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This is sensedby the mechanoreceptors which activate the myenteric nerves, and impulses are transduced to the spinalcord (and back) to relax the internal anal sphincter (IAS). The spinal cord conveys signals to the brain tostimulate the urge to defecate. These reflex actions cause the voluntary contraction of the external analsphincter (EAS) until defecation occurs. During defecation, the EAS relaxes, the person increases intraabdominal pressure, and feces are eliminated from the rectum.nCoLEGENDtr aCholecystokininVagus nerveCholeresisct iStimulatesecretiononSecretinnHClStimulate motilitynepsiFoodfattriG asPepsin oInhibitsecretionnpgeStimulatesecretionThick line indicatesprimary actionThin line indicatessecondary actionFooddistentionInhibit motilityEnzymes SecretinWater,bicarbonateFoodfatFoodfatCholecystokininMotilinNeuroendocrine cellFigure 22.11 Effect of Major GI Hormones on GI Motility Themain effects of GI hormones on GI motility are depicted in this scheme.
Whilemany hormones have effects on gastric motility, a few stimulate motility inthe small and large intestines, including motilin (small intestine only) andgastrin (both small and large intestines, not shown on figure). GIP, gastricinhibitory peptide.GIPPancreasStimulatessmoothmuscleThink about homeostasis . . . With chronic vomiting ordiarrhea, there is significant loss of fluids and electrolytes.Vomiting causes a disproportionate loss of H+ and K+(from stomach acid). If vomiting continues over an extendedtime, in addition to dehydration, the loss of H+ and K+ can leadto metabolic alkalosis and hypokalemia (low plasma K+).In contrast, chronic diarrhea results in dehydration and a disproportionate loss of HCO3-, which can result in metabolic acidosis(see Chapter 20).H2OBloodstreamH⫹Cl⫺K⫹DehydrationSystemiceffectsH⫹OH⫺CO2Peptic esophagitisH⫹Cl⫺AzotemiaandelectrolytedisturbancesNaHCO3ImpairedrenalfunctionAlkalosisKidneyNa⫹Cl⫺K⫹Diminished urine outputElectrolytedepletionVomiting Vomiting leads to a disproportionate loss of H+, Cl−, and K+, as well as loss of fluid from theextracellular space.
Prolonged vomiting results in dehydration, alkalosis, and hypokalemia (low plasma K+).268Gastrointestinal PhysiologyDiarrhea occurs when chyme and fecal matter move tooquickly through the colon. This can result from irritation ofthe lower GI tract (from bacteria or virus), diseases (irritablebowel syndrome, ulcerative colitis, Crohn’s disease), ornervous stress. Movement in the colon is usually very slow(segmental propulsion), allowing absorption of almost all ofthe water and salt from the chyme, producing feces.
If abnormal motility occurs, the fecal matter will move through thecolon with minimal absorption, producing diarrhea. Whenthis is in response to bacterial irritation, rapid motility servesto wash the irritant out of the tract, and the diarrhea abateswith the loss of the bacteria or virus.In general, osmotic diarrhea is the most common type ofdiarrhea. It is caused by hypermotility, which forces theCLINICAL CORRELATECholeraCholera is disease caused by the bacterium Vibrio cholerae, whichis contracted in a fecal-oral manner, usually through ingestion ofcontaminated water. In the small intestine, the bacteria producecholera toxin, which has devastating effects on the intestinal epithelium. The toxin modifies the G protein Gs, and as a result,GTPase activity is inhibited, causing prolonged activation ofadenyl cyclase.
The resulting high level of cAMP activates theCFTR (see “Cystic Fibrosis” Clinical Correlate in Chapter 2),which causes active Cl− secretion into the lumen of the smallintestine. The Cl− efflux is accompanied by Na+ efflux (preservingelectroneutrality), and water follows the electrolytes.
This isotonicchyme/feces through the lower GI tract too rapidly for properabsorption of fluid and electrolytes. In contrast, secretorydiarrhea is specifically caused by increased secretion of solutesinto the lumen of the gut. The hallmark example of this occurswith cholera toxin (see “Cholera” Clinical Correlate).REFLEXESAll of the reflexes ultimately serve to promote the efficientdigestion and elimination of ingested material. One of themost important reflexes, the rectosphincteric reflex, was discussed earlier in relation to defecation.
A variety of GI-relatedreflexes are described in Table 22.2.secretion of electrolytes and water depletes the vascular spacewhile maintaining plasma osmolarity. In this manner, the vascularspace is rapidly contracted, causing severe dehydration and shock.Antibiotic therapy and intravenous hydration is the most desirable therapy; otherwise, oral rehydration therapy (ORT, containing water, electrolytes, and glucose) from an uncontaminatedsource can be given. The glucose in the ORT promotes sodiumand electrolyte absorption and actually draws more of the secretedNa+ and Cl− back into the vascular space, along with water.
