Digestive System: Pathophysiology and Therapeutics

  • Created by: rkerri200
  • Created on: 01-01-21 17:29

Overview of GI System

Mouth - chewing and hydrolysis to make a bolus that can be swallowed.

eosophagus - propel bolus

stomach - churning, hydrolysis, storage, make chyme (melt down bolus into a more fluid substance.

small intestine - hydrolysis, absorption of nutrients.

large intestine (colon) - absorption of water, ions, vit K etc

Rectum - storage

Anus - expulsion

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GI tract control

The digestive tract has its own nervous system - the enteric nervous system. It doesnt need to send signals to the brain or spinal cord to perform its function. When food is eaten and makes its way to the stomach it initiates the gastrocolic reflex. So when food hits the stomach it alerts the colon to empty and make roo for the new food being digested. Hormones also regulate the GI tract. Gastrin is released when we notice food in the stomach and is released from the stomach to the blood stream to cause the release of gastric juices in the stomach. Gastrin is released from mucosal cells to cause the release of hydochloric acid from parietal cells in the stomach. Pepsinogen is going to be released from chief cells in the stomach. This is the inactive form of pepsin that when active can digest protein. Gastrin also increases stomach motlity to churn the food and produce chyme and send it to the duodenum. Gastrin release into the bloodstream is mediated by the pH of the stomach, when this hits 3 gastrin release is reduced. 

When chyme is delivered to the duodenum, secretin is released into the bloodstream. It goes to the pancreas to cause the release of a bicarbonat-rich solution to neutralise the acid in the chyme as it just came from the stomach. Secretin also goes to the stomach to cause ihibition of motility and pepsinogen release and aicd release. Another hormone released is cholecystokinin from the intestinal mucosa into the blood stream and to the pancreas to stimulate the release of pancreatic enzymes. One of these enzymes is lipase which breaks down lipids. Cholecystokinin also goes to the gallbladder to make it contract and pump bile into the cystic duct and down throught he bile duct into the duodenum to emulsify fat. Cholecystokinin also decreases stomach motility to slow down the release of chyme and allow what is already in the duodenum to be processed. It is the fat content in chyme that triggers the release of cholecystokinin to be released. The hydrochloric acid in the chyme causes secretin to be released. 

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The enteric nervous system

The principle conponents are 2 netwroks of neurons embedded in the wall of the GI tract. The first network is the myenteric plexus and the second is the submucosal plexus. They are located in the wall of the GI tract bewteen the duodenum and ileum. The wall of the small intestine is made up of 4 layers of tissue: mucosa is the inner layer of epithelial tissue and absorbs nutrients from chyme; submucosal layer composed of lymphatic vessels and nerves to support the mucosa; muscularis externa is  2 smooth muscle layers - one circular and one longitudinal; the serosa is the outer layer of the wall. The myenteric plexus is located between the smooth muscle layers of the muscularis enterna. The submucosal plexus is located in the submucosa. The myenteric plexus increases the tone of the gut and the speed and force of contractions. The submucosal plexus is involved in local secretions and blood supply which facilitates absorption and also muscle movement. 

The ENS works autonomously using the local reflex and secondly comunicates with the sympathetic and parasympathetic nervous system. The myenteric plexus contains 3 types of neurons: ascending, descending and sensory. The sensory neurons receive stimuli from smooth muscle and are assimilated by the chemicals in the food and stimulate the other neurons. Food is consumed and travels through the GI tract as a bolus. The intestine distends (this further stimulates the neurons in the yenteric plexus) and stretches (peristalsis) the intestinal smooth muscles. The ascending neurons release neurotransmitter e.g. acetylcholine and Substance P to the circular smooth muscle causing them to contract behind the bolus. Simultaneously, the decending neurons release neurotransmitters e.g. nitric oxide and VIP causing relaxation of the longitudinal muscle behind the bolus and circular muscle ahead of the bolus. 

