diarrheal disease malabsorption syndromes suboptimal absorption of different nutrients, electrolytes...

DIARRHEAL DISEASEDIARRHEAL DISEASE

MALABSORPTMALABSORPTION SYNDROMESION SYNDROMES Suboptimal absorption of different nutrients, electrolytes Suboptimal absorption of different nutrients, electrolytes

&/or water as a result of disturbance in intraluminal &/or water as a result of disturbance in intraluminal digestion, absorption, terminal (brush border) digestion &/or digestion, absorption, terminal (brush border) digestion &/or transepithelial transport.transepithelial transport.

Digestion of food occurs mostly in stomach & small Digestion of food occurs mostly in stomach & small intestine, while absorption occurs mostly in duodenum & intestine, while absorption occurs mostly in duodenum & jejunumjejunum

Malabsorption may be caused by a variety of diseasesMalabsorption may be caused by a variety of diseases Small intestinal biopsy is an important diagnostic tool: may Small intestinal biopsy is an important diagnostic tool: may

show characteristic findings, normal or nonspecific changesshow characteristic findings, normal or nonspecific changes c/o weight loss, anorexia, abdominal distension, muscle c/o weight loss, anorexia, abdominal distension, muscle

wasting and passage of abnormally bulky, frothy, greasy, wasting and passage of abnormally bulky, frothy, greasy, yellow or gray stools (steatorrhea)yellow or gray stools (steatorrhea)

CONSEQUENCES OFCONSEQUENCES OF

MALABSORPTMALABSORPTION SYNDROMESION SYNDROMES Anemia: iron, pyridoxine, folate or vit. B12 deficiencyAnemia: iron, pyridoxine, folate or vit. B12 deficiency Bleeding: vitamin K deficiencyBleeding: vitamin K deficiency Osteopenia & tetany: Ca, Mg, vitamin D deficiencyOsteopenia & tetany: Ca, Mg, vitamin D deficiency Amenorrhea, impotence, infertitlity: generalized Amenorrhea, impotence, infertitlity: generalized

malnutritionmalnutrition Hyperparathyroidism: Ca & vitamin D deficiencyHyperparathyroidism: Ca & vitamin D deficiency Purpura & petechiae: vitamin D deficiencyPurpura & petechiae: vitamin D deficiency Edema: protein deficiencyEdema: protein deficiency Dermatitis & hyperkeratosis: vit A, Zn, eFA, niacinDermatitis & hyperkeratosis: vit A, Zn, eFA, niacin Mucositis: vitamin deficienciesMucositis: vitamin deficiencies Peripheral neuropathy: vit A & B12 deficiencyPeripheral neuropathy: vit A & B12 deficiency

CLASSIFICATION OFCLASSIFICATION OF

MALABSORPTMALABSORPTION SYNDROMESION SYNDROMES Defective intraluminal digestion: pancreatic Defective intraluminal digestion: pancreatic

insufficiency; Z-E syndrome; defective bile secretion insufficiency; Z-E syndrome; defective bile secretion due to biliary obstruction, hepatic or ileal dysfunction; due to biliary obstruction, hepatic or ileal dysfunction; bacterial overgrowthbacterial overgrowth

Mucosal cell abnormalities: lactose intolerence, Mucosal cell abnormalities: lactose intolerence, bacterial overgrowth, abetalipoproteinemiabacterial overgrowth, abetalipoproteinemia

Reduced small intestine surface: Celiac sprue, CrohnReduced small intestine surface: Celiac sprue, Crohn’’s s ,short –gut syndrome,short –gut syndrome

Lymphatic obstruction: lymphoma, tuberculosisLymphatic obstruction: lymphoma, tuberculosis Infection: enteritis, tropical sprue, WhippleInfection: enteritis, tropical sprue, Whipple’’s diseases disease Iatrogenic: surgeries, drug inducedIatrogenic: surgeries, drug induced

