16.3 Large Intestine, Rectum & Defecation

16.3 Large Intestine, Rectum & Defecation

The large intestine represents the terminal organizing framework of the human alimentary canal. Framing the convoluted loops of the small intestine on the superior, lateral, and inferior margins, the large intestine extends from the ileocecal valve in the right lower quadrant to the external anal orifice. Measuring approximately 1.5 meters (5 feet) in length and roughly 6.5 cm (2.5 inches) in diameter—considerably shorter but significantly broader in caliber than the small intestine—the large intestine executes vital final homeostatic functions essential for water-electrolyte balance and waste elimination.

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Primary Functions of the Large Intestine

Unlike the stomach and small intestine, the large intestine does NOT participate in significant chemical digestion of food macromolecules and secretes no digestive enzymes of its own. By the time chyme passes through the ileocecal valve, virtually all digestible carbohydrates, lipids, and proteins have already been catabolized and absorbed. Instead, the large intestine executes five major physiological activities:

1. Water Absorption: Approximately 1.5 to 2.0 liters of fluid chyme enter the cecum daily from the small intestine. The large intestine reabsorbs approximately 90% of this remaining water (roughly 1.3 to 1.8 liters per day), concentrating the liquid residue into solid or semi-solid feces. Only about 100 to 200 mL of water is excreted daily in normal stool.
2. Electrolyte Reabsorption: Actively absorbs sodium ($Na^+$) and chloride ($Cl^-$) ions across its mucosal epithelium via active transport pumps, with water following osmotically, maintaining systemic hydration and electrolyte homeostasis.
3. Bacterial Vitamin Synthesis and Absorption: Houses an expansive symbiotic bacterial flora that metabolizes residual nutrients, synthesizing Vitamin K (essential for hepatic blood clotting factor production) and several B-complex vitamins (biotin and Vitamin $B_5$ / pantothenic acid), which are absorbed across the colonic mucosa.
4. Mucus Secretion and Fecal Lubrication: Abundant goblet cells continuously secrete a thick, alkaline, mucin-dense fluid that lubricates the passage of drying, abrasive fecal matter and shields the mucosa from bacterial metabolic acids.
5. Fecal Compaction, Storage, and Defecation: Compacts indigestible plant fiber, sloughed epithelial cells, billions of dead and living bacteria, and bile pigments (stercobilin, which imparts the characteristic brown color of stool) into cohesive feces, temporarily storing them in the sigmoid colon and rectum prior to controlled elimination via defecation.

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Three Unique Gross Anatomical Features of the Large Intestine

The external surface of the large intestine displays three distinctive macroscopic anatomical specializations that immediately distinguish it from the small intestine:

Unique Gross Anatomical Features of the Large Intestine

1. TENIAE COLI
   └── Three ribbon-like longitudinal bands of smooth muscle
       representing a modified, concentrated outer longitudinal muscularis layer.

2. HAUSTRA
   └── Series of pocket-like pouches / sacculations puckered along the colon wall
       by the sustained tonic contraction of the teniae coli.

3. EPIPLOIC (OMENTAL) APPENDAGES
   └── Small, fat-filled peritoneal teardrop pouches that dangle
       from the visceral serosal surface of the colon.

1. Teniae Coli: In the small intestine, the outer longitudinal smooth muscle layer of the muscularis externa forms a uniform cylinder encircling the entire tube. In the large intestine (from the cecum through the sigmoid colon), this outer longitudinal layer is concentrated into three discrete, narrow, ribbon-like longitudinal bands measuring about 1 cm in width, designated the teniae coli ("colonic ribbons").
2. Haustra: Because the teniae coli are shorter than the underlying mucosal, submucosal, and circular muscular layers, their sustained resting muscle tone puckers and gathers the colon wall into a sequential series of distinct, pocket-like sacculations or pouches called haustra (singular: haustrum). These pouches expand as they fill with fecal residue, facilitating localized mixing and water extraction.
3. Epiploic (Omental) Appendages: Small, teardrop-shaped, fat-filled pouches of visceral peritoneum that dangle externally from the serosal surface along the length of the colon. Although their exact physiological role remains under investigation, they serve as localized fat storage depots and may provide protective cushioning during peristaltic contractions.