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interstitial cells of Cajal

The ICCs are found in the intestinal tract. There are different types with different functions. The myenteric interstitial cells of cajul create the bioelectrical slow wave potential that leads to contraction of smooth muscle. It contrls the rate of peristalis and acts as a pacemaker in the gut. The intramuscular interstitial cells of cajal are involved in the stimulation of smooth muscle cells and neurotransmitters act through them. 

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Irritable bowel syndrome

IBS: chronic symptoms e.g., abdominal pain, bloating usually accompanied by an altered bowel habit. It is a precondition that no changes are present that are characteristic of other diseases that are likely to be the cause of the symptoms. It is diagnosed after other conditions are ruled out. Prevalence - 10-20% in West and more so in women than men, the reason unknown. The etiology is unknown. It is characterised by altered intestinal motility (leads to pain, bloating, faecal consistency), visceral hypersensitivity (decreased pain tolerance, when gut distends. alteration of the sensitivity of the receptors through nociceptor recruitment caused by symptoms of IBS. There may also be increased sensitivity and excitability in the autonomic nervous system), altered intestinal microbiome (increased risk after infection - campylobacter, shigella and salmonella- this increases lymphocytes and serotonin secreting enteroendocrine cells), diet (food sensitivity, although debated as research is of no significance) and psychological factors e.g. stress (anxiety and depression are common in IBS patients. A stressful event is linked in ~50% of cases but not the only cause). Symptoms - abdominal pain, altered bowel function, bloating, abdominal distention, tenesmus, and increased mucous. Associated with lethargy, fatigue, insomnia, fibromyalgia, dyspareunia, and backache. It is benign and does not lead to a possibility of developing cancer or collitis. It is a diagnosis of elimination and patient history (bowel movement journal). Treatment is first to tackle lifestyle  e.g. more fibre for constipation and less caffeine for diarrohea and increase exercise and diet e.g. cut out trigger foods. Pharmacological intervention is symptom based and not an umbrella tretament e.g. anti-spasmodics (mebeverine), linaclotide, menthol, antidepressents (amitriptyline) and SSRIs (sluoxetine) for pain-predominant IBS. Polydimethylsiloxane (dimethicone), probiotics and Iberis amara for meteorism (gas build-up) predominant. Ispaghula husk, psyllium and loperamide for diarrohea predomiant. Ispaghula husk, psyllium, linaclotide, probiotics, iberis amara, oxmotic laxitives (polyethylene glycol), stilulating laxitives (bisocodyl, sodium picosulfate) and CO2 laxatives (suppositories) to support evacuation. 

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diverticular disease

diverticular disease is when there are out-pouching of the colonic mucosa and underlying connective tissue through the colon wall. diverticular disease is acquired outpounching making it a false divertigula. The large intestine or colon has 6 main sections: caecum (beginning); ascending; transverse; descending; sigmoid and rectum (end). The sigmoid is wheremost divertigula occur in the west and in the east it is around the ascending/transverse section. A diverticulum is one outpouching, divertigula is plural. Diverticulosis is divertigula with no symptoms. diverticular disease can present as asymptomatic or symptomatic and is an umbrella term for diseases involving divertigula. The colon is made up of the lumen, longitudinal muscle (taenia coli) and blood vessels surrounding the colon wall (branches of IMA - inferior mesenteric arteries). In diverticular disease there is diverticulosis (presence of outpouches within the colon). These can be true or false divertigula. True divertigula involves all the layers of the colon wall in the outpouching (infants). In a false diverticula it is only the mucosa and submucosa of the colon wall that is present in the outpouching (adults). Diverticulosis is the presence of lots of diverticula making it predominantly asymptomatic. Diverticular disease usually has symptoms caused by diverticulitis causing diarrhea, cramping, bowel irritability, intense pain, bleeding, bloating and fever. The cause of diverticular disease is unknown but is hypothesised to be associated with a lack of fibre. One theory is that the pressure builds from straining during constipation and causes the colon to balloon between muscle bundles creating outpouching. It is diagnosed through patient history and possibly a colonoscopy to check for outpouching if there isnt a flare up of symptoms increasing the risk of bowel perforation. In this case a CT or virtual colonoscopy scan may be done instead. Blood tests can check the level of inflammation in the body. Management is a well-balanced diet with high fibre and lots of fluid, to soften stool and prevent pressure uilding in the colon. However, if there is diverticulitis fibre will need to be restricted and liquid only diet consumed, rest, pain medication and possibly antispasmodics. Antibiotics are often given but may not be needed if it isnt associated with infection. In severe cases hospitilisation occurs and intravenous feeding required to rest the bowel. If frequent surgical removal may be necessary. Diverticula disease is not curable. 

