PROBLEM 3 Devin Alexander

405160054
 LI 1
ANATOMY, HISTOLOGY, PHYSIOLOGY,
BIOCHEMISTRY OF LOER GI TRACT
ANATOMY
JEJUNUM - ILEUM
Jejunum
 begins at the duodenojejunal flexure where the
alimentary tract resumes an intraperitoneal
course

Ileum
 ends at the ileocecal junction, the union of the
terminal ileum and the cecum
Source: netter’s
clinical anatomy
3ed.
COLON
ARTERY &
VEINS IN
COLON

Source: netter’s
clinical anatomy
3ed.
RECTUM & ANUS
ARTERY &
VEIN
RECTUM &
ANUS
HISTOLOGY
 Jejunum
Jejunum
•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.
Ileum
Ileum

•This is very similar to the duodenum except Brunner’s glands are absent
•The villi are present as are the crypts of Lieberkuhn
•The 2 layers of smooth muscle (TM) and the submocusa (SM)
•Contains lymphatic nodules called Peyer’s patches that are found in the
mucosa
Appendix
Appendix

•Epithelium lining, with goblet cells and underlying submucosa and

smooth muscle
•It also contains lymphatic nodules and other diffuse lymphatic tissue.
Colon
Colon
RECTUM
ANORECTAL JUNCTION
PHYSIOLOGY
SMALL INTESTINE (MOTILITY)
Smal intestine motility includes segmentation and the migrating motility complex
SMALL-INTESTINE
(SECRETION)
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
No digestive enzymes are secreted into the intestinal juice
SMALL-INTESTINE
(DIGESTION)
Digestion within the small-intestine lumen is accomplished by the pancreatic
enzymes, with fat digestion being enhanced by bile secretion
Carbohydrate and protein digestion are completed within the confines of the
brush border
SMALL INTESTINE
(ABSORPTION)
All products of carbohydrate, protein, and fat digestion, as well as most of the
ingested electrolytes, vitamins, and awater, are normally absorbed by the
small intestine indiscriminately
Usually only the absorption of calcium and iron is adjusted to the body’s need
Most absorption occurs in the duodenum and jejunum
LARGE INTESTINE
The large intestine consits:
Colon
Cecum
Appendix
Rectum
LARGE INTESTINE (MOTILITY)
The colon’s main motility is haustral contractions initiated by the
autonomous rhythmicity of the colonic smooth muscle cells
Movement of the large intestine are slow and nonpropulsive, as is appropriate
for its absorptive and storage functions
These contractions, which throw the large intestine into haustra, are similar to
small-intestine segmentations but occur much less frequently
Haustral contraction are largely controlled by locally mediated reflexes
involving the intrinsic plexuses
Mass movements: the massive contractions to drive the colonic contents into the
distal part of the large intestine, where material is stored until defecation occurs
When food enters the stomach, mass movements are triggered in the colon primarily
by the gastrocolic reflex
Feces are eliminated by the defecation reflex
LARGE INTESTINE
(SECRETION & DIGESTION)
Large intestine does not secrete any digestive enzymes because digestion is
completed before the chyme ever reaches the colon
Colonic secretion consits of an alkaline (NaHCO3) and mucus
No digestion takes place within the large intestine because there are no
digestive enzymes
LARGE INTESTINE
(ABSORPTION)
The colon normally absorbs salt and H2O. The colon absorbs token amount
of other electrolytes as well as vitamin K synthesized by colonic bacteria
Through absorption of salt and H2O, a firm fecal mass is formed
BIOCHEMISTRY
CARBOH
YDRATE
PROTEIN
LIPID
 LI 2
DEHYDRATION
PEDIA
TRICS
https://www.cdc.gov/mmwr/preview/mmwrhtml/rr5216a1.htmm
CHIL
D&
ADUL
TS
 TREAT
MENT

https://www.ncbi.nlm.nih.gov
/books/NBK143745
 LI 3
GASTROENTERITIS
GASTROENTERITIS
inflammation of the mucus membranes of the gastrointestinal tract and is
characterized by diarrhea or vomiting. It is a common childhood disease.
Etiology:
1. Viruses are the most important etiology
2. rotavirus is still the most common virus
3. Bacteria  cholera
CHOLERA
Etiology : V. cholerae
Epidemiology : both endemic and epidemic patterns. endemic in many areas of Asia and
Africa. In Asia, cholera occurs seasonally before and after the monsoon rains, and the incidence
of disease peaks in children younger than five years, and may occur in neonates
Spread through contaminated water/ food, in epidemic, can spread through contaminated stool
Pathophysiology:
1. ingestion of V. Cholerae  the majority are killed by gastric acid  Surviving organisms
colonize the small intestine and elaborate cholera toxin
2. Cholera toxin  protein exotoxin that consists of a single A subunit associated with five B
subunits
3. the A subunit is translocated intracellularly, enzimatically activate adenylate cyclase and
elevate intracellular cAMP  leads to chloride secretion through the apical chloride
channel and secretory diarrhea
Sign & symptons :
1. Acute watery diarrhea  “rice water” appearance
2. Nausea & vomitting
3. Dehydration
4. Electrolyte imbalance  muscle cramps & shock  most serious
complication
5. In children  seizures
Work up :
1. Isolation and identification of Vibrio cholerae serogroup O1 or O139 by culture
of a stool specimen remains the gold standard
2. Ideal for transport media  cary blair
3. Ideal for isolation & identification  thiosulfate-citrate-bile salts agar (TCBS)
4. Stool examination  (-) stains & check under the dark field microscope  spiral
shape & shooting star motility pattern microorganism
5. Rectal swab  isolation
Diagnosis
a case of cholera should be suspected when:
1. a patient aged 5 years or more develops severe dehydration or dies from acute
watery diarrhea, even in an area where cholera is not known to be present
2. a patient aged 2 years or more develops acute watery diarrhea in an area known
to have cholera
3. V. cholerae infection can be confirmed by isolation of the organism from stool on
selective media, followed by biochemical tests, as well as serogrouping and
serotyping with specific antibodies
4. Dark field microscope  rapid exam
 Treatment
1. Rehydration
2. Antibiotics :
Prognosis :
Can be fatal if
don’t diagnostic
immediately

