Problem 5

Delmy sanjaya
405150007
LARGE INTESTINE
• 500 mL of chyme, consisting
of indigestible food residue,
unabsorbed biliary
component, remaining fluid
• Extracts more water and
salt
• The remaining: feces
• Primary function of the
large intestine : store feces
before defecation
 LARGE INTESTINE
• The outer longitudinal smooth muscle consists only of
the taeniae coli  run the length of large intestine
• Haustra  underlying layer of taenia coli, gathered into
sacs
– Actively change location bc contraction of smooth muscle
• Colon’s main motility  haustral contaction
– Initiated by autonomous rhythmicity of smooth muscle
– Similar to segmentation, at much slower rate
– Controlled by local reflex involving the intrinsic plexuses
 MASS MOVEMENTS
• Increased motility in which large segments of the
ascending and transverse colon contract
simultaneously
• Massive contraction : mass movement
• GASTROCOLIC REFLEX, trigger mass movement in
colon when food enter stomach
– Mediated by gastrin and extrinsic autonomic reflex
• GASTROILEAL REFLEX, move contents farther, make
way for new food
 DEFECATION REFLEX

Initiated by distention of rectum  stimulate

stretch receptor  defecation reflex

Internal + external anal sphincter relax

DEFECATION OCCURS
 FLATUS
• Source of air : swallowed air (+/- 500mL during
meal), gas produced by bacterial fermentation
• Gurgling sound (borborgymi)  because gas that
leak through the luminal content
• Eructation (burping)  remove swallowed air
from stomach
• To expel gas: voluntarily contract the abdominal
muscle and external anal sphincter
 LARGE INTESTINE SECRETION
• NaHCO3 protect large intestine mucosa from
mechanical and chemical injury; neutralize acid from
local bacteria fermentation
– Secretion increased bc mechanical and chemical
stimulation, mediated by short reflexes and
parasymphatetic innervation
• Mucus : lubricate passage of feces
• No digestive enzyme. Colonic bacteria digest cellulose
for their use
 LO 2
Hirschprung’s disease and anal
atresia
 Hirschprung’s disease
Definition & etiology Hirschsprung disease is a
result of the failure of neural crest cells
(precursors of ganglion cells) to complete their
caudal migration during normal colonic
development  causing functional obstruction
Mostly happen in newborn child
 Innervation of intestine 
Submucosal( meissner) plexus, Enteric nervous
myenteric(Auerbach) plexus, system
smaller mucosal plexus (ENS)/second
brain
Extrinsic signal including enteric
ganglia
w/ or w/out

Adequate
Motility  Intrinsic Intestinal smooth muscle
bowel
neuron contraction & relaxation
function

ENS activation  muscle Extrinsic neural afferents to

NO and
relaxation the ENS 
enteric
cholinergic(contraction)
neurotran
and adrenergic
smitter
fibers(inhibition)
 Myenteric and ↑ muscle tone is
submucosal absent unopposed Uncoordinated peristalsis,
imbalance of smooth muscle
contractility and functional
Aganglionosis obstruction
Loss of intrinsic
enteric relaxing
ENS reflexes, impulses
control of intestinal
smooth muscle 
extrinsic ↑ smooth muscle
tone
Activity of
cholinergic and
Adrenergic >>
adrenergic is 2-3x
cholinergic system
normal intestine
 Cogenital pathophysiology
Enteric ganglion cells are derived from the neural crest during embryonic
development.
In normal development, neuroblasts are found in the esophagus  by the fifth week
of gestation  they migrate to the small intestine  by the seventh week  to the
colon by the twelfth week.
One possible etiology of Hirschsprung disease is the arrest of aboral neuroblast
migration.
Alternatively, although normal cell migration may occur, neuroblasts may be subject to
apoptosis, failure of proliferation, or improper differentiation within the affected distal
intestinal segment.
