Abnormal Physiology That Occurs in Bulbous Villi Disorder - Case Study Example

Student’s name Institution Course Lecturer Task: Date This assignment explores the abnormal physiology that occurs in Bulbous Villi Disorder. It begins by reviewing the relevant gross anatomy, histology and physiology of the small intestines. This is followed by evaluation of the possible pathophysiology of this disorder and how it might cause the symptoms observed including; low intensity abdominal discomfort, slight anaemia, occasional elevated white blood cell counts and vitamin deficiency. The long term clinical implication of this condition on the health of the affected individual is also discussed. Other possible complications such as malignancies, possibility it being presentation of a systemic disease and some differential diagnoses of bulbous villi are reviewed. Finally a conclusion of the discussion is given at the end. The intestinal tract is one of the most complex and important organ systems. Lying at the mid segment, the small intestine is 6 meters long consisting of 3 regions; duodenum which is the C shaped first part of the small intestine that receives billiary and pancreatic secretions, jejunum that occupies the upper left part of the abdominal cavity, and ileum that the ileum tends to occupy the lower right part of the abdominal cavity and the pelvic cavity. This part of the midgut is supplied by the superior mesenteric artery and drains to hepatic portal vein via superior mesenteric veins (Standring et al, 2005). It is the site of terminal digestion, nutrient absorption by cells of the epithelial lining, and endocrine secretion. The small intestine has a general structure of the digestive tract comprising four layers; the mucosal lining, submucosa, muscularis mucosa and serosa with its specific features reviewed below. The lining of the small intestine has a series of folds, plicae circulares consisting of mucosa and submucosa, especially the jejunum less in the duodenum and ileum. Intestinal villi are outgrowths of the mucosa (epithelium plus lamina propria) ranging from 0.5- to 1.5-mm-long projecting into the lumen. They have a leaf shape in the duodenum and assume fingerlike appearance in the ileum. The epithelium of the villi is continuous with that of the intestinal glands that contains stem cells, absorptive cells, goblet cells, Paneth's cells, and enteroendocrine cells (Junqueira & Carnreiro, 2005). The absorptive cells or enterocytes are tall columnar type, each an oval basal nucleus. Each of the cells form a homogeneous layer at the apex called the striated or brush border. Under the electron microscope, the striated border has a layer of densely packed microvilli which is a cylindrical protrusion of the apical cytoplasm consisting of the cell membrane enclosing cytoskeleton proteins such as actin (Junqueira & Carnreiro, 2005). Each enterocyte has about 3000 microvilli whose physiological function is to increase the surface area of nutrient absorption. In between the intestinal villi are small openings of intestinal glands of Lieberkühn which are important sites of electrolyte and water secretion. These secretions flush away bacterial products and toxins from the epithelial surface playing an important role in mucosal defences (McPhee & Ganong, 2006). Several substances stimulate fluid and electrolyte secretion such as VIP, acetylcholine, bradykinin, serotonin, and products of immune cells such as histamine and prostaglandins. These columnar intestinal cells are involved in digestion and absorption the nutrient molecules produced by the digestive process. The absorptive cells secrete disaccharidases and peptidases that are bound to microvilli in the brush border and they hydrolyze the disaccharides and dipeptides into monosaccharides and amino acids that are absorbed through secondary active transport. The digestion of lipids occurs mainly due to the action of pancreatic lipase and bile mostly in the duodenum and upper jejunum. Each layer of columnar epithelium contains a network of capillaries and a lymphatic vessel (lacteals) that transport absorbed nutrients and drain to the portal system. Absorption can occur by molecules passing across the epithelial cells (transcellular route) or between the epithelial cells lining the intestine (paracellular route) to gain entry into the portal system (McPhee & Ganong, 2006). The lamina propria of the small intestine is composed of loose connective tissue with blood and lymph vessels, nerve fibers, and smooth muscle cells. The smooth muscle cells are responsible for the rhythmic movements of the villi that are responsible for absorption. There are the lymphoid follicles of Peyer's patches that are involved in immune function. The small intestine is innervated by both intrinsic (myenteric and submucosal plexus) and extrinsic nervous system which together with neuroendocrine secretions regulate intestinal activity (Junqueira & Carnreiro, 2005). In bulbous villous disorder, the affected people have the same number of villi per square millimetre. The villi are of normal length but each villus has a bulbous, expanded ‘head’ on it that projects into the intestinal lumen with no signs of