Primary Sclerosing Cholangitis

One of these symptoms is jaundice, which is characterized by yellowish skin and eyes because of an inability of the liver to remove bilirubin from the blood. Patient with cirrhosis also suffering from itching, due to deposited bile's products in the skin. This patient also suffers from accumulation of fluid in legs that is called edema. As a result of the blockage of blood flow via the liver, fluid accumulation in abdomen which is worsen by the decrease in protein production. Other symptoms include fatigue, weakness, loss of appetite, weight loss and nausea. As the disease progress, complications may develop ,such as varices that happens with cirrhosis patient when the blood flow through the liver slows, so the blood from intestine go back to the vessels of the stomach and esophagus, these vessels are not meant to carry this much of blood so they dilate (varices), with increasing

This essay will examine the functions of the liver and discuss the role of bile acids in OC. The pathophysiology of OC will be explored. The role of the midwife within a multidisciplinary team, alongside the physical care that is offered to women

Chrohn's disease is a type of inflammatory bowel disease. As many as 700,000 Americans have Chrohn's disease. ...Chrohns disease most commonly occurs in the small intestine and the colon.

Crohn’s is a chronic inflammatory bowel disease where the aetiology is unknown (Bullock & Hales, 2013, p. 823). Inflammation commonly occurs in the terminal ileum, jejunum and large bowel but can be present anywhere in the digestive tract from mouth to anus (Chang & Johnson, 2014, p. 447). CD disrupts all four layers of the intestine: Epithelium, subepithelium, muscularis and serosa (Bullock & Hales, 2013, p. 825). Inflammation triggers ulcers to develop in the epithelium and this results in deep fissures, fistulas or abscesses to form and extend into the peritoneum (Farrell & Dempsey, 2014, p. 917). Granulomas in the bowel do not appear constant on the wall and separations lie between normal and diseased bowel (Chang & Johnson, 2014, p. 447). Once the subsequent layers of the small intestine become oedematous from inflammation, in an attempt to heal, the damaged tissues produce scarred fibrotic tissue (Bullock & Hales, 2013, p. 825). The chronic scarring causes the intestinal lumen to become thick and narrow (Farrell & Dempsey, 2014, p. 917).

There have been confirmed cases of rheumatoid, peripheral, and axial arthritis as well as ankylosing spondylitis. Bone loss is also an extremely common complication of CD. Long term use of corticosteroids is thought to be the cause. A number of eye conditions can also be associated with Crohn’s disease. It is speculated that a number of these eye complications can be associated with the medications used in treatment. Due to the chronic inflammation of the intestinal tract, colorectal cancer is also a serious concern of those with CD. Patients affected with CD who have been experiencing symptoms for 8 years or longer are at a higher risk. While those whom are at a younger age typically do not develop cancer at a young age, they are at a higher risk to develop cancer later on in life.

In order to explain the significance of oral aphthous ulcers in Crohn’s disease, we need to first look at the pathophysiology of the disease itself.   Crohn’s disease is a relapsing inflammatory bowel disease which can affect the entire gastrointestinal tract. The cause of the disease is not well understood. However, it is believed that the inflammatory response is mainly due to a combination of genetics, an over-reactive immune response, and environmental factors. These factors lead to an inappropriate inflammatory response against enteric bacteria (Bartels et al., 2013).  In Crohn’s disease, there is an abnormal and exaggerated response to bacteria within the gut.  As we have learned in previous lectures, an inflammatory response is a defense

