagnostic.

 Trichuris trichiura
• T. trichiura,4-cm long whipworm, occurs most commonly
in tropical areas but is also found in subtropical areas
(e.g., southern U.S.).
• Clinical manifestations:
– Most individuals are asymptomatic
– Diarrhea
– Tenesmus
– Weight loss
– Anemia
– Prolapsus ani
– Peripheral eosinophilia
• Diagnosed: by seeing eggs on microscopic stool examis
diagnostic.
 Cryptosporodiosis
• Ex: Cryptosporidium parvum
• Oocysts contain naked sporozoites not
surounded by sporocyst
• Was likely a cause of human diarrheal
disease ( Nime et al. 1976)
• Normal & immunocompromised patients
were suspectible to diarrhea caused by
cryptosporodiosis
• ~60% from AIDS patient’s stool
 Clinical features
• 2 major syndromes
– Immunocompetent 
• Acute watery self limited diarrhea,
• Nausea, vomiting, fecal urgency, abdominal
cramps & discomfort
• Low or high grade fever
– Immunocompromised 
• Life-threatening diarrheal illness, relapsing
diarrhea
• Biliary tract infection
 Treatment
• Oral rehydration solution
• Nitazoxanide
• AIDS patients 
– Paramomycin (1g twice daily) & azithromycin
(600 mg twice daily)
– Prophylaxis  Clarithromycin & Rifabutin
 Isosporiasis
• Ex: Isospora belii
• Invades the host cell’s cytoplasm restricted to the
apical surface of the cell  the excreted oocysts not
fully sporulated  not immediately infective for man
• Most cases  oocysts’ maturation occurs outside the
human host & amplification of the infection in human
(autoinfection ~C. parvum)

• Epidemiology
– From tropical & subtropical areas
– Transmitted by contaminated food or water; person-person
 oral-anal contact
– AIDS  persistent & chronic diarrhea
 Clinical features
• A non spesific watery diarrheal illness, +
abdominal cramps, nausea, malaise,
anorexia, weight loss
• Severe illness  dehydration (6 liters of
stool)
• Strikingly protracted illness
• Malabsorption
• AIDS
– Disseminated infection
 Treatment & Prevention
• Maintaining adequate hydration parenterally
• Drug of choice  Cotrimoxazole  resolution
of diarrhea for 2 days
• Ciprofloxacin (500mg twice daily for 7 days)
 intolerate Cotrimoxazole

• Prevention
– Resistant to many disinfectans
– survive for months in the environment under
moist, cool condition
 Cyclospora
• An acid-fast, autofluorescent large Cryptosporidium
like parasite in the stools of a patient with HIV infection

• Epidemiology
– Seasonal occurence of infections among expatriates in
Nepal
– Association with drinking contaminated water & with foods
such as imported raspberries, mesclun lettuce and basil
– Require an obligatory phase of maturation in the
environment after they are excreted in the feces
– Unlikely to be transmitted directly from person to person
– Seasonality infection
 Clinical features
• Substantial symptoms of
– Diarrhea
– Striking fatigue
– Weight loss
– Abdominal cramps
 Treatment
• Treatment
– Cotrimoxazole b.i.d
– Tinidazole, diloxanide, quinacrine,
azithromycin  Ineffective
– Trimethoprim  patient who allergic to
sulfametoxazole
– Ciprofloxacin
 Blastocystis
• Ex: Blastocystis hominis
• Morphology
– Vacuolar form
• Nuclei & mitochondria are seen in the peripheral rim of the cell
surounding the central vacuole (fx  metabolism & storage)
– Granular form
• Numerous small granules on the central vacuole
– Multivacuolar form
• Smaller than vacuolar forms, numerous vacuoles are seen
– Avacuolar form (rare)
– Cyst form
• Condensed cytoplasm contains many vacuoles & often large
reserves of glycogen & lipid
– Amoeboid form (rare)
 Clinical features
• GI infections
– Diarrhea, abdominal pain, cramps or
discomfort, nausea, flatulence, fever
– Rectal bleeding, faecal leukocytes,
eosinophilia, hepato & splenomegaly,
cutaneus rashes & itching
• Extraintestinal infections
– Infection to synovial fluid  joint pain &
swelling
• Symptomless infections
Treatment, Prevention & control
• General anti-protozoal drugs (5-
nitroimidazoles)
• Anti-bacterial compounds (ampicillin,
penicillin, streptomycin, gentamycin, colistin,
ceftizoxime, vancomycin)
• Metronidazole  persist  Cotrimoxazole

