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Ulcerative intestine

This document discusses ulcerative lesions of the intestines, including peptic ulcer disease, infectious causes like typhoid and tuberculosis, and inflammatory bowel disease like ulcerative colitis and Crohn's disease. It provides details on the definition, sites, epidemiology, etiology, pathogenesis, clinical features, investigations, management and complications of these conditions. Peptic ulcer disease is most commonly caused by H. pylori infection or NSAID use. Typhoid causes circumscribed ulcers in the ileum due to Salmonella typhi infection. Tuberculosis can cause ulcers in the ileocecal region. Ulcerative colitis causes continuous ulcers in the colon, while Crohn's disease causes transm

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ULCERATIVE LESIONS OF INTESTINES Dr.Saurav singh Guide:Dr.PM Pagaro
Overview    Peptic Ulcer Disease Infectious Causes (Typhoid, T.B, Amoebic ulcers) Inflammatory bowel disease (Ulcerative colitis & Crohns disease)
PEPTIC ULCER DISEASE   DEFINITION A circumscribed ulceration of the gastrointestinal mucosa occurring in areas exposed to acid and pepsin. Sites:      Duodenum Stomach Oesophagus Gastro-enterostomy stoma Related to ectopic gastric mucosa (e.g. in Meckel’s diverticulum)
Epidemiology of PUD        Prevalence about 5-10% Higher prevalence in low socioeconomic classes and with certain diseases Duodenal ulcer M/F: 3:1 Gastric ulcer equal in both sexes but increases with age Family history: 3-4 increased risk . Cigarette smoking: ulceration increased Emotional disturbances and Stress: increase gastric acid secretion
Etiopathogenesis   • • • • • •   H. Pylori: 70% of all cases. Other causes include NSAIDS Alcohol Gastritis Socioeconomic status Genetic factors Stress –shock, sepsis or severe trauma Burns(curling ulcer) Head trauma (cushing ulcer)
Helicobacter factors in pathogenesis   Some strains are more pathogenic than others. The Cag A (cytotoxic) antigen is one important virulence factor Human variability also plays a part (e.g. individuals who produce high levels of IL-1 in inflammation get pan gastritis and Gastric ulcer, lower levels associated with antral gastritis and Duodenal ulcer)
Duodenal Ulcers         duodenal sites are 4x as common as gastric sites most common in middle age  peak 30-50 years Male to female ratio—4:1 Genetic link: 3x more common in 1st degree relatives more common in patients with blood group O associated with increased serum pepsinogen H. pylori infection common  up to 95% smoking is twice as common
Gastric Ulcers       common in late middle age  incidence increases with age Male to female ratio—2:1 More common in patients with blood group A Use of NSAIDs - associated with a three- to four-fold increase in risk of gastric ulcer Less related to H. pylori than duodenal ulcers – about 80% 10 - 20% of patients with a gastric ulcer have a concomitant duodenal ulcer
 Symptoms of duodenal ulcer disease:  epigastric pain 2 hours after meal or on a empty stomach or during night  pyrosis  good nutrition  obstipation  seasonal dependence (spring, autumn)
 Symptoms of gastric ulcer disease:  epigastric pain after meal or during meal  upper dyspeptic syndrome – loss of appetite, nauzea, vomiting, flatulence  vomitting brings relief  reduced nutrition  loss of weight
 Complications:  Bleeding  Perforation  Penetration  Stenosis
Diagnosis  Stool for fecal occult blood  Labs: CBC , liver function test, amylase and lipase.  Upper GI Endoscopy: Any pt >50 yrs with new onset of symptoms or those with alarm markings including anemia, weight loss, or GI bleeding.
Helicobacter pylori detection  Invasive( through endoscopy)      Gastric biopsy and staining culture of Bx specimen Tests using urease enzyme in Bx specimens Bacterial DNA detection by PCR Non-invasive:     Urea breath test H.pylori antibodies Stool antigen Salivary antigen
Staining methods of Helicobacter pylori    Warthin–Starry stain- The Warthin Starry stain (WS) is a silver nitrate based staining method Leung stain- It is a novel Alcian yellow-toluidine blue (Leung) stain for H.pylori. Methylene blue
Biopsy of peptic ulcer:     Biopsy is necessary to distinguish between benign and malignant ulcers. Biopsy should be taken from the ulcer edge, at least from each quadrant. Upto 10-12 biopsies may be taken to exclude cancer. Repeat endoscopy may be necessary if biopsies are negative and there is high index of suspicion.
Morphology of peptic ulcers    Clean, non-elevated edge Granulation tissue base (floor) Underlying fibrosis
Chronic Gastric Ulcer
Duodenal ulcer
 1. 2. 3. 4. Four histological zones are present in a peptic ulcer. Necrotic zone Nonspecific acute inflammation Granulation tissue Fibrosis
Microscopic features Thickening of vessels caused by subendothelial fibrous proliferation.  Hypertrophy of nerve bundles.  Mucosa surrounding the ulcer is pyloric type.  Necrotic surface shows superimposed infection by candida albicans.  In case of H. pylori infection following features are noted at the ulcer edge : loss of apical portion of cells, dropout of epithelial cells, erosion, cellular tufts. 
Healing process     Regenerating epithelium grows over the surface. Intestinal metaplasia May contain chief and parietal cells (ulcer in the fundus area) Gastritis remains after ulcer has healed. Cellular atypia may be present.
