Diseases of the GI tract Flashcards
1
Q
Describe the normal structure of the GI tract - and the parts of the GI tract (what separates the different parts of the GI tract?)
A
- The gut is a hollow tube connecting the mouth and anus. It is composed (in order) of the esophagus, stomach, small bowel and large bowel.
- The small bowel has three parts: duodenum (strategic for digestion - enzymes, etc.), jejunum, ileum.
- The large bowel can be subdivided into several parts (in order): cecum, ascending colon, transverse colon (right side to left side), descending colon, sigmoid colon, rectum. The appendix is attached to the cecum.
- Muscular valves help control the movement of food and bowel contents. The esophagus and stomach are separated by the lower esophageal sphincter, the stomach and duodenum by the pyloric valve, and the ileum and cecum by the ileocecal valve. The entire gut has a muscular wall and a mucosal lining. This lining varies throughout due to the differing functions of the various parts of the gut.
2
Q
Describe the normal function of the GI tract
A
- The function of the gut is digestion (stomach, duodenum and pancreas) and absorption (food -entire small bowel, bile, water and electrolytes - large bowel).
- Food and bowel contents are propelled through the gut by coordinated contractions of the muscle layer, called peristalsis. The esophagus only moves food from the mouth to the stomach.
- In the stomach, digestion begins. The stomach lining produces acid and pepsin (breaks down protein).
- In the duodenum, most of the digestion occurs. The pancreas releases digestive enzymes into the duodenum. Bile produced by the liver is also released into the duodenum, and is important in the absorption of fat. The entire small bowel is important in absorption of digested food.
- When the bowel contents reach the large bowel at the cecum, they are quite liquid. The role of the large bowel is to absorb water and electrolytes, producing formed stools. Normally, bacteria are found only in the large bowel.
3
Q
What are the signs and symptoms of disease within the GI tract?
A
Diseases of the gut may be silent (asymptomatic) or produce the following signs and symptoms:
- Loss of appetite (anorexia)
- Nausea
- Vomiting
- Diarrhea
- Pain (specifically abdominal pain, also potentially chest pain - e.g. heartburn)
- Bleeding
- Obstruction
4
Q
Describe gastrointestinal bleeding
A
- Vomiting of blood is call hematemesis
- Blood in the stools is black (melena) if the bleeding is from the stomach or duodenum, because of the action of acid and digestive enzymes on the blood.
- Bleeding from the rest of the small and large bowel results in red blood in stools (hematochezia).
- Bleeding is said to be occult (hidden) if the amount is too small to be seen with the naked eye, but can still be detected by a chemical or immunochemical test for blood.
5
Q
Describe cancer of the esophagus
A
In Canada, cancer of the esophagus accounts for 6% of GI tract cancers. Incidence is highest in males older than 50.
Two main types: Adenocarcinoma (60%) and squamous cell carcinoma (40%) of the esophagus -> differ in pathogenesis.
6
Q
Describe adenocarcinoma
A
- Longstanding gastroesophageal reflux may result in the following sequence of events in the lower esophagus:
- Intestinal metaplasia (known as Barrett esophagus) -> dysplasia -> adenocarcinoma.
- Example: 48 year old female, 15 mm adenocarcinoma arising in Barrett esophagus, invading muscle layer, metastases in 2 lymph nodes
- Adenocarcinoma may be diagnosed at an earlier stage because the preceding long period of reflux is usually associated with heartburn, prompting earlier referral to a specialist. Overall 5 year survival rate is 5-10%.
7
Q
Describe squamous cell carcinoma
A
The major risk factors for squamous cell carcinoma in Canada are alcohol and tobacco; reflux does not play a role.
- Patients usually present with difficulty swallowing (dysphagia). Unfortunately, by the time that the tumour causes symptoms, it is often not curable by surgery due to invasion through the wall of the esophagus and spread to lymph nodes.
- Late diagnosis
- Poor prognosis
8
Q
Describe peptic ulcer disease (what are the major causes? Where do they frequently occur?)
A
- A peptic ulcer is a break in the mucosal lining of the gastrointestinal tract produced by the action of gastric secretions (i.e. acid and pepsin). Normal mucosa has an impermeable epithelial cell covering and layer of mucus.
- Peptic ulcers result when the mucosa is damaged, leaving it susceptible to breakdown by gastric acid and pepsin. Most peptic ulcers are in the stomach and duodenum.
- Peptic ulcers are very common, affecting 10% of the population at some time. Duodenal ulcers are 4 times more common than gastric ulcers. Although peptic ulcers may occur at any age, duodenal ulcers are most frequent around age 20 and gastric ulcers around 40. Duodenal ulcers are more common in males, while gastric ulcers occur equally in both sexes.
