PEMICU 3

CANTIKA MONICA
405200189
13
LI 1
MM. Anatomi saluran cerna bawah (jejunum-anus)
LI 2
MM. Histologi saluran cerna bawah (jejunum-anus)
HISTOLOGI JEJENUM

• This is very similar to the duodenum

except Brunner’s glands are absent
• Extensive villi are present as are the
crypts of crypts of Lieberkuhn
• The pilcae cicularis are permanent
folds in the intestinal mucosa
• There are 2 layers of smooth muscle:
longitudinal and circular
• Mucosa consists of simple columnar
epithelium with goblet cells.

Junqueira’s Basic Histology : Text and Atlas, 13 th Edition

HISTOLOGI ILEUM
● The ileum has proportionally more goblet cells than more
proximal sections of the small intestine.  (The proportion
of goblet cells generally increases as one progresses down the
GI tract, with the highest proportion found in the lower tract.)
 The ileum also displays an increase in the amount of
mucosal lymphoid tissue, which forms conspicuous clusters
Ile
of lymph nodules, called Peyer's patches. um
● The lymphoid tissue of Peyer's patches may bulge out toward
the lumen, displacing villi, and inward across the muscularis
mucosae into the submucosa.
● The epithelium overlying this lymphoid tissue is cuboidal
(rather than columnar as on villi) and includes M cells which
transport antigen across the epithelium to immune cells.
● The lymphoid tissue of Peyer's patches is similar to that
of tonsils and appendix.  These structures, together with other
more diffuse lymphoid tissue, constitute the Gut-Associated
Lymphoid Tissues, or GALT. Junqueira’s Basic Histology : Text and Atlas, 13th Edition
Large intestine

• The mucosa is penetrated by tubular instestinal gland

• The intestinal lumen are lined by goblet and absorptive cells, with
a small number of enteroendocrine cells

• The columnar absorptive cells or colonocytes have irregular

microvilli and dilated intercellular spaces indicating active fluid
absorption

• The lamina propria is rich in lymphoid cells and in lymphoid

nodules that frequently extend into the submucosa

• Intraperitoneal portions of the colon are covered by serosa, which

is characterized by small, pendulous protuberances of adipose
tissue.

Junqueira’s Basic Histology : Text and Atlas, 13th Edition

COLON
• No vili in tunica mucosal
• A lot of goblet cells among the epithel
• + Cryptus Liberkuhn
• Panneth cells and Argentaffin cells
• Solitaire lymphonodus spread among lamina
propria

Junqueira’s Basic Histology : Text and Atlas, 13th Edition

Anal Canal

• At the anal canal the simple columnar epithelium lining the rectum shifts
abruptly to stratified squamous epithelium of the skin at the anus.
• The mucosa and submucosa of the anal canal form several longitudinal folds,
the anal columns, in which the lamina propria and submucosa include sinuses
of the rectal venous plexus.
• Near the anus the circular layer of the rectum’s muscularis forms the internal
anal sphincter, with further control exerted by striated muscle of the external
anal sphincter

Junqueira’s Basic Histology : Text and Atlas, 13th Edition

LI 3
MM. Fisiologi saluran cerna bawah  (jejunum-anus)
Molitility
● Includes segmentation and the migrating motility complex.
a. Segmentation
○ the small intestine’s primary motility during digestion of a meal, both mixes and slowly
propels the chyme.
○ Segmentation consists of oscillating, ringlike contractions of the circular smooth
muscle along the small intestine’s length; between the contracted segments are
relaxed areas containing a small bolus of chyme.
○ In this way, the chyme is chopped, and thoroughly mixed

Sherwood L. Human physiology: from cells to systems. 8th ed. Belmont: Brooks/ Cole Cencage Learning; 2013.
b. Migrating Motility Complex
●During periods of short fasting, the stomach and small intestine exhibit a unique
motor activity and are replaced by the migrating motility complex (MMC)
●The MMC cycles through the following phases in a repetitive pattern about every 1.5
hours as long as a person is fasting:
○Phase I: A long period lasting about 40 to 60 minutes of relative quiet with very few
contractions
○Phase II: A 20- to 30-minute period with some peristaltic contractions, with the time
varying between contractions
○Phase III: The shortest phase, where intense peristaltic contractions begin in the
upper stomach and propagate (migrate) through to the end of the small intestine.
The contractions rhythmically repeat for 5 to 10 minutes. During this period, the
pyloric sphincter relaxes and opens completely.

Sherwood L. Human physiology: from cells to systems. 8th ed. Belmont: Brooks/ Cole Cencage Learning; 2013.
Secretions
● Each day, the exocrine gland cells in the small-intestine mucosa secrete
into the lumen about 1.5 liters of an aqueous salt and mucus solution
called succus entericus.
● Secretion increases after a meal in response to local stimulation of the
small-intestine mucosa by the presence of chyme.
● The mucus in the secretion provides protection and lubrication.
● Furthermore, this aqueous secretion provides plenty of H2O to
participate in the enzymatic digestion of food.

Sherwood L. Human physiology: from cells to systems. 8th ed. Belmont: Brooks/ Cole Cencage Learning; 2013.
Absorption
● All products of carbohydrate, protein, and fat digestion, and most of the
ingested electrolytes, vitamins, and water, are normally absorbed by the
small intestine indiscriminately. Only the absorption of calcium and iron is
adjusted to the body’s needs.
● Most absorption occurs in the duodenum and jejunum; very little occurs in
the ileum, because most absorption has already been accomplished
before the intestinal contents reach the ileum
● The mucous lining of the small intestine is remarkably well adapted for its
special absorptive function for two reasons:
- it has a large surface area
- the epithelial cells in this lining have a variety of specialized transport
mechanisms.
Sherwood L. Human physiology: from cells to systems. 8th ed. Belmont: Brooks/ Cole Cencage Learning; 2013.
 The large intestine
● Consists of the colon, cecum, appendix, and rectum
● The cecum forms a blind-ended pouch below the junction of the small
and large intestines at the ileocecal valve.
● Appendix is the small, fingerlike projection at the bottom of the cecum, a
lymphoid tissue that houses lymphocytes
● The colon, which makes up most of the large intestine, is not coiled like
the small intestine but consists of three relatively straight parts—the
ascending colon, the transverse colon, and the descending colon.
● The end part of the descending colon becomes S shaped, forming the
sigmoid colon and then straightens out to form the rectum
Sherwood L. Human physiology: from cells to systems. 8th ed. Belmont: Brooks/ Cole Cencage Learning; 2013.
LI 4
MM. Biokimia saluran cerna bawah (jejunum-anus)
Biomedical Importance in Digestive System
• Human diet (in addition to water) → must provide metabolic fuels (mainly
carbohydrates and lipids), protein, fiber, minerals, vitamins and essential
fatty acids
• Polysaccharides, triacylglycerols, and proteins that make up the bulk of the
diet → must be hydrolyzed to their constituent monosaccharides, fatty
acids, and amino acids before absorption and utilization
• Minerals and vitamins must be released from the complex matrix of food
before they can be absorbed and utilized
• Digestion of the major foodstuffs is an orderly process involving the action
of a large number of digestive enzymes