Morpholog y of duoden al ulcer
Differential Diagnosis          Neoplasm of the stomach Pancreatitis Pancreatic cancer Diverticulitis Nonulcer dyspepsia (also called functional dyspepsia) Cholecystitis Gastritis GERD MI—not to be missed if having chest pain
Natural history of PUD     PUD is a chronic episodic disease with relapses and remissions. If left untreated, 30-40 % of ulcers heal within 8 weeks. Recurrence rate without treatment is 70% during first year and 90% within 2 years. Complications develop in 20% of PUD
Infectious causes 1. TYPHOID  Acute enteric infectious disease  caused by Salmonella typhi (S.Typhi).  Clinical features : prolonged fever, Relative bradycardia, apathetic facial expressions, roseola, splenomegaly, hepatomegaly, leukopenia.  Can lead to intestinal perforation, intestinal hemorrhage
S.Typhi. 2nd bacteremia liver、spleen、gall、 BM ,ect early stage (1-3W） stomach (mono Bac. In gall nuclea r phago cytes ) Bac. In feces Lower ileum S.Typhi eliminated convalvescence stage (4-5w) peyer's patches & mesenteric lymph nodes LN Proliferate,swell necrosis defervescence stage Enterorrhagia,i ntestinal perforation （3-4w） thoracic duct 1st bacteremia (Incubation stage) 10-14d
 Pathogenesis  The amount of bacilli infection (>105bacteria)  Bacteria ingested orally  Stomach barrier (some Eliminated)  Enters the small intestine  Penetrate the mucus layer  Enter mononuclear phagocytes of ileal peyer's patches and mesenteric lymph nodes  Proliferate in mononuclear phagocytes spread to blood causing primary bacteremia (Incubation period).
 enter spleen, liver and bone marrow (reticulo-endothelial system) further proliferation occurs  A lot of bacteria enter blood again causing secondary bacteremia.  Recovery
PATHOLOGY Proliferation of RES (reticuloendothelial system )  Specific changes in lymphoid tissues and mesenteric lymph nodes."typhoid nodules―  Most characteristic lesion: Ulceration of mucosa in the region of the Peyer’s patches of the small intestine 
Peyers patches
Major findings in lower ileum  Hyperplasia stage(1st week): swelling lymphoid tissue and proliferation of macrophages.  Necrosis stage(2nd week): necrosis of swelling lymph nodes or solitary follicles.  Ulceration stage(3rd week): Oval ulcer with its long axis parallel to the small intestine , this results from sloughing and shedding of necrotic lymphoid tissue in the peyers patches leading to intestinal hemorrhage, perforation .  Stage of healing (from 4th week): healing of ulcer, no cicatrices and no contraction
2. Gastrointestinal Tuberculosis    • • • Abdominal tuberculosis is usually secondary to pulmonary tuberculosis Sites: The ileocecal region is the most common area of involvement in the gastrointestinal tract due to the abundance of lymphoid tissue. The natural course of gastrointestinal tuberculosis may be Ulcerative hypertrophic or ulcer hypertrophic.
Clinical presentation Abdominal pain mimicking peptic ulcer disease with stomach or duodenal infection;  Malabsorption with infection of the small intestine; Pain, diarrhea, or hematochezia with infection of the colon.
Investigations       Blood routine Urine routine - to detect diabetes mellitus Plain X-ray of the abdomen Laparoscopy Laparoscopic biopsy of tubercles found in the peritoneum or other parts Barium studies
Intestinal tuberculosis.
 3. AMOEBIC ULCER  The causative organism is parasitic protozoan, called Entamoeba histolytica.  Site: It usually involves caecum and ascending colon followed by sigmoid colon, rectum, and appendix. In severe cases the entire colon is involved.  The spectrum of colitis in amoebiasis ranges from mucosal thickening, to multiple cyst formation, to diffuse Inflammation / oedema, to necrosis and perforation of colonic wall.
Life cycle Mouth - Cyst ingested Excyst to trophozoite Passed in stool Amoebic disease Cyst Trophozoite Invades gut mucosa – cyst formation
Clinical presentation • • • • • • Gradual onset of bloody diarrhoea Abdominal pain and tenderness. Leucocytes and pus may be present in stool. Fever present in <40% of patients. Weight loss and anorexia can be present. Local inflammatory masses, amoebomas, may cause obstructive symptoms
    Gross features: Begin as small foci of necrosis that progress to ulcers. In the early stages the colonic ulcers have a narrow neck and thus appear as small nodules As the ulcers enlarge they always retain their undermined base but the ulcerated area of the mucosa becomes larger. The base of the ulcer is covered by grey - white exudate. There is always undenuded mucosa between the ulcers.
 Microscopic features:  The ulcer is typically 'flask- shaped' and the broad base is composed of fibrin and cellular debris. A sharp line divides the necrotic and viable mucosa Trophozoites are found on the surface of the ulcers, in the exudate and in the crater. They are frequently found in the submucosa, muscularis propria, serosa.   
― IBD is a set of chronic inflammatory conditions resulting from inappropriate and persistent activation of the mucosal immune system ,driven by the presence of normal intestinal flora.‖
HISTORY ULCERATIVE COLITIS • First officially described by Wilks and Moxon in 1875. • Before this discovery , all the diarrheal diseases were believed to be caused by infectious agents and bacteria.
Crohn’s disease • In 1913 Dr Dalziel described transmural intestinal inflammation in 13 autopsied patients. • In 1930 Burril Crohn described TERMINAL ILEITIS first .
Epidemiology of IBD Ulcerative colitis Crohn’s disease Incidence (US) 11/100 000 7/100 000 Age of onset 15-30 & 60-80 15-30 & 60-80 Male:female ratio Smoking 1:1 May prevent disease 1.1-1.8:1 May cause disease Oral contraceptive No increased risk Relative risk Appendectomy Not protective Monozygotic twins 8% concordance Protective 67% concordance
PATHOGENESIS I. GENETIC PREDISPOSITION. II. INFECTIOUS CAUSES. III. ABNORMAL HOST IMMUNOREACTIVITY.
GENETIC • Genome wide scanning with microsatellite DNA markers has identified several genetic sites as being potentially associated with UC or CD. • Significant linkages have been reported on chromosomes 1, 3, 6, 7, 12, 14, 16, and 19. • One of the clearest linkages is for IBD-1, a susceptibility locus in the pericentromeric region of chromosome 16.
