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Miscellaneous Topics in Gastroenterology Waseem Hamoudi M.D Consultant Internal Medicine Gastroenterology & Hepatology.

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Presentation on theme: "Miscellaneous Topics in Gastroenterology Waseem Hamoudi M.D Consultant Internal Medicine Gastroenterology & Hepatology."— Presentation transcript:

1 Miscellaneous Topics in Gastroenterology Waseem Hamoudi M.D Consultant Internal Medicine Gastroenterology & Hepatology

2 Peptic Ulcer Disease.Peptic Ulcer Disease. Inflammatory Bowel Disease. Acute diarrhea.

3 Peptic Ulcer Disease Peptic ulcerations are excavated defects (holes) in the gastrointestinal mucosa that result when epithelial cells succumb to the caustic effects of acid and pepsin in the lumen. Peptic ulcer disease commonly used term to refer to ulcerations of the stomach, duodenum, or both, that is caused by acid- peptic injury.

4 Histological, ulcers are necrotic mucosal defects that extend through the muscularis mucosa and into the submucosa or deeper layers. More superficial necrotic defects are named erosions.

5 History In the early part of the 20 th century, stress and diet were considered to be the pathogenetic factors for PUD, so treatment was with bed rest and diet. 1950, clinicians had focused their attention on the pathogenetic role of gastric acid, so antacid therapy had become the treatment of choice. 1970, histamine H2 receptor antagonists became available, and acid suppression with antisecretory therapy was the treatment of choice for UD. 1980, proton pump inhibitors (PPI) were discovered, with more potent acid suppression and higher rates of ulcer healing. Using alone antisecretory drugs, will have recurrence within one year in most patients

6 H. pylori was discovered in April 1982 by two Australian physicians, Dr. Barry Marshall and Dr. Robbin Warren. In 1983 the two doctors proposed that the bacterium is the cause of peptic (duodenal and gastric) ulcers. Dr. Marshall even went so far as to inoculate himself with the bacterium to prove his point. it soon became apparent just how widespread and serious the H. pylori threat is. Researches confirm that over 90 per cent of people with peptic ulcers are infected with the bacterium. In 1987 the Sydney gastroenterologist Thomas Borody invented the first triple therapy for the treatment of duodenal ulcers.

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8 Causes United Kingdome United states Duodenal ulcer Peptic ulcer disease Gastric ulcer( Benign) Gastroesophageal varices Esophagitis Angiomas Mallory-Weiss tear Gastroesophageal varices Tumors Gastritis or gastric erosions Erosions Tumors Dieulafoy's lesion

9 Jordan (Al Bashir Hospital) Duodenal ulcer 41.90% Esophageal varices 16.07% Erosive gastritis/duodenitis 14.09% Esophagitis 8.64% Gastric ulcer 5.87% Gastric and duodenal ulcers 3.60% Esophageal ulcer 3.25% Anastomotic ulcer 2.26% Mallory-Weiss tear 1.55% Esophageal tumor 1.41% Gastric tumor 1.27% Waseem H. et al. Upper G.I Bleeding in Jordan- Retrospective statistical analysis

10 Peptic Ulcer Disease. Inflammatory Bowel Disease.Inflammatory Bowel Disease. Acute diarrhea.

11 Main types of inflammatory bowel disease (IBD) Ulcerative colitis Crohn’s disease

12 Endoscopic features of ulcerative colitis (reproduced with permission, Schiller et al, 1986)

13 Anatomical location of ulcerative colitis

14 Intestinal complications of ulcerative colitis Fibrosis Shortening of the colon Bleeding Stricture Bowel perforation Toxic megacolon

15 Systemic complications of ulcerative colitis Arthritis Iritis Erythema nodosum Pyoderma gangrenosum Sclerosing cholangitis Aphthous stomatitis Thromboembolic disorders

16 Clinical presentation of ulcerative colitis Bloody diarrhoea Fever Cramping abdominal pain Weight loss Frequency and urgency of defecation Tenesmus General malaise

17 (reproduced with permission, Schiller et al, 1986) Endoscopic appearance of Crohn’s disease

18 Anatomical location of Crohn’s disease

19 Clinical presentation of Crohn’s disease Diarrhoea Abdominal pain Bleeding Pyrexia Weight loss Fistulae Perianal disease General malaise

