Small & Large Intestine Oct. 11. 2015. SMALL/LARGE INTESTINE NORMAL: Anat., Vasc., Mucosa, Endocr., Immune, Neuromuscular. PATHOLOGY: – CONGENITAL – ENTEROCOLITIS:

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Presentation transcript:

Small & Large Intestine Oct

SMALL/LARGE INTESTINE NORMAL: Anat., Vasc., Mucosa, Endocr., Immune, Neuromuscular. PATHOLOGY: – CONGENITAL – ENTEROCOLITIS: DIARRHEA, INFECTIOUS, OTHER – MALABSORPTION: INTRALUMINAL, CELL SURFACE, INTRACELL. – (I)IBD: CROHN DISEASE and ULCERATIVE COLITIS – VASCULAR: ISCHEMIC, ANGIODYSPLASIA, HEMORRHAGIC – DIVERTICULOSIS/-IT IS – OBSTRUCTION: MECHANICAL, PARALYTIC (ILEUS) (PSEUDO) – TUMORS: BENIGN, MALIGNANT, EPITHELIAL, STROMAL

SMALL/LARGE INTESTINE ANATOMY SI = 6 meters, LI = 1.5 meters Serosa/ adv. Muscle Submucosa Mucosa MALT

MUCOSA Small Intestine Large Intestine

CONGENITAL DUPLICATION MALROTATION OMPHALOCELE GASTROSCHISIS ATRESIA/STENOSIS SPECTRUM MECKEL (terminal ileum, “vitelline” duct) AGANGLIONIC MEGACOLON (HIRSCHSPRUNG DISEASE)

Omphalocele occurs when closure of the abdominal musculature is incomplete and the abdominal viscera herniate into a ventral membranous sac.

Intestinal Obstruction Infarction Tumor 20% 80%

OBSTRUCTION – ILEUS, esp. postsurgical – INFARCTION – MOTILITY DISEASES, esp., HIRSCHSPRUNG DISEASE. – Ileus is a disruption of the normal propulsive GIT motor activity from NON-mechanical mechanisms

Congenital defect in colonic innervation M>F 1/5000 Failure of migration of neural crest cells from cecum to rectum. Functional Intest obstraction Rectum and sigmoid Complications; (Colitis, perfor. Peritonitis). Hirschsprung disease Cong. Aganglionic Megacolon

The aganglionic region may have normal or narrow appearance, while the normally innervated proximal colon undergo progressive dilation. Dx; Distal intestinal segment lacks both the Meissner (submucosal) & Auerbach (myenteric) plexus (“aganglionosis”). Hirschsprung disease Cong. Aganglionic Megacolon

Hirschsprung disease

VASCULAR DISEASES ISCHEMIA/INFARCTION Hemorrhagic Venous Arterial ANGIO-”DYSPLASIA”* HEMORRHOIDS Septic shock  painful

ISCHEMIA/INFARCTION HEMORRHAGE HEMORRHAGE is the main HALLMARK of ischemic bowel disease – ARTERIAL THROMBUS – ARTERIAL EMBOLISM – VENOUS THROMBUS – CHF, SHOCK – INFILTRATIVE, MECHANICAL MUCOSAL  TRANSMURAL

Ischemic Bowel Disease Arterial (85%) Vs. venous (15%) Arterial (85%) Vs. venous (15%) Oclusive or non- oclusive Acute Acute (severe atherosclerosis, Ar. thrombosis) chronic hypoperfusion chronic hypoperfusion (watershed zones, splenic flexure), (cardiac failure, shock, dehydration, or vasoconstrictive drugs, vasculitis), Low flow. Miscellaneous: RTx, Volvolus, Herniation, truma Effect:  Effect: Severity of vascular involvement Ac or ch. The vessels affected

Ischemic Bowel Disease Mucosal Mural infarction  Mucosal, Mural infarction or Transmural infarction  Intestinal responses to ischemia in 2 phases 1. Hypoxia 2.Rreperfusion injury

ISCHEMIA/INFARCTION

Bowel infarction

Hemorrhoids Diletation of anal & perianal col. Ves. That connect portal & syst veins. External Vs. internal hemorrhoids Complication; C.P. Rx

Internal Hemorrhoids External Hemorrhoids ConstipationPregnancy Portal hypertension

Diarrheal Dis Diarrhea Steatorrhea Dysentery  Cystic Fibrosis

GLUTEN-SENSITIVE ENTEROPATHY GLUTEN-SENSITIVE ENTEROPATHY – Sensitivity to GLUTEN, protein – in wheat oat, barley, rye – Progressive mucosal “atrophy”, i.e. villous flattening – Relieved by gluten withdrawal – class II HLA-DQ2 or HLA-DQ8 – with other immune diseases. Both histologic and serologic findings is most specific for diagnosis of celiac disease.

Antigliadin (IgG or IgA) Abs Endomysial (IgA) Abs Anti -tissue transglutaminase (tTG) Abs.

Ig A Anti endomysial Ig G if Ig A is deficient tTG more accurate (screening test).

 Clinical Features Adults, celiac disease 30 and 60 Year Adults, celiac disease 30 and 60 Year silent celiac disease, silent celiac disease, anemia (due to iron deficiency, less, B12 and folate deficiency), diarrhea, bloating, and fatigue. anemia (due to iron deficiency, less, B12 and folate deficiency), diarrhea, bloating, and fatigue. Pediatric celiac disease6 and 24 months Pediatric celiac disease, 6 and 24 months classic symptoms classic symptoms dermatitis herpetiformis

Dermatitis Herpitiformis (DH) T cell lymphoma, S Int Ca. Sq cell ca. esophagus

DIVERTICULOSIS/-ITIS Pseudo diverticuli; (Colonic diverticuli);– composed of only mucosa on the luminal side and serosa externally Mucosa/submucosa herniates through muscle wall Assoc. w.: – INCREASED LUMINAL PRESSURE – AGE – L  R – FIBER – Weakening of wall

Sigmoid diverticular disease Sigmoid diverticular disease. A, Stool-filled diverticula are regularly arranged. B. the outpouching of mucosa beneath the muscularis propria. C. protrusion of the mucosa and submucosa through the muscularis propria

DIVERTICULOSIS

Sigmoid colon Asymptomatic unless complicated (infected (“diverticulitis”)), (“appendicitis” syndrome) PERFORATE  Peritonitis, local, diffuse BLEED, silently, even fatally OBSTRUCT EXTREMELY EXTREMELY COMMON NOT assoc w. neoplasm Diverticulosis

Meckle’s Diverticulum Congenital diverticulum of the distal small bowel. – 2 feet from the ileocecal valve. – 2 inches in size. – Twice as common in males

 Meckel diverticulum,  infant or child, with painless rectal bleeding.  ileum, within 2 feet of the ileocecal valve,  present in 2% of normal persons.  results from failure of the vitelline duct to close and is found on the antimesenteric border of the intestine.  Heterotopic gastric or pancreatic tissue may be present in about one-half of cases. Complications include; perforation, ulceration, intestinal obstruction, intussusception, and neoplasms, including carcinoid tumors.