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diverticular disease

Diverticula of the colon consist of outpouchings of mucous membrane through the muscle wall of the bowel. In the colon, diverticula are found most commonly in the sigmoid and descending colon. They are unusual before the age of 40 years, but they are found in about 30% of all autopsies in the elderly. Diverticulum: abnormal sac-like protrusion from the wall of the colon. Diverticulosis: presence of multiple diverticula asymptomatic. Diverticulitis: inflammation of diverticula. Diverticular Disease: Complication of diverticulosis. True (congenital) diverticuli: contain all layers of colonic wall, often right-sided (i.e Merkel’s Diverticulum). False (acquired) diverticuli: contain mucosa and submucosa, often left-sided (highest pressure). Merkel’s Diverticulum: A true diverticulum, it is a reminant of proximal part of the yolk-stalk. May present with symptoms in a small majority of patients. The colon is divided into: Caecum; Ascending colon; Transverse colon; Descending colon; Sigmoid colon and Rectum. It is composed of circular smooth muscle throughout, and incomplete bands of longitudinal muscle (taeniae coli) in colon (stops at the rectum). There are fatty appendages along taeniae (appendices epiploicae) and a folded internal mucosal appearances (haustrations). Blood supply – from superior and inferior mesenteric artery. A normal colon has a lumen, taenia coli and blood vessels that penetrate the mucosa, submucosa and serosa. Infection is caused if faecal matter gets lodged at the opening of the diverticula causing bacteria to grow. Risk Factors: >50yrs; low fibre western diet; obesity and NSAIDs. Majority is asymptomatic. Painful diverticula disease - pain and IBD (usually). Bleeding diverticular disease - excessive bleeding (ruptured peridiverticular submucosal blood vessel). Diverticulitis - nausea; fever; tachycardia; acute pain and loose stool. Tests - colonoscopy if appropriate and wont cause perforation of the colon. If it will CT scan (shows thickening of the wall, oedema and fat stranding in diverticulitis) or virtual colonoscopy; full blood count or C-reactive protein test to check for inflammatory markers and infection. Management - high fibre diet and water intake. If diverticulitis occurs IV antibiotics (infection), analgesics and fluids. Surgery (segmental colectomy) if perforated; failing to respond to meds; undrainable abscess; fistulla formation or poor quality of life. An inflamed diverticulum (diverticulitis) may do one of three things: Perforation - Into peritoneal cavity causing peritonitis, Into the pericolic tissues with formation of a pericolic abscess, Into adjacent structures (e.g. bladder, small bowel, vagina), forming a fistula; Produce chronic infection with inflammatory fibrosis, resulting in obstructive symptoms; Haemorrhage, as a result of erosion of a vessel in the bowel wall. The bleeding varies from acute and profuse to a chronic occult loss.

