UnPar-Final Modul Gastro 2013
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Transcript of UnPar-Final Modul Gastro 2013
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Dr. Agnes Kurniawan,
PhD, SpParK
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GI Module Feb 2013-AK-UniB/UnPar 2
1. To acquire knowledge on protozoa and
worms which often leads to gastrointestinal
disorders
2. To understand the life cycle, epidemiology,clinical symptoms, diagnosis, treatment and
prevention of the protozoa and worms
causing GI disorders
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Trichuris trichiura
Taenia saginata
E. histolytica
Cyclospora cayetanensis
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WORM
PROTOZOA
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= Whipworm, a roundworm/nematode, STH
Commonly infect children
Epidemiology : warm, humid climates, crowded
Mode of infection : ingested of mature eggs
Risk factor : poor hygiene, sanitation, raw vegetables
Mature egg ingested hatch in the small intestine
larvaeadult worm in caecum/ascending colon
egg adult female = 60-70 days
egg infective stage:36 wks, soil
eggs produced: 3000-10.000/day
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Adult:
- female 5 cm, male 4 cm
- anterior portion whip like- live in colon ascendens and caecum
- no lung cycle: egg ingested hatch in thesmall intestine larvae adult worm in
caecum/ascending colon
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< 10 worms asymptomatic
Heavy infection
diarrhea, dysentery,anemia, rectal prolapse,growth retarded
Note : dysentry : frequent, painfulpassage of stool that contains amixture of mucus, water, and
blood.
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The anterior part of the worm dip into the
intestinal mucosa irritation trauma and
inflammation of the intestinal mucosa and
bleeding -- sucked by the worms
anemia
Parasitology Lab Diagnosis
Microscopy :Wet smear : T. trichiura eggs in the stool
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Treatment
- Mebendazol 2x100 mg for 3 days (>2 yo)
2x200 mg for 3 days (adult)
- Albendazol 400 mg, single dose
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1. BREAK THE WORM LIFE CYCLE- environmental sanitation : use of toilet
for defecation, not using stool forfertilizer
- good personal hygine : handwashingwith soap & water, wash well the fruitsand vegetables
- mass treatment when prevalence > 30%
2. HEALTH EDUCATION
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Definitive host: man
Adult worm: in the middle third small intestine
Intermediate host : cattle
larva (cyst) in muscles Mode of infection:
- 1. in cattle: grazing on moist pasture contaminatedwith eggs ofT. saginata from human stool
- 2. in man: consuming uncooked/rare cooked beefwith larvae (cysticercus bovis)
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LIFE CYCLE
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LIFE CYCLE & PREVENTION
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Proglotid: crawling out of anus
GI complaints: nausea, diarrhea, abdominal
pain
Systemic symptoms: fatigue, hunger,
dizziness, moderate loss of weight
Rare symptoms: vomiting of segments,
obstruction of bile ducts, pancreatic ducts orappendix
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eggs in stool
proglotid crawling out
of anusTreatment
praziquantel 10mg/kg, single dose
albendazole
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EVALUATION OF TREATMENT- Relieve of symptoms- Parasitology lab examination :
1. 24 hours collected stool after th/:
scolex + proglottids
2. stool, 3 months after th/:
negative for eggs and
or segments
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E. histolytica: histo=tissue ; Lysis = dissolve,
destroyed
Aetiology of intestinal and extra intestinal
amebiasisHost : human
Habitat : colon
Distribution : cosmopolitan, in tropical and
subtropical countries
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2 stages: trophozoite and cyst
TROPHOZOITE :
- 2 forms : histolytica (pathogen) and minuta
(apathogen). Size : 10-60 um, entameba nucleus
Endoplasm: fine granules, contains bacteriaor food metabolites
If contains red blood cells erythrophago-cytosis typical for E. histolytica infection
Live 2 hours outside the host
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Size: 10-20 um
round/oval shape
Structure: cyst wall, endoplasm with 1,2 or 4
nuclei
Endoplasm : chromatoid body (cigar form) &
glycogen vacuol (food storage)
apathogenic Infective stage : mature cyst (cyst
with 4 nuclei)
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Ingestion of mature cyst
Excystation in the stomach with the help of
gastric juice trophozoite release colon
multiplication by binary fission
invadethe mucose ( cause symptoms ) or transform
into cyst stage (encystation )
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Trophozoites express gal/gal nac lectins
antigen on its surface stick to colonic
epithelial cells present amoebapores and
excrete cysteine proteinases (amebapain dan
hystolisine) lyse extracellular protein matrix
epithelial cell lysis tissue necrosis,
further invasion to submucose flask shape
ulcer
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Form : bottle shape, small opener at the top, wide
at the bottom, irregular rim, slightly elevated
Inflammation, with blood and secondary infectionwith bacteria
Progression to submucose area along the lateral
axis of colon
Excretion of trophozoite into the lumen invadeother healthy area of colon or excreted with stool
dysentric stool (mucous and blood )
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1. Carrier state:
- intestinal amebiasis
- parasite multiplies in the body
- stools : cysts ++
- clinical signs /symptoms : none
- cause : low virulent strain, low number of
infection, adequate immune status
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2. Intestinal amebiasis
- dysentery, colitis, appendicitis, toxic
megacolon, amebomas
- Abdominal pain- Diarhoea with mucous and bloody stool ,
frequency up to 10 x/day
- Fever, loss of appetite, decrease body weight
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The most common extraintestinal complication
of amebiasis (8.5% of cases).