Primary peritonitis is an infection that develops in the abdominal (ascitic) fluid of the peritoneal cavity. It is mostly seen in patients suffering from advanced liver disease with cirrhosis, where abdominal fluid builds up (ascites) in the peritoneal cavity and may become infected. Although rare in the absence of a perforation, there are many underlying conditions that can contribute to the growth of bacteria in the ascitic fluid. This type is called spontaneous bacterial peritonitis and is the most common reason of primary peritonitis. Factors that increase risk of primary peritonitis include medical procedures like peritoneal dialysis, medical conditions such as cirrhosis, kidney failure, and heart disease, and patient history of peritonitis. However, in most cases the type of infection that develops is secondary peritonitis, which is usually caused by an infection that has spread from the digestive tract after trauma or perforation of the abdominal viscera that allows infectious organisms to contaminate the sterile environment of the peritoneal cavity. Most common causes of secondary peritonitis include injury or trauma to the peritoneum, a ruptured appendix, or stomach ulcer, digestive diseases such as Crohn’s Disease, and diverticulitis, perforations of the stomach, or intestines, and abdominal trauma such as injury from a knife or gunshot wound. Both types of peritonitis are life threatening, and when left untreated can enter into the bloodstream spreading the infection throughout the entire body leading to shock and organ

Cholemia is a condition where there is an excessive accumulation of bile salts in the blood and these bile salts are circulating in the blood stream. Bile is a yellowish fluid produced by the liver. It aids by digesting the fat in your diet. Bile is stored in the gallbladder, which is located inferior to the liver. Some individuals develop Cholemia when their gallbladder has been surgically removed. As stated before, the liver makes bile and bile is stored in the gallbladder. When a person eats, their normal gallbladder constricts and lets out the stored bile salts into the small intestines. This helps with digestion. Once the food is digested and absorbed, bile salts are then absorbed again at the other end of the small intestines and recycled to be used over and over.

In this experiment, the scientists compared the amount of autoantibodies present in the digestive system of BN rats and BNm rats. An extraction of sera from BNm rats revealed the presence of autoantibodies that recognize and attacked wall components of arterioles and venules, as well as muscular layers of the intestine (Chabod et al. 2012). Furthermore, the intestinal tracts of BNm rats were noticeably marked with macroscopic lesions, multifocal infiltration, and granulomas (Chabod et al. 2012). In comparison, BN rats lacked the same autoantibodies found the mutated rats and tended to have less intestinal abrasions and abnormalities (Chabod et al. 2012). To determine whether CD4 T cells contributed to the development of IBD, the researchers experiments with wild type BN rats that were thymectomized and given anti-CD4 treatment (Chabod et al. 2012). The experimented rats showed no signs of IBD, indicating that mutation in the Themis gene is required for the development of IBD seen in BNm rats (Chabod et al. 2012). This further supports the researchers’ notion that a mutated Themis gene, along with subsequent reduction of viable CD4 T cells, is closely related to the occurrence of

This damage causes malabsorption, however its manifestation could range from classical symptoms, such as diarrhea, weight loss, abdominal pain, and sometimes bloating, to nonspecific symptoms, such as extra intestinal manifestations, as iron deficiency anemia, osteoporosis, dermatitis herpetiformis, among others (3–6). The presence of CD is also correlated with the appearance of other autoimmune diseases, (e.g. type 1 diabetes, thyroiditis, hepatitis), and its refractory feature could lead to small bowel carcinoma and lymphomas

Cholelithiasis, are the reaming’s of the digestive fluid bile, which form within the gallbladder. They vary in size and shape from as small as a grain of sand to as large as a golf ball.[1] Cholelithiasis occur when there is an imbalance in the chemical constituents of bile that result in precipitation of one or more of the components. Gallstone disease is often thought to be a major affliction in modern society.[2] However, cholelithiasis must have been known to humans for many years, since they have been found in the gallbladders of Egyptian mummies dating back to 1000 BC.[3,4] This disease is however, a worldwide medical problem, even though there are geographical variations in gallstone prevalence[5,6,7,8,9,10,11] Cholelithiasis are becoming increasingly common. They are seen in all age groups, but the incidence increases with age.[12] About a quarter of women over 60 years will develop them.[13] In mostbcases they do not

Cholecystitis is an inflammation of the gallbladder. The gallbladder is a pear-shaped organ that lies beneath the liver on the right side of the body. The gallbladder stores bile, which is a fluid that helps the body digest fats. This condition may be sudden (acute) or occur over long periods of time (chronic). Cholecystitis is serious and needs treatment right away.