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Major Anatomical Subdivisions of the Large Intestine

The large intestine is partitioned into four major anatomical subdivisions: the cecum (with its attached vermiform appendix), the colon, the rectum, and the anal canal.

Subdivisions and Flexures of the Large Intestine

Small Intestine (Terminal Ileum)
  │
[Ileocecal Valve]
  │
  ├── 1. CECUM (Blind pouch in RLQ) ── [ Vermiform Appendix ] (MALT lymphoid organ)
  │
  ├── 2. COLON
  │     ├── Ascending Colon (Retroperitoneal along right flank)
  │     ├── Right Colic (Hepatic) Flexure (90° bend under liver)
  │     ├── Transverse Colon (Intraperitoneal across abdomen; Transverse Mesocolon)
  │     ├── Left Colic (Splenic) Flexure (Acute sharp bend near spleen)
  │     ├── Descending Colon (Retroperitoneal along left flank)
  │     └── Sigmoid Colon (S-shaped loop in pelvis; Intraperitoneal)
  │
  ├── 3. RECTUM (~15 cm; Anterior to sacrum; Transverse Rectal Folds / Valves)
  │
  └── 4. ANAL CANAL (~3 cm; Stratified squamous epithelium)
        ├── Internal Anal Sphincter (Involuntary smooth muscle; Autonomic control)
        └── External Anal Sphincter (Voluntary skeletal muscle; Somatic pudendal control)
              │
            [ Anus ] (External orifice)

1. Cecum and Vermiform Appendix

• Cecum: The initial, dilated blind-ended pouch of the large intestine, measuring about 6 cm in length, situated in the right lower quadrant (iliac fossa) inferior to the level of the ileocecal junction. The terminal ileum projects into the medial wall of the cecum through the ileocecal valve (sphincter). Tonic contraction of this muscular valve prevents the retrograde reflux of bacteria-laden colonic contents back into the sterile small intestine. Following meals, gastrin release and the gastroileal reflex relax the valve, allowing chyme to empty into the cecum.
• Vermiform Appendix: A slender, worm-like, blind-ended tubular pouch measuring 2 to 20 cm (average ~8 cm) attached to the posteromedial surface of the cecum. The appendix possesses a narrow lumen and a thick wall densely packed with lymphoid follicles (MALT). It functions as an important immune organ, sampling enteric pathogens and housing a protected bacterial reservoir that repopulates the normal gut flora following severe diarrheal illness.
• Clinical Pathology: Acute Appendicitis: If the narrow lumen of the appendix becomes obstructed (most commonly by a hardened fecal mass termed a fecalith, lymphoid hyperplasia, or a foreign body), trapped bacteria proliferate rapidly. Mucus accumulation elevates intraluminal pressure, compressing venous drainage and causing ischemic necrosis, inflammation, and potential perforation into the peritoneal cavity (causing life-threatening peritonitis). Clinically, appendicitis manifests initially as dull periumbilical pain that subsequently shifts and localizes as sharp somatic pain at McBurney's point (situated one-third of the distance along a line drawn from the right anterior superior iliac spine to the umbilicus), accompanied by rebound tenderness and fever.

2. The Colon: Four Segments and Two Flexures

The colon is the expansive midsection of the large intestine, partitioned into four sequential segments and two sharp flexures:

1. Ascending Colon: Travels superiorly along the right posterior abdominal wall from the cecum to the inferior surface of the liver. It is retroperitoneal (covered by visceral peritoneum only on its anterior and lateral surfaces).
2. Right Colic (Hepatic) Flexure: At the inferior margin of the right lobe of the liver, the ascending colon bends sharply at a 90-degree angle to the left, transitioning into the transverse colon.
3. Transverse Colon: Crosses the abdominal cavity horizontally from right to left, immediately inferior to the stomach. It is intraperitoneal and highly mobile, suspended from the posterior abdominal wall by a broad peritoneal mesentery designated the transverse mesocolon.
4. Left Colic (Splenic) Flexure: Beneath the inferior border of the spleen, the transverse colon curves sharply downward. This flexure is situated significantly higher, deeper, and more posterior within the abdomen than the hepatic flexure.
5. Descending Colon: Descends inferiorly along the left posterior abdominal wall into the pelvic brim. Like the ascending colon, the descending colon is retroperitoneal.
6. Sigmoid Colon: An S-shaped intraperitoneal loop measuring about 40 cm in length that traverses the pelvic brim. Suspended by the sigmoid mesocolon, it curves medially along the pelvic floor to join the rectum at the level of the third sacral vertebra (S3). Its mobility facilitates fecal storage before defecation.

