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Fluid and Electrolyte Disturbances In Gastrointestinal and Pancreatic Disease  443


            PATHOPHYSIOLOGY OF THE                              followed by moderate-amplitude contractions in the gas-
            GASTROINTESTINAL TRACT                              tric antrum and intestine, and shortening of the
                                                                intraabdominal esophagus. Dilatation of the cardia and
                                                                lower esophageal sphincter enables transfer of gastric
            VOMITING                                            contents to the esophagus during retching and vomiting.
            Vomiting is a reflex act that is initiated by stimulation of  Retching often precedes vomiting and is characterized by
            the vomiting center in the reticular formation of the  rhythmic inspiratory movements against a closed glottis.
            medulla oblongata. The vomiting center can be       Negative intrathoracic pressure during retching prevents
            stimulated directly or indirectly via the chemoreceptor  expulsion of esophageal contents. During vomiting, the
            trigger zone (CRTZ), which is situated in the area  abdominal muscles contract and intrathoracic and
            postrema near the floor of the fourth ventricle     intraabdominal pressures are positive, resulting in force-
            (Figure 18-8). 14,34,35,61  The blood-brain barrier is lim-  ful expulsion of gastric contents from the mouth. 34
            ited at this point, enabling blood-borne substances such  Vomiting is associated with a wide range of disease pro-
            as toxins or drugs to stimulate the CRTZ, causing a reflex  cesses and, when frequent or severe, can have major
            action to expel ingested toxins, and this reflex represents a  effects on fluid, electrolyte, and acid-base balance. The
            long-preserved evolutionary survival technique for many  consequences of vomiting depend to some extent on
            species. 14  Neurologic input from the vestibular nucleus  the cause. Vomiting of gastric and intestinal contents

                                                                                                         þ
                                                                                                              þ
            can also stimulate the CRTZ in the dog or the vomiting  usually involves loss of fluid containing Cl ,K ,Na ,

            center.  14,34,35,61  Disease or irritation of the GIT, abdom-  and HCO 3 , and dehydration is accompanied to a
            inal organs, or peritoneum and cerebral diseases can  variable extent by hypochloremia, hypokalemia, and
                                                                             34,127
            directly stimulate the vomiting center via visceral  hyponatremia.    Metabolic acidosis is generally more
            receptors and vagal afferents (Figure 18-8).  14,34,35,61  common than metabolic alkalosis in dogs with gastroin-
                                                                             23
              Once the vomiting center is adequately stimulated, a  testinal disease.
            series of visceral events is initiated. This sequence of  With obstruction of the gastric outflow tract or proxi-


            events includes inhibition of proximal gastrointestinal  mal duodenum, loss of Cl can exceed that of HCO 3 ,
            motility, a retrograde power contraction in the small  and hypochloremia, hypokalemia, and metabolic alkalosis
                                                                      23,100,127
            intestine, and antral relaxation, which enables the transfer  result.  In human patients with serum bicarbon-
            of intestinal contents to the stomach. These events are  ate concentrations greater than 45 mmol/L, gastric
                                                         Drugs
                                                         Toxins                     Motion
                                                         Uremia                     sickness
                                                         Infections


                                                          CRTZ
                                  Cerebral                                         Vestibular
                                                                1
                                                   D  1,2,3 (D) H  1,2 (D) H α  1,2 (C)  Dog
                                     1   1          2     1    2  2              H  2,3  M  1,2,3  NK  2
                                  ENK μ  ω 2      5HT  1,2,3  M  1,2  NK  2,3  ENK  1,2  1  1  1
                                                     3   1   1     μ,δ
                                                         Vomiting           Cat
                                                          Center
                                                        α 2 1,2  5HT 1A 1
                                                         5HT 3 2  NK 1 3  M 1 3

                                Liver         Afferent neuron             Efferent neuron
                                Pancreas
                                Genitourinary        Gastrointestinal tract
                                                             1
                                                                      1
                                Peritoneum       5HT 3 1,2,3  NK 1 2     5HT M 2 1  NK 1 3  Mot (D)
                                                             4
                        Figure 18-8 Initiation of vomiting. CRTZ, chemoreceptor trigger zone; D, dog; C, cat. Receptors: ENK,
                        enkephalinergic; o 2 /GABA A /chloride channel complex; D, dopaminergic; H, histaminergic, a, adrenergic;
                        5-HT, serotonergic; M, cholinergic; NK, neurokinin; Mot, motilin. (From Kirk RW. Kirk's current veterinary
                        therapy XII. Small animal practice. In: Washabau RJ, Elie MS, editors. Antiemetic therapy. Philadelphia: WB
                        Saunders, 1995: 679–684. Ettinger SJ, Feldman EC. Textbook of veterinary internal medicine: diseases of the
                        dog and the cat, 7th ed. St Louis: Elsevier Saunders, 2010: 2 v. (l, 2218, lxxi p.195-200). Elwood C, Devauchelle
                        P, Elliott J, et al. Emesis in dogs: a review. J Small Anim Pract 2010;51:4–22.)
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