Problem 5 GI Tract

Regina Theodora
405150119
Learning Objectives
• Physiology of defecation
• Lower GI disorders :
adults : colitis, diverticulosis, Irritable Bowel Syndrome,
hemorrhoid, colorectal carcinoma, perianal abscess, anal fissure,
amebiasis, proscitis
child :
• organic constipation :Hirschprung’s disease, obstructive ileus,
• Functional constipation
• Anorectal abnomaly
• Anal atresia
Physiology
DEFECATION REFLEX

Initiated by distention of rectum 

stimulate stretch receptor  defecation
reflex

Internal + external anal sphincter relax

DEFECATION OCCURS
LOWER GI DISORDERS
Colitis
Etiology and Pathogenesis
• Genetically predisposed individuals
• exogenous factors (intestinal microbiota) Chronic state of dysregulated
mucosal immune function
• endogenous host factors (immune system)
• Environmental factors

Inappropriate immune response to endogenous commensal

microbiota within the intestines, with or without some components
of autoimmunity
 Pathogenesis
• Infection in normal host  full activation of GALT is superseded by
dampening of immune response and tissue repair
• In IBD – this process is not regulated normally
• Defective immune regulation
• Mucosal immune system : normally unreactive to luminal contents bc oral
altered (mucosal) tolerance
• Deletion/anergy of antigen-reactive T cells or induction of CD4+ T cells that
suppress gut inflammation
• Inflammatory pathway emerge from genetic predisposition  innate
immune sensing and reactivity to commensal bacteria + failure to activate
CD4+ T cells
(cont.)
• Some cytokines actv inflammatory cells (mø, B cells), lymphocytes,
mononuclear cells from blood  gut
• Exogenous factors
• Salmonella, Shigella, Campylobacter, Clostridium difficile  trigger
inflammation  immune fail to control  IBD
• IBD : normal microbiota perceived as if it were a pathogen
• Psychological factors  worsening of symptoms : pain, bowel dysfunction,
bleeding
ULCERATIVE COLITIS : macroscopic
• Mucosal disease, involve the rectum & colon
• Endoscopic change : backwash ileitis  superficial and mild
• Mild inflammation: erythematous mucosa, fine granular surface
(like sandpaper)*
• Severe : hemorrhagic, edematous and ulcerated
• Long standing : pseudopolyps as result of epithelial regeneration
• Fulminant disease  toxic colitis/megacolon  bowel wall thins
and mucosa is severely ulcerated  perforation
Microscopic features
• Limited to mucosa and superficial sbmucosa
• Crypt architecture of the colon is distorted, bifid crypts and reduced
in #, w a gap between crypt bases and muscularis mucosae
• Basal plasma cells and multiple basal lymphoid aggregates
• Mucosal vascular congestion, with edema and focal hemorrhage,
and an inflammatory cell infiltrate of neutrophils, lymphocytes,
plasma cells, and macrophages
Diverticulosis
Irritable Bowel Syndrome
Irritable Bowel Syndrome
• Functional bowel disorder characterized by abdominal pain and
altered bowel habits in absence of structural abnormalities.

