© 2004 Current Medicine Group Ltd FISIOLOGIA DIGESTIVA (BCM II) Clase 12: Diarrea Dr. Michel Baró Aliste.

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© 2004 Current Medicine Group Ltd

FISIOLOGIA DIGESTIVA (BCM II)FISIOLOGIA DIGESTIVA (BCM II)

Clase 12: Diarrea Clase 12: Diarrea

Dr. Michel Baró AlisteDr. Michel Baró Aliste

© 2004 Current Medicine Group Ltd

DefinicionesDefiniciones

Diarrea: aumento de la frecuencia y/o volumen de las deposicionesDiarrea: aumento de la frecuencia y/o volumen de las deposiciones

Mayor a 200 g/díaMayor a 200 g/día

PseudodiarreaPseudodiarrea

IncontinenciaIncontinencia

Aguda (<2 semanas)Aguda (<2 semanas)

Crónica (>4 semanas)Crónica (>4 semanas)

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Tipos de DiarreaTipos de Diarrea

-Osmótica (malabsortivas)-Osmótica (malabsortivas)

-Secretora (alteración de transporte de electrolitos)-Secretora (alteración de transporte de electrolitos)

-Alteración de la motilidad-Alteración de la motilidad

-Inflamatoria (disenterías)-Inflamatoria (disenterías)

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Water fluxes through the intestine

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Calculation of osmotic gap

Diarrea Secretora vs. Diarrea Osmótica

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Typical features of secretory diarrhea

TABLE 4 - 5. TYPICAL FEATURES OF SECRETORY DIARRHEA

Voluminous, watery stools

Little or no fecal osmotic gap, stool pH near 7.0

Usually persists during fasting

Usually no pus, blood, or excess fat in stools

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Effects of resection of different parts of small intestine (a)

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Effects of resection of different parts of small intestine (b)

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Effects of resection of different parts of small intestine (c)

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Effects of resection of different parts of small intestine (d)

Umbral catártico de las Sales biliares: 3 a 5 mmol/L

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Effects of resection of different parts of small intestine (e)

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Mechanisms of diarrhea in enteritis

TABLE 4 - 10. MECHANISMS OF DIARRHEA IN ENTERITIS

Decreased surface area (destruction or resection)

Disrupted mucosal barrier (exudation)

Decreased rate of absorption, caused by inflammatory mediators or enteric nervous system

Diminished electrolyte absorption

Increased electrolyte secretion

Osmotic diarrhea due to malabsorption

Carbohydrates

Fatty acids, hydroxy - fatty acids

Bile acid diarrhea

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Bile acid malabsorption can be caused by various mechanisms (a)

Ac. biliares en colon > 3 mmol/l = diarrea

Diarrea secretora porMalabsorción de ac. biliares:Mecanismos:Tránsito aumentadoResección intestinalDaño mucosa del íleon

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Laxatives and detection methods

TABLE 4 - 15. LAXATIVES AND DETECTION METHODS

Laxative Detection Method

Phenolphthalein Alkalinization of stool produces pink color; spectrophotometry

Bisacodyl Thin - layer chromatography

Ipecac Thin - layer chromatography

Senna Urinary assay for anthraquinone

Magnesium Osmotic gap in stool water; increased concentration of magnesium in stool water

Phosphate Increased concentration in stool water

Sulfate Increased concentration in stool water

Water Creation of factitious diarrhea by addition of water to stool specimen can be detected by measurement of low - stool osmolality (<< 290 mosm/kg)

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Laxative abuse suspects

TABLE 4 - 16. PATIENTS SUSPECTED OF LAXATIVE ABUSE

Type Characteristics

Patients with bulimia Usually adolescent to young adult women; concerned about weight or manifesting an eating disorder

Secondary gain May have disability claim pending; illness may induce concern or caring behavior in others

Münchausen's syndrome Typically, a peripatetic patient who "enjoys" being a challenge to doctors; may undergo extensive testing repeatedly

Polle syndrome (Münchausen by proxy)

Dependent child poisoned by parent with laxatives to show how effective parent can be as a caregiver; may have history of sibling who died with chronic diarrhea

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Diarrheal syndromes related to circulating secretagogues

