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Gastrointestinal Tract. Small & Large Intestines. Small intestine Duodenum, Jejunum & Ileum Villi & microvilli increase surface area of the mucosa crypts of Lieberkuhn =Between the bases of the villi are pits Normal villus : crypt height ratio ~ 4:1.

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  • Small intestine

  • Duodenum, Jejunum & Ileum

  • Villi & microvilli increase surface area of the mucosa

  • crypts of Lieberkuhn =Between the bases of the villi are pits

  • Normal villus : crypt height ratio ~ 4:1.

  • Digestive enzymes (brush border enzymes) are located in the membranes of microvilli.

  • Duodenum

    • common bile duct (CBD) & pancreatic duct empty into 2nd part

    • Brunner’s glands

  • Ileum

    • Payer’s patches

  • Large intestine

  • Cecum (& its appendix); colon (ascending, transverse, descending & sigmoid); rectum & anal canal.

  • lacks villi & Micovilli

  • Has numerous goblet cells in the mucosa.

  • Absorption of fluids, electrolytes & secretion of mucous


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  • Small & Large intestine – Normal

  • Arterial supply

    • up to hepatic flexure of the colon – by superior mesenteric A.

    • Remainder up to rectum- by inferior mesenteric A.

    • arterial interconnections - mesenteric arcades

    • upper rectum - superior hemorrhoidal A ( from inferior mesenteric A)

    • lower rectum –hemorrhoidal A (from internal iliac or internal pudendal artery)

  • venous drainage

    • same distribution

    • anastomotic capillary bed between superior and inferior hemorrhoidal veins forming portal and systemic connections

    • Ascending and Descending colon

      • retroperitoneal

      • Accessory Blood supply and lymphatic drainage from posterior abdominal wall

  • Lymphatics

    • Run as parallel vessels but without arcades


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    • Small & Large intestine – Normal

    • Immune System

      • lymphoid tissue (MALT)

        • ileum - Payer patches (Grossly visible )

      • M (membranous) cells

        • Transport Ag to APC in SI & LI lymphoid sites

    • Neuromuscular Function

      • Peristalsis

        • Small intestinal peristalsis- anterograde and retrograde

        • mediated by intrinsic (Myenteric plexus) and extrinsic (autonomic innervation) neural control

      • Myenteric plexus

        • Meissner plexus (in submucosa)

        • Auerbach plexus (in muscle wall layers)

    • Function


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    Small intestine – Normal

    V

    Villus : Crypt

    LM

    C

    EM

    What are these glands?


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    Intestines

    lacks villi &presence of

    numerous goblet cells

    SI

    LI


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    • Intestines- Pathology

      Symptoms:

    • General

      • Anorexia, nausea, vomiting, flatulence, bloating, abdominal discomfort, weight loss, malaise.

    • Specific

      • Esophageal -Dysphagia (difficulty in swallowing), odynophagia (painful swallowing), heartburn, regurgitation, retrosternal pain.

      • Gastric -early satiety, hematemesis, upper abdominal pain/discomfort.

      • Small Intestinal -diarrhea, steatorrhea (malabsorption), anemia, abdominal colic.

      • Large Intestinal -diarrhea, constipation, blood and mucus per rectum, tenesmus, proctalgia, anemia



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    • Intestines- Congenital Anomalies

    • Atresia  complete obstruction

      • MC site -duodenum

        • Cause of neonatal intestinal obstruction

      • jejunum and ileum - equally involved

      • colon - never involved

    • Stenosis incomplete obstruction

      • less common

    • Imperforate Anus failure of cloacal diaphragm to rupture

       neonatal intestinal obstruction

    • Meckel’s Diverticulum  True Diverticulum

    • 2% rule (2 feet from the iliocecal valve, seen in 2% of people, 2” in size)

    • asymptomatic.

    • May contain gastric or pancreatic tissues & ( peptic ulcers, diverticulitis, intestinal obstruction ,intussusception), ...