- The two major causes of peptic ulcers are Helicobacter pylori and nonsteroidal anti-inflammatory drugs (NSAIDs) such as ASA and ibuprofen. Other important risk factors for peptic ulcers are smoking and genetic predisposition.
- Peptic ulcers are usually single, small or large, shallow or deep.
- The most common symptom is upper abdominal pain, although a significant number, especially the elderly, are asymptomatic.
- Diagnosis is made with endoscopy and x-rays. Peptic ulcers may be biopsied to rule out cancer.
- Complications of peptic ulcers are bleeding (occult or massive and life threatening), obstruction due to formation of scar tissue, and perforation with peritonitis.
- Medical treatment includes antacids and drugs inhibiting acid secretion, and antibiotics to eradicate Helicobacter pylori (if present) - drugs protecting mucosa. Surgery is performed when drug therapy fails, or to treat complications.
9
Q
Describe Helicobacter pylori (HP)
A
- HP is the cause of up to 80% of gastric ulcers and over 90% of duodenal ulcers.
- In Canada, the bacterium is found in the stomach of 20% of people under age 40 and 50% over 50 years. Lifelong infection without treatment. Lifetime risk of peptic ulcer if HP+ = 10-15%
- The infection is usually acquired in early childhood by transmission from mother to child, and bacteria may remain in the stomach for the rest of the person’s life. Can occur through: Oral ingestion, Vomitus, saliva, feces (HP has been identified in saliva, feces and vomitus)
- Although HP infection always results in inflammation of the stomach lining, most people are asymptomatic and only 10-15% will develop an ulcer at some time during their life.
- Likes to infect the Antrum part of the stomach
- It is thought that ulceration is due to increased gastric acid production. The strain of the organism and a variety of host factors determine the outcome of the infection.
- HP infection can be diagnosed by antibody tests on blood, by identifying the organism in endoscopic biopsies, or by a non-invasive breath test that identifies bacterial production of an enzyme in the stomach.
- Acute and chronic inflammation of stomach lining. No symptoms if no ulcer. Outcome depends on strain (e.g. alpha) and host factors.
10
Q
Describe the role of nonsteroidal anti-inflammatory drugs (NSAIDs) in peptic ulcers
A
Of the gastric and duodenal ulcers not caused by HP infection, most are due to NSAIDs which block prostaglandin synthesis. Prostaglandins produced by the gastric mucosa are important in maintaining an intact mucosal barrier.
11
Q
Describe acute appendicitis
A
- Acute appendicitis (acute inflammation of the appendix) is a very common disease, with a lifetime risk of 10%. It is the commonest acute abdominal condition requiring surgery. May occur at any age, but most common from ages 10-25 years. Very common, risk 1 in 10.
- In 50-80% of cases, the lumen is obstructed, usually by a fecalith (hard piece of stool). Mucus continues to be produced in the obstructed appendix, leading to an increase in intraluminal pressure, compression of veins and ischemic injury. Bacterial proliferation in the presence of obstruction and ischemia increases the inflammatory reaction. In the cases without obstruction, the etiopathogenesis is unknown.
- Acute appendicitis starts within the mucosa, with acute inflammation and then ulceration. The acute inflammation spreads to involve the entire thickness of the wall (transmural acute inflammation) and purulent exudate forms on the outer surface.
-> Eventually, the entire wall may become necrotic, and at this point the appendix may perforate, spilling pus and fecal material into the area just around the appendix (periappendiceal abscess) or into the entire peritoneal cavity (generalized peritonitis).
-> The pain is first felt around the umbilicus, but when the inflammation reaches the outer surface of the appendix, the pain moves to the lower right side of the abdomen.
-> An appendectomy is performed as soon as the diagnosis is made, before the appendix perforates.
12
Q
Describe diverticular disease of the large bowel (what are the two types)
A
- A diverticulum is a medical term for an outpouching of a hollow (or fluid filled) structure in the body. Its use implies that the structure is not normally present.
- Diverticular disease includes diverticulosis (uncomplicated diverticula - simply the presence of diverticula) and diverticulitis (inflammation of diverticula).
- Low fibre diet -> low volume stools -> bowel must contract more to move feces -> increased intraluminal pressure
- Weak points in bowel muscle layer where blood vessels pass through
- These diverticula are outpouchings of the bowel lining through the muscle layer at points of weakness.
