Written by John Immel, Asheville, NC

Introduction

Deciphering and diagnosing digestive tract disorders can be difficult because of similar symptoms. Many digestive tract disorders lack a clear definition and may be variations of a single disease or syndrome. Diagnosis is often uncertain. Etiologies and pathologies are poorly understood.

Peptic ulcer, celiac disease, irritable bowel syndrome (IBS), Crohn's disease, ulcerative colitis, and diverticulosis are several such disorders that span the entire digestive tract from stomach to colon. While some of these conditions such as peptic ulcer and diverticulosis are relatively easy to diagnose, Celiac is commonly misdiagnosed as IBS. Crohn's Disease and ulcerative colitis seem to share the same many of the same risk factors, etiology, prognosis and complications.

All the pathologies in this paper involve some form of abdominal pain, changes in the color or consistency of stool, and weight loss. But the exact location of abdominal pain is often difficult to pinpoint. This paper will first present pathologies of each condition, then compare pathology, symptomatology, etiology, risk factors, and treatment. Finally, it will conclude with an attempt of a differential diagnosis of each condition.

Digestive disorders are common. Of these, peptic ulcers is the most common affecting 4 million Americans at any one time.

Basic Pathology by Location

By location, peptic ulcer is a condition of the upper GI tract, celiac sprue affects the small intestine, Crohn's disease affects the proximal colon, ulcerative colitis affects the distal colon, and diverticulosis affects primarily the sigmoid colon. The location of IBS cannot be pinpointed because IBS does not have a physiological and psychological abnormality specific to it.

Starting from the stomach and continuing to the sigmoid colon, a peptic ulcer is an erosion of digestive tract tissue by digestive enzymes. Since peptic ulcers only occur where digestive juices are present, peptic ulcers are most common in the duodenum, stomach, and possibly the esophagus (due to acid reflux or hiatal hernia). At first, the mucosal layer is ulcerated. Ulceration then extends through entire gastric epithelial layer and into muscularis. Peptic ulcers can occur anywhere exposed to peptic juices. All ulcers, regardless of location, have a typical appearance with sharply punched out, round defects of mucosa extending into deep layers. HCL keeps the ulcer clean of necrotized tissue. Margins are sharp as opposed to irregular margins of carcinomas. Acute ulcers show little healing. Chronic ulcers extend deeper into muscular layer where they provoke a healing response and formation of granulation tissue.

Moving to the small intestine, celiac sprue is an allergic reaction to gluten containing grains. The immune system attacks the villi which become flattened leading to severe malabsorption. The symptoms of celiac sprue appear in early childhood after first exposure to grains. The gluten is broken down into gliadin which provokes an immune response. Eventually the immune system also attacks the digestive enzymes and the villi, flattening them. Mucosal atrophy and flattening of villi disappear after removal of grains from the diet. Lymphoma develops in 10-15% of patients.

Crohn's disease is an inflammation of the proximal colon. Crohn's starts around the Peyer's patches but eventually inflammation spreads and becomes transmural, causing fibrosis of the muscularis and serosa. The wall of intestine becomes thick and rigid narrowing the lumen. The colon assumes a cobblestone appearance with fibrotic "seams" surrounding remaining patches of mucosa "cobbles". The inflammation can lead to adhesions / fistula. Although the descending colon is not usually affected as in ulcerative colitis, anal lesions occur in 80% of patients of Crohn's patients.

Ulcerative colitis is an inflammation of the distal colon. Ulcerative colitis starts with inflammation and ulcerations of the rectum that extend into the descending colon. The mucosa becomes sandpapered and prone to bleeding even if wiped gently. As the fragile mucosa becomes inflamed it appears flattened and pitted, like pig skin or a football. Eventually the inflammation spreads through the entire colon. The remnants of mucosa not yet destroyed appear elevated over ulcerations looking like polyps. These false polyps are perhaps an attempt by the colon to regenerate the mucosal layer and have a tendency to become malignant. As the disease progresses, the mucosa is easily infected forming crypt abscesses. Unlike Crohn's anal lesions are less common appearing in only 20% of patients.

