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Dyspepsia

CHRONIC DYSPEPSIA

Seminar Prepared by :-
Ali Abdulazeem
Shilan Adnan Abdulrahman
Alaa Shamil
Guldan Hameed


Internal Medicine
College of Medicine - University of Kirkuk

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Dyspepsia

  1. 1. Definition : *#isnotadisease *# isgroupofsymptomsratherthanonepredominantsymptom Dyspepsia (indigestion):isacollective term*forany symptomsthought to originatefromupperGIT . Itcomposesmany causesand symptomslike;heartburn, upperabdomen discomfort,nausea, regurgitation, bloating,fullness…etc And thecauseare:
  2. 2. Causesof dyspepsia Upper gastrointestinaldisorders • Pepticulcer disease • Acute gastritis • Gallstones • Oesophagealspasm • Non-ulcer dyspepsia • Irritablebowelsyndrome Othergastrointestinaldisorders • Pancreaticdisease(cancer, chronic pancreatitis) • Coloniccarcinoma • Hepaticdisease(hepatitis, metastases) Systemicdisease • Renalfailure • Hypercalcaemia Drugs • NSAIDs • Corticosteroids • Ironandpotassiumsupplements • Digoxin Others • Psychological(anxiety,depression) • Alcohol
  3. 3. Differential diagnosis
  4. 4. Differential diagnosis ●Gastroesophageal reflux disease ●Peptic ulcer ●Gastroparesis ●Gastritis(NSAIDs & H.pylori) ●Non ulcerdyspepsia(functional dyspepsia ) ●malignancy
  5. 5. a.Organicdyspepsia
  6. 6. Risk factors of dyspepsia age Fatty meal Anxiety or depression smoking obesity Family history
  7. 7. b.Functional dyspepsia isdefinedas ≥3months ofbothersome postprandial fullness, early satiety, or epigastricpainor burning withsymptom onsetat least 6 months before diagnosisin the absenceof organiccause.
  8. 8. Rome criteria ✢ TheRome criteriawereoriginallydevelopedtounderstandfunctional gastrointestinaldisorders(FGIDs),whichareconditionsthatarebasedon symptoms thatclusteras opposedtoconditionsthataredefinedbyorgan pathology(microscopic or macroscopic), such asinflammatoryboweldiseaseand celiacdisease,or byalteredmotility,suchas gastroparesisorachalasia.TheRome IVdiagnosticcriteriaarethemostrecentiterationofsymptom-basedcriteriafor FGIDsandweredevelopedinacollaborativeeffortbetween126 experts representing26 countries.Theprocess toupdate Rome III criteria,whichwere publishedin2006, beganin2008 withthecreationofworkingteamstoacquire knowledge.Between 2010 and2015, committeememberscollected, evaluated, presented,andmodifiedclinicaltrialdatainvariousareasofinterest,including differentagespatientpopulationswithirritablebowelsyndrome(IBS) andFGIDs.
  9. 9. pathophysiology ✢The pathophysiology ofdyspepsia notwellunderstood so the researchersarefocused onseveralkeyfactors :
  10. 10. Pathophysiology of functional dyspepsia Nonmotility disorder Motility disorder psychosocial
  11. 11. Motility and nonmotility disorders the diseases that can affect the motility of GIT like : GERD ( decrease th lower esophageal sphincter tone ), Impaired gastric fundus relaxation after eating… visceral afferent hypersensitivity (These individuals with functional heartburn are believed to have heightened perception of normal esophageal pH and volume) With motility disorders there is little correlation between symptoms and severity of duodenitis , and no relation between treatment and improvement of mucosal appearance on endoscopy .
  12. 12. Abnormal fundic relaxationin responsetomeal infunctional dyspepsia Motilitydisorder
  13. 13. Altered motility in dyspepsia
  14. 14. Psychosocial factors ●Patients withnonulcer dyspepsiaaremorelikelytohave symptomsofanxiety and depressionthanarehealthy patientswithulcers. ●Multiplesomaticcomplaintsalsomorecommon in patientswhohave nonulcer dyspepsia. ●Ahistoryofchildabusealsohasbeen linked with symptomsofnonulcer dyspepsia ●Stresslife events .