TABLE 4 - 17. DIARRHEAL SYNDROMES RELATED TO CIRCULATING SECRETAGOGUES

Syndrome Typical Symptoms Main Mediators

Zollinger - Ellison Pancreatic tumor, peptic ulcer, steatorrhea, diarrhea

Gastrin

Verner - Morrison (pancreatic cholera)

Watery diarrhea, hypokalemia, achlorhydria, flushing

Vasoactive intestinal polypeptide

Medullary thyroid carcinoma

Thyroid mass, diarrhea, hypermotility Calcitonin, prostaglandins

Pheochromocytoma Adrenal mass, hypertension, diarrhea Vasoactive intestinal polypeptide, norepinephrine, epinephrine

Carcinoid Diarrhea, flushing, wheezing, right - sided cardiac valvular disease

Serotonin, kinins

Somatostatinoma Nonketotic diabetes mellitus, steatorrhea, diarrhea, gallstones

Somatostatin

Glucagonoma Skin rash (migratory necrotizing erythema), mild diabetes

Glucagon

Hyperthyroidism Diarrhea, steatorrhea, weight loss, tremor Thyroxine, tri - iodothyronine

Mastocytosis Flushing, dermatographism, nausea, vomiting, diarrhea, abdominal pain

Histamine

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Zollinger-Ellison syndrome results from secretion of gastrin

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Vasoactive intestinal polypeptide-secreting tumors (a)

Sindrome de Verner-Morrisono Cólera pancreático-diarrea acuosa-hipokalemia-hipocloridia AMPc

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Vasoactive intestinal polypeptide-secreting tumors (b)

VIPoma

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Vasoactive intestinal polypeptide-secreting tumors (c)

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Vasoactive intestinal polypeptide-secreting tumors (d)

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Medullary carcinoma of the thyroid products

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Drugs associated with diarrhea

TABLE 4 - 29. DRUGS ASSOCIATED WITH DIARRHEA

Antibiotics Hypocholesterolemic drugs

Antineoplastic drugs Lovastatin

Antiarrhythmics Gemfibrozil

Quinidine Clofibrate

Procainamide Probucol

Antihypertensives Gastrointestinal drugs

Beta - blockers Magnesium - containing antacids

Angiotensin - converting enzyme inhibitors H2 - receptor antagonists

Hydralazine Prostaglandin analogues (misoprostal)

Antidepressants Sulfasalazine

Lithium Olsalazine

Fluoxetine (Prozac) Prokinetic drugs (cisapride)

Tranquilizers Miscellaneous agents

Alprazolam (Xanax) Methysergide

Meprobamate Theophylline

Anticonvulsants Diuretics

Ethosuximide Oral hypoglycemic drugs

Valproic acid Colchicine

L - Dopa Thyroid hormone

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Longstanding diabetes mellitus and chronic diarrhea

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Malabsorción - Esteatorrea

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Diseases that impair nutrient absorption

Classification of Diseases that Cause Intestinal Malabsorption

Premucosal Mucosal Postmucosal

Pancreatic insufficiency Celiac sprue Congenital lymphangiectasia

Hepatobiliary disease Tropical sprue Secondary lymphangiectasia

Bacterial overgrowth Whipple's disease

Rapid intestinal transit Eosinophilic enteritis

Gastrectomy Brush border enzyme deficiency

Lymphoma

Short - bowel syndrome

Prolonged malnutrition

Radiation enteritis

Parasitic infection

Mesenteric ischemia

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Stool fat concentrations as a clue to etiology

<6 g/día >20 g/día

9,5%

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Effect of oral pancreatic enzyme replacement (A)

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Effect of oral pancreatic enzyme replacement (B)

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Intraduodenal bile acid concentrations and fecal fat output

2,5 umol/mL

Bilirrubina pl >4,5 mg%

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Pathophysiology of bacterial overgrowth

InflamaciónAtrofia vellositaria

-Daño histológico-Malabsorción de nutrientes-Producción de toxinas

Reabsorción en yeyuno

Absorción grasa

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Multiple jejunal diverticula

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Multiple small bowel diverticula

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Scleroderma

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Billroth I and II subtotal gastrectomy

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Radiograph of a patient with a Billroth II procedure

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Pathophysiology of lactase deficiency

