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WEEK 3:
Lower GI Pathology
| Question | Answer |
|---|---|
| ligament of treitz (suspensory muscle of duodenum) | connects duodenum to jejunum - extends from duodenojejunal flexure to diaphragm |
| function of small intestines | absorption, lubrication and immune system |
| cells in small intestine (5) | Enterocytes – absorptive cells, Goblet cells, Stem cells, Paneth cells (antibacterial and phagocytic activity) and Enteroendocrine cells (regulate pancreatic, biliary and gastric juices) |
| type of epithelium in small intestine | columnar absorptive cells (with microvilli) |
| role of enteroendocrine cells | regulate exocrine juices (so has a lot) |
| describe goblet cells in small intestine | less that large intestine |
| what are at the bases of Crypts of Lieberkuhns | paneth cells (lysosome secreting to provide antibacterial and phagocytotic activity) |
| muscle found in small intestine | circular and longitudinal |
| what is found between smooth muscle in small intestine | parasympathetic plexus of Auerbach |
| Duodenum has what type of glands | Brunner's glands |
| Brunner's Glands function | secretes alkaline juices to neutralise acid from stomach |
| Jejunum lacks | Brunner's glands and no Peyer's Patches |
| ileum has | Peyer's patches and lymphoid tissue |
| small bowel infarction | highly susceptible to ischaemic injury leading to abdominal pain (necrosis causes inflammation), bloody diarrhoea (mucosal necrosis), and decreased bowel sounds (eventually as intestines become hypoactive) |
| phase 1 of vascular compromise | initial hypoxic injury at onset of vascular compromise causes some damage but epithelial cells are somewhat resistant to transient hypoxia |
| phase 2 | reperfusion injury where restoration of blood supply is more damaging (due to free radical production, neutrophil infiltration, inflammatory mediators eg complements and cytokines) |
| tropical sprue | damage to small bowel villi due to unknown organism resulting in malabsorption which arises after infectious diarrhoa and responds to antibiotics |
| where is damage most prominent in tropical sprue | jejunum and ileum |
| damage to jejunum and ileum (from tropical sprue) leads to | secondary vitamin B12 or folate deficiency |
| Coeliac disease | immune mediated damage of villi due to gluten exposure which is associated with HLA-DQ2 and DQ8 |
| clinical presentation of coeliac disease | abdominal distension, diarrhoea and failure to thrive |
| lab results and tests for coeliac disease | IgA antibodies against endomysium t TG or Gliadin and duodenal biopsy reveals flattening of villi and patients need to remain on gluten prior to test |
| damage most prominent where in coeliac disease | duodenum |
| how can you resolve symptoms in coeliac disease | gluten free diet |
| coeliac disease can lead to (3) | Abdominal distension: Due to lack of absorption of digested food. Diarrhoea: Food not fully absorbed Failure to thrive: Due to lack of absorption |
| lactose intolerance | decreased function of lactase enzyme in brush boarder of enterocytes which may be congenital or acquired and may also be seen after small bowel infection (temporary) |
| lactase breaks down lactose into | glucose and galactose |
| lactose intolerance people presents with | abdominal distension and dirrhoea upon consumption of milk products |
| clinical presentation of lactose intolerant people (3) | Abdominal distension: Due to lack of Absorption Diarrhoea: Lack of Absorption Small bowel infection: Causes damage of to brush border enzymes and therefore causes temporary lactose intolerance |
| carcinoid tumour | malignant proliferation of neuroendocrine cells |
| tumour cells contain | neurosecretory granules that are positive for chromogranin |
| where can carinoid tumour cells arise from | anywhere in gut but more particularly in small bowel (appendix being a common site) |
| what is secreted by carcinoid tumour | serotonin into portal circulation and metabolised by the liver monoamine oxidase into 5-HIAA which is then secreted into the urine |
| carcinoid syndrome (5) | Flushing, Increased heart rate, Diarrhoea, Abdominal pain and Breathlessness and wheezing due to bronchospasm |
| why do symptoms like flushing occur in people with carcinoid tumour | due to metastasis in liver (only possible as serotonin is released and is no longer metabolised by liver and it leaks into systemic circulation via hepato systemic shunts) |
| Meckel's diverticulum | outpouching of all three layers of bowel wall arising due to failure of vitelline duct to obliterate |
| epidemiology of meckels diverticulum | 2% of population with 2 inches long and located 2 feet from ileocecal valve and can present during first 2 years of life with bleeding |
| intussusception | telescoping of proximal segment of bowel forward into distal segment due to peristalsis resulting in obstruction and disruption of blood supply with infarction |