Bender, D. A., Botham, K. M., Boyle, P. J., Kennelly, P. J., Rodwell, V. W., Weil, P. A., & Weitz, M. (2018). Harper's illustrated Biochemistry, 31. McGraw-Hill Education LLC. 
Barrett, K. E., Barman, S. M., Brooks, H. L., & Yuan, J. X.-J. (2019). Ganong's review of medical physiology. McGraw-Hill Education. 
Carbohydrates
• Carbohydrates digestion → hydrolysis to liberate oligosaccharides, then
free monodisaccharides and disaccharides
• Glycemic index → the increase in blood glucose after a test dose of a
carbohydrate compared with that after an equivalent amount of glucose
consumed
• Foods that have a low glycemic index are considered to be more beneficial
since they cause less fluctuation in insulin secretion.

Bender, D. A., Botham, K. M., Boyle, P. J., Kennelly, P. J., Rodwell, V. W., Weil, P. A., & Weitz, M. (2018). Harper's illustrated Biochemistry, 31. McGraw-Hill Education LLC. 
Barrett, K. E., Barman, S. M., Brooks, H. L., & Yuan, J. X.-J. (2019). Ganong's review of medical physiology. McGraw-Hill Education. 
Barrett, K. E., Barman, S. M., Brooks, H. L., & Yuan, J. X.-J. (2019). Ganong's review of medical physiology. McGraw-Hill Education. 
Proteins
• In the small intestine, the polypeptides formed by digestion in the stomach
are further digested by the powerful proteolytic enzymes of the pancreas
and intestinal mucosa
• Endopeptidases → trypsin, chymotrypsin, and elastase
• Endopeptidases secreted as inactive proenzymes → will be activated
when they have reached their site of action, secondary to the action of
enterokinase

Barrett, K. E., Barman, S. M., Brooks, H. L., & Yuan, J. X.-J. (2019). Ganong's review of medical physiology. McGraw-Hill Education. 
Barrett, K. E., Barman, S. M., Brooks, H. L., & Yuan, J. X.-J. (2019). Ganong's review of medical physiology. McGraw-Hill Education. 
Barrett, K. E., Barman, S. M., Brooks, H. L., & Yuan, J. X.-J. (2019). Ganong's review of medical physiology. McGraw-Hill Education. 
Nucleic Acid
• Nucleic acids → split into nucleotides in the intestine by the pancreatic
nucleases
• Nucleotides → split into the nucleosides and phosphoric acid by enzymes
that appear to be located on the luminal surfaces of the mucosal cells
• Nucleosides → split into their constituent sugars and purine and pyrimidine
bases
• The bases are absorbed by active transport

Barrett, K. E., Barman, S. M., Brooks, H. L., & Yuan, J. X.-J. (2019). Ganong's review of medical physiology. McGraw-Hill Education. 
Lipids
• Most fat digestion begins in the duodenum
• Pancreatic lipase → hydrolyzes the 1- and 3-bonds of the triglycerides
(triacylglycerols) with relative ease but acts on the 2-bonds at a very low
rate → FFA and 2-monoglycerides (2-monoacylglycerols)
• Colipase → allows lipase to remain associated with droplets of dietary lipid
even in the presence of bile acids
• Cholesterol esterase → catalyzes the hydrolysis of cholesterol esters,
esters of fat-soluble vitamins, and phospholipids, as well as triglycerides

Barrett, K. E., Barman, S. M., Brooks, H. L., & Yuan, J. X.-J. (2019). Ganong's review of medical physiology. McGraw-Hill Education. 
Barrett, K. E., Barman, S. M., Brooks, H. L., & Yuan, J. X.-J. (2019). Ganong's review of medical physiology. McGraw-Hill Education. 
LI 5
MM. Kelainan yang menyebabkan mual, muntah dan diare
(Definisi, etiologi, faktor risiko, patofisiologi, tanda gejala, Alarm symptom, PF, PP
(pemeriksaan feses, intoleransi makanan, tatalaksana, komplikasi, prognosis, KIE dan
edukasi, Resep)
Demam tifoid
Infeksi parasit (entamoeba histolytica, giardia
lamblia, plasmodium falciparum, cyclospora,
strongyloidiasis, cryptosporidium parvum,
schistosomiasis, taeniasis, trichuriasis, hookworm,
ascariasis)
 Parasitic Agents

http://www.uib.cat/depart/dba/microbiologia/ADSenfcomI/material_archivos/infeccion%20gastrointestinal.pdf
entamoeba histolytica
Entamoeba hystolitica
• Amebiasis : disease caused by a one-celled parasite called Entamoeba hystolitica
• Risk factors :
• People who have traveled to tropical places that have poor sanitary conditions
• Immigrants from tropical countries that have poor sanitary conditions
• People who live in institutions that have poor sanitary conditions
• Men who have sex with men
• Contaminated if :
• Puts anything into their mouth that has touched the feces (poop) of a person who is infected
with E. histolytica.
• Swallows something, such as water or food, that is contaminated with E. histolytica.
• Swallows E. histolytica cysts (eggs) picked up from contaminated surfaces or fingers.

CDC; Center for Disease Control and Prevention

CDC; Center for Disease Control and Prevention
Symptoms
• loose feces (poop)
• stomach pain
• stomach cramping
• amebic dysentery : stomach pain, bloody stools (poop), and fever

Diagnosis
• Submit fecal (poop) samples
• Blood test

Treatment
• Antibiotics

CDC; Center for Disease Control and Prevention

Prevention

Safe to drink :
• Bottled water with an unbroken seal
• Tap water that has been boiled for at least 1 minute
• Carbonated (bubbly) water from sealed cans or bottles
• Carbonated (bubbly) drinks (like soda) from sealed cans or bottles
May not safe to eat or drink :
• Fountain drinks or any drinks with ice cubes
• Fresh fruit or vegetables that you did not peel yourself
• Milk, cheese, or dairy products that may not have been pasteurized.
• Food or drinks sold by street vendors

CDC; Center for Disease Control and Prevention

giardia lamblia
Giardia lamblia (Flagella)

Disease: giardiasis or lambliasis

Hosts: humans, beavers, wolves, cows, cats, dogs.

Geographic distribution: cosmopolitan, especially the climate of the tropics and subtropics.