• Detailed analysis has resulted in the identification of the nucleotide-binding oligomerization domain 2 (NOD2) gene and protein. • NOD2 is also known as caspase activation and recruitment domain 15 (CARD15). • This is a polymorphic gene, the product of which is involved in the innate immune system.
NOD2 PROTEIN EXPRESSED IN macrophages / monocytes FUNCTION AS AN INTRACELLULAR RECEPTOR MICROBES TRIGGER NF- kB pathway NOD2 gene mutation CYTOKINES AND OTHER PROTEINS INNATE IMMUNE DEFENSE MECHANISM DOWN REGULATION OF INNATE IMMUNITY LEADS TO INFLAMMATORY BOWEL
Abnormal host immunoreactivity  IBD is characterized by immunoregulatory defects in the mucosa, which appear to be associated with microbial exposure.  A number of theories have been advanced concerning the pathogenesis of this process: - dysfunctional immune host response to normal luminal component - infection with a specific pathogen - defective mucosal barrier to luminal antigens.
• • It is hypothesized that exposure to commensal bacteria down-regulates the inflammatory genes and blocks activation of the NF-kB pathway, thus inhibiting the inflammatory immune response of the gut to the microbes and food antigens to which it is constantly exposed.
     . Implicated pathogens include Mycobacterium paratuberculosis Paramyxovirus Listeria monocytogenes Helicobacter hepaticus.
 Defective barrier function IBD is associated with increased permeability of the epithelial lining of the gut resulting in continuous stimulation of the mucosal immune system. Luminal bacteria appear to intensify the permeability defect further, establishing a self-sustaining cycle of mucosal inflammation that allows for uptake and translocation of bacteria.
Ulcerative colitis  Is an inflammatory disease involving only the large intestine. The inner lining or mucosa of the intestine becomes inflamed and develops ulcers. Always starts in rectum and is continuous until some proximal part of the colon. Involves the mucosa and submucosa
sites     40-50% of patients have disease limited to the rectum and rectosigmoid 30-40% of patients have disease extending beyond the sigmoid 20% of patients have a total colitis Proximal spread occurs in continuity without areas of uninvolved mucosa
Ulcerative colitis – clinical presentation The major symptoms of UC are: - diarrhea - rectal bleeding - tenesmus - passage of mucus - crampy abdominal pain 
Ulcerative colitis – macroscopic features Mucosa is : - erythematous, has a granular surface that looks like a sand paper  In more severe diseases: - hemorrhagic, edematous and ulcerated   In fulminant disease a toxic colitis or a toxic megacolon may develop ( wall become very thin and mucosa is severly ulcerated)
Acute form with marked hyperemia
Ulcerative colitis – microscopic features Process is limited to the mucosa and submucosa with deeper layer unaffected  Two major histologic features: - the crypt architecture of the colon is distorted - some patients have basal plasma cells and multiple basal lymphoid aggregates 
Broad based ulceration of the mucosa in distal colon or throughout its length
Pseudopolyps in Ulcerative colitis
Ulcerative colitis featuring crypt abscesses
Chronic ulcerative colitis in remission
Ulcerativ e colitis in an active phase.
Ulcerative colitis - complications     Hemorrhage Perforation Stricture Toxic megacolon (transverse colon with a diameter of more than 5 to 6 cm with loss of haustration)
Toxic Megacolon
Crohn’s disease (CD)     Also referred to as granulomatous or regional enteritis, granulomatous ileitis, ileocolitis Can have non-continuous pattern-‖skip lesions‖, with areas of severe inflammation with intervening normal mucosa Most frequently affects distal third of small intestine and the colon Affects all layers of the affected bowel
sites  Can affect any part of GI tract from the mouth to the anus  30-40% of patients have small bowel disease alone  40-55% of patients have both small and large intestines disease  15-25% of patients have colitis alone  In 75% of patients with small intestinal disease the terminal ileum in involved in 90%
Crohn’s disease – sign and symptoms Ileocolitis - right lower quadrant pain and diarhhea - palpable mass, fever and leucocytosis - pain is colickly and relieved by defecation  Jejunoileitis - inflammatory disease is associated with loss of digestive and absorptive surface 
Crohn’s disease – sign and symptoms Colitis and perianal disease - low grade fever, malaise, diarrhea, crampy abdominal pain, sometimes hematochezia - pain is caused by passage of fecal material through narrowed and inflamed segments of large bowel  Gastroduodenal disease - nausea, vomiting, epigastric pain - second portion of duodenum is more commonly involved than the bulb 
Crohn’s disease – macroscopic features  CD is a transmural process  CD is segmental with skip areas in the midst of diseased intestine  In one –third of patients with CD perirectal fistulas, fissures, abscesses, anal stenosis are present
Skip lesion of crohns disease
Crohn’s disease – macroscopic features  mild disease is characterized by: aphtous or small superficial ulcerations  In more active disease: stellate ulcerations fuse longitudinally and transversely to demarcate island of mucosa that are histologically normal  Cobblestone appearance is characteristic of CD
SEGMENTAL INVOLVEMENT WITH TRANSMURAL SPREAD
TYPICAL COBBLESTONE APPEARANCE
M/E : Mucosal inflammation    Mucosa normal and retain mucus. Well-defined focus of inflammatory cells surrounded by non inflammed and normal mucosa As the disease establish , neutrophils infiltrate isolated crypts – abscess – ultimate destruction.
Crohn colitis
Chronic mucosal damage:     Architectural distortion manifested as villous blunting. Crypts exhibit irregularities and branching. Crypt destruction leads to atrophy Gastric antral type or paneth cell metaplasia occur
The branched crypt
A - Mucosal Granuloma eroding a crypt of lieberkhun and initiating crypt abscess formation. B - Crypt obliterated by Granuloma formation
• Non Caseating Granuloma-in ½ cases , Sarcoid Granuloma in all tissue layers. Others: • In diseased segments muscularis mucosa exhibits reduplication , strictures. thickening, irregularity's leads to like,
Crohn disease of the colon.