Fibronectin, laminin, neural cell adhesion molecule (NCAM), and neurotrophic factors
present in the intestinal stroma are necessary for normal enteric ganglion
development, whereas their absence or dysfunction may also have a role in the
etiology of Hirschsprung disease
 SS
• Delayed passage of meconium and abdominal
distention are often the presenting symptoms
in the newborn
• Chronic constipation, abdominal distention,
volvulus, or perforation may be symptoms of
the disease in a child.
 Examination
• Digital rectal examination aids in the
diagnosis.
• The rectal vault is empty in patients with
Hirschsprung disease
• Abdominal radiographs  show colonic
dilation and a paucity of gas in the rectum.
• Barium enema may suggest the presence of
a short, narrow segment or transition zone
• Newborns may have a normal-appearing
barium enema because the proximal bowel
has not had time to dilate.
 Anorectal manometry for
hirschsprung’s disease
• Anorectal manometry  useful but difficult to perform in the newborn, I/ for older infant
• Typically a normal sphincter profile (resting pressure of 40–80 mmHg and squeeze pressure of 80–
160 mmHg) and an abnormal rectoanal inhibitory reflex are seen in patients with Hirschsprung
disease.
• The rectoanal inhibitory reflex is the normal relaxation of the internal sphincter in response to
rectal distention.
• The internal sphincter does not relax in response to rectal distention in patients with Hirschsprung
disease, and an abnormal reflex during manometry aids in the diagnosis [63,64].
• This reflex is easily identified using anal manometry with a manometric catheter and a balloon to
distend the rectum.
• When the rectal balloon is distended, the manometry tracing will reveal a normal external
sphincteric contraction but no compensatory relaxation of the internal anal sphincter.
• The rectoana inhibitory reflex may be normal in patients with short segment Hirschsprung disease.
• These patients may have a short segment as their primary disease or the short segment may be
residual disease after surgery.
• High anal resting pressures and impaired rectal emptying may be seen.
• Histological evaluation  nessecary for
diagnosis of Hirschsprung disease.
• Hyperplasia or hypertrophy of nerve fibers can
be seen, but ganglion cells are absent in the
submucosa and myenteric plexus of these
patients.
 Biopsy? Which are recommended
which are not?
Recommended Unrecommended
• Suction biopsies  simple to • Mucosal pinch biopsy specimens are
perform, but the mucosa and not adequate for diagnosis
submucosa must be identifiable to
have an adequate specimen. • Routine hematoxylin–eosin staining
• Full-thickness rectal biopsy samples misses ganglion cells in almost 40%
 necessary for confirmation. of normal patients
• Acetylcholinesterase staining 
more accurate
• A positive diagnosis may be
obtained even by evaluation of
superficial suction biopsy samples
 Colonostomy
• Colostomies are usually performed after the diagnosis is made in newborns.
• This allows a period of stabilization and growth before definitive repair.
• A colostomy may be used in the older child or adult to allow hypertrophied bowel
to resume a more normal caliber.
• Pull-through operations (Swenson technique, Duhamel procedure, or Soave
procedure) have been devised to anastomose normally innervated bowel to the
anus with or without resection of the abnormal bowel
• Intraoperative biopsy results must demonstrate the presence of ganglion cells at
the level of the colostomy and the proximal margin of the colonic resection.
• Rectal myectomy may be curative in patients with short segment Hirschsprung
disease.
 Post operative treatment
• Enterocolitis, nasogastric decompression,
intravenous fluids, antibiotics, and colonic
lavage may be necessary.
• Sodium cromoglycate, a mast cell stabilizer,
has also been reported to benefit these
patients
• Botulinum toxin injections
 Diet and activity
The patient should have nothing by mouth for 6-8 hours prior
to operation.
Postoperatively patient intravenous fluids and antibiotics
however, nothing may be administered by mouth until
passage of flatus or stool signifies return of bowel function.
If a newborn undergoes creation of a diverting colostomy, the
passage of flatus or stool from the stoma is necessary prior to
institution of oral feeding.
 Diet and activity
• Upon resumption of bowel function  tube feeding or formula/breast
milk may resume.