Most distal of the mentioned pathologies, diverticulosis occurs frequently in the sigmoid colon. Diverticulosis is characterized by small pouches/hernias called diverticulum in the lining of the large intestine. The pouches tend to develop and poke through weak spots, such as the site of an artery or vein in the sigmoid colon. Diverticulum can lead to bleeding, infections, tears, perforations, blockages, and fistula. The pouches can become infected by pieces of feces leading to abscess formation. The most common fistula due to diverticulosis is between the bladder and the colon.

IBS has no specific location and is characterized by abdominal discomfort, alternating constipation and diarrhea, and by exclusion of other pathologies. IBS is characterized by abnormal gastrointestinal motility leading to abdominal pain, constipation, diarrhea and bloating. No physiologic or psychologic abnormality has been found to be specific for IBS. Some researchers suggested IBS is a low-grade inflammatory bowel disease such as Crohn's or Ulcerative Colitis. Stress and nervous system alters perceptions of food and how it stimulates the GI tract.

Differentiation of Pathologies by Layer

The intestinal wall is made up of many layers. Depending on the layer affected, we can predict two of the complications likely to occur. One, conditions affecting outer layers can lead to fistulas. Two, conditions affecting the shallow mucosal layer can cause malabsorption. Transmural conditions lead to both. In our examples, all conditions affecting deeper layers also affect the mucosa.

In ulcerative colitis and celiac, the inflammation affects only the mucosal layer. But peptic ulcers start in the mucosa and then extend deep through all layers of the digestive tract lining. Crohn's disease starts around the Peyer's patches of the ascending colon but also becomes transmural. In diverticulosis, the entire wall bulges under increased pressure in the colon caused by muscle spasms, straining, or constipation due to hard stools. IBS is not associated with any specific tissue damage in the intestine.

Differentiation of Pathologies by Symptoms & Complications

Here is a brief description of clinical presentation: Starting in the stomach, peptic ulcers present clinically by pain 1-3 hrs after meal or during the night. Celiac presents with diarrhea with malabsorption and stunted growth. IBS presents with lower abdominal pain and bloating relieved by defecation. Crohn's is characterized by diarrhea, abdominal pain, fever and weight loss. Ulcerative colitis presents with bloody diarrhea and weight loss. Diverticulosis presents with tenderness around the lower left side of the abdomen with constipation.

At a quick glance, the similarity and overlapping of symptoms shows the need for closer observation. To accomplish this, we will compare pathologies by stool, abdominal pain, obstruction, bloating, weight loss, fistulas, infection & fever, emotional components.

Regarding quality of stool, IBS presents with alternating diarrhea and constipation. Diarrhea is more common than constipation in celiac disease, Crohn's and ulcerative colitis. Constipation due to lack of a high fiber diet is common in diverticulosis. Bleeding from an upper GI tract peptic ulcer causes 'melena' dark, tarry stool due to oxidation of the blood and mixing with HCL. If peptic juices erode the vessel walls of an artery in peptic ulcer, massive hemorrhage can result. Bleeding is also common in ulcerative colitis but here the blood in the stool is fresh and red. Bleeding is less common in Crohn's disease, celiac, or diverticulosis.

Abdominal pain is common to all the conditions discussed in this paper. Pain is usually found in the area affected by the disease but sometimes the patient may not be able to locate the exact location of the pain. Abdominal pain in a peptic ulcer is usually sharp. The patient can point directly to the pain, usually in the epigastrium, which occurs 1-3 hours after food depending upon the location of ulcer, passage of food, and level of activity of digestive juices. Pain is relieved by neutralizing the acid. In IBS, abdominal pain and cramps are relieved by eating which stimulates a bowel movement. Celiac pain generally occurs in the small intestine located mid-gut. Right abdominal pain is indicative of Crohn's, left of ulcerative colitis because those conditions affect the ascending and descending colon respectively. If Crohn's is present in the ileum, it leads to sharp pain above the pubic bone. Left inguinal pain indicates ulcerative colitis or diverticulosis.