20 Intestinal complications of Crohn’s disease Fistulae Abscesses Adhesions Strictures Obstruction

21 Perianal complications of Crohn’s disease

22 Systemic complications of Crohn’s disease Arthritis Gallstones Malabsorption –Lactase deficiency –Vitamin B 12 deficiency Renal stone formation

23 Differences in clinical presentation between ulcerative colitis and Crohn’s disease Ulcerative colitisCrohn’s disease Symptoms Pain** * * General malaise* * ** Fever** Diarrhoea* * ** Stools Blood* * ** Mucus** Pus** The number of * symbols indicates the frequency with which each symptom is present

24 Pathological and anatomical features distinguishing ulcerative colitis from Crohn’s disease Ulcerative colitisCrohn’s disease LocalisationDistalSegmental, proximal Rectum affectedAlways50% of cases Intestinal wallNormal thicknessThickened AdhesionsRareCommon InflammationSuperficial layersAll layers UlcerationsSuperficialDeep Mucous membraneDenudedCobblestones Granulomas0–4%50–70% Lymphocytic infiltrationRareAlways FistulaeRareCommon

25 (reproduced with permission, the AGA Teaching Project, 1992) Geographical distribution of IBD

26 Aetiological theories of IBD Genetic Smoking Dietary Infection Immunological Psychological?

27 Pharmacological treatment of IBD 5-ASA-containing compounds –mesalazine Pentasa® Asacol® Claversal®/Mesasal®/Salofalk® –sulphasalazine Salazopyrin® –olsalazine Dipentum® Corticosteroids Immunosuppressants

28 Treatment: indications for surgery Perforation Toxic dilatation Massive haemorrhage Chronic ill-health Risk of cancer

29 Peptic Ulcer Disease. Inflammatory Bowel Disease. Acute diarrheaAcute diarrhea.

30 Normally 10 liters enter the duodenum daily, of which 1 liter is absorbed by the small intestine. Colon resorbs most of the remaining fluid with only 100 ml fluids lose in the stool. Medical definition of diarrhea: a stool weight more than 250 g/day. Practical definition: increased stool frequency more than 3 times/day or liquidity. There are 2 types of diarrhea: acute diarrhea (less than 3 weeks) and chronic diarrhea (more than 3 weeks).

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32 Acute diarrhea Acute diarrhea: acute onset of diarrhea and present for less than 3 weeks Mostly caused by infectious agents, bacterial toxins (ingested preformed in food or produced in gut) and drugs. Similar recent illness in family members suggests an infectious etiology.

33 Non-inflammatory diarrhea Fever absent. Stool without blood or fecal leucocytes. Watery stool with peri-umbilical cramps, bloating, nausea and vomiting (small bowel enteritis) caused by either a toxin or other a toxin producing toxin or other agents that disrupt the normal absorption and secretory process in the small intestine.

34 How do we recognize non- inflammatory diarrhea? By examining the absence of the leucocytes in the stool

35 What are the causes of Non- inflammatory diarrhea? Viral: Norwalk virus, Rotavirus. Protozoa: Giardia lamblia, Cryptosporidium. Bacterial: Preformed entero-toxins: Staphylococcus aureus, Bacillus cereus, and Clostridium perfringens. Intra-intestinal enterotoxin production: E. coli (enteropathogen) and Vibrio cholera. New medication. Fecal impaction.

36 Inflammatory diarrhea Presence of fever and bloody diarrhea (dysentery) indicates colonic damage caused by invasion (shigellosis, salmonellosis, yersinia and amibiasis) or a toxin (C.difficile, E. coli 0157:H7). Colonic diarrhea is a small amount diarrhea in volume (< 1l/day) and associated with left lower quadrant cramps, urgency and tenesmus. Fecal leucocytes are present in infections with invasive organisms.

37 How do we recognize inflammatory diarrhea? By examining the presence of the leucocytes in the stool

38 What are the causes of inflammatory diarrhea? Viral: Cytomegalovirus. Bacterial: 1. Cytotoxin production: E. coli 0157:H7 (enterohemorhagic), Vibrio parahemolyticcus and Clostridium difficile. 2. Mucosal invasion: Shigella, Salmonella, enteroinvasive E. coli, aeromonas and Yersinia. 3.Bacterial proctitis: Chlamydia, N. gonorrhea. Protozoa: E. histolytica. Other: Ischemic colitis, I.B.D. and radiation colitis.

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