Hepatic infection occurs because colonic
trophozoites ascend via the portal vein
invade the parenchyma
Cause : toxin release & hepatocyte damage
Usually develop within days - months after dysentri
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Symptoms : fever (>90% acute cases), dullpleuritic right upper quadrant pain radiating to
the right shoulder, hepatomegali and pleural
effusions.
Acute form: often very high fever, continuous orintermittent + chills
Chronic forms : fever is low, develops gradually,
without chills or sweating
Right / left lobe
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Occasionally spread into the overlying
abdominal wall or form portal venous amebic
thrombi.
Hematogenous dissemination to the brain israre
Diarrhea (2%), with 4 - 5 x/ day,watery stool,
with mucus and blood, tenesmus, abdominal
cramping and distension due to potassium loss
Jaundice is an unusual feature(5%)
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the abscess extends upward the diaphragm,
pleura empyema .
Invasion of the lung parenchyma by E.
histolytica development of interstitialpneumonitis, liquefaction & formation lung
abscess
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1. Microscopic Faeces : trophozoite (invasive stage) and /
cysts (non invasive stage)
The 2 stages represent two separatespecies : E. histolytica & E. dispar which
are morphologically indistinguishable
unless E. histolytica is observed with
ingested red blood cellsCysts: found in formed stool
Trophozoites: found in diarrheal stool
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Body fluid: trophozoite
Stool examination is best performed 3X in a
week to exclude false negative
2. Serology test ( Antibody detection)
IHA, ELISA
To diagnose extraintestinal amebiasis
Performed together with the microscopic
examination of the abscess fluid and radio
diagnostic
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3. Antigen Detection
ELISA
Specimens: stool, serum, abscess fluid, saliva
Specific for E. histolytica ( cannot for E.dispar)
4. Polymerase chain reaction (PCR)
to differentiate E. Histolytica from E. dispar
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TREATMENTDrugs:
- metronidazole (trophozoite & cyst form)
- chloroquine (trophozoite form)
- paromomycin (trophozoite form)
Intestinal Amebiasis: paromomycin 25-35
mg/kgbb/hari, 3x/day, 7 days
Extraintestinal Amebiasis : metronidazol 3x750mg/hari 7-10 days + abscess drain
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Improving sanitation and hygine individuals
Health education on mode of transmission
Water treatment : chlorination and filtration
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Coccidia
Host: man
Epidemiology : developing countries
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Oocyst: 8-10 um
Immature (unsporulated) oocyst excreted instools sporulation 1 several weeks inwarm and humid climate
Mature Oocyst : 2 sporocysts @ foursporozoites
Infection : ingestion of mature oocysts
Source of infection : contaminated food /
vegetables, water such as raspberry
Parasite lives intracytoplasmic develop inthe jejunal enterocytes
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Diareanorexia, flatulance, epigastric pain,
nausea, vomitus, low grade fever Immune competent : acute, light diarrheaAIDS : chronic diarrhea, severe
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1. Microscopic :
- oocyst in the stool, duodenal aspirates,duodenal/jejunal biopsy
- 3 stools every 2-3 days- safranin / acid fast stainings
2. UV fluorecense microscope
3. PCR
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Treatment : trimetoprim + sulfametoksazol,
metronidazol, siprofloksasin
Prevention : Improving sanitation and hygine
individuals, health education, watertreatment, proper washing of raw vegetables
and fruits
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THANK YOU