Category Archives: Small Intestine
Microvillus Inclusion Disease
Microvillus Inclusion Disease
Clinical presentation
- intractable watery diarrhea in infants
Histology
- atrophic villi with no inflammation
Immunohistochemistry
- CD10 blush
Electron Microscopy
- abnormal microvillus structures, intracytoplasmic inclusions lined by microvilli
Lactose Intolerance
Lactose Intolerance
Disaccharidase Deficiency, Lactase Deficiency
- located in apical cell
Congenital Lactase Deficiency
- rare; malabsorption with milk –> explosive, watery stools and abdominal distention
Acquired Lactase Deficiency
- North American Blacks causes osmotic diarrhea
Diagnosis
- increased hydrogen in breath test (bacterial fermentation of undigested lactose)
Treatment
- terminate milk and milk products
Villous Atrophy
Villous Atrophy Differential Diagnosis
Kwashiorkor
Infectious enteritis (Giardia)
Dermatitis herpetiformis
Celiac disease, CVID
Allergy to protein
Crohn’s disease
Autoimmune enteropathy
Sprue (Tropical, Whipple)
Celiac Sprue
Celiac Sprue
Celiac Disease
Clinical presentation
- sensitivity to gluten, malabsorption, weight loss
- improves following removal of gluten from diet
- associated with lymphocytic colitis, DM type I, Sjogren’s, autoimmune thyroiditis
Pathophysiology:
- abnormal cell mediated immunity
- antibody directed at gliadin, alcohol soluble moeity of gluten
- decreased absorption
Celiac Disease Diagnosis
- increased antibody and characteristic histologic findings and improvement following withdrawal of gluten from diet
- can only say “consistent with celiac sprue”
Celiac Disease Complications
1. enteropathy-associated T-cell lymphoma
2. small intestinal adenocarcinoma
3. associated dermatitis herpetiformis
4. associated diabetes mellitus type 1
Celiac Disease Histology
- overall thickness is the same
- villous atrophy and crypt hyperplasia
- increased intraepithelial lymphocytes
- none to minimal acute inflammation
Celiac Disease Bloodwork
- increased IgA, anti-gliadin, anti-endomyseal, anti-transgluataminase antibodies
Celiac Disease Genetics
- HLA DQa/b heterodimer haplotype linked to celiac disease
Agammaglobulinemic Sprue
Agammaglobulinemic Sprue
- No plasma cells in lamina propria
Malabsorption
Small Intestine Malabsorption
Biopsy site = proximal jejunum (distal to ligament of Treitz)
(a) Causes of defective intraluminal digestion
decreased digestion fats proteins: pancreatic insufficiency due to pancreatitis or CF, ZES
decreased bile secretion (decreased fat solubilization): ileal dysfunction or resection with decreased bile salt uptake, cessation of bile flow (obstruction, hepatic dysfunction), nutrient preabsorption or modification by bacterial overgrowth
(b) Causes of abnormalities in terminal digestion or (c) transepithelial transport
Disaccharidase deficiency (lactose intolerance), bacterial overgrowth, abetalipoproteinemia, defects in ileal bile acid transporter
Lower Small Intestine Obstruction
Lower Small Intestine Obstruction
Causes
-post-operation adhesions
-malignancy
-Crohn’s
-hernias
Classification
-partial or complete
-strangulated (surgical emergency – leads to bowel ischemia) or non-strangulated
Blind Loop Syndrome
Blind Loop Syndrome
Stasis syndrome or stagnant loop syndrome
Definition
-a condition in which part of the small intestine is bypassed and cut off from the normal flow of food and digestive juices. Bacterial overgrowth results, interfering with absorption of essential nutrients, often leading to diarrhea, weight loss and malnutrition.
Causes
- structural defect in or an injury to your small intestine – surgery such as Billroth II or Roux-en-Y, gastric bypass
-Crohn’s disease, intestinal lymphoma, scleroderma or diabetes – slowed transit time through intestine
-Diverticulosis of the small intestine
Presentation
Loss of appetite
Abdominal pain
Nausea
Fatty stools (steatorrhea) — frothy, foul-smelling stools indicating poor fat absorption
Bloating
An uncomfortable feeling of fullness after eating
Diarrhea
Unintentional weight loss
Complications
-abnormalites in normal bacterial flora cause poor deconjugation of bile salts, which are required for fat emulsification and digestion. Resultant steatorrhea and malabsorption of fat-soluble vitamins - ADEK
-damage to intestinal mucosa - malabsorption of most other nutrients
-B12 malabsorption
Gastrointestinal Stromal Tumors
GIST
Gastrointestinal stromal tumors
Gastrointestinal Stromal Tumors Classification
- low, intermediate and high risk of aggressive behavior
Gastrointestinal Stromal Tumors Morphology
- spindled and epithelioid types
Gastrointestinal Stromal Tumors Immunohistochemistry
- CD117+ in 90%, CD34 + in 70%, SMA can be focally positive, desmin – (desmin is positive in leiomoyomas)
Gastrointestinal Stromal Tumors Histogenesis
- can arise anywhere in the GI tract; 60-70% from stomach, 20-30% from the small intestine and <10% from elsewhere
- cells are from a proliferation of the interstitial cells of Cajal
- association with c-kit and PDGFA genes - these are receptors with tyrosine kinase intracellular domains, and mutations in these cause their constitutive activation with activation of downstream signaling, leading to cell proliferation.
Gastrointestinal Stromal Tumors Differential Diagnosis
- leiomyoma
- leiomyosarcoma
- inflammatory fibroid polyp
- fibromatosis
- schwannoma
- inflammatory myofibrobastic tumor
- solitary fibrous tumor
Gastrointestinal Stromal Tumors Reporting
- one should report size, morphologic type, mitotic count per 50 HPFs , cellular atypia., presence of any necrosis
- MIB count can also assist with reporting as in the past there was a correlation with prognosis, 0-9% MIB = low, 10-29% intermediate, 30% or higher – high risk.
Peptic Ulcer
Peptic Ulcers
Most common sites of peptic ulcers
- duodenal (small intestine) THEN gastric (stomach)
- most common site is the duodenum, the first part of the small intestine, where the small intestine emerges from the stomach
Main cause of duodenal ulcers
- Helicobacter pylori bacteria (H.pylori)
Main cause of gastric ulcers
- H.pylori
Peptic Ulcer Pathogenesis
Gastric peptic ulcers
Gastric peptic ulcers result from altered mucosal defenses
- mucosal secretion
- bicarbonate secretion
- epithelial barrier
- blood flow
- prostaglandins
Duodenal peptic ulcers
Duodenal peptic ulcers are associated with increased acid production (H.pylori live in an increased acid, low pH environment)



