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DIARRHEAL DISEASE MALABSORPT‏ION SYNDROMES Suboptimal absorption of different nutrients, electrolytes &/or water as a result of disturbance in intraluminal.

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Presentation on theme: "DIARRHEAL DISEASE MALABSORPT‏ION SYNDROMES Suboptimal absorption of different nutrients, electrolytes &/or water as a result of disturbance in intraluminal."— Presentation transcript:

1 DIARRHEAL DISEASE MALABSORPT‏ION SYNDROMES Suboptimal absorption of different nutrients, electrolytes &/or water as a result of disturbance in intraluminal digestion, absorption, terminal (brush border) digestion &/or transepithelial transport. Suboptimal absorption of different nutrients, electrolytes &/or water as a result of disturbance in intraluminal digestion, absorption, terminal (brush border) digestion &/or transepithelial transport. Digestion of food occurs mostly in stomach & small intestine, while absorption occurs mostly in duodenum & jejunum Digestion of food occurs mostly in stomach & small intestine, while absorption occurs mostly in duodenum & jejunum Malabsorption may be caused by a variety of diseases Malabsorption may be caused by a variety of diseases Small intestinal biopsy is an important diagnostic tool: may show characteristic findings, normal or nonspecific changes Small intestinal biopsy is an important diagnostic tool: may show characteristic findings, normal or nonspecific changes c/o weight loss, anorexia, abdominal distension, muscle wasting and passage of abnormally bulky, frothy, greasy, yellow or gray stools (steatorrhea) c/o weight loss, anorexia, abdominal distension, muscle wasting and passage of abnormally bulky, frothy, greasy, yellow or gray stools (steatorrhea)

2 CONSEQUENCES OF MALABSORPT‏ION SYNDROMES Anemia: iron, pyridoxine, folate or vit. B12 deficiency Anemia: iron, pyridoxine, folate or vit. B12 deficiency Bleeding: vitamin K deficiency Bleeding: vitamin K deficiency Osteopenia & tetany: Ca, Mg, vitamin D deficiency Osteopenia & tetany: Ca, Mg, vitamin D deficiency Amenorrhea, impotence, infertitlity: generalized malnutrition Amenorrhea, impotence, infertitlity: generalized malnutrition Hyperparathyroidism: Ca & vitamin D deficiency Hyperparathyroidism: Ca & vitamin D deficiency Purpura & petechiae: vitamin D deficiency Purpura & petechiae: vitamin D deficiency Edema: protein deficiency Edema: protein deficiency Dermatitis & hyperkeratosis: vit A, Zn, eFA, niacin Dermatitis & hyperkeratosis: vit A, Zn, eFA, niacin Mucositis: vitamin deficiencies Mucositis: vitamin deficiencies Peripheral neuropathy: vit A & B12 deficiency Peripheral neuropathy: vit A & B12 deficiency

3 CLASSIFICATION OF MALABSORPT‏ION SYNDROMES Defective intraluminal digestion: pancreatic insufficiency; Z-E syndrome; defective bile secretion due to biliary obstruction, hepatic or ileal dysfunction; bacterial overgrowth Defective intraluminal digestion: pancreatic insufficiency; Z-E syndrome; defective bile secretion due to biliary obstruction, hepatic or ileal dysfunction; bacterial overgrowth Mucosal cell abnormalities: lactose intolerence, bacterial overgrowth, abetalipoproteinemia Mucosal cell abnormalities: lactose intolerence, bacterial overgrowth, abetalipoproteinemia Reduced small intestine surface: Celiac sprue, Crohn ’ s,short – gut syndrome Reduced small intestine surface: Celiac sprue, Crohn ’ s,short – gut syndrome Lymphatic obstruction: lymphoma, tuberculosis Lymphatic obstruction: lymphoma, tuberculosis Infection: enteritis, tropical sprue, Whipple ’ s disease Infection: enteritis, tropical sprue, Whipple ’ s disease Iatrogenic: surgeries, drug induced Iatrogenic: surgeries, drug induced