| intussusception is associated with | leading edge (focus of traction) |
| in kids/ paediatrics, cause of intussusception is | lymphoid hyperplasia or meckels |
| in adults cause of intussusception is | usually a tumour |
| intussusception can cause (2) | abdominal pain and jelly current stool (late sign due to necrosis of mucosa) |
| function of large intestine | absorb water and salt and produce a more solid waste |
| anatomy of large intestine | Caecum Ascending colon Transverse Colon Descending colon Sigmoid colon Rectum Appendix (lymphoid tissue |
| cells in large intestine | Abundant cells for lubrication, Enterocytes (for Absorption) and Enteroendocrine cells (some) (to control digestive juices) |
| ;'folds' in large intestine | no villi but still have crypts |
| describe crypts in large intestine | they are arranged as tubular glands (crypts of liebrkuhn) but no villi and is deeper than small intestines as they dont need a large surface area |
| epithelium in large intestine | tall columnar absorptive cells (with microvilli) |
| amount of enteroendocrine cells in large intestine | less (needed to regulate exocrine juices) |
| amount of goblet cells in large intestine | more (to produce more mucus) |
| cells lacking in large intestine | paneth cells BUT has aggregates of lymph nodes but more scattered |
| muscles in large intestine | longitudinal, circular and taenia coli muscles |
| what is between muscles in large intestine | parasympathetic plexus of Auerbach |
| slower rate of transit leads to | Constipation due to dehydration/lack of fibre Consequence can be diverticulosis |
| faster rate of transit leads to | IBS and diarrhoea |
| blocked rate of transit leads to | obstruction |
| why can the bowel tolerate slow progressive blood loss | since GIT has collateral vessels |
| acute compromise of any major vessel can lead to | infarction of large segments of bowel |
| ischaemic damage in mucosa and submucosa can be | acute or chronic infarction |
| transmural infarction in large intestine | involves all 3 layers of wall (acute infarction) |
| Watershed zones | intestinal segments at end of their respective arterial supplies that are particularly susceptible to ischaemia |
| splenic flexure | Superior and inferior mesenteric arteries terminate |
| sigmoid colon and rectus | Where inferior mesenteric, pudendal and iliac arteries Terminate |
| types of vessel disease (3) | Severe Atherosclerosis Aortic Atheromas Aortic aneurysm |
| other sources of embolus | Embolisation of cardiac vegetation |
| hypercoaguable state | Due to hereditary disease Oral contraceptive use (Iatrogenic) |
| intestinal hypoperfusion causing mucosal infarcts can also cause | Cardiac Failure Shock Dehydration Vasoconstrictive drugs Systemic Vasculitis Mesenteric Venous thrombosis (Uncommonly causes ischemic disease) Trauma Invasive neoplasm |
| ischaemic bowel disease occurs with | coexisting cardiac or vascular disease |
| symptoms of ischaemic bowel disease | Sudden severe abdominal pain and tenderness Nausea Vomiting Bloody diarrhoea Muscular spasm creates a board like rigidity on the abdominal wall (Peritonitis) |
| danger of symptoms of ischaemic bowel disease | overlap with other abdominal pathology so diagnosis can be delayed or missed |
| as mucosal barrier breaks down during ischaemic bowel disease what happens | bacteria enters circulation and can cause sepsis and mortality may exceed 50% |
| underlying causes of ischaemic enteritis | |
| infective enterocolitis (bacterial) | |
| infective enterocolitis (viral) | |
| IBD (inflammatory bowel disease) | chronic condition causing relapsing inflammation of bowel |
| types of IBD | Crohn's and ulcerative colitis |
| causes of IBD | not fully understood |
| where does IBD present in | young people teens - 30 |
| IBD causes and presents what | systemic effects and presents as recurrent bouts of bloody diarrhoea and abdominal pain |
| diagnosis of IBD | |
| what would you see in Crohns | |
| what would you see in ulcerative colitis | |
| risk of cancer between crohns and ulcerative colitis | |
| presentation differences between crohns and ulcerative colitis | |
| peak incidence between crohns and ulcerative colitis | |
| gender differences between crohns and ulcerative colitis | |
| adhesions and strictures differences between crohns and ulcerative colitis | |
| wall and lumen differences between crohns and ulcerative colitis | |
| what is seen on the walls of vessels between crohns and ulcerative colitis | |
| what can form between crohns and ulcerative colitis | |
| Crohn's can affect what organs | |
| appearance of Crohn's | skip lesions and cobblestone appearance |
| more on slide 49** | |
| more on slide 50** |
Created by:
22tango
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