• Clear liquids are delivered by mouth, and the diet may be advanced until
feeding goals are met.
• Feedings are usually initiated 24-48 hours after the creation of a
colostomy.
• The patient may be discharged from the hospital upon attaining full
feedings.
• Diets consisting of fresh fruits, vegetables, and high-fiber articles may
improve postoperative bowel function.
• With regard to activity, limit physical activity for about 6 weeks to allow
incisions to heal properly (applies more to older children).

http://emedicine.medscape.com/article/178493-treatment#d5
 Anal Atresia/ imperforate anal
• Imperforate anus occurs in 1 in 20 000 live births
and is associated with other congenital anomalies
in 50% of cases.
• Genitourinary anomalies and sacral abnormalities
are frequently seen.
• Cardiac and gastrointestinal anomalies (primarily
esophageal atresia) are also associated with
imperforate anus.
 Classifications
• Imperforate anus is classified according to the relationship of the rectum
to the levator ani muscles
• High lesions are those in which bowel of normal or greater caliber
terminates above the levator muscle complex.
• The rectum often ends in the prostatic urethra in males.
1. In low lesions, the rectum terminates distal to the levators, often ending
in a fistula.
2. Low lesions are more common in females. Fistula tracts may connect
the distal rectum with the perineum, vagina, or other hollow organs.
3. Intermediate lesions are found within the levator complex and may be
associated with a partial anal canal or perineal fistula.
 Diagnosis, SS, and Supporting
Examination
• The diagnosis is usually made by physical examination at birth.
• Most infants with imperforate anus fail to pass meconium at birth
unless a fistula is present.
• Radiography  determine the type of defect.
• Air invertograms  identify the location of the rectum in relation to
the perineum but are difficult to interpret.
• Fistulography, CT and (MRI) useful in evaluating high lesions.
• The urinary tract should be evaluated with an intravenous
pyelogram and voiding cystourethrogram because of the associated
urogenital anomalies.
 Treatment
• Treatment depends on the type of lesion
• Low lesions  dilation of fistula tracts with or without
anoplasty.
• Healthy infants with low lesions  require colostomies.
• Intermediate and high lesions  an initial diverting
colostomy to allow a period of stabilization and growth.
• A number of pull-through operations have been advocated.
 LO 3
Colitis, IBS, Diventriculitis, Ca colon & rectum,
Fistula perianal, abses perianal,
Proctitis,Amebiasis, hemorrhoid, Chron disease,
Ulcerative kolitis, Fissura perianal
 Colitis
The term colitis refers to inflammation of the colon. It may be
associated with :
• Enteritis (inflammation of the small intestine)
• Proctitis (inflammation of the rectum), or both.
Inflammatory bowel disease (IBD) is a generic term used to describe 3
idiopathic disorders that are associated with gastrointestinal (GI)
inflammation :
• Crohn disease (CD)
• Ulcerative colitis (UC)
• Indeterminate colitis
Epidemiology
 Etiology
Inflammation of the colon can be caused by
• Infection
• hypersensitivity to various allergens
• Ischemia
• Vasculitis
• Several drugs
 Classification
• Necrotizing enterocolitis (NEC)
• Allergic colitis
• Pseudomembranous colitis
• Infectious colitis (bacterial, parasitic, or viral)
• Ischemic colitis
• Colitis secondary to immune deficiency disorders
 Pathophysiology
• NEC(necrotizing enterocolitis) is a common cause of colitis in newborns
• Very small and ill preterm infants are particularly susceptible to NEC.
• NEC is multifactorial, but prematurity and the presence of bacteria in the GI tract are
significant risk factors associated with NEC.
• NEC appears to involve an inappropriate inflammatory response in an immature intestine.
• The final common pathway  the endogenous production of inflammatory mediators, such
as endotoxin lipopolysaccharide, platelet-activating factor, tumor necrosis factor, and other
cytokines, decreased epidermal growth factor, and progressive mucosal damage by free
radical production.
