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An interpretation of Endoscopic biopsy

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An interpretation of Endoscopic biopsy

  1. 1. Interpretation of the endoscopic biopsy GUIDED BY- Brig Vibha Dutta, SM Presented by Maj Ganesh Parajuli
  2. 2. OVERVIEW • • • • • Introduction Technical aspects Interpretation Pitfalls Conclusion
  3. 3. Introduction • Endoscopy : Examination of internal body cavities using a specialized medical instrument called an endoscope
  4. 4. Introduction (contd….) • Fibrooptic endoscopy and biopsy – diagnostic procedure in investigation GI disorder • The first gastroscope: George Wolf in 1911 • Semiflexible gastroscope: 1930 • Harold designed fibroscope: early 1950 • Newer technologies: chromoendoscopy, capsule endoscopy endoscopic ultrasound
  5. 5. General features of GI biopsy interpretation • GI tract: limited repertoire of response to host injuries • Diagnoses requires correlation with clinical information • Normal biopsies may be obtained from symptomatic patients • Inflammatory cells are a normal constituent of lamina propia
  6. 6. Overview comments on the GI tract 4 layers of tissue surround the lumen of the GIT Mucosa  epithelium – protective, absorbtive & secretory lamina propria – thin loose CT  muscularis mucosa – slim double layer of smooth muscle Submucosa Muscularis propria Skeletal muscle at beginning & smooth muscle at the end (inner circular; outer longitudinal layer) from lower esophagus to rectum Serosa (viseral peritoneum)
  7. 7. The major uses of mucosal biopsy includes: i. Diagnosis : either specific or in the form of an injury pattern or stage ii. Determination of the extent or severity of lesions iii. Monitoring of the clinical course of disease states with particular reference to effects of therapy iv. Detection of complication
  8. 8. Assessing any biopsy from GI tract Clinical pathological correlation is essential for diagnosisThe following clinical data should be provided : 1. Age, race and sex of the patient 2. Sign and symptoms, site of biopsy, endoscopic and radiological finding 3. History of taking drugs or alcohol 4. Medical and surgical history
  9. 9. Technical aspects • The grasp biopsy specimens obtained at flexible endoscopy typically consists only of the mucosa Regions with thicker mucosa contain only superficial portion • Suction or aspiration-type biopsy more fruitful when a larger sample or more exact location is required • Choice of fixative is usually not critical though Bouin’s may interfere with staining of the granules of Paneth cells • Multiple sections to improve the chance of detecting any focal or subtle changes
  10. 10. • For routine analysis at least 3 levels of biopsy specimen, each with 5 or more sections • When focal lesion not obtained, additional levels should be require • Cytologic preparations useful diagnostic adjunct
  11. 11. Ideal Mucosal Biopsy • At least 3 pieces of full thickness mucosa 3 mm in length • Mucosal fragments well oriented at time of embedding crypt:villous ratio can accurately evaluated
  12. 12. Abnormal esophageal Mucosal Biopsy Abnormal esophageal mucosa Non neoplastic Infections ViralHerpes simplex CMV FungalCandida Others Corrosive - lye Reflux Neoplastic Benign Squamous papilloma Malignant Squamous cell carcinoma Adenocarcinoma
  13. 13. Esophagitis The 4 most common types of esophagitis: 1. Pill esophagitis – Spectrum of injury by the ingestion of drugs – Common site anatomical narrowing – Ulcer ,granulation tissue ,polarizable foreign material and multinucleted gaint cells 2. Infectious: – HSV, CMV (BMT, solid organ transplant) – Candidal (HIV, thrush associated) Yeast and pseudohypae seen in necroinflammatory background
  14. 14. 3. Eosinonophilic esophagitis: frequently seen in childern Endoscopic finding –stricture , rings corrugation,furrows and granularity Mucosal edema ,basal cell hyperplasia with eosinophil infiltration of sq mucosa >20 eosinophil per high field
  15. 15. 4.Reflux disease • GERD the costliest GI disorder & the most common physician diagnosis GI disorder in outpatient clinic visit • GERD caused by reflux of gastric contents into esophagus Reflux of gastric acid and pepsin • Reflux of alkaline bile & pancreatic secretion moving from duodenum stomach esophagus recognized as a contributing factor to esophageal injury in GERD
  16. 16. • ‘Reflux esophagitis ‘ an example of ‘itis ‘ lack prominent component of inflammation • The pathology reflects injury to sq epithelium followed by attempts of the epithelium to regenerate • Mild features of cellular injuryballoon cells vascular lakes, mild inflammation and scattered eosinophils
  17. 17. REFLUX/GERD
  18. 18. Fairly reproducible criteria established by Fiocca et al as abnormal and associated with clinical reflux – i. Thickened basal layer(>15%) or 5 to 6 layers ii. Increased papillary length (>50%) of the squamous thickness iii. Intraepithelial eosinophil ,neutrophil (>1to 2 cells /40x field) iv. Intraepithelial mononuclear cells.(>10/40x field) v. Dilated /widened inter cellular spaces(which may appear as bubbles or ladders.