• Often overlap with other func disorders (fibromyalgia, headache,

backache, genitourinary symptoms)
Clinical features
• First symptoms <45 y
• Women > men
• Abdominal pain/discomfort. Improved by defecation and have their
onset associated w/ change in frequency / form of stool
Clinical features
• Abdominal pain
• hypogastrium (25%), right side (20%), left side (20%), epigastrium (10%)
• Episodic and crampy, sometimes constant ache during waking hours
• Severe IBS – nocturnal pain
• Pain exacerbated by eating / emotional stress; improved by passage of
flatus/stools
• Female : pain worsen during pre & menstrual phases
• Altered bowel habits  most consistent feature
• Constipation altering with diarrhea
• Hard stool, narrowed caliber*
• Sense of incomplete evacuation  repeated attempts at defecation
Clinical features
• Weeks-months constipation interrupted with brief periods of diarrhea
• Diarrhea  small volumes of <200 mL
• Aggravated by emotional stress or eating
• (+) large amt of mucus : mucous colitis
• Gas and flatulence
• Abd distention, increased belching / flatulence bc increased gas
• Impaired transit and tolerance of intestinal gas loads
• Reflux gas from distal to proximal intestine  belching
• Upper GI symptoms
• Dyspepsia, heartburn, nausea, vomiting; during diurnal period
Pathophysiology
• Colonic motor abnormalities
• Motility index & peak amplitude of high amplitude propagating
contractions (HAPCs) in diarrhea-prone IBS patients  increased
• Exhibit exaggerated sensory responses to visceral stimulation,
suggestive of visceral afferent dysfunction
• Nutrient-dependent exaggerated sensory component of
gastrocolonic response
• Increased area of referred pain after lipid ingestion
• Lipid lower thresholds for the first sensation of gas, discomfort and pain
Pathophysiology
• CNS factors – increased
perception of visceral pain
• In response to distal colonic
stimulation, the mid-cingulate
cortex shows greater activation.
• Activation of prefrontal lobe
• Abnormal psychiatric features
• Exaggerated symptoms in
response to visceral distension
• Psychological and stress alters
sensory thresholds
Pathophysiology
• GI infection
• Initial infection : campylobacter, salmonella, shigella
• Those with campylobacter infection who are toxin-positive  IBS
• After campylobacter enteritis : increased rectal mucosal enteroendocrine
cell, T lymphocyte and increased gut permeability
• 5HT containing enterochromaffin cells  increased in IBS-D
patients
• Serotonin  important in GI motility and visceral perception
Hemorrhoids
Anatomy and Pathophysiology
• Hemorrhoidal cushions vasculature prevents damage to the
sphincter muscle
• Main hemorrhoidal complexes :
• Left lateral, right anterior and right posterior
• Straining  prolapse of this tissue into anal canal
• Over time, the support system weakens, exposing this tissue to the outside
of the anal canal where it is susceptible to injury
Presentation and Evaluation
• Bleeding and protrusion
• Pain : dull ache from engorgement of the hemorrhoidal tissue
• Severe pain  thrombosed hemorrhoid
• Bright red blood
• Physical examination
Anorectal abscess
Anatomy and physiology
• Men 3 : 1 women, 3rd to 5th decade
• Abnormal fluid-containing cavity in the anorectal region
• Results from infection involving the glands surrounding the anal
canal.
• N: release mucus into the anal canal, aids in defecation
• Stool accidentally enters anal glands  infected  abscess develop
• Location : perianal (40-50%),
ischiorectal (20-25%),
intersphincteric (2-5%),
supralevator (2,5%)
Presentation and evaluation
• Perianal pain, fever
• Difficulty voiding and have blood in stool
• PE: large fluctuant area, usually visible
• Routine lab : elevated WBC
• CT/MRI : 80% accurate
• Treatment : drainage
Anal fissure
Anal Fissure
• Common in 3rd to 5th decades
• Pathophysiology
• Trauma to anal canal following defecation
• In the anterior / posterior anal canal
• Irritation  Increased resting pressure of internal anal sphincter
• Blood supply to the sphincter and anal mucosa enters laterally. Therefore,
increased anal sphincter tone  ischemia in region of the fissure  poor
healing of anal injury
• Fissure (x) in ant/post : suspicion of TB, syphilis, Chron’s disease
and malignancy
Presentation and evaluation
• Pain, associated w/ defecation and is relentless
• Lesser bleeding than hemorrhoid
• Examination: position in ant/post
• Chronic fissure: hyperthropied anal papilla at proximal end of
fissure and skin tag at the distal end
• Circular fiber of the hyperthropied anal sphincter visible within base
of fissure
• Anal manometry : elevation in anal resting pressure and sawtooth
deformity
Carcinoma
Colon Cancer
• Colon cancer is the most common type of gastrointestinal cancer. It
is a multifactorial disease process, with etiology encompassing
genetic factors, environmental exposures (including diet), and
inflammatory conditions of the digestive tract.
Sign & Symptomps Diagnosis
• Iron-deficiency anemia • Laboratory :
• Rectal bleeding • Complete blood count
• Abdominal pain • Chemistries and liver function tests
• Serum carcinoembryonic antigen
• Change in bowel habits
• Imaging studies :
• Intestinal obstruction or perforation
• Chest radiography
• Physical findings may include the • Chest computed tomography
following:
• Abdominal barium study
• Early disease: Nonspecific findings (fatigue,
weight loss) or none at all • Abdominal/pelvic CT
• More advanced disease: Abdominal tenderness, • Contrast ultrasonography of the abdomen and liver
macroscopic rectal bleeding, palpable abdominal • Abdominal/pelvic MRI
mass, hepatomegaly, ascites
• Positron emission tomography, including fusion PET-CT
scan
• Treatment
• Surgical options include the following:
• Right hemicolectomy: For lesions in the cecum and right colon
• Extended right hemicolectomy: For lesions in the proximal or middle
transverse colon
• Left hemicolectomy: For lesions in the splenic flexure and left colon
• Sigmoid colectomy: For sigmoid colon lesions
• Total abdominal colectomy with ileorectal anastomosis: For selected
patients with hereditary nonpolyposis colon cancer, attenuated familial
adenomatous polyposis, metachronous cancers in separate colon
segments, or acute malignant colon obstructions with unknown status of
the proximal bowel
• Other therapeutic options for patients who are not surgical candidates include the following:
• Cryotherapy
• Radiofrequency ablation
• Hepatic arterial infusion of chemotherapeutic agents
• Regimens used for systemic chemotherapy may include the following:
• 5-Fluorouracil (5-FU)
• Capecitabine
• Tegafur
• Oxaliplatin
• Irinotecan
• Combinations of multiple agents (eg, capecitabine or 5-FU with oxaliplatin, 5-FU with leucovorin and oxaliplatin)