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The colon is 3-5ft in length. The muscles in its wall contract and produce motility to move stool out of the body. The colon absorbs water and salts fromwaste; propels waste; stores waste; and evacuates waste. Constipation is a back up in the digestie system. Stools are passed irregularly and are often hard, lumpy and like rabbits droppings. It is often accompanied by straining. The small intestine delivers stool comprisin gof ingested food, bile and digestive juices to the caecum. Once in the colon the fluid is removed from the stool. The longer this journey through the colon takes the more reabsorption occurs and the more solid the stool becomes. In the sigmoid colon a final stage of reabsorption occurs before the stool enters the rectum, distending its walls and telling the internal anal sphincter to rlax and allow the stool to be expelled or retained. This is controlled by the pelvic floor muscles (puborectalis and external anal sphincter). The puborectalis is a sling-like structure around the rectum in an anal-rectal angle. When you relax the external anal sphincter, the stool is expelled. During constipation the stool is either moving to slowly through the colon and being dried out too much and/or the pelvic floor muscle are malfunctioning preventing elimination of the stool from the rectum as the muscles are too tight or the pelvic organ has prolapsed (the anal-rectal angle becomes narrower). Constipation is determined using the Bristol Stool Chart (type 1-7 getting increasingly wetter). Diet and lifestyle changes such as increased fibre and water and exercise help eliviate this. If not laxatives may help. 

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The bodies solid waste contains more fluid than usual and more often expelled. It can be mild to life-threatening. It can be caused by a virus - norovirus or rotavirus; bacteria such as campylobacter and E.coli; Parasites - giardiasis from contaminated water; psychological factors; food allergy/sensitivity; medication or be part of another condition e.g. IBS. Symptoms - Loose watery bowel movement 3 or 4 times a day, tenamus, abdominal pain and cramping, change in colour of stools, mucous, blood, pus or fat in stools; vomiting; lethargy and fatigue. It can also cause dehydration - life-threatening (lethargy, fatigue, anorexia, nausea, light-headedness, dizziness, dry tongue, sunken eyes, muscle cramps and tachycardia). Diagnosis - blood test - FBC. Stool test - bacteria or parasite. Flexible sigmoidoscopy or colonoscopy - lining of colon and or biopsy. Treatment - clears on its on in a few days. Life-style changes and OTC remedies. Antibiotics if infection, fluid replacement and salt replacement. Diarrohea acn be caused by stool moving through the colon too quickly and the fluid not being absorbed. Secretory diarrohea is the intestinal epithelial cells actively secret water and electrolytes sue to secretagogue (cholera). Osmotic diarrohea - ingested solutes poorly absorbed. Motility disorders - increased motility or decreased transit time or bacterial overgrowth. Decrease surface area - decreae solute absorption and decreased transit time. 

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Coeliacs Disease

inflammatory disease that is triggered by wheat proteins (gluten) in susceptible individuals. More specifically the protein gliadin. It is characterised by weight loss, anaemia, abdominal pain and discomfort, bloating stinky and fatty stool, diarrohea and a failure to thrive in children. Coeliacs disease is asymptomatic in 1/3 of individuals. Aphihous ulcers develop around the mouth and  atrophic glossitus as well as anorexia. Dermatitis herpitaformis is a chronic blistering skin condition that can also develop. Tests - FBC (anaemia or infection), EUC (electrolyte-urea creatinine - malabsorption and electrolyte imbalance); LFT (rule out disease that affects the liver or billiary tree). Blood smear to check the type of anaemia. Serology tests can be used to test for autoantibodies for transglutaminase, endomysin and gliadin. Endoscopy (gold standard for diagnosis). In coeliacs disease the tissue of the small intestine has increased lymphocytes. There is hypertrophy of the crypts and atrophy of the villi. Management - gluten-free diet. Malabsorption is treated with supplements (calcium, iron and vits). In acute flare ups (cilia crisis) quick treatment is important as it is life-threatening but rare. It presents with sever diahorrea, malabsorption and electrolyte imbalance. Treatment is rehydration and corticosteroids to reduce inflammation and pain. In the lumen of the jejunum (after the duodenum), the food will pass through. The jejunum is made of enterocytes above the lamina propria and above the enterocytes is the mucous layer. The small intestine forms crypts and villi. The enterocytes of the small intestine also have microvilli (small finger-like projections) that increase the surface area and increase absorption. The mucous protects the enterocytes and has IgA dimeric antibodies on top of it. IgA is the mucosal immune system and protects against infection. In the lamina propria there are APC which communicate between the innate and adaptive immune system. Risk factors - family history of coeliacs disease; autoimmune thyroid disease; type 1 diabetes; IgA deficiency and IBD. There are also Peyers patches and mesenteric lymphnodes in the lamina propria which help activate an immune response. These tissues contain naive T cells  The current theory for coeliacs disease is that gluten containing food is broken down and gliadin is absorbed. Gliadin through tissue transglutaminase gets deaminated into diaminated gliadin peptides. The APC pick up the deaminated gliadin peptides to the HLA DQ2 or HLA DQ* molecules and present it to the naive T cells in the Peyers patches or mesenteric lympnodes. This activates the naive T cells into CD8 T killer cells or CD4 T helper cells. CD8 T cells promote inflammation when in contact with gliadin. CD4 T cells help activate B cells and allow them to mature into plasma cells. which produce antibodies against gliadin and endomycin and tissue tranglutaminase. The plasma cells will promote inflammation when in contact with these. Inflammation in the small intestine causes abdominal pain and discomfort, diarrohea and bloating and also damages the lining of the small intestine (crypts and microvilli) preventing normal absorption. If there is damage to the mucosa, ions and vits cannot be absorped properly or nutrients and carbs leading to anaemia and weightloss and failure to thrive in children. Fat will not be absorbed and will remain in the stool making it stinky and fatty. Complications - anaemia, tumour development (GI T cell lymphomas), hyposleenism, osteoporosis, neuropathy and dermititis herpatiformis. 