3. Rectum

The rectum (from Latin rectus, meaning "straight") is a muscular tube approximately 15 cm (6 inches) in length situated anterior to the sacrum and coccyx in the pelvic cavity. Despite its name, the human rectum follows the anterior-posterior curve of the sacrum (the sacral flexure).

Internally, the rectal wall features three prominent, permanent, crescentic horizontal mucosal folds termed transverse rectal folds (rectal valves of Houston). These valves project into the lumen (two on the left, one on the right) and serve an essential mechanical purpose: they physically support the weight of the accumulated fecal column while allowing flatus (gas) to pass freely without the simultaneous involuntary discharge of solid feces.

4. Anal Canal & the Dual Sphincter Mechanism

The anal canal is the terminal 3 cm of the alimentary tract, completely external to the abdominopelvic cavity in the perineum. It descends posteroinferiorly, terminating at the anus. Its mucosa features longitudinal mucosal ridges called anal columns (columns of Morgagni), between which lie mucus-secreting anal sinuses that lubricate the anal canal during defecation.

The anal canal is encircled by two powerful muscular sphincters that maintain continence through continuous tonic contraction:

• Internal Anal Sphincter: The deeper, superior sphincter consisting of a thick ring of involuntary smooth muscle (a direct continuation and thickening of the circular smooth muscle layer of the muscularis externa). It is governed entirely by the autonomic nervous system: sympathetic fibers from the hypogastric plexus maintain tonic resting closure, while parasympathetic fibers from the pelvic splanchnic nerves (S2-S4) trigger reflexive relaxation during defecation.
• External Anal Sphincter: The superficial, inferior sphincter consisting of a broad ring of voluntary skeletal muscle that merges with the levator ani and pelvic floor musculature. It is governed entirely by the somatic motor nervous system via somatic motor neurons traveling through the pudendal nerve (S2-S4). This voluntary sphincter allows an individual to consciously clamp the anal canal shut and postpone defecation even when the involuntary internal sphincter has reflexively relaxed.

Comparative Profile of Internal vs. External Anal Sphincters

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Microscopic Histology: Crypts and Mucus Architecture

The microscopic architecture of the large intestine reflects its dual specialization for water absorption and frictionless transit of compacted waste:

• Epithelial Transition: The mucosa of the cecum, colon, and rectum consists of a uniform simple columnar epithelium dedicated to absorption. However, at the pectinate (dentate) line of the anal canal, this delicate simple columnar lining abruptly transitions into non-keratinized stratified squamous epithelium, which resists the heavy mechanical shearing forces of solid stool. At the external anal margin, it transitions into keratinized stratified squamous epithelium (skin) containing hair follicles and sebaceous glands.
• Absence of Plicae and Villi: In stark contrast to the small intestine, the mucosal wall of the large intestine possesses NO circular folds (plicae circulares) and NO villi. Because organic macronutrient absorption is already finished, extensive surface area amplification is biologically unnecessary.
• Deep Intestinal Crypts Packed with Goblet Cells: The mucosal surface of the colon is completely flat, indented by millions of deep, straight, tubular intestinal crypts (Crypts of Lieberkühn) that extend all the way down to the muscularis mucosae. These crypts are exceptionally rich in goblet cells, which outnumber absorptive enterocytes (colonocytes). The goblet cells continuously secrete an abundance of thick, viscous, alkaline mucus. This mucus fulfills two indispensable roles: it binds and lubricates dehydrated fecal particles to prevent mucosal abrasion, and its bicarbonate content shields the epithelial cells from irritating organic acids produced by resident bacterial fermentation.