- Diverticular disease increases with age, and is found in 50% of people over age 60. The two important pathogenetic factors are increased intraluminal pressure (due to low fiber diets) and foci of muscular weakness in the bowel wall (where blood vessels pass through the muscle layer).
- Most diverticula are found in the sigmoid colon.
- Diverticulosis is often asymptomatic, but may be associated with crampy pain
- Diverticulitis begins with a tiny perforation at the tip of a diverticulum. This allows fecal material to escape, producing acute inflammation. The result may be an abscess, inflammation and scarring causing bowel narrowing (stricture) and obstruction, or generalized peritonitis. An inflamed sinus tract may develop, eventually leading to a small bowel, bladder, or vagina producing an abnormal communication (fistula). Bleeding may also occur. Patients with diverticulitis have fever, pain and often a tender mass - the classic triad presentation includes: left lower quadrant pain, fever and leukocytosis (increased white blood cell count)
-> Complications: abscess, stricture -> bowel obstruction, fistula to bladder, vagina, small bowel…, rupture -> peritonitis, bleeding
-> Treatment: bowel rest (rest from eating), antibiotics, surgery for recurrent acute attacks or complications
13
Q
Describe inflammatory bowel disease (IBD)
A
Includes two diseases of unknown etiology:
1. Ulcerative colitis (UC)
2. Crohn’s disease (CD)
- Both are chronic inflammatory diseases, with a peak age of onset between ages 15 and 35. Both diseases are characterized by chronic diarrhea, with lifelong exacerbations and remissions, and extraintestinal problems involving liver (liver disease), joints (inflammatory arthritis), skin and the eye. Non curable
- IBD is felt to be due to an unregulated and exaggerated local immune response to gut microbes in genetically susceptible individuals.
- Pathogenesis:
-> abN immune reaction to gut flora in genetically susceptible person: About 15% of IBD patients have an affected first degree relative. There is up to 50% concordance in monozygotic twins with CD.
-> Too much activation of T-cells
-> Too little control by regulatory T-cells
- Although the gut flora is important, no specific microbe has been identified. The microbes may exacerbate or trigger the abnormal immune response. The exaggerated immune response is due to too much T-cell activation and/or too little control by regulatory T-cells.
14
Q
Describe ulcerative colitis (UC)
A
- Involves only the large bowel, most commonly the rectum and left colon, but may involve the entire large bowel.
- Affects only the lining of the large bowel, and is not transmural like CD.
- The rectum is always involved, and the area affected extends proximally in a continuous manner with no skip areas.
- Microscopically, the bowel lining shows acute and chronic inflammation and ulcers (shallow and broad). Granulomas are not seen. During exacerbations, the mucosal lining is red, swollen and bleeding with small to large shallow ulcers. Because the disease is not transmural, strictures, abscesses and fistulas do not occur.
- Clinical features: Typically, patients have chronic bloody diarrhea and pain.
- Severity ranges from mild to severe, and may sometimes be fatal. Patients with longstanding UC are at an increased risk of developing large bowel cancer. Therefore, periodic colonoscopy and biopsies are done to detect premalignant change and early malignancies.
- Medical treatment: involves anti-inflammatory agents/ drugs. The entire large bowel is removed (colectomy) if drug therapy fails or if complications develop. This cures the disease in the large bowel, but does not cure extra-intestinal problems. Surveillance for dysplasia - risk of neoplasia + cancer
15
Q
Describe Crohn’s disease
A
- Any part of the gut from mouth to anus (“mouth to bum”) may be involved, but most commonly the small bowel (especially the far end called the terminal ileum) and/or large bowel are affected. Segments of the involved bowel are separated by normal bowel (segmental involvement with “skip” lesions).
- This disease affects all layers of the bowel wall and produces chronic inflammation and scarring (transmural chronic inflammation and fibrosis).
- Granulomas are frequently present. Type of inflammation
- The early lesions are tiny ulcers. With progression, the ulcers enlarge and become long, serpentine, and fissuring (go deep into the bowel wall). The bowel wall thickens and there is narrowing of the lumen (stenosis). With time the fissures may lengthen to form sinuses leading to abscesses or fistulas to other bowel loops or other organs.
- Complications: stenosis, abscesses, sinuses, fistulas (quite similar to diverticulitis)
- Clinical features: Patients have episodes of diarrhea, pain and fever. There may be overt or occult blood in the stools, but massive bleeding is uncommon (usually nonbloody diarrhea).
- Medical treatment: involves anti-inflammatory agents/ drugs. CD cannot be cured by surgery. Surgery is therefore limited to resection of complications (fistulas, stenosis) and over a lifetime several operations may be necessary.