It is widely agreed upon in medicine that time is of the essence when it comes to diagnosis and treatment of disease. The pediatric disease, biliary atresia (BA) is no different in this regard, as it has been well accepted for several decades that the timely recognition and repair of BA is essential1. BA is a progressive, idiopathic disease characterized by extensive fibrosis of the extrahepatic biliary tree resulting in blockage of bile flow. BA is the most common cause of surgically correctable jaundice. It may also clinically manifest as scleral icterus, acholic stools, and urobilinogen; eventually leading to cirrhosis and hepatic failure if the disease is left untreated. BA is often fatal before the age of one year old if left untreated and as a result has become the most common indication for liver transplant in children1,2. The hypothesized pathogenesis of BA includes viral, immunologic, and genetic etiologies but currently no definitive cause for BA is known. The gold standard in diagnosing BA is intraoperative cholangiogram, which allows for direct progression to surgical correction of the anomaly if characteristic findings of BA are seen. The most common surgery performed in patients with BA is the Kasai Portoenterostomy (KP); which is intended to restore bile flow to the liver and proximal small bowel3,4. An early indication of a successful KP is resolution of jaundice demonstrating return of bile flow; the earlier in infancy this occurs the better the

Although the gut microbiota are involved in a range of functions within the human body, this essay will focus on their role in the development of Irritable Bowel Disease (IBD). The human gut microbiota play a significant role in the metabolic health of individuals with irritable bowel diseases such as Ulcerative Colitis (UC) and Crohn’s Disease (CD). IBD, UC and CD are chronic gastrointestinal illnesses, all of which have an uncertain etiology. Symptoms of these illnesses can include diarrhoea, weight loss, ulceration, proliferation and even total obstruction of the gastrointestinal (GI) tract. (1). However the causes of these diseases are not strictly known(2). There are a vast number of bacterial species that reside within the GI tract, some of which can play a role in producing inflammation. It is believed that microbial patterns may play a role in causing IBD. The innate immune system may play a role in altering the gut microbiota profile. Certain pathogens have also been found to play a role in the development of IBD. Finally, diet and nutrition play a role in IBD, however certain nutrients are believed to have both positive and negative effects. This essay will aim to critically explore what is responsible for IBD: both internal and external factors that influence the human gut microbiota, and hence trigger IBD, or more specifically; an abnormal immune response in a vulnerable individual, or a deviation in immune function that leads to an altered immune response

The GIT is a complex environment involving constant interaction between microbiota (infectious & commensal), mucus layer, epithelial cell layer (made of diverse secretory cells), mucosal immune system (innate & adaptive cells), and lymphatic system (Peyer’s patches). Mucus layer and epithelial barrier prevent the direct interaction of the contents with underlying layers, but regulate/modulate the passage of contents across the intestinal barrier. IBD is characterized by intestinal inflammation of unknown etiology. Various theories have been proposed to identify the immune cells, microbiome and elucidate pathways leading to chronic intestinal inflammation. Three main theories35 were proposed & investigated as underlying causes for IBD inflammation - 1.Reaction to persistent inflammation in intestine, 2.Defective intestinal barrier to luminal antigens and 3.Dysregulated host immune responses to normal GIT contents. The mucosal immune system of GIT has co-evolved with several layers to maintain the fine balance between tolerance and vigilance.36 Mucosal immune system and microbial flora of GIT have co-evolved36 and development of mucosal immune cells is dependent upon the presence of specific microbial species without which differentiation & functioning of immune cells is affected. For example differentiation of Th17 cells is dependent upon presence of single species of segmented filamentous bacteria Candidatus arthromitus.38,39 in mice studies. Animal model studies have also