    • Persistent segment of the vitelline duct (h connects the yolk sac + gut lumen)



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    • Aganglionic Megacolon (Hirschsprung’s Disease)

    • Caused by=Arrested migration of nerve elements into distal part of gut

    • Absence of ganglion cells in the large bowel (Aurbach’s &Meissner’s plexus)

    • 50% of familial & 15% of sporadic cases are due to mutations in the RET gene

      • RET-promote survival and growth of neurite & direction to migrating neural crest cells

    • Characterized by =Aganglionic (aperistaltic) segment narrow

    • unaffected proximal colon  dilatation and hypertrophy (megacolon)

    • Clinically =↑risk withDown syndrome

      • Affects 1 in 8000 live births, M : F = 4 : 1

      • Presents as meconium ileus, abdominal distension, constipation, diarrhea (Enterocolitis) & perforation (rare).

    • Diagnosis=Histological demonstration of absence of ganglion cells in intestinal submucosa

      • stained for acetyl cholinesterase.

    • Differential Diagnosis = any Acquired megacolon

      • Chagas disease

      • Obstruction( neoplastic) or inflammatory stricture of the bowel

      • Toxic megacolon - ulcerative colitis or Crohn disease

      • functional causes



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    • Diarrhea = frequent passage of loose watery stools.

      • Secretory Diarrhea = passage of >500 ml/day watery stools, isotonic with plasma (intestinal secretion).

      • Osmotic Diarrhea = >500 ml/d stools, the osmolality of which exceeds that of plasma by >50 mOsm.

      • Exudative Diarrhea = frequent passage of loose, purulent, bloody stools.

    • Dysentery = painful bloody diarrhea (tenesmus)

    • Malabsorption = bulky stools with excess fat (floats on water) & increased osmolality



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    Intestines - PathologyEnterocolitis (EC)


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    Intestines - PathologyEnterocolitis (EC)


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    • Acute, self-limited infectious diarrhea

      • major cause of morbidity among children

      • MCC - enteric viruses

    • Viral EC

    • Characterized by:

      • Food & water infections Damage of small intestinal epithelium with shortening of villi

      • Diarrhea for 1-7 days.

    • MCC are:

      • Rotavirus (Group A) outbreaks in children 6-24months

      • selectively infects and destroys mature enterocytes in the small intestine, without infecting crypt cells

      • Norwalk viruses food-borne nonbacterial outbreaks in school children & adults

      • Adenoviruses  outbreaks in infants


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    • Bacterial EC

      • Morphologic changes depend upon the causative agent

    • Pathogenic mechanisms:

    • Ingestion of preformed toxins present in contaminated food by

      • Staph. aureus, Clost. Perfringens, Vibrios

    • Infection by toxigenic organisms

      • Proliferate within the gut lumen and elaborate an enterotoxin

        • Enteroinvasive organisms (E. coli, Shigella, Salmonella)

      • Proliferate, invade, and destroy mucosal epithelial cells

      • Enterotoxins are either:

        • Secretagogues (cholera toxin)

        • Cytotoxins (Shiga toxin)

    • Clinical features:

      • Ingestion of preformed toxins

        • Develop within a matter of hours

        • Explosive diarrhea

        • Acute abdominal distress

        • Passes in a day or so

      • Infection with enteric pathogen:

        • Incubation period of several hours to days

        • Followed by diarrhea and dehydration


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    • Bacterial EC

    • Complications:

      • Massive fluid loss or destruction of intestinal mucosal barrier

      • Include dehydration, sepsis, and perforation

    • Feces contaminated beef and chicken

      • major sources of Salmonella inUSA

    • improperly cooked chicken

      • Campylobacter jejuni ( Common than Shigella & Salmonella)

    • Cholera toxin

      • Causes secretory diarrhea by

      • 1. Permanently activate GTP  persistent activation of adenylate cyclase  high levels of intracellular cAMP  stimulates secretion of chloride and bicarbonate

      • 2. Chloride and sodium Resorption - inhibited


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    • Pseudo-membranous colitis= Antibiotic-associated colitis (EC)

      • acute colitis

    • Caused by=Enterotoxins of Clostridium dificile

      • Due to toxins A & Bcytokine production cell apoptosis

    • Characterized by=The formation of an adherent necrotic membrane (pseudomembrane) overlying extensive mucosal inflammation

      • Pseudo membrane is composed of mucus, fibrin & inflammatory debris

    • Similar fibrino-purulent necrotic pseudomembrane forms in enteroinvasive infections & in ischemic EC

    • Clinical features=Presents as an acute diarrhea while on antibiotic therapy

      • toxin detectable in stools.