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Intestinal fluid accumulation with a lactose-containing meal

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Effect of unabsorbed carbohydrate on stool water output

3,5 g H2O / mmol de molécula no absorbida (carbohidrato, ácido orgánico, catión)

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Celiac sprue (A) – Enfermedad Celíaca

Gluten: trigo, centeno, avena

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Celiac sprue (B)

Tres meses después de dieta libre de gluten

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Molecular pathophysiology of celiac sprue (A)

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Molecular pathophysiology of celiac sprue (B)

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Molecular pathophysiology of celiac sprue (C)

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Molecular pathophysiology of celiac sprue (D)

HLA-DQ2 or HLA-DQ8

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Molecular pathophysiology of celiac sprue (E)

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Molecular pathophysiology of celiac sprue (F)

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Detecting celiac sprue (A)

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Detecting celiac sprue (B)

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Classic moulage pattern of celiac sprue

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Tropical sprue

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Whipple's disease

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Eosinophilic gastroenteritis

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Massive small-bowel resection

Predicted Nutritional Outcome in Patients who have had Massive Intestinal Resection

Remaining Jejunal length, cm Colon Nutritional outcome

0 - 50 - TPN

+ TPN

51 - 100 - IVFM/TPN

+ Modified oral diet

101 - 150 - Regular or modified oral diet

+ Regular diet

151 - 200 - Modified oral diet

+ Regular diet

>200 - or + Regular diet

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Jejunal length and sodium-water absorption (A)

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Jejunal length and sodium-water absorption (B)

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Rehydration therapy enhances sodium and water absorption

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Sodium balance after different sodium-containing test solutions

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Oral rehydration therapy and high-volume ostomy output

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Radiation enteritis

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Lymphangiectasia

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Selected symptoms and signs of nutrient deficiencies

Selected Symptoms and Signs of Nutrient Deficiencies

Symptoms or sign Possible nutrient deficiency

General Weakness, weight loss, muscle wasting Protein, calorie

Skin Pallor Folate, iron, vitamin B12

Follicular hyperkeratosis Vitamin A, vitamin C

Perifollicular petechiae Vitamin C

Dermatitis Protein, calorie, niacin, riboflavin, zinc, vitamin A, essential fatty acids

Bruising, purpura

Hair Easily plucked, alopecia Vitamin C, vitamin K

Corkscrew hairs, coiled hair Protein, zinc, biotin

Eyes Night blindness, keratomalacia, photophobia Vitamin C, vitamin A

Conjunctival inflammation Vitamin A

Mouth Glossitis Vitamin A, riboflavin

Bleeding or receding gums, mouth ulcers Riboflavin, niacin, folate, vitamin B12, protein

Decreased taste Vitamin A, vitamin C, vitamin K, folate

Burning or sore mouth and tongue Zinc, vitamin A

Angular stomatitis or cheilosis Vitamin B12, vitamin C, niacin, folate, iron

Neurologic Tetany Riboflavin, niacin, pyridoxine, iron

Paresthesias Calcium, magnesium

Loss of reflexes, wrist drop, foot drop, loss of vibratory and position sense

Thiamine, pyridoxine, vitamin B12, vitamin E

Dementia, disorientation Niacin, vitamin B12

Ophthalmoplegia Vitamin E, thiamine

Depression Biotin, folate, vitamin B12

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D-xylose to evaluate small-intestine absorptive function

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Enfermedad Inflamatoria Intestinal

•Colitis Ulcerosa•Enfermedad de Crohn

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Endoscopic features of active ulcerative colitis (B)

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Microscopic features of specimen in Fig 4-8 (B)

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Endoscopic features of Crohn's disease (A)

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Specimen from patient with Crohn's colitis (B)

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Inflammatory bowel disease etiology

TABLE 4 - 26. THEORIES OF INFLAMMATORY BOWEL DISEASE ETIOLOGY

Toxic response to luminal contents

Specific microbial pathogen

Abnormal luminal constituents

Increased absorption of luminal macromolecules

Enhanced immunologic response to normal constituents

Autoimmune response

To epithelial cell or mucus glycoproteins

Molecular mimicry (cross - reactivity of intestinal microflora and epithelia)

To immune cells

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Infliximab

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