4 MALABSORPTION SYNDROMES PANCREATIC INSUFFICIENCY Major cause of defective intraluminal digestion Major cause of defective intraluminal digestion Due to: Due to: –Chronic pancreatitis –Cystic fibrosis Osmotic diarrhea, steatorrhea Osmotic diarrhea, steatorrhea

5 MALABSORPTION SYNDROMES BACTERIAL OVERGROWTH Pathologic colonization of jejunal lumen by an abnormally large population of both anaerobic and aerobic organisms qualitatively similar to those present in the colon Pathologic colonization of jejunal lumen by an abnormally large population of both anaerobic and aerobic organisms qualitatively similar to those present in the colon Impairs intraluminal digestion & can damage mucosal epithelium in proximal small intestine Impairs intraluminal digestion & can damage mucosal epithelium in proximal small intestine Occurs in patients with: Occurs in patients with: –Intestinal luminal stasis: strictures, fistula, blind loops or pouches –Post-operative states associated with inadequate gastric acidity –Immunologic deficiencies –Mucosal disease of small intestine

6 MALABSORPTION SYNDROMES LACTOSE INTOLERANCE Deficiency of lactase is mostly acquired Deficiency of lactase is mostly acquired Lactose cannot be broken down to glucose & galactose; unabsorbed lactose exerts an osmotic pull leading to watery diarrhea & malabsorption Lactose cannot be broken down to glucose & galactose; unabsorbed lactose exerts an osmotic pull leading to watery diarrhea & malabsorption Familial inborn error of metabolism: presents at birth with initiation of milk feeding with explosive watery frothy stools & abdominal distension Familial inborn error of metabolism: presents at birth with initiation of milk feeding with explosive watery frothy stools & abdominal distension In adults, occurs with bacterial and viral gastroenteritis & other GIT disorders In adults, occurs with bacterial and viral gastroenteritis & other GIT disorders Dx: intestinal biopsy is normal; breath hydrogen testing by gas chromatography Dx: intestinal biopsy is normal; breath hydrogen testing by gas chromatography

7 MALABSORPTION SYNDROMES CELIAC SPRUE aka: Gluten-sensitive enteropathy aka: Gluten-sensitive enteropathy Sensitivity to gluten, the component of wheat & related grains (oat, barley & rye) that contain water insoluble gliadin peptides Sensitivity to gluten, the component of wheat & related grains (oat, barley & rye) that contain water insoluble gliadin peptides Pathology: when exposed to gluten, the proximal small intestinal mucosa accumulates large numbers of B cells & plasma cells, resulting in epithelial damage & total flattening of villi Pathology: when exposed to gluten, the proximal small intestinal mucosa accumulates large numbers of B cells & plasma cells, resulting in epithelial damage & total flattening of villi Patients: 1: in white Europeans; familial & viral links Patients: 1: in white Europeans; familial & viral links Presentation range from infancy to mid- adulthood; diarrhea and malnutrition Presentation range from infancy to mid- adulthood; diarrhea and malnutrition Rx: Gluten-free diet Rx: Gluten-free diet Px: Increased risk of developing malignancies Px: Increased risk of developing malignancies

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14 MALABSORPTION SYNDROMES TROPICAL SPRUE Celiac-like disease occurring almost exclusively in the tropics Celiac-like disease occurring almost exclusively in the tropics An infectious etiology is implicated. No definite microorganism has been identified. An infectious etiology is implicated. No definite microorganism has been identified. c/o malabsorption symptoms following an acute diarrheal infection c/o malabsorption symptoms following an acute diarrheal infection Pathology: minimal to severe diffuse enteritis with villous flattening Pathology: minimal to severe diffuse enteritis with villous flattening Rx: Broad-spectrum antibiotics Rx: Broad-spectrum antibiotics

15 MALABSORPTION SYNDROMES WHIPPLE’S DISEASE Rare systemic infection, mainly in intestine, CNS & joints Rare systemic infection, mainly in intestine, CNS & joints Pathology: small intestinal mucosa is full of macrophages in lamina propria, with minimal inflammation Pathology: small intestinal mucosa is full of macrophages in lamina propria, with minimal inflammation Macrophages contain Tropheryma whipelii (Gram + actinomycete). Macrophages contain Tropheryma whipelii (Gram + actinomycete). Patients: males yrs; lymphadenopathy, polyarthritis, CNS symptoms Patients: males yrs; lymphadenopathy, polyarthritis, CNS symptoms Rx: antibiotics Rx: antibiotics