      • Responds to appropriate antibiotics

    • Bacterial Overgrowth Syndrome

    • Cause= Surgical procedures -decreasing the time for exposure of ingested bacteria to gastric acid

      • bacterial overgrowthin the small intestine

    • Clinically=present with chronic diarrhea, abdominal pain, Malabsorption, and weight loss

    • Diagnosis=Breath tests for volatile bacterial byproducts

      • clinical history

      • demonstration of bacteria in the proximal small intestine by direct culture


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    • Parasitic EC (EC)

    • Nematodes

      1. Ascaris lumbricoides- MC

      • obstruct the intestine or biliary tree

      • pneumonitis

      • hepatic abscess

      • Diagnosis -detection of the eggs in the feces

        2. Strongyloides

      • pulmonary infiltrates with eosinophilia

      • Autoinfection in immunosuppressed

        3. Hookworm (Necator duodenale and Ancylostoma duodenale)

      • intestinal mucosa -erosions, focal hemorrhage

      • Long-term infection lead to IDA

        4. Enterobius vermicularis (pinworms)

      • perineal pruritus – worms migrate to the anal orifice deposits eggs

      • Diagnosis -perianal skin tape

        5. Trichuris trichiura (whipworm)

      • Heavy infections - cause bloody diarrhea and rectal prolapse

      • in young children


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    • Cestodes (EC)

    • never invade beyond the intestinal mucosa

    • No eosinophilia

    • Diphyllobothrium latum (fish tapeworm)

    • Taenia solium (pork tapeworm)

    • Hymenolepsis nana (dwarf tapeworm)

    • Protozoa

    • Amebiasis (Entamoeba histolytica )

    • Giardiasis


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    Amebiasis (EC)

    L I (cecum & A. colon)

    Dysentery

    flask-shaped ulcer

    trophozoites have one nucleus

    No flagella

    Giardiasis

    SI (duodenum )

    Diarrhea

    No Ulcers

    trophozoites have two nuclei

    Flagellated

    Amebiasis vs. Giardiasis

    Rx –Same for both


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    • Necrotizing Enterocolitis (EC)

    • MC acquired gastrointestinal emergency of neonates

    • Particularly premature or LBW Babies

    • Characterized by =Necrotizing inflammation of the small and large intestine

    • Due to =Immaturity of gut immune system

    • Initiation of oral feeding  elicits release of cytokines (PAF) inflammatory response

    • Gut colonization with bacteria

    • Mucosal injury

    • Morphology =Primarily affects terminal ileum and ascending colon( Gas in intestinal walls - radiology)

    • Clinical Features =Mild gastrointestinal disturbance or as a fulminant illness with intestinal gangrene, perforation, sepsis, and shock

    • Collagen & Lymphocytic EC

    • Collagen EC =patches of band like collagen deposits under the surface epithelium, common in middle-aged and older women (W>M)

    • Lymphocytic EC =intraepithelial infiltrate (M:F=1:1)

    • In Both the conditions

      • Endoscopy -normal

      • Radiology - unremarkable

      • Clinically - characterized by chronic watery diarrhea

      • Clinical course - benign in nature


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    • Miscellaneous EC (EC)

    • Neutropenic Colitis (Typhlitis) =acute inflammatory destruction of the mucosa

    • compromised blood flow

    • Commonly at cecal region

    • Pathogenesis = impaired mucosal immunity

    • life-threatening

    • Solitary Rectal Ulcer Syndrome

    • Inflammation of the rectum

    • impaired relaxation &sharp angulation of the anterior rectal shelf

    • inflammatory polyp

    • Characteristic triad

      • rectal bleeding

      • mucus discharge from the anus

      • superficial ulceration of the anterior rectal wall



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    • Malabsorption Syndromes (EC)

    • Characterized by =Deficient absorption of fats, proteins & carbohydrates, as well as electrolytes, minerals, fat soluble vitamins & water. vit. Deficiency, tetany

    • Caused by=Deficient digestion (Biliary-pancreatic disease)

      • Deficient absorption (small intestinal disease)

    • Clinical findings =Weight loss, flatulence & diarrhea with bulky, frothy, greasy stools

    • In prolonged cases =Anemia, petechiae, hemorrhages, dermatitis, bone aches, latent tetany, menstrual disturbances, impotence or infertility.