Submucosal nonnecrotizi ng granulomas
Complications of Crohn's Disease:  Perianal fistulas  Perianal skin ulceration  Increased incidence of gall and kidney stones (due to malabsorption of fats and bile salts)
Extraintestinal manifestations of IBD       Iritis Episcleritis Arthritis Skin involvement Pericholangitis Sclerosing cholangitis
Risk of Malignancy in IBD   In Crohn’s disease, increased risk of cancer of the affected areas is seen In ulcerative colitis, 8-10 years after initial diagnosis, there is a steady, significant increased risk of developing cancer  Prognostic factors increasing malignancy risk in UC: • Duration of disease 10 yrs or more • Pancolonic involvement • Continuous progressive disease • Severe initial onset • Associated liver disease
Gross :  Thick mucosa with finely nodular or velvety surface configuration.  Lesion polypoid , elevated , nodular or villous formation.
M/E :  Adenocarcinoma with varying degree of differentiation .  Always accompanied by dysplastic changes .
Evaluation of Dysplasia  1 - Negative for Dysplasia.  2 - Indefinite for Dysplasia,probably Negative.  3 - Indefinite for Dysplasia, Unknown.  4 - Indefinite for Dysplasia,probably Positive.  5 - Positive for Dysplasia,Low Grade.  6 - Positive for Dysplasia,High Grade.
Lab Findings in IBD     CBC’s:  Anemia is common due to blood loss or malabsorption  Leukocytosis & thrombocytosis also common ESR typically elevated; monitors disease activity Abnormal LFTs may represent pericholangitis or sclerosing cholangitis Low serum albumin (protein-losing enteropathy) suggests extensive colitis
Features UC CD Rectal Bleeding Common Inconspicuous  Abdominal mass Practically never 10-15% Abdominal pain Left sided Right sided Sigmoidoscopy Abnormal 95% Abnormal <50% Free perforation 12% 04% Colon CA 2% Rare Anal complications Minor 75%, fissures, fistulas, ulceration Response to steroid 75% 25% Result of surgery Good Fair Clinical
Features UC CD Sparing of rectum Exceptional 90% Involvement of ileum Rare Common Strictures Absent Present Skip areas Absent Common Internal fistula Absent May be present Longitudinal and transverse ulcers Exceptional Common Fissuring Absent Common Radiographic
Features UC CD Distribution of involvement Diffuse Focal Mucosal atrophy Marked Minimal Cytoplasmic Mucin Diminished Preserved Lymphoid aggregates Rare Common Edema Minimal Marked Hyperemia May be extreme Minimal Granulomas Absent Present in 60% Fissuring Absent Present Crypt abscesses Common Rare Rectal involvement Practically always 50% Morphologic
REFERENCES  Robbins and Cotran.  Surgical Pathology – Rosai and Ackerman’s.  Sternburg.  Harrison’s Textbook of Internal Medicine.  Internet
Ulcerative intestine

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Ulcerative intestine

  • 1.
  • 2.
    Overview    Peptic Ulcer Disease InfectiousCauses (Typhoid, T.B, Amoebic ulcers) Inflammatory bowel disease (Ulcerative colitis & Crohns disease)
  • 3.
    PEPTIC ULCER DISEASE   DEFINITION Acircumscribed ulceration of the gastrointestinal mucosa occurring in areas exposed to acid and pepsin. Sites:      Duodenum Stomach Oesophagus Gastro-enterostomy stoma Related to ectopic gastric mucosa (e.g. in Meckel’s diverticulum)
  • 5.
    Epidemiology of PUD        Prevalenceabout 5-10% Higher prevalence in low socioeconomic classes and with certain diseases Duodenal ulcer M/F: 3:1 Gastric ulcer equal in both sexes but increases with age Family history: 3-4 increased risk . Cigarette smoking: ulceration increased Emotional disturbances and Stress: increase gastric acid secretion
  • 6.
    Etiopathogenesis   • • • • • •   H. Pylori: 70%of all cases. Other causes include NSAIDS Alcohol Gastritis Socioeconomic status Genetic factors Stress –shock, sepsis or severe trauma Burns(curling ulcer) Head trauma (cushing ulcer)
  • 8.
    Helicobacter factors in pathogenesis   Somestrains are more pathogenic than others. The Cag A (cytotoxic) antigen is one important virulence factor Human variability also plays a part (e.g. individuals who produce high levels of IL-1 in inflammation get pan gastritis and Gastric ulcer, lower levels associated with antral gastritis and Duodenal ulcer)
  • 9.
    Duodenal Ulcers         duodenal sitesare 4x as common as gastric sites most common in middle age  peak 30-50 years Male to female ratio—4:1 Genetic link: 3x more common in 1st degree relatives more common in patients with blood group O associated with increased serum pepsinogen H. pylori infection common  up to 95% smoking is twice as common
  • 10.
    Gastric Ulcers       common inlate middle age  incidence increases with age Male to female ratio—2:1 More common in patients with blood group A Use of NSAIDs - associated with a three- to four-fold increase in risk of gastric ulcer Less related to H. pylori than duodenal ulcers – about 80% 10 - 20% of patients with a gastric ulcer have a concomitant duodenal ulcer
  • 11.
     Symptoms of duodenalulcer disease:  epigastric pain 2 hours after meal or on a empty stomach or during night  pyrosis  good nutrition  obstipation  seasonal dependence (spring, autumn)
  • 12.
     Symptoms of gastriculcer disease:  epigastric pain after meal or during meal  upper dyspeptic syndrome – loss of appetite, nauzea, vomiting, flatulence  vomitting brings relief  reduced nutrition  loss of weight
  • 13.
  • 14.
    Diagnosis  Stool for fecaloccult blood  Labs: CBC , liver function test, amylase and lipase.  Upper GI Endoscopy: Any pt >50 yrs with new onset of symptoms or those with alarm markings including anemia, weight loss, or GI bleeding.
