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Small & large gut

This document provides information on small and large intestine pathology. It discusses the normal anatomy and features of the small and large intestines. It then covers various pathologies that can affect the intestines including celiac disease, tropical sprue, Whipple's disease, amebic colitis, cryptosporidiosis, bacterial enterocolitis, ulcers of the intestine, granulomatous lesions, solitary rectal ulcer, Hirschsprung's disease, acquired megacolon, and appendicitis. For each condition, it provides details on pathogenesis, gross and microscopic pathology, clinical features, and diagnosis.

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SMALL & LARGE INTESTINE PATHOLOGY
Normal Small Intestine
NORMAL COLON
Important features ► Villous to crypt length ratio is 3:1, 5:1 ► One lymphocyte per five enterocytes ► Paneth cells secrete defensins present up to ascending colon ► Peyer patches , M cells ► Small intestine 6 meters (25cm duodenum) ► Large intestine 1.5 meters (20cm Rectum) ► Anal canal 4cm ► Enteritis(duodenitis, ileitis), Colitis(typhilitis, proctitis), Cryptitis
Major Causes of Malabsorption Defective Intraluminal Digestion • Pancreatic insufficiency- pancreatitis or cystic fibrosis • Zollinger-Ellison syndrome- inactivation of pancreatic enzymes by excess gastric acid • Ileal dysfunction or resection, with decreased bile salt uptake • Cessation of bile flow from obstruction, hepatic dysfunction Primary Mucosal Cell Abnormalities Defective terminal digestion • Disaccharidase deficiency (lactose intolerance) • Bacterial overgrowth, with brush border damage Defective epithelial transport • Abetalipoproteinemia • Primary bile acid malabsorption owing to mutations in the ileal bile acid transporter Reduced Small Intestinal Surface Area Gluten-sensitive enteropathy (celiac disease) Crohn disease Lymphatic Obstruction Lymphoma,Tuberculosis and tuberculous lymphadenitis Infection Acute infectious enteritis or Parasitic infestation Tropical sprue, Whipple disease (Tropheryma whippelii) Iatrogenic Subtotal or total gastrectomy Short-gut syndrome, following extensive surgical resection or by pass
CELIAC DISEASE ► Celiac disease (celiac sprue, gluten- sensitive enteropathy) a chronic disease, characteristic mucosal lesion of small intestine and impaired nutrient absorption, which improves on withdrawal of wheat gliadins and related grain proteins from diet ► Celiac disease occurs largely in Caucasians and is rare or nonexistent among native Africans, Japanese, and Chinese ► Infants, yet adults in 5 th decade of life may seek attention
Pathogenesis Sensitivity to gluten, alcohol-soluble, water-insoluble protein component gliadin (protein found in gluten fraction of wheat) and closely related grains (oat, barley, and rye) Interplay between genetic predisposing factors, host immune response, and environmental factors is central to disease pathogenesis ► Exposure to gliadin results in T-cell mediated chronic inflammatory reaction with accumulation of intraepithelial CD8+ T cells and large numbers of lamina propria CD4+ T cells, which are sensitized to gliadin results in circulating antibodies against gliadin ► Epithelial cells secrete large amount of IL5 that activate CD8+ T cells (increases risk of T cell lymphoma) ► Family history important in celiac disease, almost all individuals with celiac disease share major histocompatibility complex class II HLA-DQ2 or HLA- DQ8 haplotype ► Proposed that gliadin is deamidated by enzyme transglutaminase into peptides which binds to DQ2 and DQ8, recognition of these peptides by CD4+ T cells leads `to secretion of Gamma interferon which damages intestinal wall
CELIAC DISEASE Gross: Duodenal folds are absent or reduced Microscopy:  Atrophic villi (Usually complete)  Normal thickness of mucosa  Villous crypt ratio decreased  Crypt hyperplastic-elongated tortuous  Increase mitoses  Increase in no of lymphocytes, plasma cells, eosinophils, macrophages  Intraepithelial leucocytes  Vacuolar degeneration and loss of brush borders of surface epithelium
Out come of Celiac Disease ► Intestinal Non Hodgkin T-cell lymphoma ► Chronic nonspecific duodenojejunoileitis ► Small intestine adenocarcinoma ► Squamous cell carcinoma of esophagus ► Dermatitis herpitiformis blistering skin lesion
Diagnosis of Celiac Disease ► Clinical malabsorption (Diarrhea ,flatulence, wt loss, fatigue, failure to thrive in childern ► Small bowel biopsy Villous atrophy ► Responds to gluten with drawl from diet ► Antigliaden or antiendomysial antibodies ► Antitransglutiminase IgA, IgG ► Antireticulin antibodies
Normal/Celiac sprue
Celiac
TROPICAL SPRUE ► Definite geographic distribution ► Bacterial etiology with or with out additive effects of fat. ► Unaffected by gluten ingestion, responds to folic acid, vit B12, tetracycline. ► There is partial villous atrophy
WHIPPLE’S DISEASE ► Male to female ratio 10:1 ► Large macrophages in lamina propria, distorting the villi, alternating with empty spaces. ► Histiocytes cytoplasm contains diastase-resistant PAS positive & gram positive abundant bacilli Tropheryma whippelii ► Diagnosis by PCR, immuno, electron microscopy. ► Biopsy of peripheral lymph nodes – presence of typical macrophages.
