When Warteg Gives Him More

By : Group 12
Tutor : dr. Veronica Wiwing
FAKULTAS KEDOKTERAN UNIVERSITAS TARUMANAGARA
Member of Group 12
Leader : Melia Sugiarto 405070009
Secretary : Hadiyanti 405070125
Scriber : Nazrien 405070133
Anggota : Arianto Leonardi 405070072
Viencensia 405070090
Diah Permatasari 405070156
Iman Teguh 405070109
Apolonia Aurensya 405070130
Wahyu Wijasena Adhi 407070106
Gladys Sudiyanto 405070123
Ferdy Halim 405070082
Grace 405070080
Scenario
Mr.Surip, a 26-year-old previously healthy
male, has been in Jakarta for about 2 weeks
since he came home from his study in the
States. Ever since, he has eaten any kinds of
Indonesian food, and Warteg is always his
favorite, especially the one across his old
school.
Scenario
Today, Mr.Surip presents to your clinic reporting
a 2-day history of watery diarrhea and he has
noticed that theres blood in his stool. He has
up to 8 bowel movements per day. He has had
intermitten abdominal cramps as well. For the
past 2 days, he also feels nauseated, but no
vomiting. His vital signs are normal, his bowel
sounds are hiperactive and the remainder of
the physical exam is remarkable only for mild,
diffuse abdominal tenderness.
Learning Objectives
Explain about diarrhea, nausea, and vomitting
Describe the most likely mechanism for diarrhea, nausea,
and vomiting
Describe the most likely diagnosis
Describe the expected cause of the disease
Describe the expected corfirmation of the diagnosis
Describe the expected differential diagnosis
Describe the expected risk factor
Describe the expected complication associated with the
disease
Describe the expected management
Describe the expected treatment and health education
NAUSEA AND VOMITING
Definition
Nausea is the subjective feeling of a need to vomit.
Vomiting ( emesis) is the oral explusion of
gastrointestinal contents resulting from contractions
of gut and thoracoabdominal wall musculature.

PATOPHYSIOLOGY
Mechano- and chemoreceptors located in the stomach,
jejunum and ileum are involved with the detection of emetic
stimuli in the gastrointestinal tract.
Mechanoreceptors are tension receptors that initiate emesis
in response to distension and contraction e.g. from bowel
obstruction.
Chemoreceptors respond to a variety of toxins in the
intestinal lumina. It is thought that the afferent neuronal
pathways from the abdomen are the same regardless of the
stimulus.
The final common pathway for efferent responses that
produce emesis is the Vomiting Centre, which controls the act
of vomiting.
Numerous neuronal pathways converge on the Vomiting
Centre in the medulla (part of the hind brain) where the
vomiting reflex is initiated.
The Vomiting Centre is not a discrete anatomical site, but
represents inter-related neuronal networks.
As described above inputs to the Vomiting Centre include
vagal sensory pathways from the gastro-intestinal tract and
neuronal pathways from the labyrinths, higher centres of the
cortex, intracranial pressure receptors and the
Chemoreceptor Trigger Centre (CTz).
When activated the Vomiting Centre induces vomiting via
stimulation of the salivary and respiratory centres and the
pharyngeal, gastrointestinal and abdominal muscles.

The Chemoreceptor Trigger Centre (CTZ) in the area
prostrema of the 4
th
ventricle of the brain acts as the entry
point for emetic stimuli and humeral substances. The CTZ is
outside the blood-brain barrier and therefore responds to
stimuli from either the cerebral spinal fluid (CSF) or the blood.
A representation illustrating the approximate anatomical
relationship between the different parts of the brain involved
with nausea and vomiting is shown in Figure 2.