MALABSORPTION SYNDROMESMALABSORPTION SYNDROMES

PANCREATIC INSUFFICIENCYPANCREATIC INSUFFICIENCY Major cause of defective intraluminal Major cause of defective intraluminal

digestiondigestion Due to:Due to:– Chronic pancreatitisChronic pancreatitis– Cystic fibrosisCystic fibrosis

Osmotic diarrhea, steatorrheaOsmotic diarrhea, steatorrhea


BACTERIAL OVERGROWTHBACTERIAL OVERGROWTH Pathologic colonization of jejunal lumen by an Pathologic colonization of jejunal lumen by an

abnormally large population of both anaerobic abnormally large population of both anaerobic and aerobic organisms qualitatively similar to and aerobic organisms qualitatively similar to those present in the colonthose present in the colon

Impairs intraluminal digestion & can damage Impairs intraluminal digestion & can damage mucosal epithelium in proximal small intestinemucosal epithelium in proximal small intestine

Occurs in patients with:Occurs in patients with:– Intestinal luminal stasis: strictures, fistula, Intestinal luminal stasis: strictures, fistula,

blind loops or pouchesblind loops or pouches– Post-operative states associated with Post-operative states associated with

inadequate gastric acidity inadequate gastric acidity – Immunologic deficienciesImmunologic deficiencies– Mucosal disease of small intestineMucosal disease of small intestine


LACTOSE INTOLERANCELACTOSE INTOLERANCE Deficiency of lactase is mostly acquiredDeficiency of lactase is mostly acquired Lactose cannot be broken down to glucose & Lactose cannot be broken down to glucose &

galactose; unabsorbed lactose exerts an osmotic galactose; unabsorbed lactose exerts an osmotic pull leading to watery diarrhea & malabsorptionpull leading to watery diarrhea & malabsorption

Familial inborn error of metabolism: presents at Familial inborn error of metabolism: presents at birth with initiation of milk feeding with explosive birth with initiation of milk feeding with explosive watery frothy stools & abdominal distensionwatery frothy stools & abdominal distension

In adults, occurs with bacterial and viral In adults, occurs with bacterial and viral gastroenteritis & other GIT disordersgastroenteritis & other GIT disorders

Dx: intestinal biopsy is normal; breath hydrogen Dx: intestinal biopsy is normal; breath hydrogen testing by gas chromatographytesting by gas chromatography


CELIAC SPRUE CELIAC SPRUE aka: Gluten-sensitive enteropathyaka: Gluten-sensitive enteropathy Sensitivity to gluten, the component of wheat & Sensitivity to gluten, the component of wheat &

related grains (oat, barley & rye) that contain related grains (oat, barley & rye) that contain water insoluble gliadin peptideswater insoluble gliadin peptides

Pathology: when exposed to gluten , the proximal Pathology: when exposed to gluten , the proximal small intestinal mucosa accumulates large small intestinal mucosa accumulates large numbers of B cells & plasma cells, resulting in numbers of B cells & plasma cells, resulting in epithelial damage & total flattening of villiepithelial damage & total flattening of villi

Patients: 1:2000-3000 in white Europeans; familial Patients: 1:2000-3000 in white Europeans; familial & viral links& viral links

Presentation range from infancy to mid-Presentation range from infancy to mid-adulthood; diarrhea and malnutritionadulthood; diarrhea and malnutrition

Rx: Gluten-free dietRx: Gluten-free diet Px: Increased risk of developing malignanciesPx: Increased risk of developing malignancies


TROPICAL SPRUETROPICAL SPRUE Celiac-like disease occurring almost exclusively Celiac-like disease occurring almost exclusively

in the tropicsin the tropics An infectious etiology is implicated. No definite An infectious etiology is implicated. No definite

microorganism has been identified.microorganism has been identified. c/o malabsorption symptoms following an acute c/o malabsorption symptoms following an acute

diarrheal infectiondiarrheal infection Pathology: minimal to severe diffuse enteritis with Pathology: minimal to severe diffuse enteritis with

villous flattening villous flattening Rx: Broad-spectrum antibioticsRx: Broad-spectrum antibiotics