Morphology: divided into 2 forms

1. vegetative / trophozoid (14 microns), bilaterally symmetrical like a guava fruit, the anterior part holds and the
posterior is tapered. Ventrally there is 1 large suction vanity. There are 2 nuclei with a large karyosome in the
middle and 4 pairs of flagella.
2. Cyst (10-14 microns), oval shape, thin walled but strong, with 2 nuclei in young cysts and 4 nuclei in mature
cysts.

Atlas Parasitologi Kedokteran Juni Prianto L.A.

Buku Ajar Parasitologi Kedokteran FKUI Edisi Keempat
Atlas Parasitologi Kedokteran Juni Prianto L.A.
Life cycle: G. lamblia lives in the small intestine cavity, namely the duodenum and the
proximal jejunum. When the mature cyst is swallowed by the host, it excysts in the
duodenum, then the cytoplasm divides and the flagellum grows from the axoneme to form a
trophozoid. With the rapid movement of the flagellum, the trophozoid can move from the
intestinal villi to other sites. if trophozoid remain in the intestinal villi, trophozoid attach
themselves with their sucking vanes to the intestinal epithelium. The trophozoid then
reproduces by longitudinal pairs. Encystation (cyst formation) occurs on the way to the colon,
when the stool begins to solidify, the cyst will immediately come out with the stool.
infection happen when the mature cyst swallowed through contaminated water and food.

Clinical pathology: this parasite attaches to the mucosa of the duodenum and jejunum by
sucking vanity.
abnormalities that are often found in the form of irritation. If the parasite covers most of the
intestinal mucosa, the absorption of fat will be disrupted.
Atlas Parasitologi Kedokteran Juni Prianto L.A.
The incubation period lasts 9-15 days.
Buku Ajar Parasitologi Kedokteran FKUI Edisi Keempat
https://i2.wp.com/ http://3.bp.blogspot.com/-
upload.wikimedia.org/wikipedia/ rHhUOSdJpKM/T7SNSes39BI/
commons/thumb/d/db/ AAAAAAAAAJ4/
Giardia_life_cycle_en.svg/628px- zjwCZXrx8Qw/s1600/
Diagnosis: established by finding the form of trophozoites in watery stools or duodenal fluid. cyst
forms in solid stool. antigen detection, biopsy of the small intestine in the area of ​the duodeno-
jejunal junction, microscopic examination.

Treatment/therapy:
drug of choice is
Tinidazole in a single dose of 2 g in adults or 30-35 mg/kg in children.
metronidazole 250 mg 3 times daily for 7 days for adults and 5 mg/kg 3 times daily for 7 days for
children.

Other drugs are quinacrine 100 mg 3 times a day for 7 days for adults and a dose of 2 mg/kg 3
times a day for 7 days for children. It is also the drug of choice for pregnant women in
combination with paromomycin.

furazolidone is the only drug available in liquid form, so it is useful for infants and young children.
a dose of 100 mg 4 times a day for 7 days for adults and a dose of 1.25 mg/kg 4 times a day for 7
days for children.
Atlas Parasitologi Kedokteran Juni Prianto L.A.
Buku Ajar Parasitologi Kedokteran FKUI Edisi Keempat
plasmodium falciparum
cyclospora
strongyloidiasis
Strongiloidiasis
Geographic distribution
Strongyloides stercoralis is broadly distributed in tropical and subtropical areas across the globe

Risk factor
• areas with poor sanitation
• rural and remote communities
• among socially marginalized groups.

Infected if :
• infective filariform larvae that can penetrate either the intestinal mucosa or the skin of the
perianal area, resulting in autoinfection
• Filariform larvae in contaminated soil penetrate human skin when skin contacts soil

CDC; Center for Disease Control and Prevention

CDC; Center for Disease Control and Prevention
Clinical presentation
• localized pruritic, erythematous rash at the site of skin penetration
• trachea irritation and dry cough
• diarrhea, constipation, abdominal pain, and anorexia.
• Up to 75% of people with chronic strongyloidiasis have mild peripheral
eosinophilia or elevated IgE levels.
• In imunnocompromaised patient ( consume corticosteroid, HIV ) can cause
hyperinfection ( we can find adult worm in all GIT and larvae in many organ
such as lung, liver, gall bladder )
Diagnosis
• identification of Strongyloides stercoralis larvae (rhabditiform and occasionally
filariform) in the stool, duodenal fluid, and/or biopsy specimens, and possibly
sputum in disseminated infections.

CDC; Center for Disease Control and Prevention

Treatment
• albendazole 400 mg 1/2 times a day for 3 days
• mebendazole 100 mg 3 times a day for 2-4 weeks

Prognosis
Hyperinfection can lead to death

CDC; Center for Disease Control and Prevention

cryptosporidium parvum
Cryptosporidium parvum (Sporozoa)

Hosts: mammals (humans, cattle, sheep, pigs, mice, rabbits, monkeys, dogs, cats), birds and reptiles (snakes).

Disease: cryptosporidiosis

Geographic distribution: in humans found cosmopolitan.

Morphology: meront and oocysts measuring 4-5 microns.

Diagnosis: the discovery of oocysts in the stool. Ziehl-Neelsen staining modification (good way to identify oocysts,
oocyst color is red, yeast cells are round or oval in blue), if the number of oocysts is small, concentration can be
done by flotation with sugar or formalin ether or formalin ethylacetate.
Tissue biopsy of the gastrointestinal mucosa was performed with hematoxylin-eosin staining.
PCR with Ziehl-Neelsen staining.

Epidemiology: cosmopolitan

Buku Ajar Parasitologi Kedokteran FKUI Edisi Keempat

Clinical pathology: in humans this parasite is found in the pharynx, esophagus, duodenum,
jejunum, ileum, appendix, colon, rectum, gallbladder, pancreatic duct.
for immunocompetent patients (intestine and appendix) while immunocompromised patients
(along the gastrointestinal tract, hepatobiliary system, respiratory tract). The heaviest infections
are found in the jejunum.
This parasite is only found on the surface of epithelial cells.
Cryptosporidium is the main cause of diarrhea in children in developing countries (under 1 year),
this is supported by the presence of malnutrition in children.
In humans, the severity of the disease is determined by the immune status. for
immunocompetent patients (asymptomatic or self-limiting infection), while for
immunocompromised patients (chronic diarrhea that continues until death).
Diarrhea in immunocompetent patients lasts 1 month while in immunocompromised patients it
lasts 4 months or more. Other clinical symptoms: heartburn, nausea, vomiting, anorexia, low-
grade fever.
In AIDS patients there are 4 clinical manifestations of cryptosporidiosis: cholera-like diarrhea,
chronic diarrhea, intermittent diarrhea, and transient diarrhea.