  19. 19. BARRETT’S ESOPHAGUS • Defined as intestinal metaplasia of a normally SQUAMOUS esophageal mucosa. • The presence of GOBLET CELLS in the esophageal mucosa is DIAGNOSTIC. • SINGLE most common RISK FACTOR for esophageal adenocarcinoma • 10% of GERD patients get it • “BREACHED” G-E junction
  20. 20. BARRETT’S ESOPHAGUS
  21. 21. Gastritis • No widely accepted classification of gastritis • Updated Sydney System Published in 1997 • Attempted to combine topographical, morphological and etiological information • Largely unused bec of inadequate sampling & clinical information ,poor endoscopic & histologic correlation and ethic and geographic variation of the disease Operative Link for Gastritis Assessment (OLGA) staging system: Based on extent and severity of atrophic gastritis and provide relevant clinical information regarding the gastric cancer risk. However, atrophic gastritis is a difficult histopathological diagnosis of which the interobserver agreement is low.
  22. 22. H pylori associated gastritis • Helicobacter pylori (H pylori) common bacterium that is present in millions of people worldwide • found in mucous lining of stomach. It is known to be responsible for 60% to 80% of gastric ulcers and 70% to 90% of duodenal ulcers • The recognition of an association between this bacterium and peptic ulcer disease by Barry Marshall and John R. Warren, in 1983, and they were awarded the Nobel prize in 2005 • Another varient called H. heilmannii (less than 1% isolates) • Like H pylori it produces antral predominant gastritis ,less sev, than H. pylori gastritis
  23. 23. • Histologically shows organisms within the surface mucus layer and foveolar epithelium • Abundant, lymphoplasmacytic , chronic inflammation of lamina propria • Presence of lymphoid follicles (MALT) almost always indicative of infection
  24. 24. A simplified pathology report of gastritis include the following parameters: a. Type of mucosa b. Grade of lymphoplasmacytic infiltration (4 M) c. Presence or absence of active inflammation with degree of activity(if present) d. Extent of intestional metaplasia or atrophy(if present) e. Presence or absence of H pylori microorganism
  25. 25. Normal histology • Finger-like villi • C:V ratio (assessed where 4 well-oriented crypts and villi are seen) • Normal C:V ratio 1:3 or more • C:V ratio lower in children and elderly • C:V ratio usually uniform in a biopsy
  26. 26. Evaluation of small intestinal mucosal biopsy Low power • adequacy of biopsy • crypt villous architecture • degree of inflammation High power • Specific features in lumen, epithelium and lamina propria
  27. 27. Indications for biopsy: • Evaluation for patients with malabsorption • Investigation for patients with iron deficiency anemia, diarrhoea particularly in whom infections is suspected with AIDS • Diagnosis of neoplasia • Confirmation of ulceration induced by NSAID or in cases of bleeding from unknown site.