WHIPPLE’S DISEASEWHIPPLE’S DISEASE Rare systemic infection, mainly in intestine, CNS Rare systemic infection, mainly in intestine, CNS

& joints& joints Pathology: small intestinal mucosa is full of Pathology: small intestinal mucosa is full of

macrophages in lamina propria, with minimal macrophages in lamina propria, with minimal inflammationinflammation

Macrophages contain Macrophages contain Tropheryma whipeliiTropheryma whipelii (Gram + actinomycete).(Gram + actinomycete).

Patients: males 30-50 yrs; lymphadenopathy, Patients: males 30-50 yrs; lymphadenopathy, polyarthritis, CNS symptomspolyarthritis, CNS symptoms

Rx: antibioticsRx: antibiotics


ABETALIPOPROTEINEMIAABETALIPOPROTEINEMIA Rare autosomal recessive inborn error of metabolism, Rare autosomal recessive inborn error of metabolism,

with inability to synthesize apoproteins required for with inability to synthesize apoproteins required for export of lipoproteins from mucosal cellsexport of lipoproteins from mucosal cells

Free fatty acids & monoglycerides enter absorptive Free fatty acids & monoglycerides enter absorptive cells and are normally re-esterified but cannot be cells and are normally re-esterified but cannot be synthesized into chylomicronssynthesized into chylomicrons

Pathology: mucosal cells have vacuolated lipid Pathology: mucosal cells have vacuolated lipid inclusionsinclusions

Severe hypolipidemia (decreased chylomicron, VLDL, Severe hypolipidemia (decreased chylomicron, VLDL, LDL)LDL)

c/o: diarrhea, steatorrhea, failure to thrive c/o: diarrhea, steatorrhea, failure to thrive Peripheral blood picture: RBCs show characteristic Peripheral blood picture: RBCs show characteristic

burr cells (acanthocytosis)burr cells (acanthocytosis)

PROTOZOAL ENTEROCOLITISPROTOZOAL ENTEROCOLITIS

Giardia lambliaGiardia lamblia WorldWorld’’s most prevalent pathogenic gut protozoans most prevalent pathogenic gut protozoan Asymptomatic carrier state is commonAsymptomatic carrier state is common Trophozoites live in duodenum & give rise to infective Trophozoites live in duodenum & give rise to infective

cysts that are shed into the stoolscysts that are shed into the stools Spread by fecal contaminated waterSpread by fecal contaminated water Parasite attaches to small intestinal mucosa but does Parasite attaches to small intestinal mucosa but does

not invadenot invade Pathology: intestinal villi may be normal or blunted Pathology: intestinal villi may be normal or blunted

with a mixed inflammatory cell infiltrate in lamina with a mixed inflammatory cell infiltrate in lamina propriapropria

Malabsorptive diarrheaMalabsorptive diarrhea

VASCULAR DISORDERS OF INTESTINESVASCULAR DISORDERS OF INTESTINES

ISCHEMIC BOWEL DISEASEISCHEMIC BOWEL DISEASE aka: mesenteric ischemiaaka: mesenteric ischemia Involves small &/or large intestines depending on Involves small &/or large intestines depending on

particular vessel(s) involved (celiac, superior & inferior particular vessel(s) involved (celiac, superior & inferior mesenteric arteries)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 thrombosis: severe atherosclerosis, ...– Arterial embolism: cardiac vegetations, ...Arterial embolism: cardiac vegetations, ...– Venous thrombosis: hypercoagulable statesVenous thrombosis: hypercoagulable states– Nonocclusive ischemia: heart failure, shock, ..Nonocclusive ischemia: heart failure, shock, ..– Miscellaneous: radiation, volvulus, herniation, ...Miscellaneous: radiation, volvulus, herniation, ...