Thisis effective in reducing the diarrhea and maintaining hydration.Without antibiotics, and with availability of uncontaminatedwater, the bacteria will be cleared from the GI tract in 7 to 10 days,as the enterocytes slough off and are replaced by new cells.Vibrio choleraeABCholera toxinGM1Cl–Na+H2OCFTRRetrogradeendocytosisGsαAdenylatecAMPcyclaseCyclic AMPGi Epithelial cellEnkephalinActions of Cholera Toxin in Intestinal CellsMotility through the Gastrointestinal TractCLINICAL CORRELATESmooth Muscle Disorders: Achalasia andHirschsprung’s DiseaseThe enteric nervous system (ENS) can be thought of as the centralprocessing center responding to a variety of signals and makingthe appropriate connections. Because of this, if the ENS is absentfrom an area in the tract, pathology ensues.
Smooth muscle diseases such as achalasia and Hirschsprung’s disease involve aganglionic areas of the digestive tract (loss of nerves in some areas).Achalasia is a loss of the ENS in the lower part of the esophagusand always involves the lower esophageal sphincter. The aganglionic region is not able to stimulate contractions and cannottransduce the signal to relax the lower esophageal sphincter.
As aresult, the sphincter tone is very high. Because the lower esophageal sphincter is not able to relax, the food and fluid can takehours, rather than seconds, to leave the esophagus. Over time(months to years) this causes dilation of the esophagus. This condition is very painful and can eventually lead to anorectic behavior. Also, because the ingested food sits in the esophagus for longperiods of time, partial digestion occurs, and the contents can269further damage the esophageal mucosa. The etiology of achalasiais unknown, and treatment usually only partially alleviates theproblem. Pharmacologic intervention with nitrites (isosorbidedinitrite) or calcium channel blockers (nifedipine or verapamil)is used but has limited efficacy, and the primary treatment is byballoon dilation or surgically cutting the sphincter (esophagomyotomy).
This allows food and fluids to pass through the loweresophageal sphincter into the stomach but usually producesgastric reflux, and the patients must be treated with oral medication for GERD (gastroesophageal reflux disease).Hirschsprung’s disease (or megacolon) is a congenital disease thatinvolves the loss of the ENS in the distal part of the colon andalways involves the internal anal sphincter (IAS). The normaldefecation reflex mediated by the myenteric plexus (feces inrectum → stretch → relaxation of IAS) does not occur, so verylittle defecation occurs and feces build up in the rectum and colon.This dilates the colon, and symptoms include little or no bowelmovements and vomiting. Drugs are not effective; surgical removalof the aganglionic region typically restores the ability todefecate.Tremendous distentionand hypertrophy ofsigmoid and descendingcolon; moderate involvementof transverse colon;distal constricted segmentTypical abdominal distentionHirschsprung’s Disease (Megacolon)This page intentionally left blank271CHAPTER23Gastrointestinal SecretionsSALIVARY SECRETION AND REGULATIONSalivary Gland SecretionSalivary secretions make foods easier to ingest (and digest) bylubricating, cooling, and adding digestive enzymes to thefood.
There are three sets of salivary glands producing thesecretions: the parotid, the submandibular, and the sublingual. Secretion from these glands is under the control ofcranial nerves VII and IX (Figs. 23.1 and 23.2 and Table 23.1).There are a few unique aspects of salivary gland secretion thatbear noting:■■■■A large volume of fluid is produced by relatively smallglands.Saliva is always hypotonic to plasma.Compared with plasma, saliva is relatively rich in K+.Salivary secretion is primarily regulated by cranial parasympathetic nerves, which control blood flow to theglands.Approximately 1.5 liters (L) of saliva is secreted daily, most ofwhich occurs with eating.
When food enters the mouth, salivation is stimulated. The saliva serves to:■■■■■■Lubricate the food (water and mucins).Start digestion.Protect the mouth and gastrointestinal (GI) tract bycooling hot foods.Protect the tract through the antimicrobial actions ofwhite blood cells (WBCs), IgA, and opsonins.Aid coagulation by secreting platelet-activating factor.Provide oral hygiene by buffering and cleansing the oralcavity—swallowing and spitting allow us to get rid ofbacteria, whereas low flow while we sleep allows bacteriato accumulate, causing halitosis (bad breath).Digestion of starch and lipids begins in the mouth.
The serousglands secrete salivary a-amylase (or, ptyalin), which beginsstarch digestion by breaking α1-4 linkages of glucose polymers (oligosaccharides). This is the same enzyme as pancreatic α-amylase. In addition, Von Ebner’s glands of the tongueproduce a serous secretion that includes the enzyme linguallipase, which is active at low pH and can hydrolyze dietarytriglycerides (TGs) in the stomach, yielding free fatty acids(FA) and diglycerides. This is the same as gastric lipase but isdifferent from pancreatic lipase (which hydrolyzes TGs to twoFAs and one monoglyceride).Production of SalivaSalivary glands are exocrine glands, with secretions drainingthrough ducts.
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