Pemicu 3 GIT

Mudita dewi
405150016
ANATOMY
Rectum
HISTOLOGY
 Colon
• No vili.
• Plicae semilunaris consists of
Tn.mucosa, Tn.submucosa &
Tn.muscularis circularis.
• Absorptive cells have striated
border; numbers of goblet
cells among epithelial cells.
• Spec. feature : limfonodus
solitarius from lamina propria
to submucosa.
• Tn. muscularis longitudinalis
 3 longitudinal ribbon,
taenia coli.
 Appendix vermiformis
• Is the diverticulum of the
caecum.
• Same structure with
colon.
• Spec. feature : aggregate
limfonodulus in lamina
propria, reach tn
submucosa; look like rings
surround the lumen.
• Tn muscularis mucosa 
rudimenter
 Rectum
• Superior : colon-like
structure with longer
cryptus & all
surrounded by goblet
cells.
• Inferior : anal-canal.
• Rectum – anus : linea
pectinata.
Rectum
PHYSIOLOGY
Segmentation
Sfingter
Villus
Carohydrates
Protein
Lipid
Iron
Colon
BIOCHEMISTRY
Biochemistry

Source: Sherwood L. Introduction to

Human Physiology. 8th Ed. USA:
Carbohydrates

Source: Sherwood L. Introduction to Human Physiology. 8th Ed. USA:

Protein

Source:
Sherwood
L.
Introductio
n to
Human
Physiology.
8th Ed.
Sourcer: Sherwood L. Introduction to Human Physiology. 8th Ed. USA:
 Fat

Source:
Sherwood
L.
Introductio
n to
Human
Physiology.
8th Ed.
Iron

Source: Sherwood L.
Introduction to Human
Physiology. 8th Ed. USA:
Lactose Intolerance
GASTROENTRITIS
 Diare
• Buang air besar dgn tinja berbentuk cair dan
setengah cair, kandungannya biasanya > 200gr
atau 200 ml/24jam.
• Atau buang air besar encer > 3x per hari
Klasifikasi :
• Lama waktu diare: akut atau kronik
• Mekanisme patfis osmotik atau sekretorik
• Berat ringan diare: kecil atau besar
• Penyebab infeksi atau tidak
• Penyebab organik atau fungsional
Acute Diarrhea
 Diarrhea
• Passage of abnormally liquid or unformed stools at an increased
frequency
• For adults on a typical Western diet, stool weight >200 g/d can
generally be considered diarrheal
– Acute: < 2 weeks or 15 days
– Persistent: 2-4 weeks
– Chronic: > 15 days or 1 month
 Acute diarrhea
• 90% of cases of acute diarrhea are caused by
infectious agents
• Accompanied by vomiting, fever, and abdominal pain
• 10% or so are caused by medications, toxic
ingestions, ischemia, and other conditions
ETIOLOGI
 Definiton, classification and ethiology
• Dysentery is bloody diarrhoea, i.e. any
diarrhoeal episode in which the loose or
watery stools contain visible red blood.
• Dysentery is most often caused by Shigella
species (bacillary dysentery) or Entamoeba
histolytica (amoebic dysentery).
• Shigella is a gram-negative bacteria which
does not form spores. Unlike E.coli, it is not
mobile and unable to form gas from sugar.
http://www.who.int/topics/dysentery/en/
 Bacilliary dysentry [Shigellosis]
• Shigella sonnei (the most common species in
the United States)
• Shigella flexneri
• Shigella boydii
• Shigella dysenteriae
 Pathogenesis
• Contamination of shigella is through the oral
route.
• The bacterias are resistent to the low pH of the
stomach.
• Watery diarrhea from the bacterial infection is
arised from the increased secretion and the faulty
in the water resorbtion. This is caused by the
enterotoxins.
• Dystenry syndrome is noted by the bloody
mucopurulent feses. It is a sign in which the
bacteria invades the mucous layer.
 Signs and symptoms
Symptoms of shigellosis typically start 1–2 days
after exposure and include:
• Diarrhea (sometimes bloody)
• Fever
• Abdominal pain
• Tenesmus (a painful sensation of needing to
pass stools even when bowels are empty)
 Laboratory Diagnosis
• Increased PMN
• GOLD STANDARD ; Isolation nad pathogen
identificatiion in feses
 Therapy
Antibiotic therapy for shigelosis
Therapy Regimens
Drugs Children Adults
First line