• Hypoxic ischemia and aggressive enteral feedings  associated w/ NEC.
• Varying degrees of mucosal or transmural necrosis of the intestine and colon are recognized.
• The distal ileum and proximal colon are most frequently involved; in severe cases, gangrene
may involve the whole bowel from the rectum to the stomach.
• NEC presents with the gas accumulation in the submucosa of the bowel wall  progress to
necrosis  leading to perforation of the bowel, peritonitis, and sepsis.
• Histological changes in NEC  mucosal edema, hemorrhage, coagulation necrosis, and
mucosal ulceration.
 Pseudomembranous
• Pseudomembranous colitis is a form of inflammatory colitis characterized by the
pathologic presence of pseudomembranes consisting of mucin, fibrin, necrotic
cells, and polymorphonuclear leukocytes (PMNs).
• This form of colitis is pathognomonic of infection by toxin-producingClostridium
difficile and develops as a result of altered normal microflora (usually by antibiotic
therapy) that favors overgrowth and colonization of the intestine by Clostridium
difficile and production of its toxins.
• Although every antibiotic has been reported to be associated with
pseudomembranous colitis, cephalosporin and beta-lactam antibiotics are most
frequently implicated in children.
• Cases in children with underlying comorbid conditions, IBD in particular, are also
common
 Inflamatory bowel disease
• The etiology of IBD is poorly understood. Genetic and environmental influences are involved in the pathogenesis.
IBD may present either as UC or as CD. Indeterminate colitis is a term to describe a chronic idiopathic colitis that
cannot be separated based on conventional diagnostic modalities to either Crohn colitis or ulcerative colitis.
• A study by Starr et al sought to identify proteins that enable differentiation between CD and UC in children with
new onset IBD. The study found two panels of candidate biomarkers for the diagnosis of IBD and the
differentiation of IBD subtypes to guide appropriate therapeutic interventions in pediatric patients.[4]
• UC is characterized by inflammation and ulceration confined to colonic mucosa, whereas CD is manifested by
transmural inflammation and granulomas that may affect any segment of the GI tract, including the colon.
• UC invariably involves the rectum and extends proximally without skipping segments. In contrast, CD has
discontinuous patchy involvement of the GI tract, with the ileum being the most commonly affected segment.
• Growth failure results from malabsorption and loss of proteins from inflammation and damage to the mucosa; it is
3 times more likely to occur in children with CD than in children with UC.
• The diarrhea also results from mucosal damage, bile acid malabsorption, bacterial overgrowth, and protein
exudation from mucosa.
• Extraintestinal manifestations, which are slightly more common in CD than in UC, result from bacterial products
and inflammatory mediators (eg, cytokines, prostaglandins, and reactive oxygen metabolites) entering and
subsequently being deposited in various tissues and organs, such as the eyes (uveitis), skin (erythema nodosum),
liver (cholangitis, hepatitis), and joints (arthritis)
 Infectious colitis
Infectious colitis is the most common cause of pediatric colitis, particularly beyond the first year of life. It can be caused by bacterial, viral, and parasitic
pathogens.
Bacterial colitis
• The most common bacterial causes of colitis in children are Escherichia coli(including both enterohemorrhagic E coli [EHEC] and enteroinvasive E
coli [EIEC]) and species of Shigella, Salmonella, Campylobacter, and Yersinia.
• Salmonella infections can be divided into those that cause typhoid (enteric) fever and those that do not.
– In more industrialized countries, infection with nontyphoid Salmonella accounts for a significant proportion of cases of food
poisoning.Salmonella infections are typically spread via the fecal-oral route; outbreaks are commonly associated with contaminated eggs, dairy
products, and meats. Gastric acid is usually lethal to the organism, but susceptibility to infection is increased with decreased GI motility, rapid
emptying of the stomach after gastrectomy, a large quantity of ingested bacteria, malnutrition, antibiotic use, and achlorhydria.
