51: Colon and Urinary Excretion Flashcards
- List the main areas of the bladder and describe the sequence of events occurring during reflexive micturition, differentiating events under involuntary and voluntary control.
Urine produced in the kidneys continually passes to the bladder via the ureters (~1-2L/day). Smooth muscles in the ureter walls contract regularly to draw urine into the bladder. Normally, the urinary bladder is completely emptied during voiding and urine is sterile until it reaches the urethra.
The bladder is a smooth muscle chamber composed of the rough/folded body (where the urine collects), and the neck/posterior urethra (a funnel-shaped extension of the body that connects to the urethra and includes the internal sphincter). The smooth trigone area lies on the posterior wall of the bladder between the orifices of the ureters.
The body of the bladder is composed of smooth muscle called the detrusor. Contraction of the detrusor muscle is a major step in bladder emptying. The trigone and internal sphincter are also composed of smooth muscle which relaxes during bladder emptying.
Beyond the posterior urethra, the urethra passes through the urogenital diaphragm containing a layer of skeletal muscle that is under voluntary control, called the external sphincter. Stretch signals from the posterior urethra are particularly strong and primarily involved in triggering the bladder emptying reflexes. However, this response is normally inhibited and control of this voluntary reflex is learned during childhood.
The pontine micturition center controls the detrusor muscle and urinary sphincters. In turn, suprapontine centers control the pontine micturition center providing voluntary control.
Involuntary: sensory fibers detect stretch in bladder wall wall & transmit signal to spinal cord, PNS then mediates detrusor muscle contraction and internal sphincter relaxation.
Voluntary: somatic fibers control external sphincter by Pudendal nerve.
The pelvic nerves connect with the spinal cord through the sacral plexus. These nerves contain both sensory (afferent stretch) and motor (efferent parasympathetic) fibers. PNS fibers terminate on ganglion cells in the bladder wall. Short postganglionic nerves innervate the detrusor muscle to stimulate contraction + internal sphincter relaxation during voiding. The presynaptic PNS neurons are inhibited by efferent impulses in the brain (a learned reflex). Skeletal motor fibers in the pudendal nerve innervate the external sphincter. Voiding begins with voluntary relaxation of the external urinary sphincter, followed by the internal sphincter. When a small amount of urine reaches the proximal (posterior) urethra, afferents signal the cortex that voiding is imminent. The micturition reflex now continues as pontine centers no longer inhibit the parasympathetic preganglionic neurons that innervate the detrusor muscle. As a result, the bladder contracts, expelling urine.
SNS fibers inhibit contraction of the detrusor (B-adrenergic response) and stimulate contraction of the internal sphincter muscles (a-adrenergic). They also regulate blood vessels in the bladder.
Abnormalities of micturition include:
1. atonic bladder & incontinence caused by destruction of sensory nerve fibers (e.g.
crush injuries)
2. automatic bladder caused by spinal cord damage above the sacral region
3. uninhibited neurogenic bladder caused by lack of inhibitory signals from the brain (e.g. partial damage in cord or stem)
2B. Describe how disorders of motility can lead to diarrhea, constipation, megacolon, and irritable bowel syndrome.
Relaxation of the ileocecal sphincter occurs with or shortly after eating. This reflex has been termed the gastroileal reflex. It is not clear whether the reflex is mediated by gastrointestinal hormones (gastrin and cholecystokinin) or extrinsic autonomic nerves to the intestine. Note that the gastroileal reflex is named with the origin of the reflex first (gastro) and the target of the reflex named second (ileal). This method of naming is characteristic of all the gastrointestinal reflexes. The enterogastric reflex involves signals from the colon and small intestine that inhibit gastric motility and gastric secretion. The gastrocolic reflex causes the colon to evacuate when the stomach is stretched. The intestino-intestinal reflex causes a bowel segment to relax when it is overstretched. The rectosphincteric reflex is also called the defecation reflex.
The gastroileal reflex intensifies peristalsis in the ileum, and emptying of ileal contents into the cecum via the ileocecal valve (sphincter) that separates the small and large intestine.
The ascending colon travels up the right side of the body and is involved in extraction of water and electrolytes. However, dwell time of chyme is comparatively short. The transverse colon runs across the body from right to left, and functions primarily to remove electrolytes and water. Dwell time is long (~24 hrs). The descending colon runs down the left side of the body; it functions mainly to store stool. The sigmoid colon moves stools between the descending segment and the rectum. The rectum is the last ~8 inches of the colon and stores stools until defecation occurs. The anus is the exterior opening and is controlled by internal and external sphincters.
Disorders of motility:
Constipation results from poor motility which leads to greater absorption of liquids from the feces which yields hard feces. In most cases, dietary fiber promotes normal colonic function i.e. there is a direct correlation among increased dietary fiber, increased colonic intraluminal bulk, and enhanced transit through the colon.