    • MCC= Celiac sprue, chronic Pancreatitis, Crohn’s disease, tropical sprue, Whipple’s disease, bacterial overgrowth, Disaccharidase deficiency & Abetalipoproteinemia

    • 1. Celiac Sprue

    • 2) Tropical sprue


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    • 3) Whipple’s disease = (EC)Rare systemic disease

    • involves intestines, joints & CNS

    • Caused by = Gram-positive actinomycetes Tropheryma Whippelii (not yet cultured)

    • Affects= white Males (M:F=10 :1), 30-50 yrs

    • Hallmark features= distended macrophages in lamina propria contain

      PAS+ve granules (tiny rod-shaped bacilli in EM)

    • Clinical features =malabsorption syndrome, fever, joint pains, cardiac & neurologic S&S

      • Wt. Loss – MC presenting feature

    • Rx-broad-spectrum antibiotic therapy

    • 4. Disaccharidase deficiency

    • Apical membrane enzyme that cleaves lactose.

    • deficiency accumulation of lactose in the gut lumen; exerting an osmotic “purgative” effect  diarrhea & malabsorption.

    • Congenital forms = infants on exposure to milk or milk products.

    • acquired form = more common & affects adults, blacks > whites, (probably related to intestinal infections)

    • Intestinal mucosa shows no morphologic abnormalities


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    • 5. Abetalipoproteinemia (EC)

    • Congenital deficiency of beta lipoprotein which is required for intestinal transport of chylomicrons.

    • The inability to synthesize apoprotein (required to assemble lipoproteins) by the enterocytes leads to accumulation of triglycerides in the cells, with lipid Vacuolation.

    • Results in marked lowering of serum LDL, VLDL & chylomicrons defective lipid-membranes of cells, including red blood cells acanthocyticerythrocytes (burr cells), and widespread cell injury.

    • Presents in infancy with malabsorption & wasting.

    Normal

    Malabsorption



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    Idiopathic Inflammatory Bowel Diseases (EC)

    • Etiology & Pathogenesis

    • Characterized by= A chronic, relapsing inflammatory conditions

    • unknown etiology.

    • speculations involve= Genetic factors, unknown infectious agents, special susceptibility factors, altered immuno-reactivity to dietary or infectious antigens & altered regulatory controls of the inflammatory responses

    • Distinguished into two clinicopathologic entities:

      • Crohn’s disease (CD)

      • Ulcerative colitis (UC)

    • Crohn’s disease (CD)

    • Transmural granulomatous inflammation of the bowel, with mucosal ulcerations, fissures & fistulas in Young (20s)whites Females

    • Skip lesions (cobble stone app.)

    • Ulcerative colitis (UC)

    • crypt abscesses, psudopolyps & ↑risk of carcinoma (adenocarcinoma)



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    Intestines - Pathology Crohn’s & Ulcerative Colitis Idiopathic Inflammatory Bowel Diseases

    Fissuring Ulcer

    noncaseating granulomas

    (UC)

    (CD)


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    Intestines - Pathology Crohn’s & Ulcerative Colitis


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    Types of Ischemic Bowel Diseases Crohn’s & Ulcerative Colitis


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    • Angiodysplasia Crohn’s & Ulcerative Colitis= Tortuous dilated sub mucosal veins in the cecum

    • May cause massive bleeding.

    • Occurs in old age

    • Hemorrhoids =Dilated varicose veins of the perianal plexuses

    • Affect 5% of adults

    • Due to Chronic constipation, Pregnancy, Liver cirrhosis

    • two types which may occur singly or together:

    • External (inferior hemorrhoidal plexus)- painful

    • Internal (superior hemorrhoidal plexus)- painless

    • May cause hemorrhage, inflammation, thrombosis & fissures

    • Diverticular Disease= Multiple, flask like outpouchings

    • > 60 years.

    • Characterized by= protruding into the appendices epiploicae, in the distal colon.