Obstruction has many causes, including narrowing of the intestinal lumen, hard stools that cannot pass, lack of peristalsis, and others. Obstruction due to narrowing of the intestinal lumen occurs in peptic ulcer, Crohn's, and diverticulosis. Obstruction in cases of peptic ulcers can be due to inflammatory edema. Repeated inflammation causes fibrosis and thickening of the intestinal wall in peptic ulcer, Crohn's and diverticulosis. Lack of proper peristalsis causes obstruction in Celiac and IBS. Obstruction is less common in ulcerative colitis where the intestinal lining is not thickened and diarrhea is common. Constipation can cause obstruction in diverticulosis.

Bloating can be due to some form of obstruction mentioned above in the GI tract leading to fermentation of undigested or partially digested food. Bloating increases when nutrient rich microchyle is not absorbed leaving opportunity for explosive bacteria growth. In ulcerative colitis the quick elimination of fecal matter (diarrhea) leaves little opportunity for formation of gas or absorption of fluids and electrolytes from fecal matter. Nearly all of the above disorders are associated with some form of malabsorption, especially celiac where the villi are systematically destroyed by the immune system.

Weight loss can be due to loss of blood as in a peptic ulcer or ulcerative colitis. Weight loss can also be due to malabsorption. As mentioned above, malabsorption symptoms results when the lining of the digestive tract is damaged or when stools are eliminated too quickly before absorption can occur (diarrhea). Diarrhea as in Celiac, IBS, Crohn's and ulcerative colitis can also cause dehydration. All forms of malabsorption can result in kidney and gall bladder stones.

Fistulas are perforations of the intestinal wall. They are common in transmural conditions like peptic ulcer, Crohn's and diverticulosis. Celiac and ulcerative colitis affects the mucosal layer only and rarely leads to fistulas.

Inflamed and disrupted tissues are easily infected causing acute or low grade fever. Infection by H pylori is one of the causes of peptic ulcer. However, the bottom layer of the ulcer is usually sterile due to action by digestive enzymes. One in four Crohn's patients have infectious abscesses causing fever. Infection can occur when pieces of stool get caught in diverticulum. Fistulas and perforation can cause intestinal bacteria to infect the rest of the body. It is speculated that one cause of ulcerative colitis is the inability of the colon to rebalance the growth of normal flora after infection by parasite or some alteration of flora as in malabsorption.

Ulcers and IBS are believed to have an emotional component. While H Pylori is necessary for the formation of an ulcer, stress ultimately contributes to hyper acid secretion. IBS is thought to have a strong emotional component and psychological therapy is a standard treatment. Stress specifically inhibits peristalsis in the small intestine.

Etiology

The etiology of many digestive disorders is poorly understood by western medicine. Infection is listed as a possible trigger for peptic ulcer, IBS, Crohn's and ulcerative colitis. The presence of an H. Pylori bacterial infection may be a prerequisite to many cases of ulcers, but exposure to gastric juices, stress and other factors plays a role. For example hyperacidity with rapid emptying of the stomach may overwhelm duodenum's ability to neutralize acid. Many digestive disorders have a multi-factorial etiology. They are generally considered to be an imbalance in the forces that could damage the mucosal barrier and the forces that protect it. Since antibiotics provide sustained relief from IBS in certain cases, IBS is also thought by some to be an infection by an undiscovered pathogen. Others consider IBS to be a low grade form of IBD. IBS often develops after an infectious illness, fever, vomiting or diarrhea.

Stress and psychological factors are implicated in both ulcers, IBS, possibly IBD, and diverticulosis (stress induced constipation). Crohn's, ulcerative colitis and celiac are all thought to involve an auto-immune component. Crohn's is thought to be an autoimmune disorder since the pathology starts around the Peyer's patches, lymph nodes containing white blood cells in the digestive tract. Ulcerative colitis is often treated as an auto-immune disease but there is no consensus of the etiology. Celiac is a genetic auto-immune disease caused by an allergic reaction to Gliadin.

