Bases da Fisiopatologia da Diarreia (The Pathophysiology of Diarrhea)

Warren, Cirle Alcantara

doi:10.5151/9788580391893-30

Bases da Fisiopatologia da Diarreia (The Pathophysiology of Diarrhea)

Warren, Cirle Alcantara

Resumo:

Diarrhea is one of the most common complaints of patients seeking medical attention. It is commonly described as increased liquidity or decreased consistency (“loose or watery”) of stool1, 2. Other authors have defi ned diarrhea in terms of increased in stool frequency or fecal weight but in general, increased in defecation alone is not regarded as diarrhea and patients may have loose or watery stool with normal weight. The differential diagnosis for diarrhea is broad and the basic mechanism involved depends on the underlying etiologic cause. Understanding the basic physiology of the gastrointestinal tract is essential in the understanding of the mechanisms of gut dysfunction and the development of diarrhea.

The gastrointestinal tract is a delicate balance of 4 basic physiologic functions: secretion, absorption, barrier function and motility. All of these processes aim to facilitate extraction of nutrients or needed substances from food and excretion of excess, refuse and toxic materials. Intestinal absorption of water is crucial to maintain hydration for normal bodily functions. Moreover, the intestinal epithelium undergoes constant regeneration. As discussed in Chapter 16, intestinal cell proliferation occurs in the crypt, which actively supplies the sloughing enterocytes at the villus, where most absorption occurs. The entire intestinal epithelium may be replaced in 2-3 days.

Download (PDF)

