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8/12/2019 Group 12 Case 2b
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When “Warteg” Gives Him More
By : Group 12
Tutor : dr. Veronica Wiwing
FAKULTAS KEDOKTERAN UNIVERSITAS TARUMANAGARA
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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 407070106Gladys Sudiyanto 405070123
Ferdy Halim 405070082
Grace 405070080
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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.
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Scenario
Today, Mr.Surip presents to your clinic reportinga 2-day history of watery diarrhea and he hasnoticed that there’s blood in his stool. He has
up to 8 bowel movements per day. He has hadintermitten abdominal cramps as well. For thepast 2 days, he also feels nauseated, but novomiting. His vital signs are normal, his bowel
sounds are hiperactive and the remainder ofthe physical exam is remarkable only for mild,diffuse abdominal tenderness.
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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 thedisease
• Describe the expected management
• Describe the expected treatment and health education
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NAUSEA AND VOMITING
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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.
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• 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 neuronalpathways 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 actof vomiting.
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• 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, butrepresents 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 thecortex, 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 thepharyngeal, gastrointestinal and abdominal muscles.
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• The Chemoreceptor Trigger Centre (CTZ) in the area
prostrema of the 4th 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.
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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.
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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 deteriorationof enterocyte plus inflammation
• Nonspecific inflammation ulcerative colitis and chrondisease
• Specific inflammation Diarrhea with blood
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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 3,43Rotavirus 2,86
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Epidemiology
Etiology Frequency (%)
Candida sp 1,71
Vibrio NAG 1,14
Trichruris trichiura 1,14
Plesiomonas shigelloides 0,57Ancylostoma duodenalis 0,57
Blastocystis hominis 0,57
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Etiology
• Infection
– Enteral• Bacteria : shigella sp, e.coli patogen, salmonella sp,
vibrio cholera, yersinia enterocolytica, campylobacter jejuni, v.parahaemoliticus, V.NAG, staphylococcusaureus, streptococcus, klebsiella, pseudomonas,aeromonas, proteus.
• Virus : rotavirus, adenovirus, norwalk virus, norwalklike 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.
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Etiology – Parenteral
•Acute otitis media
• Pneumonia
• Traveler’s diarrhea : e.coli, giardia lamblia, shigella,
entamoeba histolytica
•
Food – Food intoxication
– Allergy
– Malabsorption
•
Imunodeficiency – Hypogamaglobulinemia
– Panhypogamaglobulinemia
– Chronic granulomatous disease
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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
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Pathophysiology Chronic Diarrhea
Process of defect mechanism and enzymatic
Mucous defect
Problem with
transportation of
electrolite and H2O(DEHYDRATION) Faecesconsistency
Metabolic acidosis
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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 isoootonicvoluminal
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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]
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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 drinkingsubstances that are contaminated with bacteria orviruses.
The germs settle in the small intestine and causeinflammation and swelling, which may lead toabdominal pain, cramping, diarrhea, fever, anddehydration.
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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
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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
NauseaVomiting 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
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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.
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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
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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.
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• 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 nonbacterialfoos-borne epidemic gastroenteritis in older
children and adults. Infection in youngchildren is unusual.
• Additional viruses accounting for infectiousdiarrhea in children,almost always by person-
to-person contact, include several subtypes of
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Bacterial Enterocolitis
• Ingestions of preformed toxin, present incontaminated food.
• Major offenders of food poisoning are
Staphylococcus aureus, Vibrio spp, andClostridium perfringens.
• One may also ingest preformed neurotoxins,
exemplified by Clostridium botulinum.• Infections by toxigenic organisms, which
proliferate within the gut lumen and elaboratean enterotoxin.
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• Infections by toxigenic organisms, whichproliferate within the gut lumen and elaborate
an enterotoxin. • Infection by enteroinvasive organisms, which
proliferate , invade, and destroy mucosal
epithelial cells.
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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. Thedisease may also affect the intestines, liver, or other parts of
the body.
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Symptoms
• Acute: Frequent dysentery with necrotic
mucosa and abdominal pain.
• Chronic: Recurrent episodes of dysentery with
blood and mucus in the feces.
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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 ofinfecting others by person-to-person contact or by contaminating food or waterwith cysts that others may ingest, for example, by preparing food with unwashedhands.
• CHRONIC NON-DYSENTERIC INFECTION. Individuals may experience symptomsover a long period of time during a chronic amebiasis infection and experiencerecurrent episodes of diarrhea that last from one to four weeks and recur over aperiod of years. These patients may also suffer from abdominal cramps, fatigue,and weight loss.
• AMEBIC DYSENTERY. In severe cases of intestinal amebiasis, the organism invadesthe lining of the intestine, producing sores (ulcers), bloody diarrhea, severeabdominal cramps, vomiting, chills, and fevers as high as 104-105°F (40-40.6°C). Inaddition, a case of acute amebic dysentery may cause complications, includinginflammation of the appendix (appendicitis), a tear in the intestinal wall(perforation), or a sudden, severe inflammation of the colon (fulminating colitis)
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PATOPHYSIOLOGY
• Enterotoxinwatery diarrhea baciller dysentery
small intenstinecolon
• Incubation 2-4 days until 1 week
• Small intestine ileum terminal colon
inflammation peptic ulcer
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THERAPY
•
Self limited disease• Ciprofloksasin
• Ampisilin
• Tetrasiklin
• Trimetoprim-sulfometoksazol
Salmonella typhi
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Salmonella typhi
• Salmonellamild 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 C li
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E. Coli
• echericia 2 species:
–
E. Coli – E. Hermanii
• E. Coli flora normalcolon
• 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
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THERAPY
• Antimicroba
• Balance with electrolite
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peptic typhoid Basiler
dysentery Amoeba dysentry Microscopic Macrophage
proliferation
PMN - PMN +++
Necrotic
Hypersecretion bleeding
Necrotic
Amoeba
MNEosinophilic
Clinical
manifestation Fever
Splenomegali
Headache
leucopenia
Diarrhea
Fever
Blood, mucous
tenesmus
Diarrhea
Blood, mucous
Tenesmus
complication Bleeding
perforation Stricture
Prolaps liver abces
perforation
amoeboma
DIFFERENTI L DI GNOSIS
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What are the symptoms of giardiasis?
• Giardia infection can cause a variety of intestinal signs orsymptoms, 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 nosymptoms at all.
• Symptoms of giardiasis normally begin 1 to 2 weeks(average 7 days) after becoming infected.
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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
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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 moresusceptible 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 careproviders about fluid replacement therapy optionsfor infants.
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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 whichshould be considered.
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Suggestion
• Washing hands properly
• Food and water sanitation
• Give education and therapy
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REFERRENCE
• Brooks GF, Butel JS, Morse SA. Lange Jawetz, Melnick& Naelberg’s Medical Microbiology. 23rd ed. USA: Mc.Graw Hill Medical, 2004.
• Kumar V, Abbas AK, Fausto N. Robbins and Cotran
Pathologi Basis Of Disease. 7th
Ed. Philadelphia:Elsevier Saunders, 2005.
• Sherwood L. Human physiologi. 5th 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.