  • 15.
    Helicobacter pylori detection  Invasive(through endoscopy)      Gastric biopsy and staining culture of Bx specimen Tests using urease enzyme in Bx specimens Bacterial DNA detection by PCR Non-invasive:     Urea breath test H.pylori antibodies Stool antigen Salivary antigen
  • 16.
    Staining methods ofHelicobacter pylori    Warthin–Starry stain- The Warthin Starry stain (WS) is a silver nitrate based staining method Leung stain- It is a novel Alcian yellow-toluidine blue (Leung) stain for H.pylori. Methylene blue
  • 19.
    Biopsy of pepticulcer:     Biopsy is necessary to distinguish between benign and malignant ulcers. Biopsy should be taken from the ulcer edge, at least from each quadrant. Upto 10-12 biopsies may be taken to exclude cancer. Repeat endoscopy may be necessary if biopsies are negative and there is high index of suspicion.
  • 20.
    Morphology of pepticulcers    Clean, non-elevated edge Granulation tissue base (floor) Underlying fibrosis
  • 21.
  • 22.
  • 23.
     1. 2. 3. 4. Four histological zones arepresent in a peptic ulcer. Necrotic zone Nonspecific acute inflammation Granulation tissue Fibrosis
  • 24.
    Microscopic features Thickening ofvessels caused by subendothelial fibrous proliferation.  Hypertrophy of nerve bundles.  Mucosa surrounding the ulcer is pyloric type.  Necrotic surface shows superimposed infection by candida albicans.  In case of H. pylori infection following features are noted at the ulcer edge : loss of apical portion of cells, dropout of epithelial cells, erosion, cellular tufts. 
  • 25.
    Healing process     Regenerating epitheliumgrows over the surface. Intestinal metaplasia May contain chief and parietal cells (ulcer in the fundus area) Gastritis remains after ulcer has healed. Cellular atypia may be present.
  • 26.
  • 27.
    Differential Diagnosis          Neoplasm ofthe stomach Pancreatitis Pancreatic cancer Diverticulitis Nonulcer dyspepsia (also called functional dyspepsia) Cholecystitis Gastritis GERD MI—not to be missed if having chest pain
  • 28.
    Natural history ofPUD     PUD is a chronic episodic disease with relapses and remissions. If left untreated, 30-40 % of ulcers heal within 8 weeks. Recurrence rate without treatment is 70% during first year and 90% within 2 years. Complications develop in 20% of PUD
  • 29.
    Infectious causes 1. TYPHOID  Acuteenteric infectious disease  caused by Salmonella typhi (S.Typhi).  Clinical features : prolonged fever, Relative bradycardia, apathetic facial expressions, roseola, splenomegaly, hepatomegaly, leukopenia.  Can lead to intestinal perforation, intestinal hemorrhage
  • 30.
    S.Typhi. 2nd bacteremia liver、spleen、gall、 BM ,ect earlystage (1-3W） stomach (mono Bac. In gall nuclea r phago cytes ) Bac. In feces Lower ileum S.Typhi eliminated convalvescence stage (4-5w) peyer's patches & mesenteric lymph nodes LN Proliferate,swell necrosis defervescence stage Enterorrhagia,i ntestinal perforation （3-4w） thoracic duct 1st bacteremia (Incubation stage) 10-14d
  • 31.
     Pathogenesis  The amount ofbacilli infection (>105bacteria)  Bacteria ingested orally  Stomach barrier (some Eliminated)  Enters the small intestine  Penetrate the mucus layer  Enter mononuclear phagocytes of ileal peyer's patches and mesenteric lymph nodes  Proliferate in mononuclear phagocytes spread to blood causing primary bacteremia (Incubation period).
  • 32.
     enter spleen, liverand bone marrow (reticulo-endothelial system) further proliferation occurs  A lot of bacteria enter blood again causing secondary bacteremia.  Recovery
  • 33.
    PATHOLOGY Proliferation of RES(reticuloendothelial system )  Specific changes in lymphoid tissues and mesenteric lymph nodes."typhoid nodules―  Most characteristic lesion: Ulceration of mucosa in the region of the Peyer’s patches of the small intestine 
  • 34.
  • 35.
    Major findings inlower ileum  Hyperplasia stage(1st week): swelling lymphoid tissue and proliferation of macrophages.  Necrosis stage(2nd week): necrosis of swelling lymph nodes or solitary follicles.  Ulceration stage(3rd week): Oval ulcer with its long axis parallel to the small intestine , this results from sloughing and shedding of necrotic lymphoid tissue in the peyers patches leading to intestinal hemorrhage, perforation .  Stage of healing (from 4th week): healing of ulcer, no cicatrices and no contraction
  • 36.
    2. Gastrointestinal Tuberculosis    • • • Abdominaltuberculosis is usually secondary to pulmonary tuberculosis Sites: The ileocecal region is the most common area of involvement in the gastrointestinal tract due to the abundance of lymphoid tissue. The natural course of gastrointestinal tuberculosis may be Ulcerative hypertrophic or ulcer hypertrophic.
  • 37.
    Clinical presentation Abdominal painmimicking peptic ulcer disease with stomach or duodenal infection;  Malabsorption with infection of the small intestine; Pain, diarrhea, or hematochezia with infection of the colon.
  • 38.
    Investigations       Blood routine Urine routine- to detect diabetes mellitus Plain X-ray of the abdomen Laparoscopy Laparoscopic biopsy of tubercles found in the peritoneum or other parts Barium studies
  • 39.
  • 40.
     3. AMOEBIC ULCER  Thecausative organism is parasitic protozoan, called Entamoeba histolytica.  Site: It usually involves caecum and ascending colon followed by sigmoid colon, rectum, and appendix. In severe cases the entire colon is involved.  The spectrum of colitis in amoebiasis ranges from mucosal thickening, to multiple cyst formation, to diffuse Inflammation / oedema, to necrosis and perforation of colonic wall.