Treatment/therapy: in AIDS patients, the ideal treatment is to improve the immune system with
Buku Ajar Parasitologi Kedokteran FKUI Edisi Keempat
Life cycle :

https://image.slideserve.com/1281338/
cryptosporidium-parvum-n.jpg

Buku Ajar Parasitologi Kedokteran FKUI Edisi Keempat

schistosomiasis
Schistosomiasis
• Known as bilharzia

Epidemiology and risk factors

• most commonly in places with poor sanitation
• school-age children who live in the area of poor sanitation
• live in, or travel to, areas where schistosomiasis is found and are exposed to
contaminated freshwater

CDC; Center for Disease Control and Prevention

Areas where human schistosomiasis is found include:
• Schistosoma mansoni
• Africa: Nile River valley in Sudan and Egypt
• South America: Brazil, Suriname, and Venezuela
• Caribbean (risk is very low): Dominican Republic, Guadeloupe, Martinique,
and Saint Lucia
• S. haematobium
• Africa: Nile River valley in Egypt and the Mahgreb region of North Africa
• areas of the Middle East
• Corsica.
• S. japonicum
• Indonesia, parts of China and Southeast Asia.
• S. mekongi
• Cambodia and Laos.
• S. intercalatum
• Central and West Africa.
CDC; Center for Disease Control and Prevention
CDC; Center for Disease Control and Prevention
• Left : Biomphalaria sp. (intermediate host for S. mansoni)
• Center : Adults of S. Mansoni
• Right : Bulinus sp. (intermediate host for S. haematobium, S. guineensis and S.
intercalatum)
• Oncomelania (S. japonicum)

CDC; Center for Disease Control and Prevention

Clinical presentation
Symptoms caused by the body’s reaction to the eggs
• Local cutaneous hypersensitivity reaction following skin penetration by cercariae
• Small, itchy maculopapular lesions
• Acute schistosomiasis (Katayama fever) : fever, cough, abdominal pain, diarrhea,
hepatosplenomegaly, eosinophillia
• Children who are repeatedly infected : anemia, malnutrition, learning difficulties
• Chronic schistosomiasis : abdominal pain, enlarged liver, blood in the stool or urine,
problems passing urine, portal hypertension, liver fibrosis, bladder cancer, in brain
(seizures, paralysis, spinal cord inflammation

Diagnosis
• Find egg in Stool or urine sample or biopsy
• Blood (serological) test

CDC; Center for Disease Control and Prevention

Treatment
• Praziquantel, taken for 1-2 days
Prevention
No vaccine is available
• Avoid swimming or wading in freshwater
• Drink safe water
• Water used for bathing should be brought to a rolling boil for 1 minute to kill any
cercariae, and then cooled before bathing to avoid scalding. Water held in a storage
tank for at least 1 – 2 days should be safe for bathing
• Vigorous towel drying after an accidental, very brief water exposure may help to
prevent parasites from penetrating the skin. However, do not rely on vigorous towel
drying alone to prevent schistosomiasis

CDC; Center for Disease Control and Prevention

Treatment

Note :
• Treatment in pregnancy : praziquantel is in group B
• Treatment in pediatrics :  infected children as young as 1 year old can be effectively treated without serious
side effects

CDC; Center for Disease Control and Prevention

taeniasis
 Taeniasis
Symptom
• The most visible symptom of taeniasis is 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.

CDC; Center for Disease Control and Prevention

CDC; Center for Disease Control and Prevention
 Diagnosis
• Diagnosis of Taenia tapeworm infections is made by
examination of stool samples. Tapeworm eggs can be
detected in the stool 2 to 3 months after the tapeworm
infection is established. ( search for proglotid / eggs )

Treatment
praziquantel or niclosamide ( or albendazole )

CDC; Center for Disease Control and Prevention

trichuriasis
Trichuriasis
Causal agent : Trichuris trichiura

Epidemiology
• Areas with tropical weather and poor sanitation practices, among children.

Risk factors
• Using fuman feses as fertilizer
• Defecation onto soil
Spread from person to person by fecal-oral transmission or through feses-
contaminated food

CDC; Center for Disease Control and Prevention

CDC; Center for Disease Control and Prevention
Clinical Presentation
• Light infections  no symptoms
• Heavy infections  frequent and painful passage of stool, contains mucus, water, and blood, in
children (severe anemia, growth retardation, impaired cognitive development)
• Rectal prolapse

Diagnosis
• Identifying the eggs in stool sample

Treatment
• Antihelminthic (DOC : albendazole & mebendazole) treated for 3 days

CDC; Center for Disease Control and Prevention

Prevention
• Avoid ingesting soil that may be contaminated with human feces, including where human fecal
matter (“night soil”) or wastewater is used to fertilize crops.
• Wash your hands with soap and warm water before handling food.
• Teach children the importance of washing hands to prevent infection.
• Wash, peel, or cook all raw vegetables and fruits before eating, particularly those that have been
grown in soil that has been fertilized with manure.
• Not defecating outdoors.
• Effective sewage disposal systems

CDC; Center for Disease Control and Prevention

Treatment

Note :
• Treatment in pregnancy : albendazole, mebendazole, ivermectin are in group C
• Treatment in pediatrics :
• Albendazole : can be used in children as young as 1 year old
• Mebendazole :  intended for the use of children up to 12 years of age
• Ivermectin : children less than 3 years old been safely treated

CDC; Center for Disease Control and Prevention

hookworm
Hook worm
Geographic distribution
• The geographic distributions of the hookworm species that are intestinal parasites in
human, Ancylostoma duodenale and Necator americanus, are worldwide in areas with warm, moist
climates and are widely overlapping

Infected if :
•Filariform larvae in contaminated soil penetrate human skin when skin contacts soil
• infection by A. duodenale may probably also occur by the oral

Disease :
 The most serious effects of hookworm infection are the development of anemia and protein
deficiency caused by blood loss at the site of the intestinal attachment of the adult worms
When children are continuously infected by many worms, the loss of iron and protein can retard
growth and mental development.

CDC; Center for Disease Control and Prevention

CDC; Center for Disease Control and Prevention
Diagnosis
• Find egg ( or larvae ) in feses. To identify which species ( A.duodenale or N.americanus ) use harada mori
culture method

Treatment
Anthelminthic medications (drugs that rid the body of parasitic worms), such as albendazole and
mebendazole, are the drugs of choice for treatment of hookworm infections. Infections are generally
treated for 1-3 days. The recommended medications are effective and appear to have few side effects. Iron
supplements may also be prescribed if the infected person has anemia

Or with pyrantel pamoat 10 mg / Kg BB

CDC; Center for Disease Control and Prevention

Hook worm; zoonosis
Epidemiology and Risk Factors
• Dog and cat hookworms : warmer climates
• Zoonotic hookworms : tropical and subtropical regions
• Cutaneous larva migrans (CLM) : returning travelers to tropical regions who have had soil and/or sand
exposures in places where dogs and cats are likely to have hookworms