      • They are lined by mucosa but no muscularis propria.

    • Caused by= Focal anatomic defect in the bowel wall at the site of penetration of blood vessels.

      • Increased intraluminal pressure is a contributory factor (constipation & increased peristalsis).

    • Complications are=Bleeding, Diverticulitis, pericolic abscess, peritonitis


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    Intestines - Pathology Crohn’s & Ulcerative Colitis


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    Intestinal Obstruction Crohn’s & Ulcerative Colitis

    • MC site =small intestine ( why?)

    • Hernias

      • Protrusion of peritoneal “hernial” sac into a defect in the abdominal wall (inguinal, femoral, umbilical, surgical scars & retroperitoneal space).

      • Viscera become trapped incarceration, obstruction, strangulation

    • Adhesions:

      • Twisting of bowel loops around peritoneal fibrous bands

      • Caused by previous surgery, infection, endometriosis or radiation

    • Intussusceptions:

      • A segment of the gut telescopes into the distal one

      • May be caused by tumors

    • Volvulus:

      • Complete twisting of a bowel loop around its mesenteric base

      • MC =sigmoid colon


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    Intestines - Pathology Crohn’s & Ulcerative ColitisTumors


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    Intestinal Neoplasms Crohn’s & Ulcerative Colitis

    • Small intestine= neoplasms are rare

    • Benign tumors

      • MC = Adenoma

      • MC site - ampulla of Vater

      • Complaints= occult blood loss/ rarely-obstruction or intussusceptions

      • Associated with familial polyposis

      • Rx =surgical excision difficult

      • Clinical Course=premalignant

    • Malignant tumors

      • MC= Adenocarcinoma

      • MC site - duodenum

      • clinical -intestinal obstruction

      • occult blood loss -only sign

      • if involves ampulla of Vater -cause fluctuating obstructive jaundice

      • risk factors

        • most tumors -no identifiable factor

        • Crohn’s, celiac disease, FAP, HNPCC& Peutz - Jeghers syndrome)


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    Intestines - Pathology Crohn’s & Ulcerative ColitisTumors

    Malignant

    Benign


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    Intestinal Neoplasms Crohn’s & Ulcerative Colitis

    • Large intestine= neoplasms are common

    • Benign tumors

    • MC = Adenoma= Polyp

    • MC site of GI Polyps= Colon

    • Types

      • Non-neoplastic (Hyperplastic, inflammatory, hamartomatous)

      • Neoplastic or adenomatous( Tubular, Villous, Tubulo-villous)

    • Malignant risk of adenomatous polyps correlates with:

      1) polyp size ( > 4cm)

      2) degree of dysplasia

      3) extent of villous component (More villous= more cancerous)


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    Intestinal Neoplasms Crohn’s & Ulcerative Colitis

    • Large intestine=Neoplastic or adenomatous( Tubular, Villous, Tubulo-villous)

    • True neoplasms

    • Cause occult bleeding, anemia, protein loss, obstruction

    • FAP syndrome= 100 polyps and 100% malignant risk

      • Autosomal dominant inheritance

      • innumerable polyps (minimum 100, may be >1000) in the colon & other parts of the GIT

      • 100% risk of progression to adenocarcinoma in 10-15 years (indication for prophylactic pancolectomy).

      • Onset in adolescence (bleeding & anemia)

    • Gardner’s syndrome:

      • FAP syndrome associated with abnormal dentition, epidermal cysts, desmoid tumors, osteomas, duodenal & thyroid cancers

    • Turcot’s syndrome:

      • FAP syndrome associated with CNS gliomas.


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    Intestinal Neoplasms Crohn’s & Ulcerative Colitis

    • Large intestine= Colorectal carcinoma

    • Epidemiology:

      • One of the MC malignancies

      • Peak age –

        • 60 - 70 years for sporadic cases

        • 30 - 40 years– for FAP syndromes

    • Etiology/Pathogenesis:

      • Arise in preexisting adenomas

      • Related to:

        • Genetic factors

        • ***Diet

          • rich in carbohydrates & fats and

          • low in vegetables & Fruits & vitamins (A, C & E).