Diarrhea is the rapid movement of fecal matter through the large intestine. In a healthy individual, short-term diarrhea is not problematic, but it can be fatal in infants. The availability of oral rehydration solutions has reduced infant mortality. There are two types of diarrhea:
The osmotic form of diarrhea results from non-absorbable solutes in the lumen (e.g., lactase deficiency/lactose not broken down to glucose and galactose)
The secretory form of diarrhea results from excessive secretion of fluids by crypt cells due to bacterial overgrowth (e.g., cholera toxin).
Common causes of diarrhea are: bacterial infections, viral infections, food intolerances, parasites, intestinal diseases, reactions to medications, functional bowel disorders, psychogenic factors, long distance running.
The ileocecal sphincter prevents fecal backflow from colon to ileum. Emptying is regulated by stretch, composition, and the fluidity of chyme.
Distension/pressure or irritation (e.g. inflamed appendix) of the cecum inhibits ileal peristalsis and excites sphincter contraction, delaying emptying. These reflexes are mediated locally by the myenteric plexus, and extrinsically by the SNS.
*Appendicitis is a medical emergency acutely presenting as severe gastric pain, followed by vomiting, then fever. It is typically due to an obstruction of the appendix lumen by calcified fecal matter. Often, the appendix is surgically removed. Left untreated, ischemia and tissue necrosis may lead to peritonitis, septicemia and death.
Hirschsprung’s Disease (Megacolon): Hirschsprung’s disease is congenital/present at birth. It results from a lack of ENS in the distal part of the GI tract (‘‘aganglionosis’’). The aganglionic segment is tonically contracted due to lack of inhibitory motor neuron function. As a consequence the proximal segment becomes distended with fecal matter that cannot be passed. The affected segment extends cranially from the anus and encompasses a variable portion of the gut. The lack of propulsive movements may lead either to an early obstructive syndrome in infants (life-threatening) or to severe constipation. In mild cases, Hirschsprung’s disease may not be detected until later in life. Hirschsprung’s disease is treated with surgery to remove the affected portion of the colon. After surgery, most children pass stool normally.
Irritable bowel syndrome: IRB is a common G.I. disorder that leads to crampy pain, bloating, gassiness, and altered bowel habits (diarrhea predominant, Constipation predominant, or alternating between both). There’s no evidence of an organic disorder. It’s higher in women. It’s often associated with a high stress and anxiety. Symptoms are treated with opioids and serotonin receptor antagonist in diarrhea predominant cases. Symptoms are treated with selective serotonin receptor agonists and/ or soluble fiber in constipation predominant cases. Cramping pain symptoms are treated with tricyclic antidepressants and antispasmodics. No cure but not life-threatening.
- Describe the sequence of events in the colon and anal sphincter regulation during reflexive defecation, differentiating those movements under voluntary control and those under autonomic control.
The rectum is usually empty. This results partly from a weak functional sphincter ~20 centimeters from the anus at the juncture between the sigmoid colon and the rectum. There is also a sharp angulation here that contributes additional resistance to filling of the rectum. Tension in the wall of the rectum typically signals the urge to defecate. Movement of stool from sigmoid colon to rectum causes increased pressure due to passive distention. In turn, this triggers active contraction of rectal smooth muscles in conjunction with relaxation of internal anal sphincter.
Fecal incontinence is involuntary defecation. The pathophysiology is often related to trauma, injury to the pelvic floor such as during childbirth or surgery, or a prolapsed rectum. The rectophincteric reflex are typically normal, but the pathology is with the external* anal sphincter. Treatments include bulking agents, surgery, and strengthening the pelvic floor or sphincter muscles.
Defecation. The sequence of events leading to defecation: The defecation (or rectosphincteric) reflex is triggered by distension of the rectum by feces. This is sensed by the mechanoreceptors which activate the myenteric nerves, and impulses are transduced to the spinal cord (and back) to relax the internal anal sphincter (IAS). The spinal cord conveys signals to the brain to stimulate the urge to defecate. These reflex actions cause the voluntary contraction of the external anal sphincter (EAS) until defecation occurs. During defecation, the EAS relaxes, the person increases intra-abdominal pressure, and feces are eliminated from the rectum.
The cerebral cortex controls the act of defecation through connections in the spinal cord.
Ordinarily, defecation is initiated by defecation reflexes. One of these is an intrinsic reflex mediated by the local ENS in the rectal wall (a myenteric reflex). This can be described as follows: When feces enter the rectum, distention of the rectal wall initiates afferent signals that spread through the myenteric plexus to initiate peristaltic waves in the descending colon, sigmoid, and rectum, forcing feces toward the anus. As the peristaltic wave approaches the anus, the internal anal sphincter is relaxed by inhibitory signals from the myenteric plexus; if the external anal sphincter is also consciously, voluntarily relaxed at the same time, defecation occurs.
The intrinsic myenteric defecation reflex functioning by itself normally is relatively weak. To be effective in causing defecation, it is fortified by another type of defecation reflex, a parasympathetic defecation reflex that involves the sacral segments of the spinal cord. When the nerve endings in the rectum are stimulated, signals are transmitted first into the spinal cord and then reflexly back to the descending colon, sigmoid, rectum, and anus via PNS fibers in the pelvic nerves. These signals greatly intensify the peristaltic waves and relax the internal anal sphincter, thus converting the intrinsic myenteric defecation reflex from a weak effort into a powerful process of defecation that is sometimes effective in emptying the large bowel all the way from the splenic flexure of the colon to the anus!