  15. 15. Investigation
  16. 16. Alarming signs
  17. 17. Specific investigation ✢ Dependoncausesand history forexample: ✢ Peptic ulcerwith hx ofsmoking andNSAIDs (endoscopy) ✢ Gastric duodenal ulcer with hx of unexplained weightloss , dysphagiaandsmoking(endoscopy) ✢ Gastric cancer(endoscopy) ✢ H.pylori (urea breath , stool antigen,whole blood antibody , serum IgGantibody tests)
  18. 18. ✢ GERD with hx of heartburn aggrevated when supine , chronic cough (omperazole test , endoscopy and 24hrspHmonitoring)
  19. 19. endoscopy ✢ Endoscopy isa nonsurgicalprocedure usedto examineaperson'sdigestive tract ✢ Types: flexible andrigid ✢ Uses: diagnostic (e.gbiopsy taking) and therapeutic (e.g polyp remove)
  20. 20. HELICOBACTER PYLORI
  21. 21. HISTORY Dr. Robin Warren, a pathologist from Perth, Australia, observed small curved bacteria colonizing the lower part of the stomach in about 50% of patients who had their stomachs biopsied. He observed that signs of inflammation were always present in the gastric mucosa close to where he saw the bacteria.
  22. 22. Barry Marshall, a colleague, became interested in Warren’s findings and together they initiated a study of biopsies from 100 patients. Marshall succeeded in cultivating a previously unknown bacterial species – later named Helicobacter pylori – from several of these biopsies. They found that the organism was present in almost all patients with gastric inflammation, duodenal ulcer, or gastric ulcer. Based on these results, they proposed that this newly identified bacterium caused these diseases. Until that time, so entrenched was the belief that lifestyle caused ulcers that, even with their evidence, it was difficult for these two researchers to convince the world of H. pylori’s role in ulcer disease.” To provide even more conclusive evidence, in 1985 Marshall deliberately infected himself with the bacterium and established his own stomach illness. Eradication therapy was then employed with mixed success, but both received the Nobel Prize for Medicine and Physiology in 2005..
  23. 23. Helicobacter pylori a gram-negative bacillus that has naturally colonized humans for at least 100,000 year and probably throughout human evolution. It lives in gastric mucus, with a small proportion of the bacteria adherent to the mucosa and possibly avery small number of the organisms entering cells or penetrating the mucosa Its spiral shape and flagella render H. pylori motile in the mucus environment. The organism has several acid-resistance mechanisms, most notably a highly expressed urease that catalyzes urea hydrolysis to produce buffering ammonia. H. pylori is microaerophilic (i.e., requires low levels of oxygen), is slow-growing, and requires complex growth media in vitro
  24. 24. Prevalence and Risk Factors • Theprevalenceof H.pyloriamong ✢ adultsis<30% inmostpartsoftheUnitedStatesandin otherdeveloped countries • >80% inmostdeveloping countries. • IntheUnitedStates,prevalence varieswithage: up to50%of 60-year-oldpersons, • ~20% of 30-year-oldpersons, • andfewerthan10% ofchildrenarecolonized. H
  25. 25. Transmission ✢ Humansarethe onlyimportant reservoir of H.pylori. ✢ Childrenmayacquiretheorganismfromtheirparents(most oftenthe primarycaregiver) orfrom other children ✢ Whether transmissiontakes place more often ✢ by thefecal-oral or theoral-oral route is unknown, ✢ but H.pyloriiseasilycultured from vomitus and gastroesophageal refluxate andis lesseasilycultured from stool
  26. 26. ✢ Most H.pylori–colonizedpersonsdo notdevelop clinicalsequelae. ✢ Thatsome persons develop overt diseasewhereas others do notis related to acombination of factors: 1. bacterial straindifferences, 2. hostsusceptibility to disease, 3. and environmentalfactors
  27. 27. CLINICAL MANIFESTATIONS
  28. 28. Peptic Ulcer Disease Worldwide, >80% of duodenal ulcers and>60% of gastric ulcers are related to H. pylori colonization However, in particular, the proportion of gastric ulcers caused by aspirin and nonsteroidal anti-inflammatory drugs (NSAIDs) is increasing, and in many developed countries these drugs have overtaken H. pylori as a cause of gastric ulceration. The main lines of evidence supporting an ulcer-promoting role for H. pylori are that (1) the presence of the organism is a risk factor for the development of ulcers, (2) non-NSAID-induced ulcers rarely develop in the absence of H. pylori, (3) eradication of H. pylori virtually abolishes long-term ulcer relapse, and (4) experimental H. pylori infection of gerbils can cause gastric ulceration.