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19 MALABSORPTION SYNDROMES ABETALIPOPROTEINEMIA Rare autosomal recessive inborn error of metabolism, with inability to synthesize apoproteins required for export of lipoproteins from mucosal cells Rare autosomal recessive inborn error of metabolism, with inability to synthesize apoproteins required for export of lipoproteins from mucosal cells Free fatty acids & monoglycerides enter absorptive cells and are normally re-esterified but cannot be synthesized into chylomicrons Free fatty acids & monoglycerides enter absorptive cells and are normally re-esterified but cannot be synthesized into chylomicrons Pathology: mucosal cells have vacuolated lipid inclusions Pathology: mucosal cells have vacuolated lipid inclusions Severe hypolipidemia (decreased chylomicron, VLDL, LDL) Severe hypolipidemia (decreased chylomicron, VLDL, LDL) c/o: diarrhea, steatorrhea, failure to thrive c/o: diarrhea, steatorrhea, failure to thrive Peripheral blood picture: RBCs show characteristic burr cells (acanthocytosis) Peripheral blood picture: RBCs show characteristic burr cells (acanthocytosis)

20 PROTOZOAL ENTEROCOLITIS Giardia lamblia World ’ s most prevalent pathogenic gut protozoan World ’ s most prevalent pathogenic gut protozoan Asymptomatic carrier state is common Asymptomatic carrier state is common Trophozoites live in duodenum & give rise to infective cysts that are shed into the stools Trophozoites live in duodenum & give rise to infective cysts that are shed into the stools Spread by fecal contaminated water Spread by fecal contaminated water Parasite attaches to small intestinal mucosa but does not invade Parasite attaches to small intestinal mucosa but does not invade Pathology: intestinal villi may be normal or blunted with a mixed inflammatory cell infiltrate in lamina propria Pathology: intestinal villi may be normal or blunted with a mixed inflammatory cell infiltrate in lamina propria Malabsorptive diarrhea Malabsorptive diarrhea

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22 VASCULAR DISORDERS OF INTESTINES ISCHEMIC BOWEL DISEASE aka: mesenteric ischemia aka: mesenteric ischemia Involves small &/or large intestines depending on particular vessel(s) involved (celiac, superior & inferior mesenteric arteries) Involves small &/or large intestines depending on particular vessel(s) involved (celiac, superior & inferior mesenteric arteries) Usually elderly patients; may be acute or insidious Usually elderly patients; may be acute or insidious Causes: Causes: –Arterial thrombosis: severe atherosclerosis,... –Arterial embolism: cardiac vegetations,... –Venous thrombosis: hypercoagulable states –Nonocclusive ischemia: heart failure, shock,.. –Miscellaneous: radiation, volvulus, herniation,...

23 TYPES OF ISCHEMIC BOWEL DISEASE Ischemic bowel disease is divided according to the severity of injury: Ischemic bowel disease is divided according to the severity of injury: –1) Mucosal infarction & 2) Mural infarction (hemorrhagic gastroenteropathy): usually due to hypoperfusion, damaging only the inner layers of the GIT; multifocal or continuous lesions; hemorrhage, edema & ulceration; intact serosa –3) Transmural intestinal infarction: dark red hemorrhagic bowel segment of variable length; ischemia starts in mucosa and extends outwards, with edema, hemorrhage, necrosis, mucosal sloughing followed by gangrene & perforation