sprue. These changes in the villi might account for the low intensity abdominal discomfort (especially after large meals) through several ways. When one feeds, phasic contractions restricted to short lengths of intestine occurs mixing and propelling food through the small intestine. This is accompanied by relaxation of adjacent segments as these contractions alternate. The chyme is forced in both directions, mixed with intestinal cell secretions, and brought in contact with luminal surface (Ganong, 2003). This facilitates both absorption and peristalsis towards the distal segments. In bulbous villi this process could be disrupted with local stasis of chime, this could account for the discomfort of felt postprandial due to local distension and stretching of the intestinal walls. The cytoskeletal proteins in the microvilli may become dysfunctional as the apical aspect is expanded in this bulbous disorder causing ineffective mixing and also accumulation of secretions in between the spaces created by the expanded base. The peristaltic activity is also influenced by local hormones (Jensen, 2002) as those explained above whose secretion could be altered in bulbous villi and hence slight changes in peristaltic activity resulting in the discomfort above. The local stasis around the villi and accumulation of chyme results in bacterial proliferation resulting in irritation from local inflammatory changes that may result. This can cause can cause a powerful rapid peristalsis called peristaltic rush. This result from nervous reflexes from both the autonomic nervous system, brain stem and the myenteric plexus reflexes within the intestinal walls. These contractions attempt to relieve the irritative effects chyme and excessive distention from stasis (Guyton, 2006). This could possibly contribute to chronic abdominal discomfort. The muscularis mucosa exhibits some movements of the individual fibers which extend into the intestinal villi and cause them to contract intermittently. This originates from local nervous reflexes in the submucosal nerve plexus when there is chyme in the intestinal lumen. These contractions of the villi cause sequential shortening and elongation squeezing the villi to allow lymph flow from the lacteals of the villi into the lymphatic system. It is possible that with bulbous villi, there could be local stasis of chyme and secretions causing constant stimulation of these movements that could be ineffective due to altered villi kinetics. All these could contribute to abdominal discomfort perceived chronically by these patients. (Guyton, 2006) The slight anaemia observed may result from reduced absorption due to reduced paracellular absorption from the obstructed apical segments only limiting mode of absorption to transcellular route. This might reduce the absorption of both water and fat soluble vitamins. Due to stasis and bacterial accumulation that may accompany it vitamin B12 deficiency can arise from bacterial consumption causing macrocytic anemia. Other nutrients whose deficit may account for anaemia are folic acid and iron. Iron deficiency anemia will cause mucosal lesions such as glossitis, mucositis, angular cheilitis and spooned and brittle nails (Fauci et al, 2008, McPhee & Ganong, 2006). The peyers patches are local immune surveillance mechanism of the small gut. In bulbous villous disorder, occasional elevation of white blood cell counts could be due to decreased secretions out of the intervillous spaces. The enterocyte secretions area involved in washing away the bacteria and toxins (Johnson, 2001), this may accumulate in this condition resulting in bacterial proliferation at mucosal surfaces resulting in leukocyte response and hence observed increase in these cells. Stasis can also cause the antigens in the food materials activate the lymphoid cells resulting in their increase. The associated fluid losses that occur due to possible reduction of paracellular pathways lead to fluid losses through secretion and solvent drag causing haemoconcentration and could possibly account for the relative leukocytosis. Slight vitamin deficiency could result from altered absorption leading to deficiency of water soluble vitamins. Interference of fat absorption could cause the deficiency of fat-soluble vitamins (vitamins A, D, E, and K) accounting for the deficiency. Other reasons that could explain this deficiency include bacterial overgrowth that utilizes vitamin B12. Reduction of food intake to avoid postprandial discomfort could also explain the vitamin deficiency. Some of long term implications that might develop in bulbous villi disorder are discussed next including nutritional deficiency and weight changes, anemia, and possible lymphoma among others. Due to what might appear as altered normal paracellular transport of the villi, nutrient absorption may be reduced. This may lead to deficiency of proteins, calories and other essential nutrients resulting in some weight loss or inability to gain weight if absorption is affected significantly. This can result in angular stomatitis, glossitis and poor wound healing can also occur. This nutritional deficiency can also result from reduced intake of meals that occurs to avoid the discomfort