• http://emedicine.medscape.com/article/277496
Rectal Cancer
• Rectal cancer is a disease in which malignant (cancer) cells form in the
tissues of the rectum.
• Risk factors for rectal cancer:
• Being aged 50 or older.
• Having certain hereditary conditions, such as familial adenomatous
polyposis (FAP) and hereditary nonpolyposis colon cancer (HNPCC or
Lynch syndrome).
• Having a personal history of any of the following:Colorectal cancer.
• Polyps (small pieces of bulging tissue) in the colon or rectum.
• Cancer of the ovary, endometrium, or breast.
• Having a parent, brother, sister, or child with a history of colorectal
cancer or polyps
Sign & Symptomps
• Blood (either bright red or very dark) in the stool.
• A change in bowel habits.Diarrhea.
• Constipation.
• Feeling that the bowel does not empty
completely.
• Stools that are narrower or have a different
shape than usual.
• General abdominal discomfort (frequent gas
pains, bloating, fullness, or cramps).
• Change in appetite.
• Weight loss for no known reason.
• Feeling very tired.
Diagnosis
• Pysical exam and history : An exam of the
body to check general signs of health,
including checking for signs of disease, such
as lumps or anything else that seems
unusual.
• Digital rectal exam (DRE): An exam of the
rectum.
• Colonoscopy : A procedure to look inside the
rectum and colon for polyps (small pieces of
bulging tissue), abnormal areas, or cancer.
• Carcinoembryonic antigen (CEA) assay : A
test that measures the level of CEA in the
blood.
Stage 0 (rectal carcinoma in situ). Abnormal
cells are shown in the mucosa of the rectum
wall.
Stage I rectal cancer. Cancer has spread from
the mucosa of the rectum wall to the muscle
layer.
Stage II rectal cancer. In stage IIA, cancer has spread through the
muscle layer of the rectum wall to the serosa. In stage IIB, cancer
has spread through the serosa but has not spread to nearby organs.
In stage IIC, cancer has spread through the serosa to nearby organs.
Stage IIIA rectal cancer. Cancer has spread through the mucosa of
the rectum wall to the submucosa and may have spread to the
muscle layer, and has spread to one to three nearby lymph nodes or
tissues near the lymph nodes. OR, cancer has spread through the
mucosa to the submucosa and four to six nearby lymph nodes.
Stage IIIB rectal cancer. Cancer has spread through the muscle layer of the
rectum wall to the serosa or has spread through the serosa but not to nearby
organs; cancer has spread to one to three nearby lymph nodes or to tissues near
the lymph nodes. OR, cancer has spread to the muscle layer or to the serosa,
and to four to six nearby lymph nodes. OR, cancer has spread through the
mucosa to the submucosa and may have spread to the muscle layer; cancer has
spread to seven or more nearby lymph nodes .
Stage IIIC rectal cancer. Cancer has spread through the serosa of the rectum
wall but not to nearby organs; cancer has spread to four to six nearby lymph
nodes. OR, cancer has spread through the muscle layer to the serosa or has
spread through the serosa but not to nearby organs; cancer has spread to seven
or more nearby lymph nodes. OR, cancer has spread through the serosa to
nearby organs and to one or more nearby lymph nodes or to tissues near the
lymph nodes .
Stage IV rectal cancer. The cancer has spread through the
blood and lymph nodes to other parts of the body, such as
the lung, liver, abdominal wall, or ovary.
Hirschprung disease
Hirschsprung Disease
• Developmental disorder (neurocristopathy) of the enteric nervous
system
• Absence of ganglion cells in the submucosal and myenteric plexus
• The most common cause of lower intestinal obstruction in neonates
1:5.000 live births and male : female ratio  4 : 1 for short segment
diseases, and approx. 2 : 1 with total colonic aganglionosis
• May be associated with other congenital defects
 Inadequate
Absence of ganglion
relaxation of the
cells in the bowel Intestinal obstruction
bowel wall and bowel
wall
wall hypertonicity
• The aganglionic segment is limited
• Rectosigmoid 80% patients
• Long-segment (prox. To the sigmoid colon) disease 10-15% of patients
• Total bowel aganglionosis is rare, approx. 5% of cases
Clinical Manifestations
• Distented abdomen
• Failure to pass meconium
• Bilious emesis or aspirates with feeding intolerance
Diagnosis
• Rectal suction biopsy  gold standard
• Anorectal manometry: evaluated the internal anal sphincter while a
balloon is distented in the rectum
• Barium enema
Treatment
• Operative intervention
• Temporary ostomy  definitive surgery until the child was older
Prognosis
• Prognosis of surgically treated Hirschprung disease is generally
satisfactory  the great majority patients achieve fecal continence