      • Site= distal colon

    • All are invasive adenocarcinomas

    • Clinical Presentation:

      • Iron deficiency anemia (occult bleeding), abdominal discomfort, progressive bowel obstruction, weight loss and liver metastases.

    • Prognosis:

      • Depends upon ***clinical stage

      • staging system = Astler-Coller modification of Duke’s staging system


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    Intestines - Pathology Crohn’s & Ulcerative ColitisL I Tumors Astler-Coller modification of Duke’s staging system

    • A - Limited to mucosa

    • B1 - Extending to (not penetrating) muscularis propria; no LNs

    • B2 - Penetrating the muscularis propria, but with no LNs

    • C1 - Extending to (not penetrating) muscularis propria+ LNs.

    • C2 - Penetratingthrough muscularis propria+ LNs.

    • D - Distant metastatic spread.

    • Surgery is the only hope for cure.

    • Prognosis ( 5-year survival )

      • Stage A (100%),

      • B1 (65%), B2 (55%),

      • C1 (45%), C2 (25%)


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    Intestinal Neoplasms Crohn’s & Ulcerative Colitis

    • Carcinoid Tumors:

    • MC site = Appendix

    • Represent one-half of small intestinal malignancies.

    • Peak Age= sixth decade.

    • Arise from Neuroendocrine cells, secrete active amines or peptides (gastrin  Zollinger-Ellison syndrome, insulin  hypoglycemia, ACTH  Cushing’s syndrome, serotonin  carcinoid syndrome).

    • Liver Metastasis – what is the clinical implication ?

      • Appendiceal & rectal carcinoids rarely metastasize.

      • Ileal, gastric & colonic carcinoids commonly metastasize

    • Prognosis=5-year survival

      • 90% without metastases

      • 50% with metastasis


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    Case - 1 Crohn’s & Ulcerative Colitis

    • A 31-year-old woman has had a 10 year history of intermittent, bloody diarrhea. Radiographic studies and sigmoidoscopy revealed a friable, ulcerated colonic mucosa extending to the splenic flexure . The descending colon along with sigmoid colon and rectum were resected. The gross specimen shown is from another case with even more severe disease, in which the ulceration extends nearly to the ileocecal valve. Image reveals the appearance of the mucosa on closer inspection. Microscopic examination reveals the appearance.


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    1.1 Crohn’s & Ulcerative Colitis


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    1.2 Crohn’s & Ulcerative Colitis


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    1.3 Crohn’s & Ulcerative Colitis


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    1.4 Crohn’s & Ulcerative Colitis


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    Case -2 Crohn’s & Ulcerative Colitis

    • A 27-year-old man has had recurrent attacks of abdominal pain, diarrhea, and low-grade fever for several months. He has also developed steatorrhea. Colonoscopy revealed erythema and erosions of the terminal ileum (image 2.1). Radiographic studies demonstrate an enteroenteric fistula that bypassed much of the small intestine, which was the cause of the malabsorption and steatorrhea (image 2.2). He was taken to surgery where a portion of small intestine was resected. The gross specimen is shown in image 2.3. The microscopic appearance is seen in images 2.4 and 2.5).


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    2.1 Crohn’s & Ulcerative Colitis


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    2.2 Crohn’s & Ulcerative Colitis


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    2.3 Crohn’s & Ulcerative Colitis


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    2.4 Crohn’s & Ulcerative Colitis


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    2.5 Crohn’s & Ulcerative Colitis


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    Case - 3 Crohn’s & Ulcerative Colitis

    • A 43-year-old man came in to the emergency room because of intense abdominal pain associated with abdominal swelling which had developed over the past two days. A plain film radiograph of the abdomen showed numerous dilated loops of small intestine. A laparotomy was performed. The lower ileum was found to have a palpable mass lesion involving the muscular wall that obstructed the lumen (image 6.1). A segmental resection of ileum was performed. The opened bowel specimen from surgery shows a segment of buckled small bowel. At the apex of the buckle, the mucosa is ulcerated. Beneath this can be seen the lesion (images 6.2 to 6.3).


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    3.1 Crohn’s & Ulcerative Colitis


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    3.2 Crohn’s & Ulcerative Colitis


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    3.3 Crohn’s & Ulcerative Colitis


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