GI Path Lab 2

GI Path Lab 2
Reading Assignments (Robbins: Pathologic Basis of Disease, 8th Ed.)
791 - 793	Ischemic bowel disease. Of the causes listed on page 821, low arterial flow through compromised arterial lumens is probably the most important cause for colonic ischemia. For small intestinal ischemia, mesenteric arterial emboli may be more important.
810 - 811	Crohn's disease. Skip the clinical parts and read them in the Medicine text.
793 - 796	Malabsorption syndromes (through Celiac Sprue). Skip the clinical part and get it from the discussion in lecture.
811 - 813	Ulcerative colitis. Skip the clinical parts and read them in the Medicine text.
803 - 804	Pseudomembranous colitis
826 - 827	Acute appendicitis. The discussion on morphology is silly. Acute appendicitis begins in the mucosa as one or more acute ulcers. From there, the inflammation extends deeper into the wall, often reaching the serosal surface, producing a coat of pus on that surface. If the disease is caught when the inflammation is still superficial, that is, confined to the mucosa and submucosa, the patient still has acute appendicitis even without neutrophils in the muscularis.
814 - 815	Diverticular disease
Areas of Concentration Ulcerative colitis Crohn's disease Ischemic bowel disease Pseudomembranous colitis Appendicitis Diverticular disease, especially in the colon Upon completion of this exercise, you should be able to: Recognize that there are different patterns of inflammation and injury that occur in different intestinal diseases. Identify changes in these diseases that correlate with the clinical features (signs and symptoms). Understand how the destruction of the appendiceal wall in acute appendicitis leads to complications. Understand the gross features and morphologic complication of colonic diverticulosis.
Slide 87 [WebScope] [ImageScope] Ulcerative Colitis The changes are limited mainly to the mucosa. Instead of the usual straight test tube-shaped crypts, many of these crypts have bulbous projections or branches or have other peculiar shapes and sizes. This is distortion, one manifestation of chronicity. Occasional crypts have neutrophils within their epithelium, that is, cryptitis, evidence of activity. Some of the peculiar crypts contain pus within their lumens. The lamina propria is highly cellular with many plasma cells and eosinophils extending from beneath the surface to the muscularis mucosae and even into the superficial submucosa. These cells also are also evidence of chronicity. There is no deeper inflammation, except for a few lymphoid nodules arranged in a row in the junction between the mucosa, muscularis mucosae, and superficial submucosa. This is an example of the type of ulcerative colitis that does not cause significant ulcers but, instead, the disease nibbles away at the mucosa, producing more and more distortion and eventual loss of crypts, that is, atrophy. What is the cause of ulcerative colitis? Who is at risk to get it? Why do you think this colon was resected? Had this colon remained in situ until the disease was 12 years old, what special program would be recommended to the patient? Slide 86 [WebScope] [ImageScope] Crohn's Disease of the Small Intestine The small intestinal villi are strikingly distorted. Many are huge, edematous structures, while others are elongated and filled with a mixture of inflammatory cells including many plasma cells. The crypts are also irregularly shaped, and at the base of the mucosa, some of them have epithelium, which contains granular pink-staining mucus, identical to that seen in glands in the gastric antrum or in Brunner's glands of the duodenum. This is a metaplasia that only seems to occur at the edges and bases of ulcers in the intestines, especially the small intestine. Some of the mucosa is ulcerated and converted to granulation tissue covered by pus. The muscularis mucosae are irregularly thickened, with muscle fibers and bundles extending into the submucosa in various directions and producing occasional lumps. The submucosal nerves are huge, that is, hypertrophied. Finally, there are aggregates of lymphoid cells or lymphoid nodules scattered throughout the submucosa. A few of these penetrate the muscularis propria, and rare ones can be found in the subserosa. Occasional slides may have loose granulomas with macrophages and even giant cells in the submucosa. This small intestinal Crohn's disease is not transmural in these slides, although it was transmural in other parts of the small bowel. What is the cause of Crohn's disease? This inflammatory and proliferative process has thickened the wall dramatically. What is likely to be the clinical result? What are the common sites of involvement by Crohn's Disease? Slide 88 [WebScope] [ImageScope] Acute Ischemic Colonic Diseases Most of the abnormalities are confined to the mucosa. There are several patches of mucosa in which the lamina propria appears granular and debris-filled, and the crypts have disappeared. Nevertheless, the outline of the mucosa persists and is of the same thickness as the intact mucosa. In other similar areas, neutrophils fill this mucosal outline. In still other areas, there are a few residual basal crypts that are small and are lined by epithelium with enlarged nuclei and very little cytoplasmic differentiation. These are regenerative, and they are trying to reconstitute the mucosa. Other evidence of regeneration is the syncytial surface epithelium that seems to be trying to cover denuded mucosa. In a few places, especially at the base of the totally necrotic mucosa, neutrophils extend into the submucosa and occasionally even into the muscularis propria where they are associated with loss or lysis of muscle fibers. In all sections, the submucosa is thick and edematous. What is the most common cause of colonic ischemic injury? How does the submucosal edema help the radiologists to diagnose acute ischemic injury? Had this colon not been resected, what do you think might have happened in the areas in which the necrosis involved the full thickness of the mucosa or deeper? Why is ischemic bowel disease important in our society? Slide 20 [WebScope] [ImageScope] Pseudomembranous Colitis There are several patches in which the mucosa is both partly or completely necrotic and replaced by neutrophils. In the partially necrotic areas, some of the superficial crypts are dilated and filled with a mixture of pus and mucin that pours onto the surface as an exudate that covers the surface. In the areas of complete mucosal necrosis, neutrophils extend into the submucosa. Why does the disease have this strange name? What are the likely causes? How do you treat it? Why was this colon resected? The importance of clinical history comes into full focus in a case such as this. Note the location of the damage. How does this type of damage account for the clinical presentation? Slide 18 [WebScope] [ImageScope] Appendix: Acute Appendicitis What has happened to the mucosa? What has happened to the muscularis propria? What might have happened to this appendix had it not been removed? What histologic feature correlates with the location of the pain to the right lower quadrant? The answers to the path lab questions will be posted approximately 48-72 hours after the lab sessions. These are abbreviated answers, not a full discussion of the topics. You can find them in the M2 CTools site resources. In the folder for each sequence the will be a folder called 'Path Lab Resources'

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