43 downloads

Sistema, digestório

DOI: 10.5151/9788580391893-30

Referências bibliográficas

TALLEY, N. J.; WEAVER, A. L.; ZINSMEISTER, A. R.; MELTON, L. J.;
III. Self-reported diarrhea: what does it mean? Am. J. Gastroenterol. 89(8):
1160-1164, 1994.
WENZL, H. H.; FINE, K. D.; SCHILLER, L. R.; FORDTRAN, J. S. Determinants
of decreased fecal consistency in patients with diarrhea. Gastroenterology. 108(6):
1729-1738, 1995.
BARRETT, K. E. Water and Electrolyte Absorption. In: BARRETT, K. E.
(ed.). Gastrointestinal Physiology. The McGraw Hill Companies, 2006.
PRESTON, G. M.; AGRE, P. Isolation of the cDNA for erythrocyte integral
membrane protein of 28 kilodaltons: member of an ancient channel family.
Proc. Natl. Acad. Sci. USA. 88(24): 11110-11114, 1991.
ALCANTARA, W. C.; DESTURA, R. V.; SEVILLEJA, J. E. et al. Detection of
epithelial-cell injury, and quantifi cation of infection, in the HCT-8 organoid
model of cryptosporidiosis. J. Infect. Dis. 198(1): 143-149, 2008.
KIRK, K. L.; HALM, D. R.; DAWSON, D. C. Active sodium transport by
turtle colon via an electrogenic Na-K exchange pump. Nature. 287(5779):
237-239, 1980.
RIORDAN, J. R.; ROMMENS, J. M.; KEREM, B. et al. Identifi cation of the
cystic fi brosis gene: cloning and characterization of complementary DNA.
Science. 245(4922): 1066-1073, 1989.
SHARP, G. W.; HYNIE, S. Stimulation of intestinal adenyl cyclase by cholera
toxin. Nature. 229(5282): 266-269, 1971.
GLENN, G. M.; FRANCIS, D. H.; DANIELSEN, E. M. Toxin-mediated
effects on the innate mucosal defenses: implications for enteric vaccines.
Infect. Immun. 77(12): 5206-5215, 2009.
HODSON, C. A.; AMBROGI, I. G.; SCOTT, R. O.; MOHLER, P. J.;
MILGRAM, S. L. Polarized apical sorting of guanylyl cyclase C is specifi ed
by a cytosolic signal. Traffi c. 7(4): 456-464, 2006.
SCHULZ, S.; GREEN, C. K.; YUEN, P. S.; GARBERS, D. L. Guanylyl cyclase
is a heat-stable enterotoxin receptor. Cell. 63(5): 941-948, 1990.
BASU, N.; ARSHAD, N.; VISWESWARIAH, S. S. Receptor guanylyl cyclase
C (GC-C): regulation and signal transduction. Mol. Cell Biochem. 334(1-2):
67-80, 2010.
TAKAHASHI, A.; SATO, Y.; SHIOMI, Y. et al. Mechanisms of
chloride secretion induced by thermostable direct haemolysin of Vibrio
parahaemolyticus in human colonic tissue and a human intestinal epithelial
cell line. J. Med. Microbiol. 49(9): 801-810, 2000.
LORROT, M.; VASSEUR, M. How do the rotavirus NSP4 and bacterial
enterotoxins lead differently to diarrhea? Virol. J. 4: 31, 2007.
KARAKI, S. I.; KUWAHARA, A. Regulation of intestinal secretion involved
in the interaction between neurotransmitters and prostaglandin E2.
Neurogastroenterol. Motil. 16(Suppl 1): 96-99, 2004.
PETERSON, J. W.; OCHOA, L. G. Role of prostaglandins and cAMP in the
secretory effects of cholera toxin. Science. 245(4920): 857-859, 1989.
HOGLUND, P.; HAILA, S.; SOCHA, J. et al. Mutations of the Downregulated
in adenoma (DRA) gene cause congenital chloride diarrhoea. Nat.
Genet. 14(3): 316-319, 1996.
GILL, R. K.; BORTHAKUR, A.; HODGES, K. et al. Mechanism underlying
inhibition of intestinal apical Cl/OH exchange following infection with
enteropathogenic E. coli. J. Clin. Invest. 117(2): 428-437, 2007.
HODGES, K.; ALTO, N. M.; RAMASWAMY, K.; DUDEJA, P. K.; HECHT,
G. The enteropathogenic Escherichia coli effector protein EspF decreases
sodium hydrogen exchanger 3 activity. Cell Microbiol. 10(8): 1735-1745,
2008.
DEAN, P.; MARESCA, M.; SCHULLER, S.; PHILLIPS, A. D.; KENNY, B.
Potent diarrheagenic mechanism mediated by the cooperative action of three
enteropathogenic Escherichia coli-injected effector proteins. Proc. Natl.
Acad. Sci. USA. 103(6): 1876-1881, 2006.
BEAU, I.; BERGER, A.; SERVIN, A. L. Rotavirus impairs the biosynthesis
of brush-border-associated dipeptidyl peptidase IV in human enterocyte-like
Caco-2/TC7 cells. Cell Microbiol. 9(3): 779-789, 2007.
HATHAWAY, L. J.; KRAEHENBUHL, J. P. The role of M cells in mucosal
immunity. Cell Mol. Life Sci. 57(2): 323-332, 2000.
PARSOT, C. Shigella spp. and enteroinvasive Escherichia coli pathogenicity
factors. FEMS Microbiol. Lett. 252(1): 11-18, 2005.
JACEWICZ, M. S.; ACHESON, D. W.; BINION, D. G. et al. Responses of human intestinal microvascular endothelial cells to Shiga toxins 1 and 2 and
pathogenesis of hemorrhagic colitis. Infect. Immun. 67(3): 1439-1444, 1999.
O’BRIEN, A. D.; NEWLAND, J. W.; MILLER, S. F.; HOLMES, R. K.;
SMITH, H. W.; FORMAL, S. B. Shiga-like toxin-converting phages from
Escherichia coli strains that cause hemorrhagic colitis or infantile diarrhea.
Science. 226(4675): 694-696, 1984.
ZHANG, X.; MCDANIEL, A. D.; WOLF, L. E.; KEUSCH, G. T.; WALDOR,
M. K.; ACHESON, D. W. Quinolone antibiotics induce Shiga toxin-encoding
bacteriophages, toxin production, and death in mice. J. Infect. Dis. 181(2):
664-670, 2000.
SANDVIG, K.; BERGAN, J.; DYVE, A. B.; SKOTLAND, T.; TORGERSEN,