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short bowel syndrome

This condition occurs when either both or one of the small or large intestine become physically shorter than normal. This can be due to surgery. It can also become functionally shorter if part of it damaged and no longer works. This leads to poor water absorption and poor nutrient absorption. Food is ingested at the mout and travels to the stomach to be broken down by stomach acid, enzymes and churning. It then goes to the duodenum where pancreatic enzymes and bile (absorbs fat) from the liver and gallbladder are added to breakdown macronutrients like proteins, carbs and fat. This is also where calcium, iron and magnesium absorption starts. The jejunum has crypts and villi giving it a large surface area for absorption of the breakdown products from the macronutrients from the duodenum (zinc, water-soluble vits and fat soluble vits - A,D,E and K). The next section is the ileum with tight intercellular junctions for fluid absorption and starts to concentrate the intestinal content. It can also adapt its structure to compensate for the jejunum if it has to and help with absorption. The next section is the terminal ileum that absorbs vit B12 and bile salts to be recycled and through the ileocecal valve which facilitates the quantity entering the large intestine and prevents backflow. The colon absorbs water, electrolytes (potassium and sodium), short-chain fatty acids and the bacteria within it produce vit K. Symptoms are dependent on which section is involved. Diarrohea - content moving to fast and food intolerences (loss of enzymes) and can lead to life-threatening dehydration. Certain vits and minerals can be poorly absorbed and lead to a range of symptoms. Malabsorption of macronutrients leads to weight loss and malnutrition. It can be present at birth but usually occurs after surgical removal of part of the small intestine. Surgery is required for necrotising entercolitis in infants and chrohns disease in adults and any condition that effects the function of the small intestine even if it is of a normal length. Diagnosis - history, lab tests (nutrient and electrolyte deficiencies or anaemia. Imaging (Xrays, barium study and MRi). Endoscopy of the upper and lower intestines. Treatment depends on symptoms. Mild symptoms may require dietry adjustments like slowly increasing food and water intake, supplements and diarrohea meds. Sever cases may need total parenteral nutrition (intravenous) and small intestine transplant.   