  29. 29. Pathogenesis of duodenal ulceration Gastric colonization causes duodenal ulceration is now becoming more clear. H. pylori– induced inflammation of the gastric antrum diminishes the number of somatostatin producing D cells. Because somatostatin inhibits gastrin release, gastrin levels are higher than in H. pylori– ve , and these higher levels lead to increased meal-stimulated acid secretion from the relatively spared gastric corpus.
  30. 30. How this situation increases duodenal ulcer risk remains controversial, but the increased acid secretion may contribute to the formation of the potentially protective gastric metaplasia found in the duodenum of duodenal ulcer patients. Gastric metaplasia in the duodenum may become colonized by H. pylori and subsequently inflamed and ulcerated.
  31. 31. Gastric Adenocarcinoma and Lymphoma Prospective nested case-control studies have shown that H. pylori colonization is a risk factor for adenocarcinomas of the distal (noncardia) stomach . Long-term experimental infection of gerbils also may result in gastric adenocarcinoma. Moreover, H. pylori may induce primary gastric lymphoma, although this condition is much less common. Many low-grade gastric B-cell lymphomas are dependent on H. pylori for continuing growth and proliferation, and these tumors may regress either fully or partially after H. pylori eradication. However, they require careful short- and long-term monitoring, and some necessitate additional treatment with chemotherapeutic agents.
  32. 32. Pathogenesis of gastric ulceration and gastric adenocarcinoma The pathogenesis of these conditions is less well understood, although both arise in association with pan- or corpus predominant gastritis. The inflammation in the gastric corpus means that it produces less acid (hypochlorhydria) despite hypergastrinemia. Gastric ulcers usually occur at the junction of antral and corpus-type mucosa, an area that is often particularly inflamed. Gastric cancer probably stems from progressive DNA damage and the survival of abnormal epithelial cell clones. The DNA damage is thought to be due principally to reactive oxygen and nitrogen species arising from inflammatory cells, perhaps in relation to other bacteria that survive in a hypochlorhydric stomach. Longitudinal analyses of gastric biopsy specimens taken years apart from the same patient show that the common intestinal type of gastric adenocarcinoma follows stepwise changes from simple gastritis to gastric atrophy, intestinal metaplasia, and dysplasia. A second, diffuse type of gastric adenocarcinoma found more commonly in younger adults may arise from chronic gastritis without atrophic changes.
  33. 33. Functional Dyspepsia Many patients have upper gastrointestinal symptoms but have normal results on upper gastrointestinal endoscopy (so-called functional or nonulcer dyspepsia). Because H. pylori is common, some of these patients will be colonized with the organism. H. pylori eradication leads to symptom resolution a little more commonly (from 0 to 7% in different studies) than does placebo treatment.
  34. 34. DIAGNOSIS
  35. 35. TREATMENT
  36. 36. Treatment ✢ FIRST LINE THERAPY ✢ PPI takensimultaneouslywithtwoantibiotics(from amoxicillin, clarithromycin andmetronidazole)forat least7days ✢ Successisachievedin80–90% ofpatients ✢ SECOND LINE THERAPY ✢ quadrupletherapyregimen, consisting ✢ omeprazole(oranotherPPI),bismuthsubcitrate,metronidazoleandtetracycline (OBMT)for10–14days, ✢ recommended. In areasof clarithromycinresistanceANDsecond-line therapyto thosewhoremaininfected afterinitialtherapy
  37. 37. ✢ THIRD LINE THERAPY ✢ antimicrobial sensitivity testing, ✢ rescuetherapy(levofloxacin,PPIand clarithromycin)or ✢ long-termacidsuppression.
  38. 38. ✢ Eradication of the infectionhas provenbenefitsin several ✢ extragastric disorders, includingunexplainedB12 deficiency and ✢ iron deficiency anaemia, once sourcesofgastrointestinal bleeding ✢ have beenlooked forand excluded. Platelet countsimprove ✢ andmay normalise after eradication therapyinpatientswith ✢ idiopathic thrombocytopenic purpura ✢ Themechanism for this isunclear
  39. 39. Use of Tests to Assess Treatment Success Theureabreathtest,thestoolantigentest,andbiopsy-basedtestscanall be usedto assessthe successof treatment However,becausethesetestsare dependent on H. pylori load, their use<4 weeksaftertreatment mayyield falsenegativeresults. Furthermore, thesetests are unreliable if performed within 4 weeksof intercurrenttreatment with antibiotics orbismuth compounds or within 2 weeksof the discontinuation ofproton pump inhibitor (PPI)treatment. Inthe assessmentoftreatment success, Noninvasivetestsarenormallypreferred;
  40. 40. •However, after gastric ulceration,endoscopy should be repeated to ensure healing and to exclude gastric carcinoma by further histologic sampling. •Serologic tests are not used to monitor treatment success, as the gradual drop in titer of H. pylori specific antibodies is too slow to be of practical use.