• Prevention
– Education to maintain personal & community
hygiene standards
– Improvement in community sanitary engineering
 prevent faecal contamination & ingestion
 Fungal infectious
Candida sp
• C. albicans is most common cause of Candida enteritis
• Characterized by watery diarrhea and abdominal pain.
• Predisposing factors :prolonged antibiotic or
immunosuppressive therapy  yeast forms are
ubiquitous and occur in fecal flora of normal persons, their
presence alone is not diagnostic.
• Definitive diagnosis requires demonstration of intestinal
mucosal invasion by Candida on biopsy or isolation of
Candida from ulcerative lesions.
 VIRAL GASTROENTERITIS

6/18/2019 90
 ETIOLOGY INCUBATIO SIGN & SYMPTOMS DURATIO
N PERIOD N OF
ILLNESS
ROTAVIRUS 1-3 days vomiting, watery diarrhea, low grade 4-8 DAYS
fever, temporary lactose intolerance
may occur infants & children, elderly,
& immunocomprimised are especially
vulnerable

CALICIVIRUSE 12-48 hr Nausea, vomiting, abdominal 12-60 hr

S& cramping, diarrhea, fever, myalgia, &
NOROVIRUS some headache.

OTHER VIRAL 10-70 hr Nausea, vomiting, diarrhea, malaise, 2-9 hr

AGENT abdominal pain, headache, fever
(ADENOVIRUS,
ASTROVIRUSE
S,
PARVOVIRUSE
S)

6/18/2019 91
 LABORATORIUM TESTING TREATMENT

ROTAVIRUS Identification of virus in stool Supportive care, severe diarrhea

via immunoassay may require fluid and electrolyte
replacement

CALICIVIRUSES Routine RT – PCR & EM on Supportive care such us

& NOROVIRUS fresh unpreserved stool rehydration, good hygiene
samples. Clinical diagnosis,
negative bacterial cultures,
stools is negative for WBCs

OTHER VIRAL Identification of the virus in Supportive care usually mild

AGENT early acute stool samples, self limiting, good hygiene
(ADENOVIRUS, serology, commercial ELISA
ASTROVIRUSES
,
PARVOVIRUSES
)
6/18/2019 92
 Clinical Features of Diarrheal Diseases
Location of Infection
Small Bowel Large Bowel
V. cholerae Shigella
ETEC, EPEC, EAggEC EIEC, EHEC
Rotavirus Campylobacter
Norwalk virus E. histolytica
Pathogens Giardia