WHIPPLE
GIARDIA
AMEBIC COLITIS ► Simulate ulcerative colitis or Crohn’s disease ► Gross: ulceration covered by exudate, with normal intervening mucosa ► Site: cecum and ascending colon ► L/M: nonspecific ► Flask shaped ulcer, relative paucity of inflammatory cells beneath ulcer ► Trophozoites of E. histolytica ► Erythrocytosis by trophozoites usually present ► Can be detected by PAS stain ► Stool R/E
Ameba
Cryptosporidosis
Major Causes of Bacterial Enterocolitis Escherichia coli • ETEC EHEC EPEC EIEC Salmonella Shigella Campylobacter Yersinia enterocolitica Vibrio cholerae, Clostridium difficile Clostridium perfringens Mycobacterium tuberculosis Protozoa Amebic colitis
Pseudo membranous colitis
Ulcers of Intestine ► Oval- Salmonella typhi long axes along axes of ileum ► Linear-Salmonella paratyphi ► Flask shaped –amebic ► Irregular –Shigella ► Multiple superficial ulcers-Campylobacter jejuni ► Ulcer along transverse axes- Tuberculosis ► Early Aphthous & late long linear serpintine-Crohn ► Extensive broad base – Ulcerative colitis ► Solitary Rectal Ulcer ► Malignant ulcers
Granulomatous lesions of Intestine ► Tuberculosis caseating granulomas ► Crohn disease non-caseating granulomas ► Foreigen body granulomas ► Necrotizing granulomas-Yersinia enterocolitica, Y. pseudetuberculosis ► Oliogranuloma-against fat
SOLITARY RECTAL ULCER ► Solitary ulcerated or polypoid lesion 4-18cm from anal margin ► Associated with rectal prolapse ► S/S: passage of blood and mucus , altered bowel habits and pain L/M: superficial and irregular mucosal ulceration ► Hyperplasia of crypts, villous configuration ► Obliteration of lamina propria by fibroblasts, elastin and smooth muscles ► Thickened muscularis mucosae ► ↓ lymphocytes and plasma cells ► Chronic form– similar to colitis cystica profunda
HIRSCHSPRUNG’S DISEASE Cause: lack of coordinated Sex: 80% ♂ movements of distal large ► Association with bowel due to loss of intrinsic inhibitory intestinal atresia and innervations anorectal malformation ► Absent parasympathetic S/S: abdominal distention, ganglion cells in delayed meconium intramural and passage, tight anus submucosal plexus due to ► Proximal bowel dilatation failure of migration of & hypertrophy of muscle neural crest cells or ► Complications: acute immune mediated intestinal obstruction, neuronal necrosis enterocolitis, megacolon, ► Age: 1st yr life perforation, sepsis
HIRSCHSPRUNG’S DISEASE
HIRSCHSPRUNG’S DISEASE L/M: ► Aganglionosis in both plexus of segment of bowel ► Hypertrophied nerves, altered distribution of interstitial cells of Cajal, fibromuscular dysplasia of arteries, hyperplasia of lymphoglandular complex Biopsy types: ► Full thickness biopsy of rectum ► Biopsy should be 2cm above anal valve in infant and 3cm in older children ► Suction or mucosal rectal biopsy
TYPES 1. Classic: aganglionic segment begins in distal colorectum and extend in adjacent proximal dilated bowel 2. Short segment: involvement of rectum and rectosigmoid for few cm 3. Ultra-short: involved segment very narrow, easily missed 4. Long-segment: involves most or all of large bowel, may extend into small bowel 5. Zonal colonic aganglionosis: only short segment involved, ganglion cells present below and above aganglionic segment
HIRSCHSPRUNG’S DISEASE ► ↑Acetylcholinesterase activity in lamina propria and muscularis mucosae ► NSE, neurofilaments, highlight hypertrophied nerves and absent ganglion cells ► S-100—absent normal periganglionic satellite cells Acquired Megacolon ► IBD, Chagas disease, intestinal obstruction, psychosomatic disorders
Acquired Megacolon IBD Chagas disease Intestinal obstruction, Psychosomatic disorders
Toxic Megacolon
Normal / Inflamed Appendix
Pathogenesis Acute Appendicitis Appendiceal inflammation is associated with obstruction in 50% to 80% of cases, usually in the form of a fecalith and, less commonly, a gallstone, tumor, or ball of worms (oxyuriasis vermicularis). Continued secretion of mucinous fluid in the obstructed viscus presumably leads to a progressive increase in intraluminal pressure sufficient to cause eventual collapse of the draining veins. Ischemic injury then favors bacterial proliferation with additional inflammatory edema and exudation, further embarrassing the blood supply. Nevertheless, a significant minority of inflamed appendices have no demonstrable luminal obstruction, and the pathogenesis of the inflammation remains unknown.