Comparative Overview of Large Intestine Subdivisions

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The Human Gut Microbiome (Colonic Bacterial Flora)

The human large intestine is home to a vast, complex, metabolically active ecosystem designated the gut microbiome (colonic bacterial flora). Containing over 1,000 distinct bacterial species and roughly 40 trillion bacterial cells—about as many as the body's own cells (older textbooks claimed a 10-to-1 excess)—this symbiotic biomass accounts for roughly 30% to 50% of the dry weight of human feces. Dominant bacterial phyla include Bacteroidetes, Firmicutes (such as Lactobacillus and Clostridium), and Proteobacteria (such as Escherichia coli).

Metabolic and Physiological Roles of the Colonic Bacterial Flora

1. FERMENTATION OF INDIGESTIBLE CARBOHYDRATES
   ├── Ferments cellulose, pectin, and resistant starches that human enzymes cannot cleave.
   ├── Produces Short-Chain Fatty Acids (SCFAs: Butyrate, Acetate, Propionate).
   │     └── Butyrate serves as primary cellular fuel for colonocytes; promotes mucosal health.
   └── Generates Flatus (~500 mL/day: CO2, H2, CH4, and pungent Hydrogen Sulfide [H2S]).

2. VITAMIN SYNTHESIS
   ├── Synthesizes Vitamin K (Obligate cofactor for hepatic clotting factors II, VII, IX, and X).
   └── Synthesizes B-Complex Vitamins (Biotin and Vitamin B5 / Pantothenic acid).

3. COMPETITIVE COLONIZATION RESISTANCE
   └── Occupies ecological niches and secretes bacteriocins to block pathogen proliferation.
       Disruption by broad-spectrum antibiotics enables Clostridioides difficile colitis.

1. Fermentation of Indigestible Carbohydrates

Human digestive enzymes cannot hydrolyze structural plant polysaccharides, such as cellulose, hemicellulose, and pectin. When these complex dietary fibers reach the colon, anaerobic bacterial enzymes ferment them into absorbable Short-Chain Fatty Acids (SCFAs)—principally acetate, propionate, and butyrate:

• Butyrate is particularly vital: it is absorbed by colonocytes and serves as their primary metabolic energy source, providing roughly 60% to 70% of the daily ATP required by the colonic epithelium while promoting epithelial integrity and suppressing inflammation.
• Flatus Production: Microbial fermentation releases gaseous metabolic byproducts, producing approximately 500 mL of flatus (gas) daily. This gas consists primarily of odorless nitrogen ($N_2$), carbon dioxide ($CO_2$), hydrogen ($H_2$), and methane ($CH_4$). The characteristic pungent odor of flatulence is caused by minute concentrations of sulfur-containing gases, principally hydrogen sulfide ($H_2S$) and mercaptans produced during the breakdown of sulfur-rich amino acids.

2. Vitamin Synthesis & the Clinical Milestone of Neonatal Vitamin K

The colonic flora synthesizes vital micronutrients that are absorbed across the colonic wall into the bloodstream:

• Vitamin K: A fat-soluble vitamin synthesized in significant quantities by colonic bacteria (principally Escherichia coli and Bacteroides fragilis). Vitamin K serves as an obligate biological cofactor for hepatic gamma-glutamyl carboxylase, the enzyme responsible for activating blood clotting factors II (prothrombin), VII, IX, and X, as well as regulatory anticoagulant proteins C and S.
• Clinical Milestone: Neonatal Vitamin K Prophylaxis: At birth, a newborn infant's gastrointestinal tract is essentially sterile. Microbial colonization occurs gradually over the first days and weeks of life through breast milk, formula feeding, and environmental exposure. Furthermore, Vitamin K does not cross the human placenta efficiently, and human breast milk contains low concentrations of the vitamin. Consequently, newborn infants experience a physiological deficiency of Vitamin K during their first week of life. Without adequate Vitamin K, the liver cannot synthesize functional clotting factors II, VII, IX, and X, leaving the neonate vulnerable to spontaneous, life-threatening internal bleeding—a condition termed Vitamin K Deficiency Bleeding (VKDB), historically designated hemorrhagic disease of the newborn. To prevent fatal intracranial hemorrhage, pediatric standards mandate that all newborn infants receive a single prophylactic intramuscular injection of Vitamin K shortly after birth.
• B-Complex Vitamins: Colonic flora also synthesize measurable quantities of water-soluble biotin (Vitamin $B_7$) and pantothenic acid (Vitamin $B_5$), supplementing dietary intake.