Ciprofloxacin 15 mg/kg 2x a 500 mg

day for 3 days
Second line
Pivmesilinam 20 mg/kg 4x a Expensive
day for 5 days. resistence
PO 100 mg
Ceftriaxone 50-100 mg/kg
IM once a day
for 2-5 days Injected 1-1,5 mg
Azitromisin 6-20 mg/kg 1x a
day for 1-5 days
PO
 Prognosis
Possible complications from Shigella infections
include:
• Post-infectious arthritis.
• Blood stream infections.
• Seizures.
• Hemolytic-uremic syndrome or HUS.
 Amoebic dysentry
• Ethiology ; The protozoan parasite Entamoeba
histolytica, possibly other Entamoeba spp
• Transmission; fecal-oral route, either directly
by person-to-person contact (such as by
diaper-changing or sexual practices) or
indirectly by eating or drinking fecally
contaminated food or water
Life cycle
 Clinical presentation
• A wide spectrum, from asymptomatic
infection ("luminal amebiasis”)
• invasive intestinal amebiasis (dysentery,
colitis, appendicitis, toxic megacolon,
amebomas)
• invasive extraintestinal amebiasis (liver
abscess, peritonitis, pleuropulmonary abscess,
cutaneous and genital amebic lesions).
 Laboratory diagnosis
• Fresh stool: wet mounts and permanently stained
preparations (e.g., trichrome).
• Concentrates from fresh stool: wet mounts, with
or without iodine stain, and permanently stained
preparations (e.g., trichrome). Concentration
procedures, however, are not useful for
demonstrating trophozoites
• Enzyme immunoassay (EIA)
• indirect hemagglutination (IHA) testAntigen
detection
Therapy
 Risk factors
• Travelers • Immunodeficient persons
– Enterotoxigenic or – Mycobacterium species
enteroaggregative – viruses (cytomegalovirus,
adenovirus, and herpes
Escherichia coli as well as simplex)
to Campylobacter, Shigella, – protozoa (Cryptosporidium,
Aeromonas, norovirus, Isospora belli, Microsporida,
Coronavirus and and Blastocystis hominis)
Salmonella • Daycare attendees and
their family members
– Giardia, Cyclospora – Shigella, Giardia,
• Consumers of certain foods Cryptosporidium, rotavirus
– Salmonella, • Institutionalized persons
Campylobacter, or Shigella – C. difficile
– Vibrio species, or acute
hepatitis A
 Patophysiology
1. Osmotic diarhea
2. Secretoric diarhea
3. Malabsorbtion of fat and bile acid
4. Decrease the anion / transport exchange in
enterocytes
5. Abnormality of intestine motility and transit time
6. Intestine permeability problem
7. Inflamatoric diarhea
8. Infection diarhea
 Pathogenesis
• Acute diarhea (Infection)
– Agent factor
– Host factor

• Pathogenesis of diarhea:
1. Enterotoxicgenic
2. Enteroinvasive
dehydration
 Dehydration
Definition
The loss of body water, with or without salt, at a rate greater
than the body can replace it.
http://www.ncbi.nlm.nih.gov/pubmed/18519109

The condition that results from excessive loss of body water

. In severe acute malnutrition, dehydration is caused by
untreated diarrhoeal disease which leads to the loss of water
and electrolytes.
http://www.who.int/elena/titles/bbc/dehydration_sam/en/

Loss of free water in greater proportion than the loss of

sodium
http://emedicine.medscape.com/article/801012-overview#a5
 Etiology

• The mechanisms of dehydration :

(1) decreased intake due to diseases such as stomatitis,
(2) increased output from diarrhea or osmotic diuresis from
uncontrolled diabetes mellitus
(3) increased insensible losses such as with fever.