https://www.ncbi.nlm.n
ih.gov/pmc/articles/PM
C3761070/table/T3/?
report=objectonly
GIARDIASIS
•Etiology : G. lamblia
•Life cycle :
•Transmitted from person to person by
fecal-oral contamination with cysts or
indirectly by transmissionn water and
occasionally food
•Epid: worldwide, with higher
prevalence where sanitation is poor.
Persons of all ages are affected,
endemic areas infection is more
frequent in infants.
Both cysts and trophozoites can be found in the feces (diagnostic stages)
1. The cysts are hardy and can survive several months in cold water. Infection occurs
by the ingestion of cysts in contaminated water, food, or by the fecal-oral route
(hands or fomites)
2. In the small intestine, excystation releases trophozoites (each cyst produces two
trophozoites)
3. Trophozoites multiply by longitudinal binary fission, remaining in the lumen of
the proximal small bowel where they can be free or attached to the mucosa by a
ventral sucking disk
4. Encystation occurs as the parasites transit toward the colon. The cyst is the stage
found most commonly in nondiarrheal feces
5. Because the cysts are infectious when passed in the stool or shortly afterward,
person-to-person transmission is possible.
Sign and symptons :
1. incuation period  9-15 days
2. intestinal uneasiness, followed by nausea and anorexia
3. explosive, watery, foul-smelling, oily diarrhea
4. Flatulence
5. Cramping
6. Malabsorption
Work up:
1. Stool examination
2. direct immunofluorescence assay (DFA)  stool tagged by fluorescent marker,
check under fluorescent microscope, seen as green glowing ovoid objects
3. Enzyme immunoassay (EIA)
4. Rapid immunochromatographic cartridge assays
Diagnostic : confirmed by foung cysts/trophozoites in stool examination
Treatment
1. Metronidazole  250 mg three times a day for 7 days for adults and 5
mg/kg three times a day for 7 days for children
2. Quinacrine (Atabrine) is the most effective  100 mg three times a day
for 7 days for adults and 2 mg/kg three times a day for children.
3. Furazolidone (Furoxone)  only drug available in liquid form The adult
dosage is 100 mg four times a day for 7 days, and that for children is 1.25
mg/kg four times a day for 7 days
Prevention
1. Wash hands
2. Cooked & wash vegetables and fruits untill ripe
3. Conventional water treatment plants that use coagulationsedimentation-
filtration methods
 LI 4
TYPHOID FEVER
Etiology: Salmonella enterica serotype typhi
Pathophysiology:
SIGN & SYMPTON
The incubation period  6–30 days
a sustained fever (one that doesn’t come and go) that can be as high as 103–104° F (39–40° C).
Other symptoms of typhoid fever include :
1. Weakness
2. Stomach pain
3. Headache
4. Diarrhea or constipation
5. Cough
6. Loss of appetite
7. vomiting  not usually severe.
8. transient, maculopapular rash of rose-colored spots on the trunk
PHYSICAL EXAMINATION
1. Bradycardia in the presence of high fever  hallmark of typhoid fever, not
common.
2. The abdomen may be tender to palpation, with poorly localized
discomfort.
3. Rose-coloured spots (small maculopapular blanching lesions) appear on
the trunk of about 25% of patients with light skin.
4. The spots are less frequent and more difficult to locate in people with
darker skin
WORKUP EXAMINATION
1. Rutin blood
2. Widal test  antibody for S.typhi, aglutination beetwen aglutinin & S.typhi
antibody
3. Typhidot test  detected IgM & IgG antibody from membrane cell S.typhi
4. Blood culture  gold standard
5. Stool and urine cultures
TREATMENT
Antibiotics
1. fluoroquinolones.
2. Chloramphenicol, amoxicillin and trimethoprim–sulfamethoxazole 
when quinolones are unavailable
3. In resistant case  given to a longer duration of quinolone therapy,
azithromycin or a third-generation cephalosporin

Antipiretics, analgetic
COMPLICATION
occur in 10%–15% of cases:
1. gastrointestinal bleeding
2. perforation
3. typhoid encephalopathy are the most serious.
4. Gastrointestinal bleeding can occur in up to 10% of cases, most likely from
intestinal erosion
PREVENTION & PROGNOSIS
handwashing
sanitary disposal of human feces
provision of safe public water supplies
controlling of flies
scrupulous food preparation
and pasteurization of milk and other dairy products

Prognosis is good if the eradication is early