DIARRHEA
Definition

Passage of abnormality liquid or unformed
stools at an increased frequency (> 3x/day).
For adult, stool weight > 200 g/day can
generally considered diarrhea.
Clasification
Acute Diarrhea
Chronic Diarrhea ( > 3 weeks, for child > 2 weeks)
Osmotic diarrhea malabsorbtion, steatore
Secretoric diarrhea defect transport fluid faeces
Functional diarrhea psychology factor
Inflammation diarrhea the death and deterioration
of enterocyte plus inflammation
Nonspecific inflammation ulcerative colitis and chron
disease
Specific inflammation Diarrhea with blood
Epidemiology
Etiology Frequency (%)
E. Coli 38,29
Vibrio cholerae ogawa 18,29
Aeromonas sp 14,29
Shigella flexneri 6,29
Salmonella sp 5,71
Entamoeba histolytica 5,14
Ascaris lumbricoides 3,43
Rotavirus 2,86
Epidemiology
Etiology Frequency (%)
Candida sp 1,71
Vibrio NAG 1,14
Trichruris trichiura 1,14
Plesiomonas shigelloides 0,57
Ancylostoma duodenalis 0,57
Blastocystis hominis 0,57
Etiology
Infection
Enteral
Bacteria : shigella sp, e.coli patogen, salmonella sp,
vibrio cholera, yersinia enterocolytica, campylobacter
jejuni, v.parahaemoliticus, V.NAG, staphylococcus
aureus, streptococcus, klebsiella, pseudomonas,
aeromonas, proteus.
Virus : rotavirus, adenovirus, norwalk virus, norwalk
like virus, CMV, echovirus, virus HIV.
Protozoa : entamoeba histolytica, giardia lamblia,
cryptosporidium parvum, balantidium coli.
Worm : a.lumbricoides, cacing tambang, trichuris
trichiura, s.stercoralis, cestodiasis.
Fungus : candida, moniliasis.
Etiology
Parenteral
Acute otitis media
Pneumonia
Travelers diarrhea : e.coli, giardia lamblia, shigella,
entamoeba histolytica
Food
Food intoxication
Allergy
Malabsorption
Imunodeficiency
Hypogamaglobulinemia
Panhypogamaglobulinemia
Chronic granulomatous disease
Etiology
IgA deficiency
IgA immunodeficiency heavycombination
Pharmacology therapy
Antibiotic
Chemotherapy
Antasid
Special treatment
Gastrectomy
Gastroenterostomy
High dose therapy radiation
Others
Zollinger ellison syndrome
Neuropathy autonomic
Pathophysiology Chronic Diarrhea
Process of defect mechanism and enzymatic
Mucous defect
Problem with
transportation of
electrolite and H
2
O
(DEHYDRATION)
Faeces
consistency
Metabolic acidosis
Pathophysiology Acute Diarrhea
1. Noninvasive Bacteria
the toxin which produce by bacteria fasten with
mucosa small intestinal but not make broken in
the mucosa.
[ETEC,C.perfringers,S.aureus, dan vibrio-
nonaglutinable]
>Symptoms : Diarrhes secretoric isoootonic
voluminal

2. Enteroinvasif Bacteria
diarrhea caused small intestine damage like
necrosis and ulcer (exudative secretoric).
[EIEC, S.paratyphi B, S.typhimurium,
S.enteriditis, S.choleraesuis, shigella, yersinia
dan perfringers tipe C]
ENTERITIS
Enteritis is inflammation of the small intestine.
The inflammation can also involve the stomach
(gastritis) and large intestine (colitis).

Causes
Enteritis is usually caused by eating or drinking
substances that are contaminated with bacteria or
viruses.
The germs settle in the small intestine and cause
inflammation and swelling, which may lead to
abdominal pain, cramping, diarrhea, fever, and
dehydration.
Enteritis may also be caused by:
An autoimmune condition such as Crohn's disease
Certain drugs, including ibuprofen, naproxen sodium,
and cocaine
Damage from radiation therapy

organism symptoms
Microbe :
shigella






Campylobacter jejuni


Stphylococcus aureus







Salmonella

















Acute (sudden) abdominal pain or cramping
Acute (suden) fever
Blood, mucus, or pus in stool
Crampy rectal pain (tenesmus)
Nausea and vomiting
Watery diarrhea

Cramping abdominal pain
Fever
Watery diarrhea, sometimes bloody

Nausea
Vomiting for up to 24 hours
Diarrhea
Loss of appetite
Severe abdominal cramps
Abdominal distention
Mild fever

The time between infection and symptom
development is 8 - 48 hours.
Abdominal pain or cramping or tenderness
Chills
Diarrhea
Fever
Muscle pain
Nausea
Vomiting


Organism symptoms
Parasit
E.hystolitica



Giardia lamblia



Balantidium coli

Acute: Frequent dysentery with necrotic
mucosa and abdominal pain.
Chronic: Recurrent episodes of dysentery
with blood and mucus in the feces.