Symptoms
• Abdominal pain and discomfort
• Diarrhea

CDC; Center for Disease Control and Prevention

CDC; Center for Disease Control and Prevention
Diagnosis
• Finding red, raised tracks in the skin that are very itchy

Treatment
• Antiparasitic

Prevention and control

• Wearing shoes and taking other protective measures to avoid skin contact with
sand or soil
• Routine veterinary care of dogs and cats (regular deworming, will reduce
environmental contamination with zoonotic hookworm eggs and larvae)
• Prompt disposal of animal feces prevents eggs from hatching and
contaminating soil

CDC; Center for Disease Control and Prevention

Treatment

Note :
• Treatment in pregnancy : albendazole, ivermectin are in group C
• Children younger than 2 years of age or under 15 kg body weight may be treated with topical preparations

CDC; Center for Disease Control and Prevention

ascariasis
 Ascariasis
Epidemiology
• Ascaris lumbricoides infection  most common intestinal worm infections

Risk factors
• poor personal hygiene
• poor sanitation
• in places where human feces are used as fertilizer

Geographic Distribution
• the geographic distributions of Ascaris lumbricoides are worldwide in areas with warm, moist climates and
are widely overlapping
• Infection occurs worldwide and is most common in tropical and subtropical areas where sanitation and
hygiene are poor

CDC; Center for Disease Control and Prevention

CDC; Center for Disease Control and Prevention
Clinical presentation
• Children : stunted growth via malnutrition
• Adult worms : no acute symptoms
• High worm burdens : abdominal pain, intestinal obstruction, perforation
• Migrating adult worms : symptomatic occlusion of biliary tract, appendicitis, nasopharyngeal expulsion

Diagnosis
• Identifying Ascaris eggs in a stool

Treatment
• Antihelmintic medication (DOC : albendazole and mebendazole)
• Infections are generally treated for 1-3 days

CDC; Center for Disease Control and Prevention

Prevention and control
• Avoid ingesting soil that may be contaminated with human or pig feces, including where human fecal
matter (“night soil”), wastewater, or pig manure is used to fertilize crops.
• Wash your hands Teach children the importance of washing hands to prevent infection.
• Supervise children around pigs, ensuring that they do not put unwashed hands in their mouths.
• Wash, peel, or cook all raw vegetables and fruits before eating, particularly those that have been grown
in soil that has been fertilized with manure.

Transmission of Ascaris lumbricoides infection to others in a community setting can be

prevented by:
• Not defecating outdoors.
• Effective sewage disposal systems.

CDC; Center for Disease Control and Prevention

Treatment

Prognosis :
• Have a good prognosis, and generally self limited in 1,5 year.
• With treatment, healing presentation ( 70-99 % )

Complication :
• Obstruction
• perforation

CDC; Center for Disease Control and Prevention

Infeksi virus (Rotavirus,
Adenovirus,Norovirus)
Infeksi bakteri (salmonella typhi dan
paratyphi, shigella, cholera E. Coli,
enterobacteria, campylobacter)
salmonella typhi dan paratyphi
shigella
 Shigella
• Shigella causes an acute invasive enteric infection clinically manifested by
diarrhea that is often bloody

Pathogenesis :
• Shigella has specialized mechanisms to survive the low gastric pH. survives
the acid environment in the stomach and moves through the gut to the
colon, its target organ.
• Shigella passes the epithelial cell barrier by transcytosis through M cells
and encounters resident macrophages.
• The bacteria evade degradation in macrophages by inducing apoptosis,
which is accompanied by proinflammatory signalling
 Clinical Manifestations

• incubation period of 12 hr to several days before symptoms ensue

• Severe abdominal pain, high fever, emesis, anorexia, generalized toxicity,
urgency, and painful defecation characteristically occur
• The diarrhea may be watery and of large volume initially, evolving into
frequent, small-volume, bloody mucoid stools
• Significant dehydration is related to the fluid and electrolyte losses in
feces and emesis.
• Physical examination initially shows abdominal distention and tenderness,
hyperactive bowel sounds, and a tender rectum on digital examination
 Treatment - Adults
- Adults
• Rehydration should be oral unless the patient is comatose or presents in shock.
• Hand washing after defecation or handling of children’s feces and before handling of food is
recommended

– Child
• first concern in a child with suspected shigellosis should be for fluid and electrolyte correction and
maintenance.
• Nutrition is a key concern in areas where malnutrition is common.
• A single large dose of vitamin A (200,000 IU)
• Zinc supplementation (20 mg elemental zinc for 14 days)
• Indication for antibiotic incule; severe diarrhea, persistence for >1 week, and worsening of symptoms
cholera E. Coli
 Escherichia Coli

• Enteropathogenic E. coli (EPEC) pathogens do not make any toxins

• Enterotoxigenic E. coli (ETEC) pathogens possess colonization factors (fimbrial
adhesins)
• Enterohaemorrhagic E. coli (EHEC) isolates produce a verotoxin
• Enteroinvasive E. coli (EIEC) pathogens attach specifically to the mucosa of the
large intestine
• Enteroaggregative E. coli (EAEC) pathogens derive their name from their
characteristic attachment pattern to tissue culture cell
• Diffusely adherent E. coli (DAEC) pathogens produce an alpha haemolysin and
cytotoxic necrotizing factor 1.
 Diagnosis

• Diagnosis currently depends heavily on laboratory studies that are not

readily available to practitioners.
• Fecal leukocyte examination of the stool is often positive with EIEC or
occasionally positive with other diarrheagenic E. coli
• EIEC and STEC there may be an elevated peripheral blood
polymorphonuclear leukocyte count with a left shif
 Treatment

- adults :
• Antimicrobial therapy for STEC/EHEC/ST-EAEC infection (the presence of which
is suggested by grossly bloody diarrhea without fever) should be avoided
because antibiotics may increase the incidence of HUS
- Child :
• The cornerstone of management is appropriate fluid and electrolyte therapy
• this therapy should include oral replacement and maintenance with
rehydration solutions such as those specified by the World Health Organization
• Early refeeding (within 6-8 hr of initiating rehydration) with breast milk or
infant formula or solid foods should be encouraged
enterobacteria
campylobacter
 Campylobacter

• Campylobacter organisms are Gram-negative, curved, thin (0.2- 0.4 µm

wide), non–spore-forming rods (1.5-3.5 µm long) that usually have
tapered ends.
• They are smaller than most other enteric bacterial pathogens and have
variable morphology, including short commashaped or S-shaped
organisms and long, multispiraled, filamentous, seagull-shaped
organisms.
Pathogenesis
• Most Campylobacter isolates are acid sensitive, and should, in theory, be
eradicated in the stomach.
• pathogenesis of C. jejuni enteritis include mechanisms to transit the
 Laboratory Evaluation

