Small and Large Intestine Flashcards
Small intestine and colon
Small Intestine consists of three segments: duodenum (25 cm long), jejunum (next 40%), and the ileum (final 60%).
10 feet in length total (3.5-6.5 meters); surface area the size of a doubles tennis court; greatly increased by its circular folds, villi, and microvilli.
Duodenum-fixed, pancreatic and biliary drainage at ampulla of vater.
Primary site of digestion and nutrient absorption.
Large intestine=colon.
Allows for absorption of water and electrolytes.
Begins as the ileocecal valve enters in the sac like cecum.
The vermiform (worm like) appendix attaches to the base of the cecum.
The taenia coli are three narrow bands of longitudinal muscle that run the length of the large intestine.
Haustra are folds of circular muscle creating sac like segments along the colon.
GALT (GI Associated Lymphoid Tissue)
25% of the weight of the GI tract.
Kupfer cells- fixed macrophages in the liver.
Individual cells (intraepithelial lymphocytes), large “clumps” of immune cells (Peyer’s patches in the ileum).
Lymph nodes outside the stomach, small and large intestine.
The stomach is the most common “extra nodal” site for lymphoma.
Diarrhea
Reflects an increase in stool volume or frequency or a decrease in consistency.
Small or large bowel problems can cause this.
A volume greater than 150-200 mL / 24 hours.
Osmotic diarrhea: when CHO (lactose, sorbitol) or minerals (magnesium citrate) create an osmolar gap; water follow into the lumen to reduce this situation.
Secretory diarrhea may be secondary to toxins from infectious bacteria (Yersina, Campylobacter jejunii, Shigella, Salmonella) or gut hormones.
Constipation
A problem of the large intestine.
2 or fewer BMs/week
Sense of incomplete evacuation > 25% of the time
Hard stools >25% of the time
Straining >25% of the time.
Decreased stool frequency or increased consistency.
Causes: structural (tumor, adhesion), hormonal (hypothyroidism, diabetes), neurologic (Hirschsprung disease).
Most common cause in the Western world is poor dietary fiber intake.
Treatment: fiber, fluids, exercise, medication (polyetylene glycol-miralax), pelvic floor therapy, linaclotide, lubiprostone.
Lactose (glucose-galactose) intolerance (lactase deficiency) and Lactase persistance
The inability to breakdown the disaccharide lactose causes diarrhea, gas, and abdominal pain, bloating.
The small intestine can only absorb simple sugars (monosaccahrides).
Genrally, all animals lose the ability to make the brush border enzyme lactase around the time of weaning, this normal event does not occur in most populations (Northern Europeans), so lactose can still be ingested in large amounts.
Lactose that is not absorbed in the small bowel reaches the colon and is broken down by bacteria.
8 oz glass of milk equivalent of lactose sugar everyone tolerates, yogurt, lactose sugar is used and everyone tolerates.
Treatment: Lactase enzyme supplements (lactaid) used when eating lactase.
Celiac Disease (Sprue)
Gluten sensitive enteropathy refers to the inability to absorb certain proteins found in most grains (gladden, gluten).
Leads to severe, chronic diarrhea containing large amounts of fat (steatorrhea) with associated weight loss, anemia, and death.
Some asymptomatic and some just failure to thrive and non specific complaints.
Most now present with mild symptoms.
Degree of symptoms dependent of length of affected bowel; begins in duodenum and extend distally.
True food hypersensitivity.
Intestine shows a flattening of the normal folds and villi as well as inflammation.
Avoid these proteins brings rapid improvement.
Autoimmune disorder to the proteins glutenins and gliadins, non digestible protein fragments.
Primarily wheat, but also other similar grains like rye and barley.
Affects the small intestine, upper part more than lower due to more exposure.
Gluten is H2O insoluble.
Diagnostic gold standard is a proximal small bowel biopsy.
Pathology: mucosal inflammation, villus atrophy, crypt hyperplasia, increased intraepithelial lymphocytes.
Long term complications: increased risk of developing malignant lymphoma in patients with sprue.
Anemia (iron, folate, B12), osteogenic bone disease (Ca, it D), muscle cramps, tetany (Low Ca, Mg), Bleeding (vit k), peripheral neuropathy, menstrual abnormalities, infertility.