M. L. Endocytosis and retrograde transport of Shiga toxin. Toxicon. 56(7):
1181-1185, 2010.
IIDA, T.; NAKA, A.; SUTHIENKUL, O.; SAKAUE, Y.; GUERRANT, R.
L.; HONDA, T. Measurement of fecal lactoferrin for rapid diagnosis of
enterohemorrhagic Escherichia coli infection. Clin. Infect. Dis. 25(1): 167,
1997.
PERNA, N. T.; MAYHEW, G. F.; POSFAI, G. et al. Molecular evolution of
a pathogenicity island from enterohemorrhagic Escherichia coli O157:H7.
Infect. Immun. 66(8): 3810-3817, 1998.
JUST, I.; SELZER, J.; WILM, M.; VON EICHEL-STREIBER, C.; MANN,
M.; AKTORIES, K. Glucosylation of Rho proteins by Clostridium diffi cile
toxin B. Nature. 375(6531): 500-503, 1995.
JUST, I.; WILM, M.; SELZER, J. et al. The enterotoxin from Clostridium
diffi cile (ToxA) monoglucosylates the Rho proteins. J. Biol. Chem. 270(23):
13932-13936, 1995.
GENTH, H.; DREGER, S. C.; HUELSENBECK, J.; JUST, I. Clostridium
diffi cile toxins: more than mere inhibitors of Rho proteins. Int. J. Biochem.
Cell Biol. 40(4): 592-597, 2008.
VOTH, D. E.; BALLARD, J. D. Clostridium diffi cile toxins: mechanism of action and role in disease. Clin. Microbiol. Rev. 18(2): 247-263, 2005.
ALCANTARA, C.; STENSON, W. F.; STEINER, T. S.; GUERRANT, R.
L. Role of inducible cyclooxygenase and prostaglandins in Clostridium
diffi cile toxin A-induced secretion and infl ammation in an animal model. J.
Infect. Dis. 184(5): 648-652, 2001.
MANTYH, C. R.; PAPPAS, T. N.; LAPP, J. A. et al. Substance P activation
of enteric neurons in response to intraluminal Clostridium diffi cile toxin A in
the rat ileum. Gastroenterology. 111(5): 1272-1280, 1996.
SLACK, E.; HAPFELMEIER, S.; STECHER, B. et al. Innate and adaptive
immunity cooperate fl exibly to maintain host-microbiota mutualism. Science.
325(5940): 617-620, 2009.
KELLY, D.; CAMPBELL, J. I.; KING, T. P. et al. Commensal anaerobic gut
bacteria attenuate infl ammation by regulating nuclear-cytoplasmic shuttling
of PPAR-gamma and RelA. Nat. Immunol. 5(1): 104-112, 2004.
MAZMANIAN, S. K.; LIU, C. H.; TZIANABOS, A. O.; KASPER, D. L. An
immunomodulatory molecule of symbiotic bacteria directs maturation of the
host immune system. Cell. 122(1): 107-118, 2005.
ABRAHAM, B.; SELLIN, J. H. Drug-induced diarrhea. Curr. Gastroenterol.
Rep. 9(5): 365-372, 2007.
DONOWITZ, M.; ROOD, R. P. Magnesium hydroxide: new insights
into the mechanism of its laxative effect and the potential involvement of
prostaglandin E2. J. Clin. Gastroenterol. 14(1): 20-26, 1992.
RATNAIKE, R. N.; JONES, T. E. Mechanisms of drug-induced diarrhoea in
the elderly. Drugs Aging. 13(3): 245-253, 1998.
KAST, R. E. Acarbose related diarrhea: increased butyrate upregulates
prostaglandin E. Infl amm. Res. 51(3): 117-118, 2002.
KLES, K. A.; VAVRICKA, S. R.; TURNER, J. R.; MUSCH, M. W.; HANAUER,
S. B.; CHANG, E. B. Comparative analysis of the in vitro prosecretory effects
of balsalazide, sulfasalazine, olsalazine, and mesalamine in rabbit distal ileum. Infl amm. Bowel Dis. 11(3): 253-257, 2005.
MOLAD, Y. Update on colchicine and its mechanism of action. Curr.
Rheumatol. Rep. 4(3): 252-256, 2002.
GRAY, T. K.; BIEBERDORF, F. A.; FORDTRAN, J. S. Thyrocalcitonin and
the jejunal absorption of calcium, water, and electrolytes in normal subjects.
J. Clin. Invest. 52(12): 3084-3088, 1973.
PARFITT, J. R.; DRIMAN, D. K. Pathological effects of drugs on the
gastrointestinal tract: a review. Hum. Pathol. 38(4): 527-536, 2007.
CARON, F.; DUCROTTE, P.; LEREBOURS, E.; COLIN, R.; HUMBERT, G.;
DENIS, P. Effects of amoxicillin-clavulanate combination on the motility of
the small intestine in human beings. Antimicrob. Agents. Chemother. 35(6):
1085-1088, 1991.
WEGENER, M.; WEDMANN, B.; LANGHOFF, T.; SCHAFFSTEIN, J.;
ADAMEK, R. Effect of hyperthyroidism on the transit of a caloric solidliquid
meal through the stomach, the small intestine, and the colon in man. J.
Clin. Endocrinol. Metab. 75(3): 745-749, 1992.
DONOHOE, C. L.; REYNOLDS, J. V. Short bowel syndrome. Surgeon. 8(5):
270-279, 2010.
ORTIZ-LUCAS, M.; SAZ-PEIRO, P.; SEBASTIAN-DOMINGO, J. J. Irritable
bowel syndrome immune hypothesis. Part one: the role of lymphocytes and
mast cells. Rev. Esp. Enferm. Dig. 102(11): 637-647, 2010.
SHAKIL, A.; CHURCH, R. J.; RAO, S. S. Gastrointestinal complications of
diabetes. Am. Fam. Physician. 77(12): 1697-1702, 2008.
BURES, J.; CYRANY, J.; KOHOUTOVA, D. et al. Small intestinal bacterial
overgrowth syndrome. World J. Gastroenterol. 16(24): 2978-2990, 2010.
KEELY, S. J.; BARRETT, K. E. Regulation of chloride secretion. Novel
pathways and messengers. Ann. N. Y. Acad. Sci. 915: 67-76, 2000.

Como citar:

WARREN, Cirle Alcantara; "Bases da Fisiopatologia da Diarreia (The Pathophysiology of Diarrhea)", p. 809-826. Sistema digestório: integração básico-clínica. São Paulo: Blucher, 2016.
ISBN: 9788580391893, DOI 10.5151/9788580391893-30