  • 41.
    Life cycle Mouth -Cyst ingested Excyst to trophozoite Passed in stool Amoebic disease Cyst Trophozoite Invades gut mucosa – cyst formation
  • 42.
    Clinical presentation • • • • • • Gradual onsetof bloody diarrhoea Abdominal pain and tenderness. Leucocytes and pus may be present in stool. Fever present in <40% of patients. Weight loss and anorexia can be present. Local inflammatory masses, amoebomas, may cause obstructive symptoms
  • 43.
        Gross features: Begin assmall foci of necrosis that progress to ulcers. In the early stages the colonic ulcers have a narrow neck and thus appear as small nodules As the ulcers enlarge they always retain their undermined base but the ulcerated area of the mucosa becomes larger. The base of the ulcer is covered by grey - white exudate. There is always undenuded mucosa between the ulcers.
  • 44.
     Microscopic features:  The ulceris typically 'flask- shaped' and the broad base is composed of fibrin and cellular debris. A sharp line divides the necrotic and viable mucosa Trophozoites are found on the surface of the ulcers, in the exudate and in the crater. They are frequently found in the submucosa, muscularis propria, serosa.   
  • 47.
    ― IBD isa set of chronic inflammatory conditions resulting from inappropriate and persistent activation of the mucosal immune system ,driven by the presence of normal intestinal flora.‖
  • 48.
    HISTORY ULCERATIVE COLITIS • First officiallydescribed by Wilks and Moxon in 1875. • Before this discovery , all the diarrheal diseases were believed to be caused by infectious agents and bacteria.
  • 49.
    Crohn’s disease • In 1913Dr Dalziel described transmural intestinal inflammation in 13 autopsied patients. • In 1930 Burril Crohn described TERMINAL ILEITIS first .
  • 50.
    Epidemiology of IBD Ulcerativecolitis Crohn’s disease Incidence (US) 11/100 000 7/100 000 Age of onset 15-30 & 60-80 15-30 & 60-80 Male:female ratio Smoking 1:1 May prevent disease 1.1-1.8:1 May cause disease Oral contraceptive No increased risk Relative risk Appendectomy Not protective Monozygotic twins 8% concordance Protective 67% concordance
  • 51.
  • 52.
    GENETIC • Genome wide scanningwith microsatellite DNA markers has identified several genetic sites as being potentially associated with UC or CD. • Significant linkages have been reported on chromosomes 1, 3, 6, 7, 12, 14, 16, and 19. • One of the clearest linkages is for IBD-1, a susceptibility locus in the pericentromeric region of chromosome 16.
  • 53.
    • Detailed analysis hasresulted in the identification of the nucleotide-binding oligomerization domain 2 (NOD2) gene and protein. • NOD2 is also known as caspase activation and recruitment domain 15 (CARD15). • This is a polymorphic gene, the product of which is involved in the innate immune system.
  • 54.
    NOD2 PROTEIN EXPRESSED INmacrophages / monocytes FUNCTION AS AN INTRACELLULAR RECEPTOR MICROBES TRIGGER NF- kB pathway NOD2 gene mutation CYTOKINES AND OTHER PROTEINS INNATE IMMUNE DEFENSE MECHANISM DOWN REGULATION OF INNATE IMMUNITY LEADS TO INFLAMMATORY BOWEL
  • 55.
    Abnormal host immunoreactivity  IBDis characterized by immunoregulatory defects in the mucosa, which appear to be associated with microbial exposure.  A number of theories have been advanced concerning the pathogenesis of this process: - dysfunctional immune host response to normal luminal component - infection with a specific pathogen - defective mucosal barrier to luminal antigens.
  • 56.
    • • It is hypothesizedthat exposure to commensal bacteria down-regulates the inflammatory genes and blocks activation of the NF-kB pathway, thus inhibiting the inflammatory immune response of the gut to the microbes and food antigens to which it is constantly exposed.
  • 57.
         . Implicated pathogens include Mycobacteriumparatuberculosis Paramyxovirus Listeria monocytogenes Helicobacter hepaticus.
  • 58.
     Defective barrier function IBDis associated with increased permeability of the epithelial lining of the gut resulting in continuous stimulation of the mucosal immune system. Luminal bacteria appear to intensify the permeability defect further, establishing a self-sustaining cycle of mucosal inflammation that allows for uptake and translocation of bacteria.
  • 59.
    Ulcerative colitis  Is aninflammatory disease involving only the large intestine. The inner lining or mucosa of the intestine becomes inflamed and develops ulcers. Always starts in rectum and is continuous until some proximal part of the colon. Involves the mucosa and submucosa
  • 60.
    sites     40-50% of patientshave disease limited to the rectum and rectosigmoid 30-40% of patients have disease extending beyond the sigmoid 20% of patients have a total colitis Proximal spread occurs in continuity without areas of uninvolved mucosa
  • 61.
    Ulcerative colitis –clinical presentation The major symptoms of UC are: - diarrhea - rectal bleeding - tenesmus - passage of mucus - crampy abdominal pain 
  • 62.
    Ulcerative colitis –macroscopic features Mucosa is : - erythematous, has a granular surface that looks like a sand paper  In more severe diseases: - hemorrhagic, edematous and ulcerated   In fulminant disease a toxic colitis or a toxic megacolon may develop ( wall become very thin and mucosa is severly ulcerated)
  • 63.
  • 64.
    Ulcerative colitis –microscopic features Process is limited to the mucosa and submucosa with deeper layer unaffected  Two major histologic features: - the crypt architecture of the colon is distorted - some patients have basal plasma cells and multiple basal lymphoid aggregates 
  • 65.
    Broad based ulceration of themucosa in distal colon or throughout its length
  • 66.
  • 67.
  • 68.
  • 69.
  • 70.
    Ulcerative colitis -complications     Hemorrhage Perforation Stricture Toxic megacolon (transverse colon with a diameter of more than 5 to 6 cm with loss of haustration)
  • 71.
