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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.)