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27 CLINICAL FEATURES OF ISCHEMIC BOWEL DISEASE Transmural lesions: sudden abdominal pain, bloody diarrhea, shock, … Transmural lesions: sudden abdominal pain, bloody diarrhea, shock, … Mural & mucosal: abdominal distension, GI bleeding, gradual pain or discomfort Mural & mucosal: abdominal distension, GI bleeding, gradual pain or discomfort Dx: high index of suspicion in the appropriate setting Dx: high index of suspicion in the appropriate setting Px: mortality rate with transmural infarction is nearly 90%, largely due to delay in diagnosis; mural & mucosal infarction may not be fatal if causes of hypoperfusion are corrected Px: mortality rate with transmural infarction is nearly 90%, largely due to delay in diagnosis; mural & mucosal infarction may not be fatal if causes of hypoperfusion are corrected

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29 VASCULAR DISORDERS OF INTESTINES ANGIODYSPLASIA A misnomer; not a pre-malignant lesion A misnomer; not a pre-malignant lesion Tortuous dilations of submucosal & mucosal blood vessels, mostly in cecum & rt. colon, elderly patients Tortuous dilations of submucosal & mucosal blood vessels, mostly in cecum & rt. colon, elderly patients Blood vessels may rupture & bleed; account for 20% of significant lower GIT bleeding Blood vessels may rupture & bleed; account for 20% of significant lower GIT bleeding Difficult to diagnose: -ve Barium enema radiology; normal gross appearance. Visible by endoscopy & angiography. Difficult to diagnose: -ve Barium enema radiology; normal gross appearance. Visible by endoscopy & angiography. Isolated lesions or part of systemic disorder, e,g. Osler-Weber-Rendu syndrome & CREST syndrome Isolated lesions or part of systemic disorder, e,g. Osler-Weber-Rendu syndrome & CREST syndrome

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31 VASCULAR DISORDERS OF INTESTINES HEMORRHOIDS aka: piles aka: piles Dilated varices of anal and perianal submucosal venous plexuses Dilated varices of anal and perianal submucosal venous plexuses Patients: common in adults >50 yrs; setting of persistently elevated venous pressure within the hemorrhoidal plexus Patients: common in adults >50 yrs; setting of persistently elevated venous pressure within the hemorrhoidal plexus Predisposing factors: Predisposing factors: –Chronic constipation –Pregnancy –Portal hypertension Pathology: thin-walled dilated blood vessels covered by anal mucosa Pathology: thin-walled dilated blood vessels covered by anal mucosa

32 HEMORRHOIDS

33 CLINICAL FEATURES OF HEMORRHOIDS Types of hemorrhoids: Types of hemorrhoids: –1) Internal: above the dentate line –2) External: below the dentate line Clinical features: Clinical features: –Usually asymptomatic –Protrusion & itching –Ulceration & bleeding –Thrombosis & pain –Prolapse: internal hemorrhoids trapped by anal sphincter, with sudden pain, edema, enlargement or strangulation Rx: depends on severity; medical & surgical Rx: depends on severity; medical & surgical

34 PATHOLOGY OF SMALL & LARGE INTESTINE IDIOPATHIC INFLAMMATORY BOWEL DISEASE‏ Crohn ’ s disease & ulcerative colitis: chronic relapsing disorders of unknown cause, which are characterized by extensive bowel inflammation, tissue injury & mucosal destruction Crohn ’ s disease & ulcerative colitis: chronic relapsing disorders of unknown cause, which are characterized by extensive bowel inflammation, tissue injury & mucosal destruction Intermittent bloody diarrhea; pain; malabsorption Intermittent bloody diarrhea; pain; malabsorption Etiology: Etiology: –Genetic predisposition, IBD 1 on chromosome 16,HLA-DR –Abnormal mucosal structure, –Infectious –Abnormal host immunoreactivity ; IL-2,IL-10,TNF,IL-R

35 INFLAMMATORY BOWEL DISEASE ULCERATIVE COLITIS & CROHN’S DISEASE Ulcerative colitis and Crohn ’ s disease have common features: Ulcerative colitis and Crohn ’ s disease have common features: –Chronic recurrent inflammation –No definit cause is identified –May have extra-intestinal manifestations Integration of clinical, radiological and pathological findings are essential for diagnosis of UC or CD. Integration of clinical, radiological and pathological findings are essential for diagnosis of UC or CD. Histologic feature may be identical, particularly with small biopsies Histologic feature may be identical, particularly with small biopsies In 10-30% of cases, distinction between the two diseases cannot be made (indeterminate cases) In 10-30% of cases, distinction between the two diseases cannot be made (indeterminate cases)