  28. 28. Abnormal Small Intestinal Mucosal Biopsy Abnormal small intestinal mucosa Nonspecific changes Specific changes Celiac disease Tropical sprue Bacterial overgrowth Epithelial Cow’s milk allergy Chronic renal failure B12, folate, iron, zinc def Autoimmune enteropathy Infections Others Drugs Viral Parasitic Bacterial Lumen parasites Lamina propria Infections Lymphocytic Viral Abetalipoprot. Parasitic Microvillous inc Fungal GVHD AIDS enteropathyl Inflammatory lBD Granulomatous Collagenous Eosinophilic Immunodeficiency Autoimmune enterop Metabolic Amyloidosis Storage disorders Neoplasms Benign polyps Adenocarcinomas Endocrine Lymphomas GISTs Waldenstrom’s
  29. 29. Spectrum of Nonspecific inflammatory changes in the small intestinal mucosa Architecture • Crypt hyperplasia • Crypt hyperplasia with villous atrophy • Villous atrophy with crypt hypoplasia (rare) • Branching, broadening and fusion of villi (mild cases) Epithelium • Epithelial damage: flattening, nuclear irregularity, loss of polarity, vacuolization, basophilia • Increased intraepithelial lymphocytes • Increased apoptosis • Macrocytosis of epithelial cells Lamina propria • Chronic inflammation • Acute inflammation
  30. 30. Varying degrees of change mild mod sev
  31. 31. Celiac disease Macroscopic features • On endoscopy the mucosa appear flattened and scalloped if there is significant villous atrophy Microscopic features • Microscopic changes most severe in duodenum and decrease in severity distally • 4 small intestinal biopsies are required for absolute diagnostic confidence (Pais et el, Gastroint Endosc 2008); • May be patchy • Changes decrease with gluten withdrawal and recur when gluten is re-introduced
  32. 32. Celiac disease : Spectrum of changes Marsh’s diagnostic criteria • 0 – preinfiltrative: Dermatitis herpetiformis; no mucosal change • I More than 40 intraepithelial lymphocytes per 100 epithelial cells – infiltrative • II. Crypt hyperplasia with increased intraepithelial lymphocytes – infiltrative type 2 • • • • III. Crypt hyperplasia with increased intraepithelial lymphocytes and villous atrophy IIIa Mild villous atrophy IIIb Moderate villous atrophy IIIc Severe villous atrophy • IV Crypt hypoplasia with villous atrophy
  33. 33. Tropical sprue • Chronic malabsorptive syndrome seen in residents and visitors to tropical countries • Etiology related to chronic infections and bacterial overgrowth • Entire small intestine from duodenum to terminal ileum may be involved • Villous atrophy, crypt hyperplasia, inflammation and increased IELs • Often responds to broad spectrum antibiotics like tetracycline
  34. 34. Cow’s milk protein allergy • Temporary condition affecting young infants presented with malabsorption & dehydration requiring parenteral nutrition • Bloody diarrrhoea, vomiting, abdominal pain, weight loss • Small intestional mucosal changes similar to celiac disease but lesser extent • Intraepithelial eosinophils & peripheral eosinophil are more noted with cow’s milk
  35. 35. Nutritional deficiences Vitamin B12, protein, iron and zinc deficiency Structural abnormalities of intestional mucosa associated with malsorption • B12: villous blunting, macrocytosis, decreased mitoses • Protein deficiency • Zinc deficiency
  36. 36. AIDS enteropathy • Individuals infected with HIV with chronic diarrhoea have opportunistic infections or diffuse small intestional mucosal alterations in the absence of pathogens • Duodenal biopsies may shows crypt hyperplasia and partial villous atrophy, increased intraepithelial lymphocytes and infiltration of the lamina propria by plasma cells and lymphocytes • Crypts shows evidence of increase apoptotic activity
  37. 37. Specific changes in Small intestinal biopsies Lumen
  38. 38. Giardia Lamblia