TYPES OFTYPES OF

ISCHEMIC BOWEL DISEASEISCHEMIC BOWEL DISEASE Ischemic bowel disease is divided according to the Ischemic bowel disease is divided according to the

severity of injury:severity of injury:– 1) Mucosal infarction & 2) Mural infarction 1) Mucosal infarction & 2) Mural infarction

(hemorrhagic gastroenteropathy): usually due to (hemorrhagic gastroenteropathy): usually due to hypoperfusion, damaging only the inner layers of hypoperfusion, damaging only the inner layers of the GIT; multifocal or continuous lesions; the GIT; multifocal or continuous lesions; hemorrhage, edema & ulceration; intact serosa hemorrhage, edema & ulceration; intact serosa

– 3) Transmural intestinal infarction: dark red 3) Transmural intestinal infarction: dark red hemorrhagic bowel segment of variable length; hemorrhagic bowel segment of variable length; ischemia starts in mucosa and extends outwards, ischemia starts in mucosa and extends outwards, with edema, hemorrhage, necrosis, mucosal with edema, hemorrhage, necrosis, mucosal sloughing followed by gangrene & perforationsloughing followed by gangrene & perforation

CLINICAL FEATURES OFCLINICAL FEATURES OF

ISCHEMIC BOWEL DISEASEISCHEMIC BOWEL DISEASE Transmural lesions: sudden abdominal pain, Transmural lesions: sudden abdominal pain,

bloody diarrhea, shock, bloody diarrhea, shock, …… Mural & mucosal: abdominal distension, GI Mural & mucosal: abdominal distension, GI

bleeding, gradual pain or discomfortbleeding, gradual pain or discomfort Dx: high index of suspicion in the appropriate Dx: high index of suspicion in the appropriate

settingsetting Px: mortality rate with transmural infarction is Px: mortality rate with transmural infarction is

nearly 90%, largely due to delay in diagnosis; nearly 90%, largely due to delay in diagnosis; mural & mucosal infarction may not be fatal if mural & mucosal infarction may not be fatal if causes of hypoperfusion are correctedcauses of hypoperfusion are corrected


ANGIODYSPLASIAANGIODYSPLASIA A misnomer; not a pre-malignant lesionA misnomer; not a pre-malignant lesion Tortuous dilations of submucosal & mucosal blood Tortuous dilations of submucosal & mucosal blood

vessels, mostly in cecum & rt. colon, elderly patientsvessels, mostly in cecum & rt. colon, elderly patients Blood vessels may rupture & bleed; account for 20% Blood vessels may rupture & bleed; account for 20%

of of significant significant lower GIT bleedinglower GIT bleeding Difficult to diagnose: -ve Barium enema radiology; Difficult to diagnose: -ve Barium enema radiology;

normal gross appearance. Visible by endoscopy & normal gross appearance. Visible by endoscopy & angiography.angiography.

Isolated lesions or part of systemic disorder, e,g. Isolated lesions or part of systemic disorder, e,g. Osler-Weber-Rendu syndrome & CREST syndromeOsler-Weber-Rendu syndrome & CREST syndrome


HEMORRHOIDSHEMORRHOIDS aka: pilesaka: piles Dilated varices of anal and perianal submucosal Dilated varices of anal and perianal submucosal

venous plexusesvenous plexuses Patients: common in adults >50 yrs; setting of Patients: common in adults >50 yrs; setting of

persistently elevated venous pressure within the persistently elevated venous pressure within the hemorrhoidal plexushemorrhoidal plexus

Predisposing factors:Predisposing factors:– Chronic constipationChronic constipation– PregnancyPregnancy– Portal hypertensionPortal hypertension

Pathology: thin-walled dilated blood vessels covered by Pathology: thin-walled dilated blood vessels covered by anal mucosaanal mucosa