Affects upper GI more than lower.
The CD Trio causes: Environmental triggers, genetic risk (HLA DQ2, HLA DQ8), Leaky gut.
Molecular Mimicry: A -gliadin, similar to E1b protein of the human adenovirus serotype 12 (Ad12), which is usually found in the human digestive tract.
E1b protein causes inflammation in celiac patients.
Diagnosis: screening antibody testing; IgA Tissue Transglutaminase, IgA Anti - endomysial antibodies.
Diagnosis: Endoscopy: scalloping or loss of circular folds in the duodenum.
Treatment: limit lactose initially, avoid all foods containing wheat, rye, and barley.
Inflammatory Bowel Disease (IBD)
NOT Irritable Bowl Syndrome.
Chronic inflammation of the bowel and often has a pattern of familial occurrence.
May be manifestations in systems outside the GI tract.
Cause not determined.
Interplay between genetic susceptibility, immune dysregulation and environmental triggers.
The Hygiene Hypothesis: people in areas endemic for intestinal parasites and other intestinal pathogens are less likely to get IBD.
The majority of them do not develop disease directly from intestinal parasites.
These organisms may play a vital role in preventing immune dysregulation in genetically susceptible people.
By ridding ourselves of relatively harmless organisms with a relevant immunoregulatory role, we may have inadvertently produced an immunoregulatory imbalance and thus have become prey to autoimmune diseases like IBD.
Ulcerative Colitis (UC) and Ulcerative proctitis
A specific type of IBD
Ulcers in the colon exclusively.
Most commonly develops in young adults peaking in incidence in the 30s.
Disease of the lining or mucosa of the colon; it may involved the entire organ (pancolitis) or be limited to the distal aspect (left sided colitis).
Some patients have involvement of the rectum alone and never progress further (ulcerative proctitis).
Symptoms: bloody diarrhea with frequent, small volume bowel movements, urgency, pain with defecation (tenesmus).
Cumulative incidence of UC and colorectal cancer; unlike the typical sequence, may arise from flat, non-polyp associated mucosa.
Characteristic microscopic finding is the crypt abscess.
Over time, raised islands of normal mucosa form and are known as pseudo polyps.
Severe, rapid progression of UC is known as toxic megacolon and can lead to micro perforations, sepsis, and death.
Extracolonic manifestations: arthritis, skin lesions (erythema, nodosum, pyoderma gangrenosum), primary sclerosing cholangitis, cholangiocarcinoma, uveitis.
Treatment: medications including steroids and sulfasalazine.
Colectomy is a curative surgery and also relieves most of the extra-colonic manifestations.
Chron’s Disease
A second specific type of IBD.
Most often arises in adolescents and young adults.
May be seen in family clusters.
May affect any part of the digestive tract from mouth to anus.
Most often seen in the terminal ileum and right side of the colon.
20% just in the colon and presents like UC.
1/3 just in the small bowel.
50% in the end of the small bowel and start of the colon.
Transmural process, involving the FULL THICKNESS of the bowel wall in contrast to UC.
Granulomas are typically found.
Areas of involvement are interspersed between normal appearing bowel (skip lesions).
Early lesions are small round aphthous ulcers.
May cause narrowed strictures in the small or large bowel.
Fistulae can form from the bowel to the bladder, vagina, skin, or other parts of the bowel; outer edge of bowel wall=sticky.
Perianal involvement may cause multiple abscesses and drainage tracts.
Clinical presentation is dependent on the part of the bowel involved; often, early Crohn’s is non specific and symptoms may include fever, abdominal pain, and diarrhea.
Partial obstruction, malabsorption, and bleeding are also seen.
Chronic pain and diarrhea, intestinal obstruction, acute inflammation (appendicitis-like).
Extra-intestinal manifestations: Same wide spectrum as seen in UC, through primary sclerosing cholangitis and cholangiocarcinoma are much less common.
Risk of colon cancer is increased with Crohn’s colitis.
Treatment: No curative treatment; steroids, sulfasalazine and immunosuppressives such has azathioprine may be used. Surgery is often helpful post-op, but half the patients will have recurrence.
TREATMENT FOR IBD: induce and maintain remission, mesalamine, corticosteroids oral (prednisone), IV, topical,
Immune modulators (azathioprene, methotrexate), Biologics (anti-tumor necrosis factor), infliximab, adalimumab (humira).