  41. 41. Common causes of Dyspepsia
  42. 42. Causesof dyspepsia Upper gastrointestinaldisorders • Pepticulcer disease • Acute gastritis • Gallstones • Oesophagealspasm • Non-ulcer dyspepsia • Irritablebowelsyndrome Othergastrointestinaldisorders • Pancreaticdisease(cancer, chronic pancreatitis) • Coloniccarcinoma • Hepaticdisease(hepatitis, metastases) Systemicdisease • Renalfailure • Hypercalcaemia Drugs • NSAIDs • Corticosteroids • Ironandpotassiumsupplements • Digoxin Others • Psychological(anxiety,depression) • Alcohol
  43. 43. Gastricandduodenalulcer ✢ Theprevalence of peptic ulcer (0.1–0.2%) ✢ The male-to female ratio for DU varies from 5 : 1 to 2 : 1, GU is2 : 1 or less. ✢ Chronic GU is usually single; 90% are situated on the lesser curve within the antrum or at the junction between body andantral mucosa. ✢ Chronic DU usually occurs in the first part of the duodenum and50% areon the anterior wall.
  44. 44. Pathophysiology ✢ H.pylori ✢ NSAIDs: Treatment with NSAIDs is associated with peptic ulcers due to impairment of mucosal defences ✢ Smoking: Smoking confers an increased risk of gastric ulcer and, to alesserextent, duodenal ulcer.
  45. 45. NSAIDs
  46. 46. Risk factors forNSAID-inducedulcers • Age>60yrs • Past historyof peptic ulcer • Past historyof adverse eventwith NSAID • Concomitant corticosteroid use • High-dose or multiple NSAID • High-riskNSAID(Indometacin, Ketoprofen, Piroxicam, Azapropazone)
  47. 47. Commonly usedNSAIDsandtheir relative riskofgastrointestinal bleedingand perforation Verylow risk Celecoxib, Etoricoxib Low risk Ibuprofen,Etodolac, Meloxicam, Nabumetone Medium risk Ibuprofen,Naproxen, Diclofenac Highrisk Indometacin, Ketoprofen Highest risk Piroxicam, Azapropazone
  48. 48. Functionaldyspepsia ✢ This is defined as chronic dyspepsia in the absence of organic disease. ✢ Other commonly reported symptoms include early satiety, fullness, bloating and nausea. ✢ ‘Ulcer-like’ and ‘dysmotility-type’ subgroups are often reported, but there is overlap between these and with irritable bowel syndrome. ✢ The cause is poorly understood but probably covers a spectrum of mucosal, motility and psychiatric disorders.
  49. 49. clinicalfeatures ✢ Pt. are usually young (< 40 years) and women are affected as twice as men. ✢ Abdominal discomfort is associated with other ‘dyspeptic’ symptoms (nausea,early satiety and bloating after meals). ✢ Morning symptoms arecharacteristic andpain or nauseamay occur on waking. ✢ Directenquiry may elicit symptoms suggestiveof IBS. ✢ Peptic ulcer disease must be considered, whilst in older subjects intra-abdominal malignancyisa prime concern.
  50. 50. clinicalfeatures ✢ There are no diagnostic signs, apart perhaps from inappropriate tendernesson abdominal palpation. ✢ Symptoms may appear disproportionate to clinical well- being andthere is no weight loss. ✢ Patients often appear anxious. ✢ A drug history should be taken and the possibility of a depressive illnessshould be considered. ✢ Pregnancy should be ruled out in young women before radiological studies areundertaken. ✢ Alcohol misuse should be suspected when early morning nauseaand retching areprominent
  51. 51. investigation ✢ All patients should be checked for H. pylori infection. ✢ patients over the age of 55 years should undergo endoscopy to exclude mucosal disease.