– Salmonellae can penetrate the epithelial layer to the level of the lamina propria and evoke a leukocyte response. They cause diarrhea by producing
several toxins and prostaglandins, which stimulate the active secretion of fluids and electrolytes.
• Shigella species attach to binding sites on the surface of the intestinal mucosal cells. The organism penetrates and proliferates in the cell, which leads
to cell destruction, produces mucosal ulcerations, and causes bleeding. Shigellae also elaborate the exotoxins that produce diarrhea.
• E coli may produce diarrhea in several different ways, depending on their specific pathologic characteristics. Pathologic strains of E coli have been
classified as follows:
– Enteropathogenic
– Enterotoxic
– Enteroinvasive
– Enteroaggregative
– Enteroadherent
– Enterohemorrhagic
• EHEC, including O157:H7 and O26:H11, causes hemorrhagic colitis and systemic complications (eg, hemolytic uremic syndrome [HUS]). The risk of
developing HUS after infection with E coli O157 is estimated to be 10-15% in children. In typical infectious colitis, the lamina propria of the large
intestine is infiltrated by PMNs. EIEC, on the other hand, exhibits almost exactly the same pathogenetic mechanisms as Shigella.
 Infectious colitis
Parasitic colitis
• Entamoeba histolytica is the most common cause of parasitic colitis in the world.
Transmission takes place through ingestion of trophozoites (usually from water
contamination) and person-to-person transmission (typically because of poor sanitation).
• Balantidium coli is a large ciliated protozoan that also causes colitis; balantidiasis manifests in
much the same way as amebiasis.
Viral colitis
• Colitis caused by cytomegalovirus (CMV) infection is a rare form that typically is found in
immunocompromised patients (eg, organ recipients who are receiving immunosuppressive
treatment). It results in deep round ulcerations that have a tendency to bleed easily and
profusely.
• Adenovirus infection can also cause a severe colitis in immunocompromised patients,
especially those with AIDS, although patients with solid organ and bone marrow transplants
are also at risk
 Ischemic colitis
Ischemic colitis is a form of vasculitis that results
from inflammation and ischemia of colonic
mucosa, which causes rectal bleeding and
abdominal pain. This form of colitis is common
in Henoch-Schönlein purpura (HSP), which is
considered one of the collagen-vascular
diseases.
 Congenital immune deficiency
Several primary immunodeficiency syndromes, including common
variable immunodeficiency, chronic granulomatous disease, Wiskott-
Aldrich syndrome, and IPEX (immunodysregulation,
polyendocrinopathy, enteropathy, X-linked) syndrome, have all been
associated with an IBD-like clinical and histopathological presentation.
Patients may present with clinical signs and symptoms
indistinguishable from patients with IBD, including chronic abdominal
pain, diarrhea, and colitis-like symptoms. Indeed, extraintestinal
manifestations such as failure to thrive, developmental delay and
perianal diseases are common presenting complaints.
 SS(diagnosis)
• Patients with necrotizing enterocolitis (NEC) may exhibit a wide spectrum of illness, ranging from
mild disease with only guaiac-positive stools to severe disease with peritonitis, perforation, shock,
coagulopathy, and death. The onset is usually insidious, but illness may progress rapidly. The first
sign is abdominal distention with gastric retention, emesis, and discomfort. Illness may progress to
hemodynamic compromise. A plain film radiograph of the abdomen can assist in the diagnosis.
• Infants with allergic colitis present with blood and mucus in the stool, vomiting, and diarrhea after
introduction of milk when they are aged approximately 1 week to 3 months. The symptoms may
also be mild and may be indistinguishable from esophageal reflux. The syndrome is also known to
occur in exclusively breastfed infants, as a reaction to food allergens present in the mother’s diet
and appearing in the breast milk.
• The typical presentation of milk-protein sensitivity colitis is the acute onset of blood-streaked
mucoid diarrheal stool in a well-appearing infant younger than 6 months. The infants do not appear
sick or dehydrated, and weight gain is typically within normal limits.
pseudomembranous colitis typically present
with profuse watery or mucoid diarrhea,
tenesmus, fever, abdominal cramps, and
tenderness, usually within 1 week of antibiotic
therapy. The stools may be frankly bloody or
guaiac-positive.