• Diagnosis ussualy confirmed by identification of organism in cultures of

stool or rectal swabs.
• For rapid diagnosis of campylobacter enteritis, direc carbol fuchsin stain of fecal
smear, indirect fluroscence antibody test, dark field microscopy, or latex
agglutination.
Complication :
• Reactive arthritis – with patients who are + HLA-B27
• Trigger the disease patient with GBS (Guillain-Barre Syndrome)
• IgA nephropathy and
• Immunce complex glomerulonephritis
Infeksi jamur (candida albicans)
 Oral Candidiasis
• Oral candidiasis is a common opportunistic infection of the oral cavity caused by an
overgrowth of Candida species, the commonest being Candida albicans.
• Oral candidiasis is the most common human fungal infection especially in early and
later life.
• The incidence of C albicans isolated from the oral cavity has been reported to be
45% in neonates,6 45%–65% of healthy children, 30%–45% of healthy adults, 50%–
65% of people who wear removable dentures, 65%–88% in those residing in acute
and long term care facilities, 90% of patients with acute leukaemia undergoing
chemotherapy, and 95% of patients with HIV.
• In immunocompromised patients, infection can spread through the bloodstream or
upper gastrointestinal tract leading to severe infection with significant morbidity
and mortality. Systemic candidiasis carries a mortality rate of 71% to 79%.

Akpan A, Morgan R. Oral candidiasis. Postgraduate Medical Journal 2002;78:455-459.

 Predisposing
factors

THOMAS, J. E., & LLOYD, P. M. (1985). Oral

candidiasis in the elderly. Special Care in Dentistry,
5(5), 222–225. doi:10.1111/j.1754-
 Classification
Oral candidiasis can be classified as follows:
1.Acute candidiasis
1. Acute pseudomembranous candidiasis (thrush).
2. Acute atrophic (erythematous) candidiasis.
2.Chronic candidiasis
1. Chronic hyperplastic candidiasis (candidal leukoplakia).
2. Denture induced candidiasis (chronic atrophic (erythematous) candidiasis).
3. Median rhomboid glossitis.
3.Angular cheilitis (stomatitis)

Akpan A, Morgan R. Oral candidiasis. Postgraduate Medical Journal 2002;78:455-459.

 Pseudomembranous candidiasis (thrush)
• characterised by extensive white pseudomembranes consisting
of desquamated epithelial cells, fibrin, and fungal hyphae.
• occur on the surface of the labial and buccal mucosa, hard and
soft palate, tongue, periodontal tissues, and oropharynx.
• The membrane can usually be scraped off with a swab to expose
an underlying erythematous mucosa.
• Diagnosis is usually straightforward as it is easily seen and is one
of the commonest forms of oropharyngeal candidiasis
accounting for almost a third.
• Diagnosis can be confirmed microbiologically either by staining a
smear from the affected area or by culturing a swab from an oral
rinse.
• Predisposing factors: extremes of age, diabetes mellitus,
HIV/AIDS or leukaemia, those using steroid aerosol inhalers,
broad spectrum antibiotics, and psychotropic drugs, and
patients who are terminally ill.
Akpan A, Morgan R. Oral candidiasis. Postgraduate Medical Journal 2002;78:455-459.
 Acute atrophic candidiasis
• Acute atrophic candidiasis is usually
associated with a burning sensation in
the mouth or on the tongue.
• The tongue may be bright red similar to
that seen with a low serum B12, low
folate, and low ferritin.
• A swab from the tongue/buccal mucosa
may help diagnosis.

THOMAS, J. E., & LLOYD, P. M. (1985). Oral candidiasis in the elderly. Special Care in
Dentistry, 5(5), 222–225. doi:10.1111/j.1754-4505.1985.tb00577.x 
https://image.slidesharecdn.com/candidiasis-151002183830-lva1-
Akpan A, Morgan R. Oral candidiasis. Postgraduate Medical Journal 2002;78:455-459. app6892/95/candidiasis-13-638.jpg?cb=1443811177
 Chronic hyperplastic candidiasis
• Chronic hyperplastic candidiasis characteristically
occurs on the buccal mucosa or lateral border of the
tongue as speckled or homogenous white lesions.
• There is an association with smoking and complete
resolution appears to be dependent on cessation of
smoking.
• This condition can progress to severe dysplasia or
malignancy and is sometimes referred to as candidal
leukoplakia.
• This condition may be confused with lichen planus,
pemphigoid/pemphigus, and squamous cell
carcinoma.

Akpan A, Morgan R. Oral candidiasis. Postgraduate Medical Journal 2002;78:455-459.

 Chronic atrophic candidiasis
• Chronic atrophic candidiasis also known as
“denture stomatitis” is characterised by
localised chronic erythema of tissues covered
by dentures.
• Lesions usually occur on the palate and upper
jaw but may also affect mandibular tissue.
• Diagnosis requires removal of dentures and
careful inspection; swabs may be taken for
confirmation.
• quite common with incidence rates of up to https://d3i71xaburhd42.cloudfront.net/
d3240dfcda250d3062f697328428cd59272e8b75/3-Figure1-1.png
65% reported.

Akpan A, Morgan R. Oral candidiasis. Postgraduate Medical Journal 2002;78:455-459.

 Median rhomboid glossitis
• Median rhomboid glossitis is a chronic
symmetrical area on the tongue anterior to
the circumvallate papillae. It is made up of
atrophic filiform papillae.
• The classic symptom of this condition is a
diamond-shaped area of erythema or slight
mucosal nodularity on the posterior
middorsum of the tongue
• Biopsy of this area usually yields candida in
over 85% of cases. It tends to be associated
with smoking and the use of inhaled steroids. https://upload.wikimedia.org/wikipedia/
commons/thumb/f/f6/Glossitis.jpg/300px-
THOMAS, J. E., & LLOYD, P. M. (1985). Oral candidiasis in the elderly. Special Care in
Glossitis.jpg
Dentistry, 5(5), 222–225. doi:10.1111/j.1754-4505.1985.tb00577.x 
Akpan A, Morgan R. Oral candidiasis. Postgraduate Medical Journal 2002;78:455-459.
 Angular cheilitis
• Angular cheilitis is an erythematous fissuring at one or
both corners of the mouth, and is usually associated with
an intraoral candidal infection.
• Facial wrinkling at the corners of the mouth and along
the nasolabial fold especially in older people leads to a
chronically moist environment that predisposes to this
lesion.
• This wrinkling is worse in long term denture wearers
because there is resorption of bone on which the
dentures rest leading to a reduction in height of the
lower face when the mouth is closed.
• Other factors implicated in the aetiology of this condition
are iron deficiency anaemia and vitamin B12 deficiency.

Akpan A, Morgan R. Oral candidiasis. Postgraduate Medical Journal 2002;78:455-459.