  • 72.
    Crohn’s disease (CD)     Alsoreferred to as granulomatous or regional enteritis, granulomatous ileitis, ileocolitis Can have non-continuous pattern-‖skip lesions‖, with areas of severe inflammation with intervening normal mucosa Most frequently affects distal third of small intestine and the colon Affects all layers of the affected bowel
  • 73.
    sites  Can affect anypart of GI tract from the mouth to the anus  30-40% of patients have small bowel disease alone  40-55% of patients have both small and large intestines disease  15-25% of patients have colitis alone  In 75% of patients with small intestinal disease the terminal ileum in involved in 90%
  • 74.
    Crohn’s disease –sign and symptoms Ileocolitis - right lower quadrant pain and diarhhea - palpable mass, fever and leucocytosis - pain is colickly and relieved by defecation  Jejunoileitis - inflammatory disease is associated with loss of digestive and absorptive surface 
  • 75.
    Crohn’s disease –sign and symptoms Colitis and perianal disease - low grade fever, malaise, diarrhea, crampy abdominal pain, sometimes hematochezia - pain is caused by passage of fecal material through narrowed and inflamed segments of large bowel  Gastroduodenal disease - nausea, vomiting, epigastric pain - second portion of duodenum is more commonly involved than the bulb 
  • 76.
    Crohn’s disease –macroscopic features  CD is a transmural process  CD is segmental with skip areas in the midst of diseased intestine  In one –third of patients with CD perirectal fistulas, fissures, abscesses, anal stenosis are present
  • 77.
  • 78.
    Crohn’s disease –macroscopic features  mild disease is characterized by: aphtous or small superficial ulcerations  In more active disease: stellate ulcerations fuse longitudinally and transversely to demarcate island of mucosa that are histologically normal  Cobblestone appearance is characteristic of CD
  • 80.
  • 81.
  • 82.
    M/E : Mucosal inflammation    Mucosanormal and retain mucus. Well-defined focus of inflammatory cells surrounded by non inflammed and normal mucosa As the disease establish , neutrophils infiltrate isolated crypts – abscess – ultimate destruction.
  • 83.
  • 84.
    Chronic mucosal damage:     Architecturaldistortion manifested as villous blunting. Crypts exhibit irregularities and branching. Crypt destruction leads to atrophy Gastric antral type or paneth cell metaplasia occur
  • 85.
  • 86.
    A - Mucosal Granuloma erodinga crypt of lieberkhun and initiating crypt abscess formation. B - Crypt obliterated by Granuloma formation
  • 87.
    • Non Caseating Granuloma-in½ cases , Sarcoid Granuloma in all tissue layers. Others: • In diseased segments muscularis mucosa exhibits reduplication , strictures. thickening, irregularity's leads to like,
  • 88.
  • 89.
  • 90.
    Complications of Crohn'sDisease:  Perianal fistulas  Perianal skin ulceration  Increased incidence of gall and kidney stones (due to malabsorption of fats and bile salts)
  • 91.
    Extraintestinal manifestations ofIBD       Iritis Episcleritis Arthritis Skin involvement Pericholangitis Sclerosing cholangitis
  • 92.
    Risk of Malignancyin IBD   In Crohn’s disease, increased risk of cancer of the affected areas is seen In ulcerative colitis, 8-10 years after initial diagnosis, there is a steady, significant increased risk of developing cancer  Prognostic factors increasing malignancy risk in UC: • Duration of disease 10 yrs or more • Pancolonic involvement • Continuous progressive disease • Severe initial onset • Associated liver disease
  • 93.
    Gross :  Thick mucosawith finely nodular or velvety surface configuration.  Lesion polypoid , elevated , nodular or villous formation.
  • 94.
    M/E :  Adenocarcinoma withvarying degree of differentiation .  Always accompanied by dysplastic changes .
  • 95.
    Evaluation of Dysplasia  1- Negative for Dysplasia.  2 - Indefinite for Dysplasia,probably Negative.  3 - Indefinite for Dysplasia, Unknown.  4 - Indefinite for Dysplasia,probably Positive.  5 - Positive for Dysplasia,Low Grade.  6 - Positive for Dysplasia,High Grade.
  • 99.
    Lab Findings inIBD     CBC’s:  Anemia is common due to blood loss or malabsorption  Leukocytosis & thrombocytosis also common ESR typically elevated; monitors disease activity Abnormal LFTs may represent pericholangitis or sclerosing cholangitis Low serum albumin (protein-losing enteropathy) suggests extensive colitis
  • 100.
    Features UC CD Rectal Bleeding Common Inconspicuous  Abdominal mass Practicallynever 10-15% Abdominal pain Left sided Right sided Sigmoidoscopy Abnormal 95% Abnormal <50% Free perforation 12% 04% Colon CA 2% Rare Anal complications Minor 75%, fissures, fistulas, ulceration Response to steroid 75% 25% Result of surgery Good Fair Clinical
  • 101.
    Features UC CD Sparing of rectum Exceptional 90% Involvementof ileum Rare Common Strictures Absent Present Skip areas Absent Common Internal fistula Absent May be present Longitudinal and transverse ulcers Exceptional Common Fissuring Absent Common Radiographic
  • 102.
    Features UC CD Distribution of involvement Diffuse Focal Mucosalatrophy Marked Minimal Cytoplasmic Mucin Diminished Preserved Lymphoid aggregates Rare Common Edema Minimal Marked Hyperemia May be extreme Minimal Granulomas Absent Present in 60% Fissuring Absent Present Crypt abscesses Common Rare Rectal involvement Practically always 50% Morphologic
  • 104.