• Pediatric dehydration  ↑ output from gastroenteritis

 characterized by vomiting and
diarrhea

http://emedicine.medscape.com/article/801012-overview#a5
 Pathophysiology

Diarrhea  excess loss of fluids and essential electrolytes

from the body  fluid lost in the stools is not replaced 
dehydration
Signs of dehydration in Signs of dehydration in
adults babies and young children

• Being thirsty • dry mouth and tongue

• Urinating less often than • crying without tears
usual • no wet diapers for 3 hours
• Dark-colored urine or more
• Dry skin • a high fever
• Feeling tired • being unusually sleepy or
• Dizziness and fainting drowsy.

https://medlineplus.gov/dehydration.html
Signs and Symptoms
 Degree of Dehydration
%
Sign & General Mouth/
Eye Thirst Skin Weight Extremity
symptom Appearance tongue
Loss

No Skin turgor
Fine Normal Wet Not thirsty <3 Warm
dehydration normal

Skin turgor
Mild reduced
Worse Sunken Dry Look thirsty 3–9 Cold
dehydration (back after
< 2 seconds
Skin turgor
Lethargic, worse
Severe Deeply Can’t drink Cold,
consciousness Very dry (back after >9
dehydration sunken well cyanotic
decrease >2
seconds)
 Scoring System
Degree of dehydration

Score 0 1 2
General condition Healthy Irritability, Delirium, coma or
sleepy, apathy shock
Skin elasticity Normal Decreased Very decreased
Eye Normal Sunken(ckung) Very sunken
Fontanel (ubun2) Normal Sunken Very sunken
Mouth Normal Dry Dry & cyanotic
Pulse Normal 120-140 > 140

Amount of score: 0- 2 Mild dehydration

3- 6 Moderate dehydration
7-12 Severe dehydration

Maurice King, 1974

A decrease in skin turgor is indicated when the skin (on the back of the
hand for an adult or on the abdomen for a child) is pulled up for a few
seconds and does not return to its original state. A decrease in skin
turgor is a late sign of dehydration.
 Hypertonicity

Dehydration accompanied by hypertonicity can be genarated

through:
1. Insufficiency of H2O input
2. Excessive of H2O output
3. Diabetes insipidus
 Hypotonicity

1. Patients with renal failure can not excrete dilute urine is

going to be hypotonic if they consume more H2O than
solute
2. Hypotonicity may occur transiently in healthy people if
lots of H2O enter quickly that the kidneys are not able to
remove excess H2O
3. The inappropriate of vasopresin secretion
 Treatment
• Fluid (mild cases) and electrolyte replacement
– Oral sugar-electrolyte solutions  severe diarrhea
– dehydrated patients, especially infants and the elderly  IV
rehydration
• Antimotility and antisecretory agents such as loperamide (CI: febrile
dysentery)
• Bismuth subsalicylate
– reduce symptoms of vomiting and diarrhea
• Judicious use of antibiotics
– quinolone, such as ciprofloxacin (500 mg 2x/day for 5-7 d)
– giardiasis with metronidazole (250 mg 3x/day for 7 d)
– Antibiotic prophylaxis  travelling patients (immunocompromise,
IBD, hemochromatosis, gastric achlorhydria)
– trimethoprim/sulfamethoxazole, ciprofloxacin, or rifaximin 
reduce bacterial diarrhea
 ETIOLOGY INCUBATION SIGN & SYMPTOMS DURATION
PERIOD OF ILLNESS

ROTAVIRUS 1-3 days vomiting, watery diarrhea, low grade fever, 4-8 DAYS
temporary lactose intolerance may occur
infants & children, elderly, &
immunocomprimised are especially
vulnerable

CALICIVIRUSES & 12-48 hr Nausea, vomiting, abdominal cramping, 12-60 hr

NOROVIRUS diarrhea, fever, myalgia, & some headache.