Acute Appendicitis Morphology: ► Earliest stages, scant neutrophilic exudate in mucosa, submucosa, and muscularis propria. Subserosal vessels congested, and often perivascular neutrophilic infiltrate. Normal glistening serosa changes into dull, granular, red membrane ► Later stage, a prominent neutrophilic exudate generates a fibrinopurulent reaction over the serosa , abscess formation within wall, along with ulcerations and foci of suppurative necrosis in mucosa acute suppurative appendicitis . ► Large areas of hemorrhagic ulceration of mucosa and green-black gangrenous necrosis of wall, extending to serosa, creating acute gangrenous appendicitis , followed by rupture and suppurative peritonitis ► The histologic criterion for the diagnosis of acute appendicitis is neutrophilic infiltration of the muscularis propria.
Acute Appendicitis ACUTE APPENDICITIS OBSTRUCTIVE ► fecolith ► foreign body ► calculus-gall stone ► Mucocoele ► Tumor: primary secondary--- cecum ► Diffuse lymphoid hyperplasia (10 to 19 yrs) ► Oxyuris vermicularis NON OBSTRUCTIVE ► Secondary to generalized infection (viral-Measles)
Fungal  candidiasis,  cryptosporidiosis Others  crohn disease  ulcerative colitis  sarcoidosis  yersiniosis
Acute Appendicitis
ACUTE APPENDICITIS D/D  Mesenteric lymphadenitis  Gynecologic lesions  Acute diverticulitis  Meckel’s diverticulitis  Infarction of greater omentum  Ureteric colic  Chemotherapy induced typhilitis
Tumors of Appendix Non-neoplastic: MUCOSAL HYPERPLASIA Neoplastic: MUCINOUS TUMORS Mucinous cystadenomas Mucinous cystadenocarcinoma ADENOCARCINOMA Primary secondary CARCINOID
CARCINOID ► Most common tumor of appendix ► One in 300 appendicectomies ► Peak incidence in 3rd and 4th decades of life ► Mostly incidental ► Mostly occur at the tip ► Mostly less than 1cm in diameter ► GROSS ► Firm, grayish white ► Fairly well circumscribed ► Not encapsulated ► Characteristic yellow coloration after formalin fixation.