HEMORRHOIDSHEMORRHOIDS

CLINICAL FEATURES OFCLINICAL FEATURES OF

HEMORRHOIDSHEMORRHOIDS Types of hemorrhoids:Types of hemorrhoids:– 1) Internal: above the dentate line1) Internal: above the dentate line– 2) External: below the dentate line2) External: below the dentate line

Clinical features:Clinical features:– Usually asymptomaticUsually asymptomatic– Protrusion & itchingProtrusion & itching– Ulceration & bleedingUlceration & bleeding– Thrombosis & painThrombosis & pain– Prolapse: internal hemorrhoids trapped by anal Prolapse: internal hemorrhoids trapped by anal

sphincter, with sudden pain, edema, enlargement or sphincter, with sudden pain, edema, enlargement or strangulationstrangulation

Rx: depends on severity; medical & surgicalRx: depends on severity; medical & surgical

PATHOLOGY OF SMALL & LARGE INTESTINEPATHOLOGY OF SMALL & LARGE INTESTINE

IDIOPATHICIDIOPATHIC INFLAMMATORY BOWEL DISEASE INFLAMMATORY BOWEL DISEASE CrohnCrohn’’s disease & ulcerative colitis: chronic s disease & ulcerative colitis: chronic

relapsing disorders of unknown cause, which are relapsing disorders of unknown cause, which are characterized by extensive bowel inflammation, characterized by extensive bowel inflammation, tissue injury & mucosal destructiontissue injury & mucosal destruction

Intermittent bloody diarrhea; pain; malabsorption Intermittent bloody diarrhea; pain; malabsorption Etiology:Etiology:– Genetic predisposition ,Genetic predisposition ,IBD 1 on chromosome 16 ,HLA-DRIBD 1 on chromosome 16 ,HLA-DR

– Abnormal mucosal structure ,Abnormal mucosal structure ,

– InfectiousInfectious– Abnormal host immunoreactivity ; Abnormal host immunoreactivity ; IL-2,IL-10,TNF,IL-RIL-2,IL-10,TNF,IL-R

INFLAMMATORY BOWEL DISEASEINFLAMMATORY BOWEL DISEASE

ULCERATIVE COLITIS & CROHN’S DISEASEULCERATIVE COLITIS & CROHN’S DISEASE Ulcerative colitis and CrohnUlcerative colitis and Crohn’’s disease have s disease have

common features:common features:– Chronic recurrent inflammationChronic recurrent inflammation– No definit cause is identifiedNo definit cause is identified– May have extra-intestinal manifestationsMay have extra-intestinal manifestations

Integration of clinical, radiological and pathological Integration of clinical, radiological and pathological findings are essential for diagnosis of UC or CD.findings are essential for diagnosis of UC or CD.

Histologic feature may be identical, particularly with Histologic feature may be identical, particularly with small biopsiessmall biopsies

In 10-30% of cases, distinction between the two In 10-30% of cases, distinction between the two diseases cannot be made (indeterminate cases)diseases cannot be made (indeterminate cases)


CROHN’S DISEASECROHN’S DISEASE aka: terminal ileitis, regional enteritisaka: terminal ileitis, regional enteritis Systemic disease with predominant GI involvementSystemic disease with predominant GI involvement– Any level of GIT may be involvedAny level of GIT may be involved– Associated immune extra-intestinal manifestations (iritis, Associated immune extra-intestinal manifestations (iritis,

uveitis, polyarthritis, erythema nodosum, hepatic uveitis, polyarthritis, erythema nodosum, hepatic pericholangitis, sclerosing cholangitis..)pericholangitis, sclerosing cholangitis..)