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

AGENT abdominal pain, headache, fever
(ADENOVIRUS,
ASTROVIRUSES,
PARVOVIRUSES)
 LABORATORIUM TESTING TREATMENT
ROTAVIRUS Identification of virus in stool via Supportive care, severe diarrhea may
immunoassay require fluid and electrolyte
replacement

CALICIVIRUSES & Routine RT – PCR & EM on fresh Supportive care such us rehydration,
NOROVIRUS unpreserved stool samples. good hygiene
Clinical diagnosis, negative
bacterial cultures, stools is
negative for WBCs

OTHER VIRAL Identification of the virus in early Supportive care usually mild self
AGENT acute stool samples, serology, limiting, good hygiene
(ADENOVIRUS, commercial ELISA
ASTROVIRUSES,
PARVOVIRUSES)
 Non Farmako
• Eating when you have diarrhea :
– You can bake or broil beef, pork, chicken or turkey
– Use low fat milk, cheese, or yogurt. But if the
diarrhea is very severe, you may need to stop
consuming dairy products
– Eat vegetables but avoid those that can cause gas
such as broccoli, peppers, beans
– Avoid caffeine, alcohol, and carbonated drinks
 Prevention
• Washing hands thoroughly with soap and
water or an antibacterial handwash
• Cleaning the toilet
• Not sharing towels
• Not returning to school/work until at least 48
hours after their last episode of diarrhoea or
vomiting
• Immunization against rotavirus
 Gastroentritis in Children
• Gastroenteritis is an infection of the intestine
that causes diarrhea and can also cause
vomiting, abdominal pain and other
symptoms. Although vomiting in
gastroenteritis can be lost in 1-2 days, but
diarrhea can last up to 10 days. Gastroenteritis
can result in dehydration, a dangerous
condition in infants and children.
 Causes of gastroenteritis
• Viruses, viruses remain the most common cause of
acute gastroenteritis in children, both in the
developed and developing world. Rotavirus
represents the most important viral pathogen
worldwide, responsible for 29% of all diarrhea-
related deaths.
• Viral gastroenteritis typically presents with low-grade
fever and vomiting followed by copious watery
diarrhea (up to 10-20 bowel movements per day),
with symptoms persisting for 3-8 days.
• bacterial pathogens, bacterial pathogens
[Salmonella, Shigella, and enterotoxigenic
Escherichia coli (ETEC) ] Relative to viral
gastroenteritis, bacterial disease is more likely to be
associated with high fevers, shaking chills, bloody
bowel movements (dysentery), and abdominal
cramping
• Clostridium difficile has emerged as an important
cause of antibiotic-associated diarrhea in children.
Any antibiotic can trigger infection with C difficile,
though penicillins, cephalosporins, and clindamycin
are the most likely causes.
• Since 50% of neonates and young infants are
colonized with C difficile, symptomatic disease is
unlikely in children younger than 12 months.
• Parasites remain yet another source of
gastroenteritis in young children, with Giardia and
Cryptosporidium the most common.
• Parasitic gastroenteritis generally present with
watery stools but can be differentiated from viral
gastroenteritis by a protracted course or history of
travel to endemic areas
• Malabsorption factor a. Carbohydrate malabsorption:
a disaccharide (lactose intolerance, maltose and sucrose),
monosaccharides (glucose intolerance, fructose and galactose)
in infants and children are the most important and frequently is
lactose intolerance.
b. Mal absorption of fat
c. Mal absorption of proteins: amino acids, lactoglobulin
• Dietary factors : toxic foods (lead, cyanide, allergies to food.
• Psychological Factors : fear, anxiety and stress (rare)
 patfis
• Viruses remain by far the most common cause of
acute gastroenteritis in children ,2 mechanisms
responsible for acute gastroenteritis are as follows:
– Damage to the villous brush border of the
intestine, causing malabsorption of intestinal
contents and leading to osmotic diarrhea
– Release of toxins that bind to specific enterocyte
receptors and cause the release of chloride ions
into the intestinal lumen, leading to secretory
diarrhea
 Patofisiologi Protozoa
Normally, humans are infected through mature cysts in
feces. Cysts entry through the gastrointestinal route.
Cysts are resistant to stomach acid so they can get to
the small intestine. In a state supportive environment,
cysts can turn into a pathogenic form tropozoit. The
form of this pathogen will invade the cells of the
intestinal mucosa and diarrhea.
 Signs and symptoms
• Diarrhea
• Vomiting
• Increase or decrease in urinary frequency
• Abdominal pain
• Signs and symptoms of infection - Presence of fever,
chills, myalgias, rash, rhinorrhea, sore throat, cough;
these may be evidence of systemic infection or sepsis
• Changes in appearance and behavior - Including
weight loss and increased malaise, lethargy, or
irritability, as well as changes in the amount and
frequency of feeding and in the child’s level of thirst
 Agents used in the treatment or prevention of acute pediatric
gastroenteritis include the following:

• Probiotics - Live microbial feeding supplements commonly

used in the treatment and prevention of acute diarrhea
• Zinc - To treat diarrhea;the WHO recommends zinc
supplementation for all children younger than 5 years with
acute gastroenteritis, though little data exist to support this
recommendation for children in industrialized countries
• Metronidazole - In patients infected with C difficile and
Giardia
• Tetracycline and doxycycline - For cholera (though not
generally recommended for children younger than 8 years)
• Vaccine - In February 2006, the US Food and Drug
Administration (FDA) approved the RotaTeq vaccine for
prevention of rotavirus gastroenteritis
CHRONIC DIARRHEA
 Chronic Diarrhea Definition
• Chronic or persistent diarrhea is defined as an
episode that lasts longer than 14 days.
• Chronic diarrhea is defined as a decrease in stool
consistency continuing for > 4 weeks.
• Diarrhea results when the remarkable efficiency of
the gut for absorbing water, electrolyte, and
nutrients is impaired.
• The augmented water content in the stools is due to
an imbalance in the physiology of the small and large
intestinal processes (absorption of ions, organic
substrates, and water).
 Classification
• Stool type: • Stool output:
– Watery diarrhea – High output
– Fatty diarrhea – Normal output
– Inflammatory or • Mechanism:
excudative diarrhea – Osmotic diarrhea
• Etiology: – Secretory diarrhea
– Infectious diarrhea
– Non-infectious diarrhea
• Organic:
– Organic diarrhea
– Functional diarrhea
 Pathophysiology
• In secretory diarrhea, the epithelial cells’ ion transport processes
are turned into a state of active secretion.
• The most common cause of acute-onset secretory diarrhea is a
bacterial infection of the gut.
• After colonization, enteric pathogens may adhere to or invade the
epithelium; they may produce enterotoxins (exotoxins that elicit
secretion by increasing an intracellular second messenger) or
cytotoxins.
• They may also trigger release of cytokines attracting inflammatory
cells, which, in turn, contribute to the activated secretion by
inducing the release of agents such as prostaglandins or platelet-
activating factor.
• Features of secretory diarrhea include a high purging rate, a lack of
response to fasting, and a normal stool ion gap (ie, 100 mOsm/kg
or less), indicating that nutrient absorption is intact.
 Pathophysiology
• Osmotic diarrhea is caused by nonabsorbed nutrients in the
intestinal lumen due to one or more of the following
mechanisms:
– intestinal damage (such as in enteric infection),
– reduced functional absorptive surface (such as in celiac
disease),
– defective digestive enzyme or nutrient carrier (such as in
lactase deficiency),
– decreased intestinal transit time (such as in functional
diarrhea), and
– nutrient overload exceeding the digestive capacity.
Pathophysiology
Common cause of Chronic Diarrhea
 Determine the cause of diarrhea
• Stool characteristics (eg, • Travel history (common
consistency, color, volume,
frequency) pathogens affect specific
• Presence of associated enteric regions; also consider rotavirus
symptoms (eg, nausea/vomiting, and Shigella, Salmonella, and
fever, abdominal pain) Campylobacter spp regardless
• Use of child daycare (common
pathogens: rotavirus, astrovirus, of specific travel history, as
calicivirus; Campylobacter, these organisms are prevalent
Shigella, Giardia, and worldwide)
Cryptosporidium species [spp])
• Food ingestion history (eg, • Animal exposure (eg, young
raw/contaminated foods, food dogs/cats: Campylobacter spp;
poisoning) turtles: Salmonella spp)
• Water exposure (eg, swimming
pools, marine environment, water • Predisposing conditions (eg,
source) hospitalization, antibiotic use,
immunocompromised state)
 Sign and symptoms
• Dehydration: Lethargy, depressed consciousness,
sunken anterior fontanel, dry mucous membranes,
sunken eyes, lack of tears, poor skin turgor, delayed
capillary refill
• Failure to thrive and malnutrition: Reduced
muscle/fat mass or peripheral edema
• Abdominal pain/cramping
• Perianal erythema
 Stool characteristic and source
Stool Characteristics Small Bowel Large Bowel
Appearance Watery Mucoid and/or bloody
Volume Large Small
Frequency Increased Highly increased
Blood Possibly positive but never Commonly grossly bloody
gross blood
pH Possibly < 5.5 >5.5
Reducing substances Possibly positive Negative
WBCs < 5/high power field Commonly >10/high power
field
Serum WBCs Normal Possible leukocytosis,
bandemia