The onset of IBD, with Crohn disease (CD) or ulcerative
colitis (UC), is usually insidious, consisting of
growth failure, weight loss, diarrhea, and occult rectal
bleeding.
Abdominal pain and diarrhea, with or without occult
blood, are the most common symptoms at presentation
UC  arthralgia, ankylosting spondilitys, delayed
pubertal development, apthous stomatitis, renal calciculi
and opthalmic complication
Salmonellae may cause food-borne outbreaks,
often in summer and fall. The child experiences
abdominal cramps and nausea after an
incubation period of 8-48 hours following
ingestion of a contaminated source (food or
water). The stools are watery and may contain
blood. Fever is noted in most children.
Shigellae may cause asymptomatic infection, mild
gastroenteritis, or bacillary dysentery. Bacillary
dysentery begins suddenly with fever and abdominal
pain, and diarrhea begins shortly thereafter. Stools are
frequent (10-12/day, on average) and contain mucus
and blood; tenesmus is common. Fever is noted, often
in the range of 102-104°F (39-40°C).
Amebiasis is manifested clinically as dysenteric colitis,
commonly presenting with bloody diarrhea, abdominal
pain, and fever. B coli causes symptoms similar to those
of amebiasis.
 Amebiasis
Definisi  penyakit yang
disebabkan oleh
rhizopoda – Entamoeba
histolytica
Hospes  manusia
 Tanda dan gejala
• Amebiasis kolon akut  nyeri perut, diare, tinja cair, berlendir,
berdarah, freq 10x/hari, demam(jarang), loss of appetite, BB turun
• Amebiasis kolon menahun  gejala kurang jelas  trdpt gejala
usus ringan  x enak di perut, diare diselingi obstipasi
• Amebiasis extraintestinal  demam batuk dan nyeri perut kuadran
kanan atas(hati), nyeri pleura kanan/ menjalar- kebahu, kejang otot
perut, kembung.
• Abses perianal  x diobati  myebar ke vagina dan kulit skitar
anur  ulkus
 Diagnostik
• Pemeriksaan mikroskopik
• Pemeriksaan serologi untuk menderita
antibodi
• Deteksi antigen
• PCR
 pengobatan
• Amebiasis non invasif  paromomisin
• Amebiasis invasif /amebiasis koli ringan gol
notroimidazole  metronidazole  post th/
ini sebaiknya diberikan peromomisin/
diloksanid furoat u/ eliminasi total
• u/ abses hati  drainase abses
 Obat yg bekerja pd lumen usus
1. Paromomisin  antibiotik gol aminoglikosida 
membunuh std yg ad dilumen usus  eliminasi kista
post th/ metronidazole/ tinidazole, hati2 pd ps kel
ginjal ,dosis 25-35mg/kgbb/hari terbagi 8 jam selama
7 hari
2. Diklosanid furoat  DOC u/ E. histolytic, dosis
3x500mg/hari selama 10 hari
3. Idoquinol  gol hidroksikuionolon  (X) gg fg ginjal,
dosis 3x650mg/hari selama 20 hr
 Obat yg bekerja pd jaringan
1. Emetin hidroklorida  u/ std trofozoit -> plg effctive
pemeberian IM/ subkutan slma 10 hr, dosis max org
dewasa 65 mg sehari, anak < 8 thn 10mg sehari,lama
pengobatan 4-6 hr, (x) pada bumil, ps dg gg ginjal dan jtg,
lansia trnkn dosis
2. Metronidazole  DOC u/ amebiasis koliatau abses hati
ameba  effctive u/ std trofozoite dlm dinding usus dan
jaringan  (X) MEMBUNUH STD KISTA, lumen usus hny
50% yg mati  dianjurkan kombinasi dgn obat lain, dosis :
3x750 mg/hari 7-10 hari, KI : Bumil Trimester 1