Defecation signals entering the spinal cord initiate other effects, such as taking a deep breath, closure of the glottis, and contraction of the abdominal wall muscles to force the fecal contents of the colon downward and at the same time cause the pelvic floor to relax downward and pull outward on the anal ring to evaginate the feces.
Destruction of the pathways in the spinal cord and cerebral cortex results in loss of voluntary control of defection.
Destruction of the nerves leading to the anorectal region can cause fecal retention.
- Describe the transport processes mediating recovery of water and electrolytes in the colon.
The major exchanges occurring the ascending and transverse colon: the colon absorbs sodium, chloride, & water & secretes K+ & HCO3-.
Mode of active Na+ absorption by the large intestine: Na+-H+ and Cl–HCO3 -exchange is coupled by a change in intracellular pH that results in “electroneutral NaCl absorption,” which is the primary mechanism for interdigestive Na+ absorption.
Absorption of Na+ and Cl- creates an osmotic gradient across the intestinal mucosa, promoting absorption of water
The colon is a net secretor of K+. There is passive K+ secretion through tight junctions, which occurs throughout the colon. The driving force is a lumen-negative transepithelial voltage. There is also active K+ secretion throughout in the colon (stimulated by aldosterone and cAMP). Stimulation of K+ secretion by cholera toxin (which increases cAMP) accounts for significant fecal K+ loss in diarrhea.
The tight junctions in the colon offer greater resistance to fluid flow (they are “tighter”) through the paracellular pathway than the small intestine. This prevents back-diffusion of ions and allows more complete absorption of Na+ ions, compared to the small intestine. This is enhanced when aldosterone is present.
2A. Describe the function of colonic motility, in mediating formation of haustra and hasutral shuttling, mass movements through the transverse and distal colon, and defecation.
Motility in the colon = segment mixing, propulsion, and mass movements.
Similar to the small intestine, the colon contains ICCs (interstitial cells of cajal) that provide spontaneous electrical activity, and other factors (PNS, SNS, chemical, stretch) influence the triggering of spikes/action potentials at the peaks of these slow waves. Similar to the small intestines, slow waves are not observed in the absence of ICCs.
Motility in the large intestine is characterized by slow segmental propulsion, segmental mixing, and mass movements (motility is sluggish compared to small intestine).
Haustrations (bulges) are specialized for slow segmental propulsion and mixing, allowing time for electrolyte and fluid absorption, thus solidifying the chyme. They are formed by large circular muscle constrictions and also by constriction of 3 flat bands of longitudinal muscle called taenia coli.
Each haustration reaches peak intensity in ~30 sec and disappears during the next min. The term haustration derives from the outward bulging of the baglike sacs in the unstimulated portion of the colon.
About 1-3 times a day (often following breakfast) mass movements create peristaltic movements that force the chyme/feces toward the rectum. Haustrations disappear during mass movements which persist for ~10-30 min. Mass movements typically signal the urge to defecate.
Following a meal, an increased incidence of mass movements occurs via the gastrocolic reflex.
Factors that increase motility of the colon can cause diarrhea, by limiting haustrae formation and increasing mass movements.
Autonomic Innervation of the Colon. The small intestines and colon are innervated by both sympathetic and parasympathetic nerves. Sympathetic fibers from the spinal cord lead to the celiac, superior mesenteric ganglia, and inferior mesenteric ganglia. Parasympathetic fibers arise from the vagus (innervate through transverse colon) and pelvic (innervate descending colon, sigmoid, and rectum) nerves. Sympathetic stimulation reduces motility and secretions, whereas parasympathetic stimulation increases motility, secretions, and relaxation of the internal anal sphincter.
When extrinsic autonomic nerves to the colon are removed, the gastrocolic and duodenocolic reflexes(which facilitate appearance of mass movements after a meal in response to distension of the stomach and duodenum) are weak or absent.
The gastrocolic reflex occurs when distension of the stomach (gastro) stimulates mass movements in the colon (colic). All of the gut reflexes are named with the anatomical origin of the reflex as the prefix followed by the name of the gut segment in which the outcome of the reflex is observed, that is, the gastrocolic reflex begins in the stomach and ends in the colon. The duodenocolic reflex has a similar function to the gastrocolic reflex. When the duodenum is distended, nervous signals are transmitted to the colon, which stimulates mass movements. The enterogastric reflex occurs when signals originating in the intestines inhibit gastric motility and gastric secretion. The intestino-intestinal reflex occurs when overdistension or injury to a bowel segment signals the bowel to relax.The rectosphincteric reflex, also called the defecation reflex, is initiated when feces enters the rectum and stimulates the urge to defecate.
Individuals suffering from ulcerative colitis have persistent mass movements due to irritation in the colon.