Organisms •Viral •Invasive bacteria
•Rotavirus •Escherichia Coli
•Adenovirus (enteroinvasive,
•Calicivirus enterohemorrhagic)
•Astrovirus •Shigella species
•Norovirus •Salmonella species
•Campylobacter species
•Yersinia species
•Aeromonas species
•Plesiomonas species
•Enterotoxigenic bacteriaE coli •Toxic bacteriaClostridium
•Klebsiella difficile
•Clostridium perfringens
•Cholera species
•Vibrio species
•ParasitesGiardia species •ParasitesEntamoeba
•Cryptosporidium species organisms
Pediatric Chronic Diarrhea
 Mechanism
• A paradigm of chronic
diarrhea generated by
multiple mechanisms is
provided by HIV infection,
in which immune
derangement, enteric
infections, nutrient
malabsorption, and
intestinal damage, together
with a direct
enteropathogenic role of
HIV, trigger and maintain
chronic diarrhea
Main causes
Pediatric Chronic Diarrhea Etiology
Work up
Pediatric Chronic Diarrhea Algorithm
Pediatric diarrhea
Therapeutic Approach
NUTRITION
 PREVENTING FOOD ALLERGY
Pregnancy and Infancy
• Allergen exposure
• Breastfeeding
• Choice of infant formula
• Solid food introduction
Early Diet and Immunomodulatory factors
• Antioxidants
• Folate
• Pre and Probiotics
• Polyunsaturated Fatty Acids (PUFA)
• Vitamin D
 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
– Cough and pneumonia after migration of larvae through lung scan
– Peripheral eosinophilia may occur.
• Identification of larvae in stooldiagnostic.
 Ascaris Lumbricoides
• Clinical manifestations:
• Can be asymptomatic
• Mild diarrhea
• Intermittent epigastric pain
• Anorexia
• Vomiting
• 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.
• Detecting hookworm eggs on stool smear is diagnostic.
 Schistosomiasis
• Schistosomiasis, also known as bilharzia, is a
disease caused by parasitic worms
• Most human infections are caused by
Schistosoma mansoni, S. haematobium, or S.
japonicum.
 Risk factor
• most commonly in places with poor
sanitation.
• School-age children who spend time
swimming or bathing in water containing
infectious cercariae.
• People who live in, or travel to areas where
schistosomiasis is found and are exposed to
contaminated freshwater
 Sign and symptoms
• Common symptoms  Most people have no
symptoms when they are first infected.
However, within days after becoming infected,
they may develop a rash or itchy skin. Within
1-2 months of infection, symptoms may
develop including fever, chills, cough, and
muscle aches
• Cronic schistosomiasis  Without treatment,
schistosomiasis can persist for years. Signs and
symptoms of chronic schistosomiasis include:
abdominal pain, enlarged liver, blood in the stool
or blood in the urine, and problems passing
urine. Chronic infection can also lead to increased
risk of bladder cancer.
• Rarely, eggs are found in the brain or spinal cord
and can cause seizures, paralysis, or spinal cord
inflammation.
 Diagnosis & treatment
• Stool or urine samples can be examined
microscopically for parasite eggs (stool for S.
mansoni or S. japonicum eggs and urine for S.
haematobium eggs).
• a blood (serologic) test.
• Safe and effective medication is available for
treatment of both urinary and intestinal
schistosomiasis. Praziquantel, a prescription
medication, is taken for 1-2 days to treat
infections caused by all Schistosoma species.
 Taeniasis
• Taeniasis in humans is a parasitic infection
caused by the tapeworm species Taenia
saginata (beef tapeworm) and Taenia solium
(pork tapeworm).
• Humans can become infected with these
tapeworms by eating raw or undercooked
beef (T. saginata) or pork (T. Solium)
 Symptoms
• Abdominal pain, loss of appetite, weight loss, and
upset stomach
• The active passing of proglottids (tapeworm
segments) through the anus and in the feces.
• In rare cases, tapeworm segments become
lodged in the appendix, or the bile and pancreatic
ducts.
• Infection with T. solium tapeworms can result in
human cysticercosis, which can be a very serious
disease that can cause seizures and muscle or eye
damage.
 Diagnosis
• examination of stool samples
• Stool specimens should be collected on three
different days and examined in the lab for
Taenia eggs using a microscope. Tapeworm
eggs can be detected in the stool 2 to 3
months after the tapeworm infection is
established.
• Treatment  praziquantel or niclosamide
 Food poisoning
• Occurs when swallow food or water that contains bacteria, parasites, viruses, or the
toxins made by these germs. Most cases are caused by common bacteria such as
Staphylococcus or E. coli.