Histologic Pattern of Carcinoid ► Classic insular type ► Carcinoids with glandular differentiation ► Tubular type ► Goblet cell carcinoid
Carcinoid
CLASSIC TYPE ► Solid nests of small monotonous cells with occasional acinar or rosette formation. ► Mitoses rare ► Peculiar retraction of tumor periphery from the stroma ► Invasion of muscle and lymph vessels is the rule ► Spread to the peritoneal surface not rare
IMMUNOHISTOCHEMISTRY Tumor cells are positive for: ► argentaffin ► argyrophil Ultrastructurally: filled with pleomorphic dense core secretory granules Immunohistochemically reactive for: ► neuron-specific enolase, ► chromogranin ► 5-HT
Major Causes of Intestinal Obstruction Mechanical Obstruction ► Adhesions ► Hernias, internal or external ► Volvulus ► Intussusception ► Tumors ► Inflammatory strictures ► Obstructive gallstones, fecaliths, foreign bodies ► Congenital strictures; atresias ► Congenital bands ► Meconium in mucoviscoidosis ► Parasites ► Imperforate anus Pseudo-obstruction ► Paralytic ileus (e.g., postoperative) ► Vascular—bowel infarction ► Myopathies and neuropathies (e.g., Hirschsprung)
Diverticulosis
MECKEL’S DIVERTICULUM
Ischemic Bowel Disease Acute occlusion of Celiac, superior and inferior mesenteric arteries Types ► Mucosal-hypoperfusion acute or chronic ► Mural- “ “ “ “ ► Transmural- occlusion of major mesenteric blood vessels
Predisposing conditions for ischemia ► Arterial Thrombosis- atherosclerosis, vasculitis ► Arterial Embolism-cardiac vegetations ► Venous Thrombosis-Oral contraceptives, postoperative state ► Non occlusive ischemia- cardiac failure, shock, dehydration ► Miscellaneous-radiation injury, volvulus, stricture, amyloidosis, Diabetes mellitus
Ischemic injury two phases ► Initial hypoxic injury ► Secondary reperfusion injury-generation of oxygen free radicals, neutrophils infiltration, production of inflammatory mediators
INFARCTION
INFARCTION
ISCHEMIC COLITIS Age: >50yrs—arteriosclerosis, diabetes, vascular surgery ► Younger pts—collagen-vascular diseases, Wegener’s granulomatosis, amyloidosis, oral contraceptives ► S/S: sudden onset of bleeding, abdominal pain, bloody diarrhea, vomiting ► Site: segmental disease, splenic flexure commonly involved ► D/D: IBD
ISCHEMIC COLITIS X-ray: gas within bowel wall, thumb printing Gross: pseudopolyps, ulceration and fibrosis L/M: in chronic ischemia ulcer covered by granulation tissue extending into submucosa ► Hemosiderin abundant, hyaline thrombi ► Ischemic necrosis—full thickness mucosal necrosis, hyalinized lamina propria, hemorrhage and atrophic crypts in healed stage
Inflammatory Bowel Disease Chronic relapsing inflammatory disorder-obscure origin ► Crohn disease Autoimmune, affect any part of GIT ► Ulcerative colitis Chronic inflammatory disease limited to colon & rectum Both exhibit extra-intestinal inflammatory manifestations
Etiology-Pathogenesis Idiopathic-cause unknown Two key pathogenic abnormalities ► Strong immune response against normal microbial flora in genetic susceptible individuals ► Defects in epithelial barrier function
Pathogenesis of IBD A-Genetic Susceptibility 1. Associated genes with CD are HLA- DR1/DQw5, NOD2 2. HLA-DR 2 increase in U. Colitis B-Intestinal Flora increase immune reaction by providing antigens and inducing co-stimulators and cytokines contribute to T-cell activation, defects in epithelial barrier allow luminal flora to gain access to mucosal lymphoid tissue –trigger immune response C-Abnormal T-Cell response to much T-cell activation and/or too little control by regulatory T- lymphocytes results in damaging the mucosa
Diagnosis of IBD  Clinical history  Radiographic- string sign in CD, Lead pipe in UC  Lab Findings (serum antibodies):  pANCA positive in75%of UC & 11%in CD  ASCA Elevated in CD  Tissue Diagnosis
CROHN DISEASE EPIDEMIOLOGY ► Both sexes female more than males ► All ages peak age 2nd &3rd decade ► Primarily disease of Western developed populations ► Annual incidence in USA 3per 100,000 Fully developed CD is pathologically characterized by; 1. Sharply delimited, transmural inflammatory process with mucosal damage 2. Non-caseating granulomas 3. Fissures and fistulae
GROSS ► Skip lesions ► Cobblestone appearance ► Transmural involvement, Creeping fat ► Early- aphthous ulcers ► Late-Ulcer linear, serpentine and discontinuous with intervening normal or edematous mucosa ► Healing→ long rail-track scars ► Pseudopolyps or mural bridging lesions may develop ► Stricture, fissure, fistulas ► Mesenteric lymphadenopathy
Crohn Disease MICROSCOPY ► Tranmural inflammation ► Fissures ► Non caseating granulomas ► Mucosa relatively normal, normal content of mucin ► Glandular architecture maintained ► submucosal lymph edema, lymphoid hyperplasia, patchy necrosis, atrophy or regenerative hyperplasia. COMPLICATIONS ► Intramural abscess ► Fistulas, perforation ► Occasionally carcinoma.