Diverticulosis
Colon-4.5 ft long.
The formation of mucosal outpouchings of the lining of the large bowel (pseudodiverticula).
80% have no symptoms
Acquired herniation of mucosa/submucosa through the muscularis of the colon.
Common in the western world.
Cause in part by low dietary fiber and th higher pressures the colon makes to propel stool forward.
Form over time, don’t really cause symptoms.
Complications:
1. Diverticulitis: stool and bacteria can become trapped in the pockets leading to low grade infection or even small perforations with subsequent abscess formation. Chronic infections can lead to scarring and strictures; increased WBC, fever, left lower quadrant pain; fecaliths.
Treatment: clear liquids, antibiotics (metronidazole/ciprofloxacin), low fiber diet during episode.
Complications: generalized peritonitis, Abscess, fistula (colovesical or colovaginal).
2. Bleeding: diverticula form where small arteries pierce through the bowel wall to supply the colonic lining; these may rupture and lead to severe, painless, lower GI bleeding; due to damage vasa recta.
Other common cause of lower GI bleeding is from angiodysplasia (vascular ectasia).
Diagnosis: colonoscopy, emergency angiography, nuclear scanning (tagged RBCs).
Colon polyps and cancer
Colon cancer is the second most common cause of cancer in men and third most common cause in women in the western world.
Adenomas and other polyps
A polyp is a mass that protrudes into the lumen of the gut.
They may be found throughout the length of the GI tract, but are most common in the colon.
Not ALL polyps have the potential of becoming a malignancy (examples: hyper plastic, juvenile, inflammatory, lymphoid polyps)
Adenomatous polyps (adenomas) can progress to adenocarcinoma.
Progression of polyps to cancer:
Over years, adenomas grow larder and develop changes in their microscopic structure from tubulous to villous in nature.
The larger the polyp (>1-2 cm) and the more villous in histology, the greater the chance that cancer will be found in it.
Adenoma-carcinoma hypothesis reflects he belief that polyps accumulate a number of genetic mutations over time that eventually lead to a cancer being formed.
Colorectal cancer
Number 2 cause of death of men and women in the US.
Risk factors: increased age, UC, history of colon cancer, hereditary polyposis syndrome.
Silent for majority of clinical course.
Early (curable) colon cancer has no symptoms.
Common and asymptomatic when easily curable, so that is why we screen.
Increased is the number one risk factor.
May cause very subtle, hidden occult (random) bleeding-screeing for this with stool guiaic (Hemoccult) cards should be performed yearly after age 50.
Advanced colon cancer may cause gross bleeding, obstruction, perforation, or a fistula.
Large portion of predisposing conditions is unknown.
Sequence of events: normal mucosa -> adenoma -> severe dysplasia -> cancer. (this can happen in 10-20 years).
Colorectal cancer screening:
immunohistochemical fecal occult blood test; inexpensive, non-specific.
flexible sigmoidoscopy; views left colon only.
Colonoscopy: sensitive, specific, allows for therapeutics, expensive, requires sedation.
Virtual Colonography (CT colonography)
Stool Genetic Analysis (Cologuard)
Long term outlook can be assessed by degree the tumor has advanced.
Dukes staging system one of most popular.
Dukes A refers to tumors confined to the bowel wall (within the muscular layer).
Dukes C cancer extends beyond the bowel wall.
Dukes C implies lymph node involvement.
Dukes D is distant metastasis.
TNM system also used.
Colorectal cancer screening is effective and cost-effective.
Family Cancer Syndromes
Although most colon cancers are random, 20% largely due to direct genetic influence.
1. Familial Adenomatous Polyposis (FAP)
Autosomal dominant gene, adenomatous polyposis coli (APC) is due to a specific genetic defect found on chromosome 5.
Gene ID and blood samples can be screened.
Thousands of polyps develop in the colon and colon cancer is inevitable by age 40.
Polyps also develop in the stomach and small bowel.
2. Hereditary Non-polyposis Colon Cancer
Refers to patients with small numbers of polyps but clustering of colon, pancreas, ovary, and uterus cancers. Defect in the mismatch repair gene and it allows for mistakes to happen during DNA replication.