    REFERENCES  Robbins and Cotran.  SurgicalPathology – Rosai and Ackerman’s.  Sternburg.  Harrison’s Textbook of Internal Medicine.  Internet

Editor's Notes

  • #8 The most important contributing factors are H pylori, NSAIDs, acid, and pepsin. Additional aggressive factors include smoking, ethanol, bile acids, aspirin, steroids, and stress.Important protective factors are mucus, bicarbonate, mucosal blood flow, prostaglandins, hydrophobic layer, and epithelial renewal. When an imbalance occurs, Peptic ulcer ds might develop
  • #9 --H Pylori Causes intense inflammatory and immune response. (Inter leukinL-1, IL-6, TNF, IL-8).it Enhance gastric acid secretion and impairs duodenal bicarbonate production
  • #16 --------Rapid urease tests are considered the endoscopic diagnostic test of choice. The presence of H pylori in gastric mucosal biopsy specimens is detected by testing for the bacterial product urease. One or more gastric biopsy specimens are placed in the rapid urease test kit. If H pylori are present, bacterial urease converts urea to ammonia, which changes pH and produces a color change
  • #18 Picture shows Clusters of bacteria on Warthin–Starry staining. WS stains organisms dark brown to black, and the background light golden brown/golden yellow.
  • #19 The 1st figure shows Hpylori with leung stain…2nd figure shows rod shaped bacilli satained with methylene blue in the gastric pit.
  • #21 --PETIC ulcer are 4x more common in proximal duodenum then in stomach.they are solitary in more then 80% of patient.classic peptic ulcer is round to oval sharpely punched out defect.this is endoscopic view of peptic ulcer showing….
  • #22 This is a gross view of a chronic gastric ulcer showingruggae. There is “punched-out” defect with sharp, overhanging margins
  • #23 Picture shows duodenal peptic ulcer located in first portion of duodenum
  • #27 Picture shows cross-section of a duodenal ulcer crater with an acute inflammatory exudate
  • #31 This is picture showing pathogenesis of typhoid fever…
  • #40 Picture shows circumfential ulceration which is characteristic of intestinal TB
  • #42 Entamoebahistolytica has a biphasic life cycle, existing in two forms; as an infectious cyst and an amoeboid trophozoite. Transmission is by feco-oral route.
  • #43 -----------In more severe cases fulminant amoebic colitis develops. Liver involvement is more common in these cases,
  • #44 -----------------------Muscle coat of the large intestine form a barrier to the penetrating trophozoites which fan out laterally producing a flask-shaped ulcer with narrow neck and broad base.
  • #45 --------There is little inflammatory response in the early ulcers.
  • #46 Picture showing amebic colitis,multiple undermined ulcers are present in cecum and ascending colon.
  • #47 Picture shows Histological cross section of classical flask shaped amoebic ulcer in colonic mucosa
  • #48 -----------It Refers to two chronic diseases that cause inflammation of the intestines:ulcerative colitis and Crohn&apos;s disease.
  • #51 UC- chemicals in tobacco especially nicotine has a protective effect by increasing the mucus production in the colon and rectum. It also suppresses the immune system and prevents inflammation. But in CD- such chemicals like nicotine, CO, free radicals acts as immunosuppressants on macrophages thus many harmful bacteria cannot be cleared from the gut, they may also lead to restricion in blood flow inside the gut walls thus making intestine more susceptible to develop crohnsds.
  • #55 The NOD2 gene is expressed mainly in monocyte/macrophage cell lines, where it has a role in host-signaling pathways. One effect is the activation of nuclear factor (NF)-kB Activation leads to production of a wide variety of nonspecific mediators of inflammation like cytokines, growth factors, and metabolites of arachidonic acid and reactive oxygen ultimately lead to tissue destruction
  • #57 ------Inibd Exposure to luminal micro flora triggers an inflammatory response by the cells lining the mucosa, leading to a chronic, destructive immune response.
  • #58 ------------------------ A number of reports suggest a link between Crohnds and early measles infection.
  • #64 Picture showing
  • #66 Picture shows chronic form of ulcerative colitis with mucosal ulceration and residual foci of elevated and hyperimic mucosa.
  • #69  The luminal border is irregular; the colonic crypts have lost their parallel arrangement, and they are branched and budded. The muscularismucosae is hypertrophied.
  • #70  The luminal border is irregular. Increased inflammatory cells are present within the lamina propria.
  • #72 Picture showing toxic megacolon.it is complication of ulcerative colitis..
  • #78  This slide shows a segment of intestine with Crohn’s disease. This disease does NOT involve bowel in a uniform manner, i.e., there are skip areas. It is a disease, however, in which the affected segments are involved in their entire thickness: mucosa, submucosa, muscularis, and serosa –a transmural involvement
  • #80 Figure (a) shows fat wrapping in crohnsds , in figure (b) two segments of intestine can be seen connected by fistula tract and in figure © cobblestone appearance characterized by presence of serpiginousanastomosing ulcers
  • #82 Picture shoeing Cobblestone lesions&quot; usually in terminal ileum and &quot;skip lesions&quot; which are discontinuous areas of inflammation, edema and fibrosis
  • #84 Crohn colitis demonstrating the &quot;focal active colitis&quot; pattern of injury showing infiltration of chronic inflammatory cells in the lamina propria.
  • #86  this is a picture showing chronic crohns colitis..the branched crypt is feature of chronicity..
  • #89 This is a picture showing noncaseatinggranuloma is present in the lamina propria of an uninvolved region of colonic mucosa
  • #90 This diagram shows Lymphocytic inflitration and the formation of non-caseatinggranuloma.
  • #97 Picture showing low grade dysplasia with chronic ulcerative colitis.
  • #100 Cbc-complete blood count
  • #101 This slide shows differentiating features between ulcerative colitis and crohns ds.1st clinical feature
  • #104 This diagram shows distribution of lesions in inflammatory bowel disease.the distinction between crohnds and ulcerative colitis is primarily based on morphology.Incrohnds there are skip lesions but in ulcerative colitis there is continuos colon involvement.incrohns ulceration and fissure are seen and in ulcerative there is pseudopolyp are characteristic.