• Long-term postoperative problems include constipation, recurrent

enterocolitis, stricture, prolapse, perianal abscesses, and fecal
soiling. Some children require myectomy or a redo pull-through
procedure.
Ileus
• Failure of intestinal peristalsis caused by loss of coordinated gut
motility withouch evidence of mechanical obstruction
• In children most often associated with abdominal surgery or
infection (gastroenteritis, pneumonia, peritonitis)
• Also accompanies metabolic abnorm. (uremia, hypokalemia,
hypercalcemia, hypermagnesemia, acidosis) or administration of
certain drugs (opiates, vincrinstine and antimotility (lopereamide))
• Manifestation:
• Nausea
• Vomiting
• Feeding intolerance
• Abdominal distention with associated pain
• Delayed passage of stool and bowel gas
• Bowel sounds: minimal or absent
• Abdominal radiograph:
• Multiple air-fluid levels throughout the abdomen
• Contrast radiographs: slow movement of barium through a patient lumen
• Post operative ileus generally resolve in within 72 hrs
• Treatment:
• Correcting the underlying abnormality
• Supportive care of comorbidities
• Mitigation of iatrogenic contributions
• Nasogastric decompression  relieve recurrent vomiting or abdominal
distention associated with pain
• Prokinetic agents: erythromycin (not routinely recommended),
methylnaltrexone (selective peripheral opioid antagonists, hold promise in
decreasing post-op ileus but pediatric data are lacking)