experienced after feeding. This would reduce the nutritional intake and account for some weight loss. Weight problems can lead to reproductive problems such as secondary amenorrhea, decreased libido and infertility due to protein depletion and also the resultant secondary hypopituitarism (Tierney et al, 2006). In the long run, with severe nutritional deficiency wasting of the body can occur if the demands for calories exceed the intake with resultant deterioration of the clinical state. Fluid and electrolyte imbalances due to reduced paracellular transport can occur leading to electrolyte deficits if very much of these are lost with fluids. Though compensatory mechanisms from other parts of the intestines and the kidney result in countering this deficits (McPhee & Ganong, 2006) hence this may not be experienced as often except when other conditions such as intestinal infections occur worsening the fluid deficits. Bouts of loose and heavy motions could occur following the irritant effects of chyme when local stasis occurs. This could accentuate fluid losses the episodes of bowel discomfort and alterations of bowel activity may mimic irritable bowel syndrome in its symptomatology. Anaemia resulting from above mechanisms in the long term results in chronic fatigue and reduced quality of life. If anaemia becomes severe it can complicate with high output heart failure and impaired tissue perfusion. Neurological sequelae can occur if B12 deficiency is the main underlying deficit. This can cause paraesthesia, tabes dorsalis among other neurological deficits (Tierney et al, 2006). Anemia in certain situations such as pregnancy can affect the outcome. Though this is not known, mucosal lymphoma is also a possibility in the long run following local stasis that occurs at the villi resulting in reduced flushing of toxins and bacteria. Constant stimulation of immune cells at the mucosal and sub mucosal surfaces would result in chronic activation of lymphocytes (Kumar, et al., 2007) and this proliferative state could possibly result in lymphoma and other tumors of the immune cells. Psychological effects can result from those suffering from gastrointestinal disease (Spirt, 2004) due to discomfort that occurs after meals. This could manifest as depression, feeding disorders such as anorexia nervosa and rumination syndrome. The association of food with discomfort could prime the cortical association areas thus associating food with discomfort and resulting in chronic feeding problems hence propagating its nutritional effects in the long run. Impaired appetite is also a likely consequence of the discomfort. Neoplasia has several characteristic changes including cellular differentiation as one of them and whose molecular basis is very complex (Kumar et al., 2007). Malignant transformation risk in this benign condition also remains to be determined, and these changes in the shapes of apical aspect of the villi have not been established as to whether it results from altered cellular differentiation. The bulbous changes can either be primary or secondary, the physiological abnormalities in the gut would either cause the bulbous shaped villi or the change in villi is occurs a primary problem whose underlying pathophsiology still remains elusive. Other mimics of bulbous villi disorder have to be considered including intestinal lymphangiectasia which have swollen bulbous villi with dilated submucosal lymphatics with PAS positive macrophages which are characteristic for this condition (Kapetanos, 2010). Consideration of other conditions would help detect early changes which could be a part of a spectrum of a disease process; this would give us more understanding and help to unveil the possible causes, risk factors and any neoplastic changes that may be associated with it. Moreover, these changes could be a systemic disease presenting with intestinal changes. All these possibilities should be considered and remain to be unraveled, and with more studies we expect to gain insight of this condition. Bulbous villi disorder is characterized by expanded ‘head’ of the villi with no change in the number of villi as well as absence of signs of sprue. It presents with abdominal discomfort, slight anemia, occasional elevation of leukocytes and slight vitamin deficiency. These clinical effects are possibly as a result of altered local intestinal physiology due to the observed histological changes in villi including altered motility, local stasis, altered absorption and immune stimulation. This could account nutritional deficiencies, altered feeding habits, psychological effects among others. The condition still remains elusive and hardly any publication exists on the condition showing the need for further clinical studies are needed to unravel the aetiopathogenetic mechanisms and show any possibilities of neoplasia or organ involvement as systemic disease. References Adelson, D. W & Million, M. 2004. Tracking the moveable feast: Sonomicrometry and gastrointestinal motility. Physiology, 19(1):27-32. Barrett, K. E, Keely S. J. 2000. Chloride secretion by the intestinal epithelium: molecular basis and regulatory aspects. 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