Patients: any age, peaks 2-3rd & 6-7th decades; F>MPatients: any age, peaks 2-3rd & 6-7th decades; F>M Insidious or sudden onset of symptoms which may remit Insidious or sudden onset of symptoms which may remit

spontaneously or with therapy, usually followed by relapsesspontaneously or with therapy, usually followed by relapses Marked weight loss & malabsorptionMarked weight loss & malabsorption Complications: fistulas,abdominal abscesses & peritonitis, Complications: fistulas,abdominal abscesses & peritonitis,

stricture and obstruction, bleedingstricture and obstruction, bleeding Cancer: Increased risk, but significantly less than UCCancer: Increased risk, but significantly less than UC


ULCERATIVE COLITISULCERATIVE COLITIS Ulcero-inflammatory disease of colon, limited to mucosa & Ulcero-inflammatory disease of colon, limited to mucosa &

submucosa, except in severe casessubmucosa, except in severe cases Starts in rectum & extends proximally in a continuous Starts in rectum & extends proximally in a continuous

fashionfashion Systemic disease, may be associated with polyarthritis, Systemic disease, may be associated with polyarthritis,

ankylosing spondylitis (HLA-B27+), uveitis, liver ankylosing spondylitis (HLA-B27+), uveitis, liver (pericholangitis & PSC) & skin involvement (pericholangitis & PSC) & skin involvement

Patients: any age; peak 20-25 yrs.Patients: any age; peak 20-25 yrs. Chronic relapsing & remitting disease; bloody stoolsChronic relapsing & remitting disease; bloody stools Complications: severe diarrhea & electrolyte disturbances,Complications: severe diarrhea & electrolyte disturbances,

massive hemorrhage, toxic megacolon, rupturemassive hemorrhage, toxic megacolon, rupture Cancer: depends on duration & extent of diseaseCancer: depends on duration & extent of disease


CROHN’S DISEASECROHN’S DISEASE ULCERATIVE COLITISULCERATIVE COLITIS Incidence: 1-3/100,000Incidence: 1-3/100,000 Whites, JewsWhites, Jews Small intestine 40%; Small intestine 40%;

small & large intestine small & large intestine 30%; large intestine 30%30%; large intestine 30%

Skip lesionsSkip lesions Granulomas 40-60%Granulomas 40-60% Deep linear ulcersDeep linear ulcers Cobble stone appearanceCobble stone appearance Strictures: earlyStrictures: early Fissures, sinuses & Fissures, sinuses &

fistulasfistulas

Incidence: 4-6/100,000Incidence: 4-6/100,000 WhitesWhites Rectum/rectosigmoid Rectum/rectosigmoid

80% extending proxi-80% extending proxi-mally; pan-colitis 10%mally; pan-colitis 10%

Continuous involvementContinuous involvement No granulomasNo granulomas Superficial ulcersSuperficial ulcers PseudopolypsPseudopolyps Strictures: late/rareStrictures: late/rare NoNo

MICROSCOPIC FEATURES OFMICROSCOPIC FEATURES OFCROHN’S DISEASECROHN’S DISEASE ULCERATIVE COLITISULCERATIVE COLITIS Inflammation, ulceration & Inflammation, ulceration &

chronic mucosal changeschronic mucosal changes Deep ulcers with transmural Deep ulcers with transmural

involvementinvolvement Wall thickeningWall thickening Granulomas +/-Granulomas +/- Marked lymphoid reactionMarked lymphoid reaction Marked serositisMarked serositis Fistulas or sinusesFistulas or sinuses Moderate-marked fibrosisModerate-marked fibrosis

Inflammation, Inflammation, ulceration & chronic ulceration & chronic mucosal changesmucosal changes

Ulcers with mostly Ulcers with mostly mucosal involvementmucosal involvement

Wall is usually thinWall is usually thin No granulomasNo granulomas Mild lymphoid Mild lymphoid

reactionreaction No or mild serositisNo or mild serositis No fistulas or sinusesNo fistulas or sinuses Mild fibrosisMild fibrosis

diarrheal disease malabsorption syndromes suboptimal absorption of different nutrients, electrolytes...

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