ORAL CANDIDIASIS
Symtomps and Signs • Mouth Sores
• Bad Breath
• Bad taste in the mouth
• Bleeding Gums • Numbness or Tingling in Mouth
• Burning Pain in the mouth • Pain When Swallowing
• Burning Tongue • Tongue Redness
• Cracked Corners of Lips • Toothache
• Difficulty Swallowing • White Patches in Mouth
• Dry Mouth • White Patches in Throat
• Feeling of Food stuck in throat • White Patches Inside Cheeks
• Fever • White Tongue
• Mouth Pain
• Mouth Soreness

http://www.medicinenet.com/thrush_oral_candidiasis_symptoms_and_signs/symptoms.htm
ORAL CANDIDIASIS
Medical Treatment:
• Nystatin oral suspension 100.000 IU 60 ml, 4 x 1 ml
• Miconazole cream 2% 10g, 4 x1
 Candidiasis in Elderly
• The overall mortality of candidiasis was significantly higher in older
patients
• Risk Factors for candidaemia in the elderly
• chronic pulmonary and cardiovascular disease
• chronic renal failure
• diabetes mellitus
• higher Charlson Comorbidity Index
• whilst the ‘classic’ risk factors, such as haematological malignancies,
neutropenia, transplantation and solid tumours are less common in
elderly patients

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6105183/
 Fungal infection of the colon
• Fungi are pathogens that commonly infect immunocompromised
patients. At present, the incidence of these pathogens in disease
causation is gradually increasing as a result of increased use of
immunosuppressive drugs, chemotherapy, and transplantation as well
as infections with the human immunodeficiency virus.
• The German Society for Hygiene and Microbiology (DGHM) defines an
intestinal fungal infection as the detection of 105 or more yeast
cells/g of stool.

Praneenararat, S. (2014). Fungal infection of the colon. Clinical and Experimental Gastroenterology, 415. doi:10.2147/ceg.s67776
https://www.adiclair.com/manifestations-of-candida-mycoses/fungal-infections-of-the-gastrointestinal-tract.html#:~:text=Fungal%20infections%20of%20the%20gastrointestinal
%20tract%3A%20Candida%20ssp.,those%20of%20irritable%20bowel%20syndrome.
 Fungal infection of the colon
Fungal Prevalence of Risk factors Clinical Lesions Distribution Initial treatment Response
infections colonic manifestations
involvement
Paracoccidioido 29% • Endemic area (South • Diarrhea, Ulcer, mass, Whole colon Co-trimoxazole, 71%
mycosis America) abdominal pain, polyp, stricture sulfadiazine,
• Any host fever amphotericin B,
or itraconazole

Histoplasmosis 28% • Any host • Diarrhea, Ulcer, edema Whole colon but Amphotericin B 77%
abdominal pain, mucosa mass predominantly
LGIB, fever, right side of
weight loss colon and rectum

Candidiasis 20% of • Malignancy, • Diarrhea, Ulcer, plaque, Whole colon Fluconazole or 100%
intestinal immunosuppressive abdominal pain, erosion caspofungin
candidiasis in agents, neutropenia, fever
autopsy AIDS, ESRD
• No immunocompetent
patients

Praneenararat, S. (2014). Fungal infection of the colon. Clinical and Experimental Gastroenterology,

415. doi:10.2147/ceg.s67776
 Fungal Prevalence of Risk factors Clinical Lesions Distribution Initial treatment Response
infections colonic manifestations
involvement

Cryptococcosi 17% of • AIDS, immunosuppressive • Symptoms: LGIB, Mass, perirectal Whole colon Amphotericin B 60%
s disseminated agents, hematologic fever, abdominal abscess, colonic + flucytosine ±
or pulmonary malignancy, splenectomy, pain, diarrhea, ulcer, patchy surgery
cryptococcosis Job’s syndrome, cirrhosis rectal abscess lesions, stricture,
• Immunocompetent patients • 20% polyp
(23%) asymptomatic
Aspergillosis 9.2% • Malignancy, chemotherapy, • Fever, abdominal Ulcer, necrosis Whole colon Amphotericin B or 50%
neutropenia, pain, LGIB, caspofungin ±
immunosuppressive agents, diarrhea surgery
DM, burn
• No immunocompetent patients
Penicilliosis 1.9% • Endemic area (Southeast Asia, • Fever, diarrhea, Ulcer Predominantly Amphotericin B 75%
southern China, Hong Kong, and abdominal pain, in right side of
India) LGIB colon and spare
• Mostly AIDS (75%) rectum
• No immunocompetent patients
Zygomycosis 0.85% • Immunosuppressive agent, • Abdominal pain, Ulcer, necrosis, mass Whole colon but Amphotericin B + 50%
malnutrition, renal failure, DM, abdominal predominantly surgery
hematologic malignancy distension, fever, in the right side
• I mmunocompetent patients LGIB, diarrhea of the colon
(33.3%)
Pneumocystosis Only one case • AIDS • Fever, diarrhea Edema mucosa Whole colon Pentamidine 100%
Scedosporiosis Only one case • Post-liver transplantation, • Diarrhea, Ulcer Whole colon Amphotericin B 100%
immunosuppressive agents abdominal pain

Praneenararat, S. (2014). Fungal infection of the colon. Clinical and Experimental Gastroenterology, 415. doi:10.2147/ceg.s67776
Non infeksi (malabsorbsi, alergi
makanan, food intolerance, food
intoxication, botulism)
malabsorbsi
alergi makanan
 Food Allergy
• Food allergy is defined as an immune reaction to proteins in the food
and can be immunoglobulin (Ig)E-mediated or non–IgE-mediated.
• Allergic reactions secondary to food ingestion are responsible for a
variety of symptoms involving the skin, gastrointestinal tract, and
respiratory tract. Prevalence rates are uncertain, but the incidence
appears to have increased over the past three decades, primarily in
countries with a Western lifestyle.
• Any food can cause allergy but overall only a few foods account for
the vast majority of allergies. This includes milk, eggs, peanuts,
shellfish, wheat, and nuts.