3. Colonization Resistance and Immune Education

A healthy, dense microbial flora protects the host via colonization resistance: symbiotic bacteria consume accessible nutrients, occupy mucosal attachment sites, and secrete antimicrobial compounds (bacteriocins) that competitively prevent pathogenic organisms (such as Salmonella, Shigella, and Clostridioides difficile) from establishing infection.

• Clinical Milestone: Clostridioides difficile Colitis: When a patient receives broad-spectrum antibiotic therapy (such as clindamycin or fluoroquinolones), substantial populations of the normal commensal gut flora are eradicated. Stripped of competitive inhibition, opportunistic spore-forming bacteria such as Clostridioides difficile proliferate unchecked, releasing enterotoxin A and cytotoxin B. These toxins cause severe mucosal inflammation, epithelial sloughing, and the formation of characteristic fibrinous pseudomembranes (pseudomembranous colitis), manifested clinically as severe, foul-smelling watery diarrhea, fever, and leukocytosis.

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Colonic Motility: Haustral Churning vs. Mass Movements

Motility within the large intestine is sluggish compared to the vigorous peristalsis of the small intestine, allowing ample time for water extraction. Colonic motility involves two primary motor patterns:

1. Haustral Contractions (Haustral Churning)

Haustral contractions are slow, localized, uncoordinated segmenting movements that occur approximately every 30 minutes.

• As an individual haustrum gradually fills with fecal residue, the physical distension of the wall stretches local mechanoreceptors.
• This stretch stimulates intrinsic myenteric neurons, triggering a localized contraction of the circular smooth muscle.
• The contracting haustrum compresses and rolls the fecal contents into the adjacent haustrum. This slow churning movement does not produce rapid forward propulsion; rather, it continuously turns over the fecal mass, exposing fresh surfaces to the mucosal epithelium to maximize water and electrolyte absorption.

2. Mass Movements (Mass Peristalsis)

Mass movements are powerful, high-amplitude, sweeping waves of peristaltic contraction that travel over expansive segments of the transverse, descending, and sigmoid colon.

• Unlike localized haustral churning, mass movements force large columns of compacted fecal matter rapidly toward the rectum.
• Mass movements occur only 3 to 4 times per day, typically during or immediately following a meal.
• Gastrocolic and Gastroileal Reflexes: The primary trigger for mass movements is the entry of food into the stomach. Gastric distension and partially digested proteins activate long autonomically mediated neural pathways (the gastrocolic reflex) and stimulate the release of gastrin, which accelerates colonic motility. This physiological wiring explains why individuals frequently experience the urge to defecate shortly after breakfast or heavy meals.

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The Defecation Reflex: Autonomic Mechanics and Somatic Control

Defecation is the coordinated neuromuscular reflex by which feces are evacuated from the rectum and anal canal. Under resting conditions, the rectum remains largely empty because the transverse rectal folds and the tonic contraction of the sigmoid colon hold feces back. Defecation is initiated when a powerful mass movement forces a mass of feces from the sigmoid colon down into the rectal ampulla.

Step-by-Step Sequence of the Defecation Reflex Pathway

1. FECAL ENTRY & RECTAL DISTENSION
   └── Mass movement drives feces into rectal ampulla -> Stretches rectal wall.

2. AFFERENT SENSORY SIGNALING
   └── Mechanoreceptors fire action potentials along afferent fibers to Sacral Spinal Cord (S2-S4).

3. PARASYMPATHETIC EFFERENT DISCHARGE
   └── Efferent signals descend via Pelvic Splanchnic Nerves back to colon, rectum & anus.

4. INVOLUNTARY EFFECTOR ACTIONS
   ├── Rectal smooth muscle contracts vigorously -> Increases intraluminal pressure.
   ├── Sigmoid colon contracts -> Drives additional feces downward.
   └── Internal Anal Sphincter relaxes (Involuntary smooth muscle opens).

5. CORTICAL CONSCIOUS PERCEPTION
   └── Feces enter sensitive anal canal -> Signals cerebral cortex -> Conscious urge to defecate.