  52. 52. Mangment ✢ The most important elements are explanation and reassurance, Possible psychological factors should be explored. ✢ restrictive diets are of little benefit, but smaller portions And fat restriction may help. ✢ Up to 10%of patients benefitfrom H. pylori eradication ✢ therapy also removes a major risk factor for gastric cancer ✢ but at the cost of a small risk of side effects and worsening symptoms of underlying gastrooesophageal reflux diseases
  53. 53. Mangment ✢ Antacids, suchas hydrotalcite, are sometimes helpful. ✢ Prokinetic drugs, such as metoclopramide (10 mg 3 times daily) or domperidone (10–20 mg 3 times daily), may be given before meals if nausea, vomiting or bloating isprominent. ✢ H2-receptor antagonist drugs may be tried if night painor heartburn is troublesome. ✢ Low-dose tricyclic agents, such as amitriptyline, are of value inup to two-thirds. ✢ Some patients need behavioural or other formal psychotherapy
  54. 54. Gastricca.
  55. 55. Clinicalfeatures ✢ Asymptomatic ✢ Two-thirds of patients with advanced cancers have weightloss. ✢ 50% have ulcer-likepain. ✢ Anorexia and nauseaoccur inone-third. ✢ Early satiety, haematemesis, melaena and dyspepsia aloneare less common ✢ Dysphagia ✢ Anaemia
  56. 56. Clinicalfeatures ✢ Weight loss ✢ Anaemia ✢ Palpable epigastric mass ✢ Jaundice or ascites ✢ tumour spread occurs to the supraclavicular lymph nodes (Troisier’s sign), umbilicus (Sister Joseph’s nodule) or ovaries (Krukenbergtumour). ✢ Paraneoplastic phenomena, such as acanthosis nigricans, thrombophlebitis (Trousseau’s sign) and dermatomyositis, occur rarely
  57. 57. Endoscopicimage ofasmallsuperficialpre-pyloriccancer
  58. 58. Appearance afterendoscopic mucosalresection(EMR)
  59. 59. Irritablebowelsyndrome ✢ Is characterised by recurrent abdominal pain in association with abnormal defecation in the absenceof astructural abnormality of the gut. ✢ About 10–15% of the population are affected at some time but only 10% of these consult their doctors because of symptoms. ✢ Young women are affected 2–3 times more often than men. ✢ Coexisting conditions, such as non-ulcer dyspepsia, chronic fatigue syndrome, dysmenorrhoea and fibromyalgia, arecommon.
  60. 60. Pathophysiology ✢ The cause of IBS is incompletely understood but biopsychosocial factors are thought to play an important role, along with luminal factors, such as diet andthe gutmicrobiota. ✢ Behavioural and psychosocial factors About 50% of patients referred to hospital have a psychiatric illness, such as anxiety,depression, somatisation andneurosis. ✢ Acute psychological stress and overt psychiatric disease are known to alter visceral perception and gastrointestinal motility. ✢ These factors contribute to but do not causeIBS.
  61. 61. Clinical feature ✢ The most common presentationisthat:  Recurrent abdominal discomfort , colicky or cramping in nature,felt in the lower abdomen relieved by defecation.  Abdominal bloating worsens throughout theday ✢ The cause is unknown but it is not due to excessive intestinal gas. ✢ Most patients alternate between episodes of diarrhoea and constipation, but it is useful to classify patients as having predominantly constipation or predominantly
  62. 62. Clinical feature ✢ Those with constipation tend to pass infrequent pellety stools, usually in association with abdominal painor proctalgia. ✢ Those with diarrhoea have frequent defecation but produce low-volume stools and rarely have nocturnal symptoms . ✢ Passage of mucus is common but rectal bleeding does not occur. ✢ Patients do not lose weight and are constitutionally well.
  63. 63. Diagnosis ✢ The diagnosis isclinical innature. ✢ Full blood count and faecal calprotectin, with or without sigmoidoscopy,are usually done and are normal in IBS. ✢ Colonoscopy should be undertaken in;  (over 40 yearsof age)to exclude colorectal cancer.  report rectal bleeding to exclude colon cancer and IBD.
  64. 64. Diagnosis Those who present atypically require investigations to exclude other gastrointestinal diseases. Diarrhoea predominant patientsjustify investigations to exclude: ✢ coeliac disease ✢ microscopic colitis ✢ lactose intolerance , ✢ bile acid malabsorption, ✢ thyrotoxicosis, ✢ parasitic infection.