https://www.ncbi.nlm.nih.gov/books/NBK482187/
 Etiology and Risk Factors
• Food allergy can have 2 etiology depending on the mechanism of
disease: IgE-mediated or type I hypersensitivity and other
immunologically non-IgE mediated reactions.
• The food allergens are usually water soluble glycoproteins that are
resistant to breakdown and are easily transported across the mucosal
surface in the intestine.
• Risk factors for severe food allergies or anaphylaxis include:
• Asthma
• Prior episodes of anaphylaxis
• Delay in the use of epinephrine

https://www.ncbi.nlm.nih.gov/books/NBK482187/
 Pathophysiology
• In predisposed persons exposed to certain allergens, IgE antibodies specific for food are
formed that bind to basophils, macrophages, mast cells, and dendritic cells on Fc epsilon
receptors.
• Once food allergens enter the mucosal barriers and reach cell-bound IgE antibodies,
these mediators are released and cause smooth muscle to contract, vasodilation, and
mucus secretion, which result in symptoms of immediate hypersensitivity (allergy).
• Activated mast cells and macrophages that attract and activate eosinophils and
lymphocytes release cytokines. This leads to prolonged inflammation, affecting the skin
(flushing, angioedema, or urticaria), respiratory tract (rhinorrhea, nasal pruritus with
nasal congestion, sneezing, dyspnea, laryngeal edema, wheezing), gastrointestinal tract
(nausea, oral pruritus, vomiting, angioedema, abdominal pain, diarrhea), and
cardiovascular system (hypotension, loss of consciousness, dysrhythmias)

https://www.ncbi.nlm.nih.gov/books/NBK482187/
THE MOST COMMON FOOD
ALLERGIES

Children Adult
Cow’s milk Peanuts
Hen’s egg Tree nuts
Peanuts Fish
Tree nuts Crustaceans (such as shrimp, crabs, and lobster)
Soybeans Mollusks (such as clams, oysters, and mussels)
Wheat Fruits
Vegetables
 Clinical manifestations
• Food protein-induced enterocolitis syndrome (FPIES): these patients
can present with emesis one to three hours after feeding, and
constant exposure might result in abdominal distention, bloody
diarrhea, anemia, and faltering weight and are provoked by cow’s
milk or soy protein-based formulas.
• Food protein-induced proctocolitis is known to cause blood-streaked
stools in otherwise healthy infants in the first few months of life and is
associated with breastfed infants.
• Food protein-induced enteropathy is associated with steatorrhea and
poor weight gain in the first several months of life.

https://www.ncbi.nlm.nih.gov/books/NBK482187/
 Evaluation
• Medical history, physical examination
• skin prick tests (SPTs)
• Serum tests to determine food-specific IgE antibodies (e.g., RASTs)
• provocative oral challenge

https://www.ncbi.nlm.nih.gov/books/NBK482187/
 Treatment
• Avoidance of food allergens and treatment of food allergen-induced
systemic reactions with adrenaline remain the standard of care.
• Adrenaline can reverse oedema, urticaria, bronchospasm,
hypotension and gastrointestinal symptoms within minutes.
• Other pharmaceuticals, such as antihistamines, including
diphenhydramine, or the more specific H1 receptor blockers such as
cetirizine, are used to treat localized food allergy symptoms.
Gastrointestinal symptoms can be treated with H2 receptor blockers
such as famotidine.
• Immunotherapy to desensitize individuals to potential food allergens

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5123910/
 Prognosis and Complication
• Prognosis:
• Over time, most children outgrow or become tolerant of food allergens to eggs,
milk, wheat, and soy. However, allergies to nuts and shellfish are more long-
standing.
• Close to 20% of children have a resolution of their food allergy by school age.
• The non-IgE mediated food allergies resolve within the first year of life.
Unfortunately, sporadic cases of fatal anaphylactic reactions still continue to
occur.
• Complications
• Anaphylaxis
• Respiratory distress
• Cardiac arrest

https://www.ncbi.nlm.nih.gov/books/NBK482187/
food intolerance
Lactose Intolerance
Human milk contains around 200 mmol/L (68 g/L) of lactose, which is
normally digested to glucose and galactose by the brush border enzyme
lactase prior to absorption. In most populations, enterocyte lactase activity
declines throughout childhood. The enzyme is deficient in up to 90% of adult
Africans, Asians and South Americans but only 5% of northern Europeans. In
cases of genetically determined (primary) lactase deficiency, jejunal
morphology is normal. ‘Secondary’ lactase deficiency occurs as a
consequence of disorders that damage the jejunal mucosa, such as coeliac
disease and viral gastroenteritis. Unhydrolysed lactose enters the colon,
where bacterial fermentation produces volatile short-chain fatty acids,
hydrogen and carbon dioxide.
In most people, lactase deficiency is completely asymptomatic. However,
some complain of colicky pain, abdominal distension, increased flatus,
borborygmi and diarrhoea after ingesting milk or milk products. Irritable
bowel syndrome may be suspected but the correct diagnosis is suggested by
clinical improvement on lactose withdrawal. The lactose hydrogen breath test
is a useful non-invasive investigation.Dietary exclusion of lactose is
recommended, although most sufferers are able to tolerate small amounts of
milk without symptoms. Addition of commercial lactase preparations to milk
has been effective in some studies but is costly.
Intolerance of other sugars
‘Osmotic’ diarrhoea can be caused by sorbitol, an unabsorbable
carbohydrate that is used as an artificial sweetener. Fructose contained
within fruit juices may also cause diarrhoea if it is consumed in greater
quantities than can be absorbed.
Food Allergies
Food allergies are immune-mediated disorders, most commonly due to type I
hypersensitivity reactions with production of IgE antibodies.
 Pro inflammatory content release
Common cause of allergic reaction induced by mast cell degranulation
food intoxication
Food Poisoning
Acute diarrhea, sometimes with vomiting, is the predominant symptom in infective
gastroenteritis Acute diarrhoea may also be a symptom of other infectious and non-
infectious diseases Stress, whether psychological or physical, can also produce loose
stools. In developed countries, diarrhoea remains an important problem, with the
elderly being most vulnerable.The majority of episodes are due to infections spread
by the faecal–oral route and transmitted either on fomites, on contaminated hands, or
in food or water. Measures such as the provision of clean drinking water, appropriate
disposal of human and animal sewage, and the application of simple principles of
food hygiene can all limit gastroenteritis
The clinical features of food-borne gastroenteritis vary. Some organisms (Bacillus cereus, Staph.
aureus and Vibrio cholerae) elute exotoxins that cause vomiting and/or so-called ‘secretory’ diarrhoea
(watery diarrhoea without blood or faecal leucocytes)reflecting small bowel dysfunction). In general,
the time from ingestion to the onset of symptoms is short and, other than dehydration, little systemic
upset occurs. Other organisms, such as Shigella spp., Campylobacter spp. and enterohaemorrhagic
Escherichia coli (EHEC), may directly invade the mucosa of the small bowel or produce cytotoxins
that cause mucosal ulceration, typically affecting the terminal small bowel and colon. The incubation
period is longer and more systemic upset occurs, with prolonged bloody diarrhoea. Salmonella spp.
are capable of invading enterocytes and of causing both a secretory response and invasive disease
with systemic features. This is seen with Salmonella Typhi and Salmonella Paratyphi (enteric fever),
but may occasionally be seen with other non-typhoidal Salmonella spp., particularly in the
immunocompromised host and the elderly.
botulism
LI 6
Tatalaksana
Dehidrasi → cara hitung cairan pasien saat dehidrasi (management cairan &
elektrolit)
THANK YOU