6. DUAL MOTOR PATHWAY DECISION:
   ├── CONVENIENT (Defecation Allowed):
   │     ├── Somatic motor impulses via Pudendal Nerve are voluntarily INHIBITED.
   │     ├── External Anal Sphincter relaxes (Voluntary skeletal muscle opens).
   │     └── Valsalva Maneuver engaged -> Feces evacuated externally.
   └── INCONVENIENT (Defecation Postponed):
         ├── Somatic motor impulses via Pudendal Nerve STIMULATE External Sphincter contraction.
         ├── Rectal wall undergoes receptive relaxation -> Wall stretch decreases.
         └── Defecation urge subsides until the next mass movement.

Step-by-Step Neurological and Muscular Sequence

1. Rectal Wall Distension: The arrival of feces distends the highly compliant rectal wall, stimulating stretch mechanoreceptors embedded within the muscularis.
2. Spinal Afferent Signaling: Stimulated stretch receptors fire sensory action potentials that ascend along somatic and visceral sensory neurons to the sacral segments of the spinal cord (S2, S3, and S4).
3. Parasympathetic Efferent Activation: Within the sacral spinal cord, sensory afferents synapse with preganglionic parasympathetic neurons. Parasympathetic efferent motor signals travel through the pelvic splanchnic nerves to the myenteric plexus of the descending colon, sigmoid colon, rectum, and anus.
4. Involuntary Effector Actions: The parasympathetic burst produces two simultaneous motor responses:
   • Rectal Contraction: Stimulates vigorous, coordinated contraction of the rectal and sigmoid smooth muscle walls, driving feces toward the anal orifice and elevating intraluminal rectal pressure.
   • Internal Sphincter Relaxation: Causes reflexive relaxation of the involuntary smooth muscle internal anal sphincter.
5. Conscious Perception: As the internal anal sphincter relaxes, feces slide into the proximal anal canal. Highly sensitive somatic sensory nerve endings in the anal mucosa sample the contents (discriminating between gas, liquid, and solid stool) and transmit signals to the cerebral cortex, producing the conscious urge to defecate.
6. Voluntary Decision and Evacuation vs. Postponement:
   • If Defecation is Convenient: The cerebral cortex consciously inhibits somatic motor neurons traveling through the pudendal nerve. This allows the external anal sphincter (voluntary skeletal muscle) and the puborectalis muscle to relax. The anorectal angle straightens, aligning the rectum with the anal canal. Evacuation is assisted by the Valsalva maneuver—a voluntary forced exhalation against a closed glottis paired with contraction of the abdominal wall muscles (rectus abdominis, obliques, and transversus abdominis) and diaphragm. This elevates intra-abdominal pressure, compressing the rectal walls and expelling the fecal mass through the anus.
   • If Defecation is Inconvenient: The cerebral cortex consciously commands somatic motor neurons in the pudendal nerve to maintain vigorous contraction of the voluntary external anal sphincter. The external sphincter clamps the anal canal shut, overcoming the pressure from above. Within several minutes, the rectal smooth muscle undergoes receptive relaxation (stress-relaxation phenomenon), adapting to the distension. The stretch receptors adapt, rectal wall pressure drops, and the conscious urge to defecate dissipates. The fecal mass remains stored in the rectum until the next mass movement initiates another defecation reflex (often hours later).

Clinical Correlates: Constipation vs. Diarrhea

• Constipation: Occurs when fecal residue moves through the colon too slowly. Because the colon absorbs water continuously, extended transit time allows excessive water reabsorption, rendering the stool hard, dry, compacted, and painful to pass. Common etiologies include low dietary fiber intake, inadequate fluid intake, lack of physical exercise, emotional stress, and chronic voluntary suppression of the defecation reflex (which dulls rectal mechanoreceptor sensitivity over time).
• Diarrhea: Characterized by frequent, loose, watery fecal discharges. Occurs when intestinal motility is accelerated, rushing chyme through the large intestine so rapidly that the colonic mucosa does not have sufficient time to absorb remaining water. Alternatively, osmotic agents (e.g., lactose in lactase deficiency) or bacterial enterotoxins (e.g., Vibrio cholerae stimulating mucosal cAMP) cause massive secretion of water and electrolytes into the lumen. Prolonged, severe diarrhea can rapidly produce severe systemic dehydration, hypokalemia, and metabolic acidosis (owing to profound fecal loss of bicarbonate ions).

Step-by-Step Defecation Reflex Neural Pathway and Effector Actions