Location of pain Mid abdomen Lower abdomen, rectum

Volume of stool Large Small

Type of stool Watery Mucoid

Blood in stool Rare Common

Common (except in
Leukocytes in stool Rare amebiasis)
Mucosal ulcers;
Protoscopy Normal hemorrhage; friable mucos
 Complication
• Dehydration
• Malnutrition
• Micronutrient deficiencies
• Secondary infections
 Prevention
• Promotion of exclusive breast feeding
• Improved complementary feeding
practices
• Rotavirus immunization
• Improved water and sanitary facilities
• Promotion of personal and domestic
hygiene
• Improved case management of diarrhea
LO6. EXPLAIN ABOUT THYPOID
FEVER
 Typhoid fever
• Typhoid fever is an acute illness associated with fever
that is most often caused by the Salmonella
typhi bacteria. It can also be caused bySalmonella
paratyphi, a related bacterium that usually leads to a
less severe illness.
• The bacteria are deposited in water or food by a
human carrier and are then spread to other people in
the area. Typhoid fever is rare in industrial countries
but continues to be a significant public-health issue in
developing countries.
•
Approximately 3%-5% of patients become carriers of
the bacteria after the acute illness.
•
 Epidemiology
• With an estimated 16–33 million cases of
typhoid fever annually resulting in 216,000
deaths in endemic areas, the World Health
Organization identifies typhoid as a
serious public health problem. Its
incidence is highest in children and young
adults between 5 and 19 years old.
 cause
• Salmonellae typhi bacteria.
• ingestion of contaminated food or water.
• Contact with an acute case of typhoid
fever or chronic asymptomatic carrier
• Eating food or drinking beverages that
handled by a person carrying the bacteria
 Salmonella typhi
• Structure :
– Basil like shaped
– Gram negative
– Facultative anaerob
– Equipped with capsul to prevent phagocytosis
and flagel for movement
 Salmonella typhi
• Antigen
– Antigen H
• Antigen of the flagel
• Resistance against heat (up to 60 C) and acid (up to
1,5)
• IgG will be produced to fight against it
– Antigen somatic (O)
• Antigen of the outer membrane
• Resistance against heat (up to 100 C) and acid (up to
1,5)
• IgM will be produced to fight against it
– Antigen Vi
• Located above antigen O (capsule)
• Act as capsule to prevent phagocytosis and intracellular
damage
 patphysiology
• bacteria enter through contaminated food.
• some destroyed in the stomach, and some get into the
intestines then proliferate
• When Immunity down, bacteria penetrate the intestinal
epithelial cells  lamina propria proliferate and
phagocytosis by phagocytic cells, especially
macrophages  live inside macrophages and taken to
plaque peyeri ileal mesenteric lymph nodes  through
the toraxic duct into the blood circulation (bacteremia
I).
• Spread to the reticuloendothelial organs, especially
the liver and spleen  left phagocytes  multiply
outside the cell or blood sinusoids  enter again
(bacteremia II)
• In the liver, bacteria enter to gallblader 
proliferate and secreted with bile into the
intestinal lumen  partial exit through the
feces, some into the blood circulation 
repeated cycles
• Macrophages that have been activated and
hyperactive release inflammatory mediators
 fever, malaise, myalgia, headache,
abdominal pain, vascular instability, mental
disorders and coagulation
• Macrophages hyperactive tissue
hyperplasia  erosion of blood vessels
bleeding
 Clinical symptoms
• week I : • week II:
fever fever
Headache Relative bradhycardia
Muscle aches Coated tongue
dizzines Hepatomegaly
Anorexia Splenomegaly
Nausea Meteorismus
Vomiting Somnolen
Obstipasi/diarhea Stupor
Abdominal discomfort coma
cough Delirium
epistaksis psychocis
 examination
• Routine blood test
• Widal test
• tubex test
• Typhidot test
• IgM dipstick test
• Blood cultures
 treatment
• Rest and treatment
• Diet dan adjunctive therapy
• antimicroba
 complication
• Intestinal • Ekstraintestinal
- Intestinal bleeding - Hematologycal
- Intestinal perforation complication
- Paralytic ileus - Hepatitis tifosa
- pancreatitis - Pancreatitis tifosa
- Myocarditis
- Neuropsychiatric/
tifoid toxic
 prevention
• Identification and eradication of S. typhi in
asymptomatic typhoid patients, careers
and acute
• Prevention of direct transmission from
infected patients with acute and career
S.typhi
• Protection to people at risk and infected
 vacination
• Vaksin oral : Ty21a(vivotif berna)
• Vaksin parenteral : ViCPS (typhim Vi/
pasteur merieux
DD OF TYPHOID FEVER
 Such as upper respiratory tract infection.
Abrupt onset with fever, headache, leucopenia,
sore throat, cough, coryza.
No rose spots, no enlargement of liver &
Viral infection spleen. The course of illness no more than 2
weeks.
Differential diagnosis depends on typical
manifestations and blood culture.

History of exposure to malaria.

Paroxysms(often periodic) of sequential
chill,high fever and sweating.
Headache, anorexia, splenomegaly, anemia,
Malaria leukopenia
Characteristic parasites in
erythrocytes,identified in thick or thin blood
smears.

Sudden high fever day 1-3 (above 38,5o C), in

day 3 or day 4-5 increase but not very high
(below 38,5o C)
Dengue Fever
 CONCLUSION
• We had studied learning objective :
– Anatomy, histology, physiology, biochemistry
lower GIT
– Gastroenteritis
– Typhoid fever
– Dehydration
 SUGGESTION
• Further examination:
– Blood Culture and Widal Test
– Lifestyle
– Rehydration
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Fleisher DF, Taminiau J. Childhood functional
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Lange Jawetz, Melnick & Naelberg’s Medical
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• http://emedicine.medscape.com
• http://www.cdc.gov