Many types of germs and toxins may cause food poisoning, including:

• Campylobacter enteritis

• Cholera

• E. coli enteritis

• Toxins in spoiled or tainted fish or shellfish

• Staphylococcus aureus

• Salmonella

• Shigella
 Symptoms Exam and test

• Abdominal cramps • Tests stools or the food that patient

• Diarrhea (may be bloody) have eaten to find out what type of

• Fever and chills germ is causing the symptoms. However,

• Headache tests may not always find the cause of

• Nausea and vomiting the diarrhea.

• Weakness (may be serious) • In more serious cases  sigmoidoscopy

• loss of appetite : uses a thin, hollow tube with a light on
• a high temperature (fever) the end that is laced in the anus to look

for the source of bleeding or infection.

 • Common  dehydration

• Less common, but more serious depend on the bacteria.

1. Arthritis
Complication 2. Bleeding problems

3. Damage to the nervous system

4. Kidney problems

5. Swelling or irritation in the tissue around the heart

• Most people fully recover from the most common types

of food poisoning within 12 - 48 hours. Some types of
Prognosis food poisoning can cause serious complications.

• Death from food poisoning in people who are otherwise

healthy is rare
Food allergy Food intolerance
• Usually comes on suddenly • Usually comes on gradually
• Small amount of food can trigger • May only happen when you eat a lot of the
• Happens every time you eat the food
food • May only happen if you eat the food often
• Can be life-threatening • Is not life-threatening
 REFERENCES
• Managing acute gastroenteritis among children. CDC
Morbidity and Mortality Weekly Report; 2003.
• Netter FH. Atlas of human anatomy. 6th ed. Philadelphia:
Saunders Elsevier; 2014.
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