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peptic ulcer disease overview

peptic ulcer disease describes having one or more breaks in the membrane of the stomach (gastric ulcer) or duodenum (duodenal ulcer - more common). Normally the GI tract is lined with mucosa consisting of an epithelial layer - absorbs and secretes mucus and digestive enzymes (inner), lamina propria - contains blood and lymph vessels, muscularis mucosa - smooth muscle that contracts and aids the breaksown of food (outer). The stomach has 4 regions: the cardia; the fundus; the body and the pyloric antrum. The exit is the pyloric sphincter which remains closed while food is being digested in the stomach. . The cardia has mostly foveolar cells that secrete mucus which is a mix of water and glycoprotein. The fundus and body have mostly parietal cells that secrete hydrocholric acid and chirf cells that secrete pepsinogen (becoms pepsin to digest protein). The antrum has mostly G cells (aslo found in the duodenum ad pancreas) which secret gastrin when food enters the stomach. Gastrin stimulates the parietal cells to produce hydrochloric acid and stimulates the growth of glands in the epithelial layer. The duodenum has Brunner glands that secrete mucus-rich in bicarbonate ions into the lumen. The mucus and bicarbonate ions prevent the stomach and duodenal walls from being degraded by the acid and enzymes.  The stomach has a thicker mucus layer than the duodenum. Prostaglandins get secreted in the stomach and duodenum. They stimulate mucus and bicarbonate secretion as well as vasodilation for epithelial cell growth and inhibits acid secretion.The main cause of ulceration is H.pylori bacteria (gram negative) that colonise the gastric mucosa and release adhesins (stick to foveolar cells) and proteases to damage mucosal cells. The majority of bacterial infections with H.pylori are asymptomatic but it can cause patchy damgae starting in the antrum and then the rest of the stomach and then the duodenum. Over time the damage goes deeper into the mucosa and causes an ulcer to form. Gastric ulcer and not so often duodenal ulcers can also be caused by NSAIDs which inhibit COX in the production of prostaglandins (inflammatory mediators). Doing this long-term leaves the gastric mucosa susceptible to damage and eventually ulcers will devlop. Zollinger Ellison syndrome can also cause peptic ulcer disease (rare) due to gastronomas (a neuroendocrine tumour in the duodenal wall or pancreas that secretes gastrin). This leads to excess hydrochloric acid and a decrease in normal defence mechanisms and alloe=ws ulcers to form in the first part of the duodenum or distal duodenum or jejunum. These ulcers a usually small, round holes in the mucosa. They are usually clean because constant churning keep debris away. Scar tissue and blood vessels develop beneath the ulcer and the ulcers can bleed if the erosion is deep (dangerous if an artery is nearby as haemorrage can occur and the rapid loss of blood into the GI tract can cause shock). Gastric ulcer are usually found in the lower curve of the antrum. Duodenal ulcers usually form just after the pyloric sphincter. There is usually Brunner gland hypertrophy as a consequence of the body trying to increase mucus production to prevent damage.  

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peptic ulcer disease complications, symptoms and t

A complication is perforation if an ulcer erodes all the way through the stomach or duodenum and allows GI content into the peritoneal space which is usually sterile. This is common in duodenal ulcers of the anterior wall. Perforation causes air to collect under the diaphragm irritating the phrenic nerve and sending referred pain to the shoulder. Rarely in long-standing duodenal ulcers near the pyloric sphincter can have oedema and scarring causing an obstruction in the GI tract resulting in gastric outlet obstruction leading to nausea and vomiting as the food cant leave the stomach. The main symptoms of peptic ulcer disease is epigastric pain, bloating, belching and vomiting. Gastric ulcer pain increases when eating a meal because of food presence and increased hydrochloric acid (weight loss). Duodenal ulcer pain decreases when eating a meal (weight gain). Diagnosis with upper endoscopy and biopsy to check for malignancy and H.pylori infection.  Treatment - antibiotic for infection and acid-lowering meds (proton pump inhibitors). NSAIDs, alcohol, tobacco and caffeine can worsen peptic ulcers. Surgery in extreme cases. 

