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IBD: Inflammatory Bowel Disease Hira Waris Sajid Ali.

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Presentation on theme: "IBD: Inflammatory Bowel Disease Hira Waris Sajid Ali."— Presentation transcript:

1 IBD: Inflammatory Bowel Disease Hira Waris Sajid Ali

2 What is IBD: Inflammatory Bowel Disease?  the inflammation of gastrointestinal track due to abnormal response of innate and adaptive immunity, particularly the activity of T-cells.  can also result due to improper or wrong response of intestinal microbes which again result in inflammation  That’s why IBD is called as autoimmune disease

3  The host-microbe relationship is also very important in the pathogenesis of IBD  IBD is basically the outcome of two different diseases. First one is:  Crohn’s disease  Ulcerative Colitis.  The molecular basis of these two disease are still not exactly known as IBD is polygenic disease resulting due to different factors like genetics, environment, inappropriate immune response, unhealthy or imbalanced diet and stress.

4 Ulcerative Colitis  Ulcerative Colitis is the disease of large intestine.  In this disease, mucosa or inner lining of the intestine get inflamed and lead to development of ulcers.  This disease is limited to mucosa and sub mucosa and deep layers remain unaffected.

5 Ulcerative Colitis  Ulcerative Colitis is the disease of large intestine.  In this disease, mucosa or inner lining of the intestine get inflamed and lead to development of ulcers.  This disease is limited to mucosa and sub mucosa and deep layers remain unaffected.

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7 Major symptoms  Diarrhea  Rectal bleeding  Crampy abdominal pain.

8 ulcerative colitis:the left side of the colon is affectedcolon The image shows confluent superficial ulceration and loss of mucosal architecture.

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10 Crohn’s Disease  Crohn’s affects the last part of small intestine and some part of large intestine or it can attack any part of digestive track and generally involve the whole bowel wall.  CD is trans mural process and results in formation of strictures and fistulas.  About 1.4 million people in America are affected by this per year and its prime onset is in people with years of age.

11  Cigarette smoking contributes to these diseases in different manner. Smokers have pronounced risk for Crohn’s disease making it worse while UC occurs evenly in both smokers and nonsmokers.

12 Genetics of disease  If we study genetics of this disease, it shows that genomic region which contain nucleotide domain 2 (NOD2), autophagy genes and components of interleukin-23-type 17 helper T-cells (Th 17) pathway is involved.  NOD2 protein is a sensor of bacterial peptidoglycan which is present inside the cell.  Autophagy is the process which allows cells to destroy and regulate different components or organelles present in cells including pathogens. The autophagy gene, ATG16L1 is more related with Crohn’s disease and has no role in Ulcerative colitis.

13  Many genes of interleukin-23-Th17 pathway is associated with CD and UC. IBD’s successptaibility loci, including chromosome 16q (IBD 1), 6q (IBD 3), 14q (IBD 4), 19q (IBD 6) and still there is scope of further investigation and research.  These sensitive loci may encode hundreds of different genes as well as proteins which further complicate the identification of genes and their function.  Crohn’s disease is one of the earliest diseases whose targeted genes were identified.

14  NOD2 is now renamed as CARD 15 and is present on chromosome 16. Investigators have identified the role of NF-kB in the epithelium of intestine.  It is a signaling molecule and helps cells to cope with stress conditions.  Using advance genetic methods, scientists had generated a mouse model that does not express NEMO, necessary to stimulate NF-kB, in intestinal epithelial cells.  Presence of both these disease in the same family suggests that some of genes may be common to both disorders.

15  The accumulation of leukocytes like neutrophils into the mucosa of intestine forms mucosal lesions.

16 DIAGNOSIS Mujtaba Chaudhry

17  The condition is usually diagnosed via endoscopy, in which a tiny camera on the end of a flexible tube is inserted into the bowel  A single blood test may not determine if you have inflammatory bowel disease or not.  Information from both blood and the stool tests are done and X-rays are used for diagnosing IBD.  A complete blood count test, Creatinine level, serum urea, LFT,ESR, SAT, CAS and C reactive protein.

18  Information from both blood and the stool tests are done and X-rays are used for diagnosing IBD.  A complete blood count test, Creatinine level, serum urea, LFT,ESR, SAT, CAS and C reactive protein.

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21 Antibodies Tests  Antibodies tests are also used to determine if a person suffers an inflammatory bowel disease  Crohn’s disease and Ulcerative colitis could not be diagnosed with these antibody tests.  But now an increase in ANC antibodies in UC and ASC antibodies in Crohn’s disease has been observed.

22  Confirmation of IBD can be done by the help of following test: 1) Decreased hemoglobin and human serum albumin. 2) Increased platelet count, C reactive protein level and ESR.  These characteristics of IBD are not always present there since Ulcerative colitis have been reported with normal platelets count, EST and hemoglobin.

23  Many pediatric gastroenterologists consider it important to have multiple biopsies of all segments of the colon and a full colonoscopy with terminal ileum intubation  Radioactive barium meal and then follow through are one of the best methods for assessment of small bowel or also by enteroclysis with duodenum intubation.

24  Crohn’s disease causes more growth failure as well as nutritional impairment than UC when diagnosed however in longer term both groups cause growth impairment which is characterized by delayed puberty and delayed skeletal maturation.

25 IBD and its Treatment Safana Farooq

26 Treatment of Crohn’s Disease  EEN  Corticosteroids  5-Aminosalicylates  Azathioprine  Immunosuppression  Surgery

27 EEN  EEN is the most suitable treatment in Crohn’s Disease.  Treatment lasts from 6-8 weeks.  Use of flavored and chilled drinks is recommended.  This treatment is effective where nutritional deficiency is the cause.

28 Corticosteroids  Corticosteroids are quite active in reducing infection.  Also have considerable side effects.  Especially given in intense pancolitis.  Dosage method and supplements.

29 5-Aminosalicylates  5-Aminosalicylates are effective is disease is mild or moderate.  Corticosteroids and EEN are given in addition to 5-ASA therapy.

30 Azathioprine  Azathioprine is another drug used in curing mild to moderate disease  Side effects of Azathioprine.  Care while treating with Azathioprine.

31 Immunosuppression  When conventional drugs fail to response we use immunosuppression agents like methotrexate, cyclosporine, tacrolimus, and anti-TNF monoclonal antibodies (infliximab).

32 Surgery  Least and last option when all the other drugs failed to respond.  There are chances of Reoccurrence of disease which can be avoided by constant intake of immunosuppressant and other drugs.

33 Treatment of Ulcerative Colitis  In UC same drugs are given but the exclusive eternal nutrition is not effective in this case.  Corticosteroids  5-ASA derivatives  Azathioprine  Second line Immunosuppression  Surgery

34 Stem Cell Therapy  for acquiring or having the formation of all types of mature tissues  provides great facility for tissue regeneration and for the cure of different degenerative diseases.  Embryonic stem cells have the ability to grow and differentiate as well as restore the intestinal epithelium as we have seen in mice with colitis.  Now scientists are seeking protocol for using it in humans.  Method of stem cell therapy  The epithelium is restored in every 3-5 days with stem cells present at the base of each crypt.

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