The etiology of diverticulosis is usually due to constipation, strain or spasms of the colon causing increased pressure on the colon muscle wall, weakening it. Continued pressure leads to stretches and protrusions. Diverticulitis is a condition of inflamed diverticulum. The etiology of diverticulitis is not proven but it is suspected that pieces of stool or bacteria get lodged into the diverticulum.

Risk Factors

Diet, lifestyle, age, and genetic components are risk factors in each of these pathologies. Regarding diet, all these disorders benefit from foods that reduce or do not provoke inflammation in the GI tract. An example of foods that provoke inflammation are fatty fried foods. Smoking is a risk factor in all disorders except diverticulosis. Instead of anti-inflammatories, diverticulosis benefits most from foods that encourage smooth passage of feces.

50% of peptic ulcers have a family history. The likelihood of contracting Crohn's and ulcerative colitis increases 30 times if a family member has the disorder. Celiac is caused by a genetic mutation. Thus, many digestive pathologies have a strong genetic component. IBS is not thought to have a genetic component.

Anything that reduces resistance and increases breakdown of the mucosal barrier protecting the intestinal tract could lead to peptic ulcers. Examples are shock, stress, smoking, alcohol, aspirin, and NSAIDS. Corticosteroids are also ulcerogenic. Duodenal ulcers can occur anytime in adult life but like diverticulosis, gastric ulcers typically affect an older population.

Crohn's and ulcerative colitis have the same risk factors, peak age is 15-35 yrs old, they both affect northern populations living in urban areas. Ashkenazi Jews are the highest risk group. These two forms of IBD as well as diverticulosis are more common in industrialized nations. However, in diverticulosis the reason is due to the presence of highly refined, low fiber diet causing constipation. Connective tissue disorders can also make someone more prone to diverticulosis.

The major risk factor of celiac beyond genetics is exposure to any form of gluten or gluten like proteins. Unlike the other disorders, celiac starts at a young age upon first exposure to grains.

Treatment

Diet including foods that reduce inflammation and hypoallergenics is a treatment for all the disorders mentioned. High fiber diets are useful in ulcerative colitis and diverticulosis. Good hydration helps in diverticulosis as well as avoiding nuts, popcorn, sunflower, pumpkin, caraway, sesame seeds and other food particles that might become stuck or irritate the colon. Removing the cause (gluten) is the most effective treatment for Celiac.

Anti-inflammatory drugs are used in Crohn's and ulcerative colitis. Antibiotics are effective in IBS, ulcers and intermittent infections for all the pathologies discussed in this paper. Anti-spasmodics help intestinal motility in IBS and reduces colon pressure in diverticulosis. Probiotics help normalize flora in ulcerative colitis and IBS.

Resection of the affected part of the colon can be life saving in advanced ulcerative colitis, Crohn's disease or in repeated attacks of diverticulosis.

Relieving stress and psychotherapy is helpful in peptic ulcers and IBS.

Conclusion - General symptoms by Disease and differential Diagnosis

To conclude our comparison of the several pathologies discussed, I would like to present a simple, generalized differential diagnosis. Although the differentiate diagnosis is not sufficient for all cases, hopefully it will be helpful in some.

An ulcer is diagnosed by sharp upper gastric abdominal pain 1-3 hrs after a meal. In case of bleeding ulcer, there will be black tarry stool. If stools are not tarry but there is diarrhea with blood detected, then of these conditions ulcerative colitis is suspected. If there is diarrhea but abdominal pain appears above the pubic bone or on the right side of the body with fever, then Crohn's is suspected. If cramping is mild and limited to the lower left of the body, with constipation, diverticulosis is suspected. Celiac patients get affected upon first exposure to grains at a young age and symptoms disappear with removal of gluten. If the above conditions are ruled out and patient meets the Rome Criteria III (https://www.romecriteria.org), IBS is suspected.

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