Fowl-smelling, bulky diarrhea; blood or
necrotic tissue rare

Dysentery with blood and necrotic tissue
but no abscesses.
Agents Incubation
period
Vomiting Abdominal
pain
Fever Diarrhea
Bacillus
Cereus
1-8 h 3-4+ 1-2+ 0-1+ 3-4+,watery
Vibrio
Cholera
8-72h 2-4+ 1-2+ 0-1+ 3-4+,watery
E.coli,Giardi
a,Cryptosp.
1-8d 0-1+ 1-3+ 0-2+ 1-2+,watery,
mushy
Clostridium
Difficile,He
morhagik
E.coli
12-72 h 0-1+ 3-4+ 1-2+ 1-3+, watery
and bloody
Rotavirus,
Norwalk
1-3d 1-3+ 2-3+ 3-4+ 1-3+,watery
Salmonella 12h 11 d 1-3+ 2-4+ 3-4+ 1-4+,watery
and bloody
Shigella 12h 8d 0-1+ 3-4+ 3-4+ 1-2+,bloody
Symtomatic disease is caused by
several distinct groups of viruses:
Rotavirus accounts for an estimated 130
million cases and 0.9 million deaths worldwide
per year, and constitutes approximately 60%
of chillhood enterocolitis in united states.
The affected population is children 6 to 24
months of age; spread is by fecal oral
contamination.
The prodrome for the development of
diarrhea after infections is 2 days, and the
disease lasts for 3 to 5 days.
Calciviruses, particularly the Norwalk virus,
are responsible for most cases of nonbacterial
foos-borne epidemic gastroenteritis in older
children and adults. Infection in young
children is unusual.
Additional viruses accounting for infectious
diarrhea in children,almost always by person-
to-person contact, include several subtypes of
adenovirus (Ad40 and Ad41) and astrovirus.
Bacterial Enterocolitis
Ingestions of preformed toxin, present in
contaminated food.
Major offenders of food poisoning are
Staphylococcus aureus, Vibrio spp, and
Clostridium perfringens.
One may also ingest preformed neurotoxins,
exemplified by Clostridium botulinum.
Infections by toxigenic organisms, which
proliferate within the gut lumen and elaborate
an enterotoxin.
Infections by toxigenic organisms, which
proliferate within the gut lumen and elaborate
an enterotoxin.
Infection by enteroinvasive organisms, which
proliferate , invade, and destroy mucosal
epithelial cells.
AMEBIASIS
Amebiasis is an infectious disease caused by a parasitic one-
called microorganism (protozoan) called Entamoeba
histolytica.
Persons with amebiasis may experience a wide range of
symptoms, including diarrhea, fever, and cramps. The
disease may also affect the intestines, liver, or other parts of
the body.


Life Cycle
Symptoms
Acute: Frequent dysentery with necrotic
mucosa and abdominal pain.
Chronic: Recurrent episodes of dysentery with
blood and mucus in the feces.
Intestinal amebiasis
Intestinal amebiasis can be subdivided into several categories:
ASYMPTOMATIC INFECTION. Most persons with amebiasis have no noticeable
symptoms. Even though these individuals may not feel ill, they are still capable of
infecting others by person-to-person contact or by contaminating food or water
with cysts that others may ingest, for example, by preparing food with unwashed
hands.
CHRONIC NON-DYSENTERIC INFECTION. Individuals may experience symptoms
over a long period of time during a chronic amebiasis infection and experience
recurrent episodes of diarrhea that last from one to four weeks and recur over a
period of years. These patients may also suffer from abdominal cramps, fatigue,
and weight loss.
AMEBIC DYSENTERY. In severe cases of intestinal amebiasis, the organism invades
the lining of the intestine, producing sores (ulcers), bloody diarrhea, severe
abdominal cramps, vomiting, chills, and fevers as high as 104-105F (40-40.6C). In
addition, a case of acute amebic dysentery may cause complications, including
inflammation of the appendix (appendicitis), a tear in the intestinal wall
(perforation), or a sudden, severe inflammation of the colon (fulminating colitis)