CROHN DISEASE of COLON (GRANULOMATOUS COLITIS) ►Involve large bowel in 40% cases, with or without ileal component ►Ileum involved-50% ►Anal lesions-75% Complications: Fistula, skin ulceration, toxic megacolon, colonic Ca (risk < UC)
Crohn- Cobble Stone & Sharp Demarcation
CROHN DISEASE
CROHN FISSURE
C/F of CD ► Intermittent attacks of mild diarrhea, fever, and abdominal pain spaced by asymptomatic periods lasting for weeks to many months ► Attacks precipitated by emotional stress ► Colonic involvement can result in fecal blood loss ► Sometime present as a case of acute appendicitis or acute bowel perforation ► Extensive involvement of ileum result in marked loss of albumin- protein losing enteropathy ► Malabsorption of vit B12 P.anemia ► Malabsorption of bile salts –steatorrhea ► Fistulae and Fissures with urinarry bladder, vagina, perianal skin ► Extraintestinal manifesintations migratory polyarthritis, sacroilitis, ankylosing spondylitis, erythema nodusum clubbing of fingers, hepatic primary sclerosing cholangitis
ULCERATIVE COLITIS
ULCERATIVE COLITIS ► Age: 20-30yrs ► Sex: ♂=♀ ► Etiology: unknown ► S/S: prolonged duration, many remissions and exacerbations ► Site: left sided colon, begins in rectosigmoid ► Ulcerative proctitis—disease localized to rectum ► Pancolitis—involve entire colon
ULCERATIVE COLITIS Gross: varies with stage ► Acute: mucosal surface wet and glare  Petechial hemorrhages  Ulcers undermining mucosa, mucosal bridges  Pseudopolyps ► Advanced: bowel—fibrotic, narrowed and shortened  Atrophy of all components of wall  Increased pericolic fat ► Quiescent: no ulceration, mucosa atrophic ► Back wash ileitis
ULCERATIVE COLITIS L/M: mucosal and submucosal disease ► Acute: ↑ inflammatory cells in lamina propria ► Inflammation remain above muscularis mucosae ► Crypt abscess, cyrptitis ► Marked ↓ cytoplasmic mucus, irregularly shaped glands, paneth cell metaplasia ► Atrophic and regenerative changes in glands ► Nuclear enlargement, ↑ mitosis ► Dilated blood vessels, mucosal capillary thrombi ► Ulcers covered by granulation tissue ► Pseudopolyps= granulation tissue + inflammed mucosa
ULCERATIVE COLITIS ► Submucosa—normal, inflammed, hyperemic, infiltrated by fat or fibrosed (depending on stage) ► Submucosal endarteritis obliterans (10%) ► Muscularis externa—hypertrophic/normal ► Subserosal fibrosis Quiescent stage: Mucosa grossly normal Mucin content restored, irregularly branched glands, paneth cells, neutrophils in lamina propria
ULCERATIVE COLITIS Extraintestinal manifestations: liver disease, Arthritis, Uvietis Pyoderma gangreonosum Complications: perforation, peritonitis, abscess, toxic megacolon, venous thrombosis Increase risk of dysplasia/carcinoma
Clinical Manifestation Of UC ► Relapsing disorder, asymptomatic interval of months to years ► Attacks of bloody mucoid diarrhea persist for days, weeks to months ► Initial attack may lead to serious bleeding with fluid and electrolyte imbalance ► Toxic megacolon may lead to perforation
Ulcerative Colitis
Dysplasia in Ulcerative colitis
Features UC CD Clinical Rectal bleeding Common Inconspicuous Abdominal mass Never 10-15% Abdominal pain Left sided Right sided Sigmoidoscopy 95% abnormal <50% abnormal Free perforation 12% 4% Colon CA 5-10% V rare Anal Fissures Rare, minor 75%, fissures.. Response to steroid 75% 25% Results of surgery Very good Fair Ileostomy dysfunction Rare Common