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Crohn's disease

Crohns disease is a form of IBD that causes tissue destruction anywhere along the GI tract. It is an immune related disorder meaning Crohns disease is triggered by a foreign pathogen in the GI tract like mycobacterium paratuberculosis, pseudomonas and listeria species. The immune system targets the foreign pathogen but its response is huge and out of control and destroys the cells of the GI tract. A pathogen activates the immune system via APC that present to CD$ T helper cells and release cytokines like interferon gamma, tumour necrosis factor alpha which are inflammatory mediators. These cytokines attract other immune cells like macrophages which release more inflammatory mediators like proteases, platelet-activating factor and free radicals increasing inflammation. It is hypothesised that one of these stages in the immune response is dysfunctional and produces an unregulated over the top response, resulting in the destruction of healthy tissue. This is thought to happen through genetics as there is an increased risk with family history and a number of mutations identified e.g. frameshift mutation in CARD15 gene. The intestine wall can be split into the mucosa (inner), submucosa, smooth muscle and serosa (outer). A possible defect in the mucosal wall might let pathogens through more easily in Crohns disease. As the inflammatory process starts the immune cells invade deeper intot he mucosa and produces granulomas which encapsulate any foreign material. Eventually after the inflammation and damage to healthy tissue a transmural ulcer will form in the intestinal wall from mucosa to serosa. These areas of inflammation and damage are scattered throughout the GI tract, commonly the ileum and colon. In the colon, this causes pain in the affected areas and diarrohea and blood in stool are common. This is due to damage to the intestinal wall and an inability to reabsorb water. In the small intestine this results in malabsorption as nutrient absorption is poor. Treatment - anti-inflammatories and antibiotics to reduce bacteria in the intestine and reduce the immune rsponse if they have an anti-inflammatory effect. Immunosuppresents may be used in sever cases like corticosteroids. Surgical removal of the affected tissue is possible but isnt curative as inflammation can occur anywhere n the GI tract.  

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Ulcerative Colitis

UC is a form of IBD. The inner lining of the colon becomes inflamed causing ulcers. UC affects the mucosa and submucosa of the intestinal wall. The condition evolves with recurrent flares when new ulcers form followed by symptom free periods when the ulcers heal. Symptoms include abdominal pain and diarrohea with mucus and/or blood. Some patients may have tenesmus, faecal incontinance and urgency. UC often manifests outside the intestine with inflammation of joints skin and eyes. Systemic symptoms of weight loss, nausea, vomiting and fatigue and fever are associated with severe cases. It usually starts at the end of the colon and may stay at the rectum (proctitis - mild (blood and mucus n stools)) or spread to the rectum and sigmoid colon (proctosigmoiditis) or spread through the rectum, sigmoid and descending colon (left-sided colitis) or the entire colon (pancolitis - more liquid blood mucous content). Complications - increased risk of colon cancer; toxic colitis characterised by sudden violent diarrohea, fever, abdominal pain and signs of peritonitis. Toxic colitis occurs when the inflammation extends into the smooth muscle layer of the intestinal wall, causing paralysis of the colon. This can lead to perforation and dilatation of the colon. It is associated with high levels of T helper type 2 cells. The mechanism is not fully understood but is likely a combination of genetic and environmental factors. Genes that have been identified help maintain the epithelial barrier or are involved in the immune response. A gene variant thought to play a role in increasing the risk of UC by 50% is ADCY7. It is most common in developed countries. Smoking appears to be protective for UC. Diagnosis is symptom based after ruling out infection via stool sample and colonoscopy/sigmoidoscopy with biopsy for cancers. Treatments - dietary management (raw foods avoided and occasionally non-dairy diets. Anti-diarroheal meds e.g. loperamide but not for severe flare ups. Mild to moderate cases are given topical or oral 5-aminosalicylic acid depending on locations affected. extensive UC is treated with corticosteroids, immunomodulators (azathioprine, mercaptopurine) and biologics (infliximab, adalimumab etc). Severe cases are treated in hospital with IV corticosteroids and monitored for toxic colitis. Toxic colitis is treated with high dose corticosteroids and antibiotics with possibility of surgery. Surgery is curative. The inflammation is the same mechanism as crohns disease but it is limited to one area and not spread out. 

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