DYSENTRY
Dysentery Intestinal infection marked
by diarrhea containing blood and mucus.
SHIGELLA
Shigella patogen dysentery.
4 species shigella :
S. Dysenteriae
S. Flexneri
S. Boydii
S. sonnei
PATOPHYSIOLOGY
Enterotoxinwatery diarrhea baciller dysentery
small intenstinecolon
Incubation 2-4 days until 1 week
Small intestine ileum terminal colon
inflammation peptic ulcer

THERAPY
Self limited disease
Ciprofloksasin
Ampisilin
Tetrasiklin
Trimetoprim-sulfometoksazol
Salmonella typhi
Salmonella mild gastroenteritisthypoid
3 spesies :
S. Choleraesuis
S. Typhi
S. Enteritidis
Infection : food and water borne disease
Pathophysiology: Salmonella infected epithellium cell
of ileum activate adenilal siklase secretion
diarrhea
Theraphy: kloramfenikol and ampisilin
Food and water sanitation


E. Coli
echericia 2 species:
E. Coli
E. Hermanii
E. Coli flora normal colon
Primary infection,for example travelers diarrhea
Antigen (2 fimbriae)
Tipe manosa sensitif (pili)
Tipe manosa resisten (CFAs 1 dan 2)
Enterotoxin
Toksin LT
Toksin ST
Infected bowel epithel mucous cell produce toxin
damage cell bleeding into lumen intestine



THERAPY
Antimicroba
Balance with electrolite
peptic typhoid Basiler
dysentery
Amoeba dysentry
Microscopic Macrophage
proliferation
PMN -
PMN +++
Necrotic
Hypersecretion
bleeding
Necrotic
Amoeba
MN
Eosinophilic
Clinical
manifestation
Fever
Splenomegali
Headache
leucopenia
Diarrhea
Fever
Blood, mucous
tenesmus
Diarrhea
Blood, mucous
Tenesmus
complication Bleeding
perforation
Stricture
Prolaps
liver abces
perforation
amoeboma

What are the symptoms of giardiasis?

Giardia infection can cause a variety of intestinal signs or
symptoms, which include
Diarrhea
Gas or flatulence
Greasy stools that tend to float
Stomach or abdominal cramps
Upset stomach or nausea
These symptoms may lead to weight loss and
dehydration. Some people with Giardia infection have no
symptoms at all.
Symptoms of giardiasis normally begin 1 to 2 weeks
(average 7 days) after becoming infected.

How is a Giardia infection diagnosed?
Your health care provider will likely ask you to
submit stool examination to check for the
parasite. Because Giardia can be difficult to
diagnose, your provider might ask you to
submit multiple stool specimens collected
over a few days.
Cyst/trofozoit
What is the treatment for giardiasis?

Several prescription drugs are available to treat
Giardia infection.
Although Giardia can infect all people, young
children and pregnant women might be more
susceptible to dehydration resulting from diarrhea
and should, therefore, drink plenty of fluids while ill.
Rapid loss of fluids from diarrhea can be especially
life threatening to infants.
Therefore, parents should talk to their health care
providers about fluid replacement therapy options
for infants.
Conclusion
We conclude that Mr. Surip suffers acute
diarrhea or dysentery which need specific
observation to get exact diagnosis.
Acute diarrhea should be diagnosed by proper
physical and clinical examination.
Rehydration, diet, anti diarrhea drugs, and
anti microbes drugs are the therapy which
should be considered.
Suggestion
Washing hands properly
Food and water sanitation
Give education and therapy
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Brooks GF, Butel JS, Morse SA. Lange Jawetz, Melnick
& Naelbergs Medical Microbiology. 23
rd
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Graw Hill Medical, 2004.
Kumar V, Abbas AK, Fausto N. Robbins and Cotran
Pathologi Basis Of Disease. 7
th
Ed. Philadelphia:
Elsevier Saunders, 2005.
Sherwood L. Human physiologi. 5
th
ed. Belmont:
Thomson Learning, 2004.
Sutanto I, Ismid IS, Sjarifuddin PK, Sungkar S, editors.
Buku ajar parasitologi kedokteran UI. Edisi ke-4.
Jakarta: Balai penerbit FKUI, 2008.
THANK YOU