Group 12 Case 2b

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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PATOPHYSIOLOGY

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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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DIARRHEA

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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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Life Cycle

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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.

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THANK YOU

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Group 12 Case 2b