  65. 65. Rome IIIcriteria for diagnosis of irritable bowel syndrome Recurrent abdominal pain ordiscomfort at least3days/mth inthe last 3months, associated withtwo ormore of the following: • Improvement withdefecation • Onsetassociated witha changeinfrequencyofdefecation • Onsetassociated witha changeinform (appearance)ofstool
  66. 66. Features supportingadiagnosis ofIBS • Symptoms >6mths • Frequent consultationsfor non-gastrointestinal problems • Previous medically unexplainedsymptoms • Stress worsenssymptoms Alarm features • Age>50 yrs;male gender • Weightloss • Nocturnalsymptoms • Family history of colon cancer • Anaemia • Rectal bleeding
  67. 67. Chronicpancreatitis ✢ 80% of casesin Westfrom alcohol misuse. ✢ severe chronic calcific pancreatitis occurs in non- alcoholics, possibly as a result of malnutrition and cassava consumption.
  68. 68. Chronicpancreatitis ✢ Abdominal pain, in 50%, this occurs as episodes of ‘acute pancreatitis’. ✢ Slowly progressive chronic pain without acute exacerbations affects 35% of patients, whilst the remainder have nopainbut presentwith diarrhoea. ✢ Pain may be relieved by leaning forwards or by drinkingalcohol. ✢ Steatorrhoea :> 90% of theexocrinetissue isdestroyed ✢ 30% of patients are diabetic, 70% in those with chronic calcific pancreatitis. ✢ erythema ab igne
  69. 69. Pancreaticcarcinoma ✢ 90% areadenocarcinomas from the ducts. ✢ Manypt. areasympt. until an advanced stage. ✢ They present with central abdominal pain, weight loss and obstructive jaundice ✢ The pain results from invasion of the coeliac plexus and is characteristically incessantandgnawing. ✢ It often radiates from the upper abdomen through to the back and may be eased a little by bending forwards.
  70. 70. Pancreaticcarcinoma ✢ Almost all patientslose weightand manyare cachectic. ✢ 60% of tumours in head of the pancreas, and involvement of the CBD resultsin obstructive jaundice, with severe pruritus. ✢ A few patients present with diarrhoea, vomiting from duodenal obstruction, diabetes mellitus, recurrent venous thrombosis, acute pancreatitis or depression. ✢ Weight loss, An abdominal mass, a palpable gallbladder or hepatic metastasis, A palpable gallbladder in a jaundiced patient is usually the consequence of distal biliary obstruction by a pancreatic cancer (Courvoisier’s sign).
  71. 71. Viralhepatitis ✢ Headache, myalgia, arthralgia, nausea and anorexia usually precedes the development of jaundiceby a fewdays to 2 weeks. ✢ Vomiting and diarrhoea may follow, and abdominal discomfort is common. ✢ Darkurineandpale stools may precede jaundice. ✢ Theliver isoften tender but only minimally enlarged. ✢ Occasionally, mild splenomegaly and cervical lymphadenopathy areseen.
  72. 72. Gallstones ✢ Only 10% of individualswithgallstonesdevelop clinical evidence of gallstonedisease. ✢ Symptomatic stones within the gallbladder manifest as either biliary pain (‘biliary colic’) or cholecystitis. ✢ The term ‘biliary colic’ is a misnomer because the pain does not rhythmically increase and decrease in intensitylikeother forms of colic. ✢ Combinations of fatty food intolerance, dyspepsia and flatulence‘gallstonedyspepsia’.
  73. 73. ✢ Pain is usually felt in the epigastrium (70% of patients) or rightupper quadrant (20%). ✢ Radiates to the interscapular region or the tip of the right scapula,the left upper quadrant and the lower chest. ✢ It occurs suddenly and persists for about 2 hours.
  74. 74. Colorectalcancer ✢ Left colon: freshrectal bleeding iscommon with earlyobstruction. ✢ Right colon: anaemia from occult bleeding or with altered bowel habit, but obstruction is a late feature. ✢ Colicky lower abdominal pain is present in twothirds of patients andrectal bleeding occurs in50%. ✢ Some present with either obstruction or perforation, leading to peritonitis, localised abscess or fistula formation. ✢ Ca. of the rectum usually causes early bleeding, mucus discharge or afeelingof incomplete emptying.
  75. 75. Thank you
  76. 76. Thanks for attending and listening What do you think about the first part? WhatdidyoulearnorifyouhaveAnynote,adviseorquestion? What do you think about the second part? Whatdidyoulearnorifyouhaveanynote,adviseorquestion? What do you think about the third part? Whatdidyoulearnorifyouhaveanynote,adviseorquestion? What do you think about the fourth part? Whatdidyoulearnorifyouhaveanynote,adviseorquestion? ?

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