1. Gastrointestinal Tract
2. Small & Large Intestines
3. 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.
common bile duct (CBD) & pancreatic duct empty into 2nd part
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
4. Small & Large intestine – Normal
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)
anastomotic capillary bed between superior and inferior hemorrhoidal veins forming portal and systemic connections
Ascending and Descending colon
Accessory Blood supply and lymphatic drainage from posterior abdominal wall
Run as parallel vessels but without arcades
5. Small & Large intestine – Normal
lymphoid tissue (MALT)
ileum - Payer patches (Grossly visible )
M (membranous) cells
Transport Ag to APC in SI & LI lymphoid sites
Small intestinal peristalsis- anterograde and retrograde
mediated by intrinsic (Myenteric plexus) and extrinsic (autonomic innervation) neural control
Meissner plexus (in submucosa)
Auerbach plexus (in muscle wall layers)
6. Small intestine – Normal
8. Intestines- Pathology
Anorexia, nausea, vomiting, flatulence, bloating, abdominal discomfort, weight loss, malaise.
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
9. Intestines - Pathology
10. 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
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)
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)
11. Meckel’s Diverticulum
12. 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 with Down 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
Obstruction( neoplastic) or inflammatory stricture of the bowel
Toxic megacolon - ulcerative colitis or Crohn disease
13. Intestines - Pathology
14. 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
15. Types of Diarrhea
16. Intestines - Pathology Enterocolitis (EC)
17. Intestines - Pathology Enterocolitis (EC)
18. Acute, self-limited infectious diarrhea
major cause of morbidity among children
MCC - enteric viruses
Food & water infections ? Damage of small intestinal epithelium with shortening of villi
Diarrhea for 1-7 days.
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
19. Bacterial EC
Morphologic changes depend upon the causative agent
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)
Ingestion of preformed toxins
Develop within a matter of hours
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
20. Bacterial EC
Massive fluid loss or destruction of intestinal mucosal barrier
Include dehydration, sepsis, and perforation
Feces contaminated beef and chicken
major sources of Salmonella in USA
improperly cooked chicken
Campylobacter jejuni ( Common than Shigella & Salmonella)
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
21. Pseudo-membranous colitis= Antibiotic-associated colitis (EC)
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 overgrowth in the small intestine
Clinically=present with chronic diarrhea, abdominal pain, Malabsorption, and weight loss
Diagnosis=Breath tests for volatile bacterial byproducts
demonstration of bacteria in the proximal small intestine by direct culture
22. Parasitic EC
1. Ascaris lumbricoides- MC
obstruct the intestine or biliary tree
Diagnosis -detection of the eggs in the feces
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
never invade beyond the intestinal mucosa
Diphyllobothrium latum (fish tapeworm)
Taenia solium (pork tapeworm)
Hymenolepsis nana (dwarf tapeworm)
Amebiasis (Entamoeba histolytica )
24. Amebiasis vs. Giardiasis Amebiasis
L I (cecum & A. colon)
trophozoites have one nucleus
SI (duodenum )
trophozoites have two nuclei
25. Necrotizing Enterocolitis
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
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
Radiology - unremarkable
Clinically - characterized by chronic watery diarrhea
Clinical course - benign in nature
26. Miscellaneous EC
Neutropenic Colitis (Typhlitis) =acute inflammatory destruction of the mucosa
compromised blood flow
Commonly at cecal region
Pathogenesis = impaired mucosal immunity
Solitary Rectal Ulcer Syndrome
Inflammation of the rectum
impaired relaxation &sharp angulation of the anterior rectal shelf
mucus discharge from the anus
superficial ulceration of the anterior rectal wall
27. Intestines - Pathology
28. Malabsorption Syndromes
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
30. 3) Whipple’s disease =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
31. 5. Abetalipoproteinemia
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 ? acanthocytic erythrocytes (burr cells), and widespread cell injury.
Presents in infancy with malabsorption & wasting.
32. Intestines - Pathology
33. Idiopathic Inflammatory Bowel Diseases
Etiology & Pathogenesis
Characterized by= A chronic, relapsing inflammatory conditions
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)
34. Different Clinical, Endoscopic, and Radiographic Features of Crohn’s & Ulcerative Colitis
36. Intestines - Pathology Idiopathic Inflammatory Bowel Diseases
37. Intestines - Pathology
38. Types of Ischemic Bowel Diseases
39. Angiodysplasia= 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
40. Intestines - Pathology
41. Intestinal Obstruction
MC site =small intestine ( why?)
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
Twisting of bowel loops around peritoneal fibrous bands
Caused by previous surgery, infection, endometriosis or radiation
A segment of the gut telescopes into the distal one
May be caused by tumors
Complete twisting of a bowel loop around its mesenteric base
MC =sigmoid colon
42. Intestines - Pathology Tumors
43. Intestinal Neoplasms
Small intestine= neoplasms are rare
MC = Adenoma
MC site - ampulla of Vater
Complaints= occult blood loss/ rarely-obstruction or intussusceptions
Associated with familial polyposis
Rx =surgical excision difficult
MC site - duodenum
clinical -intestinal obstruction
occult blood loss -only sign
if involves ampulla of Vater -cause fluctuating obstructive jaundice
most tumors -no identifiable factor
Crohn’s, celiac disease, FAP, HNPCC& Peutz - Jeghers syndrome)
44. Intestines - Pathology Tumors
45. Intestinal Neoplasms
Large intestine= neoplasms are common
MC = Adenoma= Polyp
MC site of GI Polyps= Colon
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)
46. Intestinal Neoplasms
Large intestine=Neoplastic or adenomatous( Tubular, Villous, Tubulo-villous)
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)
FAP syndrome associated with abnormal dentition, epidermal cysts, desmoid tumors, osteomas, duodenal & thyroid cancers
FAP syndrome associated with CNS gliomas.
47. Intestinal Neoplasms
Large intestine= Colorectal carcinoma
One of the MC malignancies
Peak age –
60 - 70 years for sporadic cases
30 - 40 years– for FAP syndromes
Arise in preexisting adenomas
rich in carbohydrates & fats and
low in vegetables & Fruits & vitamins (A, C & E).
Site= distal colon
All are invasive adenocarcinomas
Iron deficiency anemia (occult bleeding), abdominal discomfort, progressive bowel obstruction, weight loss and liver metastases.
Depends upon ***clinical stage
staging system = Astler-Coller modification of Duke’s staging system
48. Intestines - Pathology L 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 - Penetrating through 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%)
49. Intestinal Neoplasms
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
90% without metastases
50% with metastasis
50. Case - 1 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.
55. Case -2 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).
61. Case - 3 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).