  39. 39. Infections Giardiasis • Most common parasitic infection • Presence of trophozoites in fecal and duodenal biopsy specimen confirm giardia infection • Duodenum (more than 80%) followed by jejunum and ileum, rarely the stomach and colon • The mucosa is normal shows minimal changes in majority of cases with mild villous atrophy, crypt hyperplasia , loss of normal brush border shorting of villous epithelium and increase intraepithelial lymphocytes • The parasite found in lumen close to the surface of villous epithelium
  40. 40. Specific changes in Small intestinal biopsies Epithelium
  41. 41. Lymphocytic enteritis
  42. 42. Increased intraepithelial lymphocytes • • • Definition: > 30 or 40/100 villous epithelial cells Or more than 5 per 20 villous tip epithelial cells • Should be diffuse • Counting should not be done over a lymphoid follicle Causes • Infections • H.pylori infection • Tropical sprue • Celiac sprue • Refractory sprue • Protein intolerance • NSAIDs • Bacterial overgrowth • IBD • Lymphocytic enteritis • AIDS, hypogammaglobulinemia • Collagen vascular disease
  43. 43. Acute GVHD Endoscopic findings • Normal mucosa, erythema, ulcers and sloughing Histologic features • Single cell apoptosis in crypts • Villous blunting • Loss of crypts • D/D: CMV infection; chemoradiation-induced damage
  44. 44. Chronic GVHD
  45. 45. Epithelial infections Viral – nonspecific changes except CMV Bacterial – Enteropathogenic E.coli may form colonies on the brush border Parasitic • Microspora – genera Encephalitozoon, Enterocytozoon • Isospora • Cryptosporidium • Cyclospora
  46. 46. Cryptosporidiosis • Cryptosporodium parvum protozoan, highly infectious with waterborne ,person to person • Immunocompetent pts acute ,self limiting diarrhoea while immunocompromised pts including AIDs chronic watery dairrhoea • Distribution worldwide ,endemic in developing countries, found in >50%of AIDS
  47. 47. Cryptosporidiosis
  48. 48. Microsporidiasis Widespread obligate intracellular parasite Opportunistic infection in immunosuppressed organ transplant patents and those with AIDS The infection includes : Enterocytozoon bieneusi & Encephalitozoon intestinalis Histological features : In small bowel both causes a partial villous atrophy ,mild crypt hyperplasia with short blunt villi and mild increase in lymphocytes ,plasma cells & eosinophil in the lamina propria
  49. 49. Microsporidiosis Entercytozoon bieneusi Encephalitozoon intestinalis
  50. 50. Specific changes in Small intestinal biopsies Lamina propria
  51. 51. Specific changes in the lamina propria Infections Vascular IBD Others • • • • • Parasitic: Isospora Viral: CMV Bacterial: TB, MAI, Whipple’s, yersinia Fungal: Histoplasma, cryptococcus Crohn’s Allergic • • Eosinophilic enteritis Lymphocytic/collagenous enteritis Immune • Immunodeficiency syndromes • • • • • • Radiation enteritis Vasculitis Ischemia Portal hypertension Amyloidosis Lymphoma
  52. 52. CMV Macroscopic • Patchy erythema, edema, aphthous and deep penetrating ulcers Microscopic • Usually endothelial cells and other stromal cells deep in the base of ulcers and other sites; rarely epithelial • less inflammation in immunocompromised individuals • Atypical inclusions: smudged nuclei Other diagnostic tests: immunohistochemistry and PCR
  53. 53. Histoplasmosis • Macroscopic: • Nodular or ulcerating lesions in ileum • Microscopic: • Granulomas • Fungal bodies in the cytoplasm of histiocytes; small oval yeast forms with buds at the pointed ends
  54. 54. Mycobacterium Avium Complex • Commonly affects small intestine (duodenum most frequent) and colon of immunocompromised individuals (AIDS with CD4 counts <60/mm 3 • On endoscopy: coarse granularity, edema, erythema, yellowish streaks or ulcers • • On histology – immunocompetent individuals show necrotizing (up to 30%, small foci) or nonnecrotizing granulomatous inflammation; immunodeficient individuals : diffuse infiltrates of histiocytes with foamy or granular cytoplasm and minimal other inflammatory cells Regional lymph nodes enlarged with similar cells • • • AFB and PAS positive (fibrillary appearance versus granular appearance of Whipple’s) • EM: intact bacteria
  55. 55. • Mycobacterium Avium Complex • Ziehl Neelsen