Feature Crohn Disease-SI Crohn Disease-Colon Ulcerative Colitis Macroscopic ► Bowel region Ileum ± colon Colon ± ileum Colon only ► Distribution Skip lesions Skip lesions Diffuse ► Stricture Early Variable Late/rare ► Wall appearance Thickened Thin Thin ► Dilation No Yes Yes Microscopic ► Inflammation Transmural Transmural Limited in mucosa ► Pseudopolyps No to slight Marked Marked ► Crypt Abscess Not seen Common ► Ulcers Deep, linear Deep, linear Superficial ► Lymphoid reaction Marked Marked Mild ► Fibrosis Marked Moderate Mild ► Serositis Marked Variable Mild to none ► Granulomas Yes (50%) Yes (50%) No ► Fistulae/sinuses Yes Yes No ► Lymph node Granulomas Do Reactive Clinical ► Fat/vit malabsorp Yes Yes, if ileum No ► Malignant potential Rare +/- Yes ► Resp to surgery Poor Fair Good
Tumors Small & Large Intestine Non-neoplastic (Benign) Polyps ► Hyperplastic polyps ► Hamartomatous polyps • Juvenile polyps • Peutz-Jeghers polyps ► Inflammatory polyps ► Lymphoid polyps Neoplastic Epithelial Lesions Benign • Adenoma * Malignant • Adenocarcinoma * • Carcinoid tumor • Anal zone carcinoma Mesenchymal Lesions ► Gastrointestinal stromal tumor (GIST) ► Other benign lesions • Lipoma • Neuroma • Angioma ► Kaposi sarcoma Lymphoma Metastatic
Intestinal Polyps
Hyperplastic/ PJ polyp
Juvenile Rectal Polyp
Tubular adenoma
Adenomatous polyps
Villous adenoma
Villous adenoma
Familial polyposis
Gardenar syndrome
Adenocarcinoma colon
Adenocarcinoma Colon
BENIGN EPITHELIAL TUMORS BRUNNER’S GLAND ADENOMA ► Nodular proliferation of histologically normal Brunner’s glands, accompanied by ducts and scattered stromal elements, cilliated cysts and adipose tissue. ► Focal multifocal or diffuse ► Located commonly at posterior wall of duodenum at junction of first and second parts.
BENIGN EPITHELIAL TUMORS ADENOMAS ► More often In duodenum and jejunum’ single or multiple, sessile or pedunculated ► Microscopically can be villoglandular polyp, adenomatous polyp or villous adenoma. ► Malignant transformation can occur mostly when lesion is large villous or multiple. HAMARTOMATOUS POLYP Benign juvenile Rectal polyp ► Jejunoileum– (in Peutz Jeghers syndrome) ► Glands supported by broad bands of smooth muscle fibers ► Several types of epithelial cells are present. ► Associated with adenocarcinima and adenoma malignum of uterine cervix, ovarian mucinous tumors, breast carcinoma.
ADENOCARCINOMA ► Both sexes elderly population less common than counterpart in colon. ► More common in upper portion of small bowel ► Associated with hereditary nonpolyposis colorectal carcinoma syndrome, Peutz-Jeghers syndrome, Reckling- huasen’s disease, bowel duplication, Crohn’s disease, at ileostomy sites, jejunal limb of Roux-en-Y esophagojejunostomy. ► GROSS- duodenal carcinoma; papillary configuration, distal lesions; napkin-ring, polypoid or fungating appearance ► MICROSCOPY- moderately well differentiated adenocarcinoma. Mucin production, CEA reactivity is the rule ► Commonly positive for chromogranin 5-HT ► IMMUNO- COX-2, sPLA2 cPLA2.peptide hormones ► ULTRASTRUCTURE- prominent development of microvilli.
SMALL CELL NEUROENDOCRINE CARCINOMA ► Rare, ► MICROSCOPY- Small round oval cells, scanty cytoplasm, hyperchromatic nucleus. ► ULTRASTRUCTURE- dense-core granules of neurosecretory type ► IMMUNORECTIVE for neuroendocrine markers ► Deeply invasive, prone to metastasis, very poor prognosis. ANAPLASTIC CARCINOMA ► Highly bizarre tumor cells, multinucleated with abundant cytoplasm, no glandular differentiation. ► Aggressive
CARCINOID TUMORS ► Low grade neoplasm originating from the diffuse neuroendocrine system outside of pancreas and thyroid C cells. ► Adults, ► Located in ileum mostly ► GROSS- intact mucosa , tumor infiltrating the submucosa and extending to muscularis externa. ► Buckling of bowel wall due to fibrosis ► Brightly yellow color ► MICROSCOPY- solid nests of monotonous population of cells having small round nuclei scant to moderate granular cytoplasm fine nucleoli. ► Peripheral palisading common , scanty mitotic figures, lymphatic and neural invasion common. ► Microscopic types from A to E : insular, trabecular, glandular, undifferentiated, mixed.