36 INFLAMMATORY BOWEL DISEASE CROHN’S DISEASE aka: terminal ileitis, regional enteritis aka: terminal ileitis, regional enteritis Systemic disease with predominant GI involvement Systemic disease with predominant GI involvement –Any level of GIT may be involved –Associated immune extra-intestinal manifestations (iritis, uveitis, polyarthritis, erythema nodosum, hepatic pericholangitis, sclerosing cholangitis..) Patients: any age, peaks 2-3rd & 6-7th decades; F>M Patients: any age, peaks 2-3rd & 6-7th decades; F>M Insidious or sudden onset of symptoms which may remit spontaneously or with therapy, usually followed by relapses Insidious or sudden onset of symptoms which may remit spontaneously or with therapy, usually followed by relapses Marked weight loss & malabsorption Marked weight loss & malabsorption Complications: fistulas,abdominal abscesses & peritonitis, stricture and obstruction, bleeding Complications: fistulas,abdominal abscesses & peritonitis, stricture and obstruction, bleeding Cancer: Increased risk, but significantly less than UC Cancer: Increased risk, but significantly less than UC

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45 INFLAMMATORY BOWEL DISEASE ULCERATIVE COLITIS Ulcero-inflammatory disease of colon, limited to mucosa & submucosa, except in severe cases Ulcero-inflammatory disease of colon, limited to mucosa & submucosa, except in severe cases Starts in rectum & extends proximally in a continuous fashion Starts in rectum & extends proximally in a continuous fashion Systemic disease, may be associated with polyarthritis, ankylosing spondylitis (HLA-B27+), uveitis, liver (pericholangitis & PSC) & skin involvement Systemic disease, may be associated with polyarthritis, ankylosing spondylitis (HLA-B27+), uveitis, liver (pericholangitis & PSC) & skin involvement Patients: any age; peak yrs. Patients: any age; peak yrs. Chronic relapsing & remitting disease; bloody stools Chronic relapsing & remitting disease; bloody stools Complications: severe diarrhea & electrolyte disturbances, massive hemorrhage, toxic megacolon, rupture Complications: severe diarrhea & electrolyte disturbances, massive hemorrhage, toxic megacolon, rupture Cancer: depends on duration & extent of disease Cancer: depends on duration & extent of disease

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52 INFLAMMATORY BOWEL DISEASE CROHN’S DISEASE ULCERATIVE COLITIS Incidence: 1-3/100,000 Incidence: 1-3/100,000 Whites, Jews Whites, Jews Small intestine 40%; small & large intestine 30%; large intestine 30% Small intestine 40%; small & large intestine 30%; large intestine 30% Skip lesions Skip lesions Granulomas 40-60% Granulomas 40-60% Deep linear ulcers Deep linear ulcers Cobble stone appearance Cobble stone appearance Strictures: early Strictures: early Fissures, sinuses & fistulas Fissures, sinuses & fistulas Incidence: 4-6/100,000 Whites Rectum/rectosigmoid 80% extending proxi- mally; pan-colitis 10% Continuous involvement No granulomas Superficial ulcers Pseudopolyps Strictures: late/rare No

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54 MICROSCOPIC FEATURES OF CROHN’S DISEASE ULCERATIVE COLITIS Inflammation, ulceration & chronic mucosal changes Inflammation, ulceration & chronic mucosal changes Deep ulcers with transmural involvement Deep ulcers with transmural involvement Wall thickening Wall thickening Granulomas +/- Granulomas +/- Marked lymphoid reaction Marked lymphoid reaction Marked serositis Marked serositis Fistulas or sinuses Fistulas or sinuses Moderate-marked fibrosis Moderate-marked fibrosis Inflammation, ulceration & chronic mucosal changes Ulcers with mostly mucosal involvement Wall is usually thin No granulomas Mild lymphoid reaction No or mild serositis No fistulas or sinuses Mild fibrosis

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