  56. 56. Eosinophilic enteritis • Often associated with peripheral eosinophilia (75%) and allergic disorders • Eosinophilia may be confined to the mucosa or involve the muscle coat or serosa • May present with hemorrhage, chronic diarrhea, abdominal pain, malabsorption, protein losing enteropathy, obstruction or ascites • D/D: parasitic infections, vaculitis, Crohn’s disease, Gluten sensitivity, lymphomas, inflammatory fibroid polyp, magnesium, vitamin E or selenium deficiency
  57. 57. Eosinophilic Enteritis
  58. 58. (I) IBD • CROHN DISEASE (granulomatous colitis) • ULCERATIVE COLITIS
  59. 59. (I) IBD • COMMON FEATURES – IDIOPATHIC – DEVELOPED COUNTRIES – COLONIC INFLAMMATION – SIMILAR Rx – BOTH have CANCER RISK
  60. 60. (I) IBD DIFFERENCES • CROHN (CD) – – – – – – – – – TRANSMURAL, THICK WALL NOT LIMITED to COLON GRANULOMAS FISTULAE COMMON TERMINAL ILEUM OFTEN SKIP AREAS “CRYPT” ABSCESSES NOT COMMON NO PSEUDOPOLYPS MALABSORPTION • ULCERATIVE (UC) – – – – – – – – – MUCOSAL, THICK MUCOSA LIMITED to COLON NO GRANULOMAS FISTULAE RARE TERMINAL ILEUM NEVER NO SKIP AREAS “CRYPT” ABSCESSES COMMON PSEUDOPOLYPS NO MALABSORPTION
  61. 61. Intestinal TB versus Crohn’s disease Tuberculosis: Granulomas • Caseation • Confluent granulomas • Lymphoid cuff • Granulomas larger than 400 micrometer • 5 or more granulomas in biopsies from one segment • Granulomas located in the submucosa or in granulation tissue: often with palisaded histiocytes • Granulomas in the ileocecal region • Nonspecific inflammatory changes in the same and adjacent segments to those with granulomatous iflammation • Disproportionate submucosal inflammation Crohn’s disease: Granulomas • Small (<200 micrometer) • Discrete • Very few / single • Poorly organised • Commonly located in the mucosa • Granulomas in the rectosigmoid • “microgranulomas”: aggregates of histiocytes • Nonspecific inflammation more diffusely distributed and not restricted to the same segments or those adjacent to the sites of granulomatous iflammation • Crypt-centric inflammation: pericryptal granulomas and focally enhanced colitis
  62. 62. Crohn’s disease • • • • • Segmental, patchy and focal involvement Distorted crypt villous architecture, Villous atrophy Significant chronic inflammation Increased intraepithelial lymphocytes, cryptitis, ulceration Granulomas, microgranulomas
  63. 63. Amyloidosis • G.I. involvement occurs in 85 to 100% cases of systemic amyloidosis • Commonly causes ulceration, bleeding; motility disorders, stasis and malabsorption • Macroscopy: fine granularity, erosions, friability, thickening of folds
  64. 64. Take home message  Interpretation & evaluation of GI biopsy specimen requires clinicopathological correlation  Good orientation of the biopsy specimen essential for accurate histopathological assessment.  A well-oriented biopsy specimen should have at least 4-5 consecutive elongated ,well distended villi from the base of the tip  The evaluation of the villous: crypt ratio, the count and distribution of the intraepithelial lymphocytes(IELs) as well as the evaluation of the enterocytes in the tip is critical  Infections can be accompanied by subtle changes in the architecture and minimal inflammation
  65. 65. References • Biopsy Interpretation of the Gastro intestional tract mucosa , Elizabeth A. Montigomery & Lysandra voltaggia .2nd Edition • Mucosal biopsy of the Gastrointestional tract,Whitehead 2nd edition • Morson and Dowson’s Gastrointestional Pathology,David W Day 4th edition • Robbins and Cortan Pathologic Basis of Disease 8th edition • Sternberg’s Diagnostic Surgical Pathology, Stancy E.Mills 5th editon • Wheater’s Functional Histology, Barbara Young , Alan,James 5th edition
  66. 66. • Pathology illustrated, Robin Reid, Foina, Elaime. 7th edition • S serra, P A Jane. An approach to duodenal biopsies J Clin Pathol2006; • Harvey Goldman, Donald. Mucosal biopsy of the esophagus ,stomach, and proximal duodenum Human pathology • Netter’s illustrated Human Pathology, Gerhard, L.M. Buja.1st edition

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