Physiology of the Gallbladder
The gallbladder is a small storage organ located inferior and posterior to the liver. May 27, at 8: People who lack intrinsic factor, cannot absorb vitamin B and suffer from pernicious anemia. It is relatively long and has a constant diameter. Both liver damage and pancreatitis are potentially life-threatening conditions.
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The larger end of the gallbladder extends inferiorly and to the right while the tapered end points superiorly and medially. The tapered end of the gallbladder narrows into a small bile duct known as the cystic duct. The cystic duct connects to the common hepatic duct that carries bile from the liver. These ducts merge to form the common bile duct that extends to the wall of the duodenum.
The mucosa, which forms the innermost layer of the gallbladder, lines the gallbladder with simple columnar epithelial tissue. The columnar epithelial tissue contains microvilli on its surface, increasing the surface area and allowing the lining to absorb water and concentrate the dilute bile. Beneath the columnar tissue is a thin lamina propria layer made of connective tissue and capillaries that support and anchor the epithelial layer.
Deep to the lamina propria is the muscularis layer that contains smooth muscle tissue. Contraction of the muscularis pushes bile out of the gallbladder and into the cystic duct. Surrounding the muscularis is a thin layer of fibrous connective tissue that helps to reinforce and strengthen the wall of the gallbladder. Finally, the serosa forms the outermost layer of the gallbladder. The serosa is an epithelial layer that forms part of the peritoneum, or lining of the abdominal cavity.
The serosa gives the gallbladder a smooth, slick surface to prevent friction between moving organs. The gallbladder acts as a storage vessel for bile produced by the liver. Bile is produced by hepatocytes cells in the liver and passes through the bile ducts to the cystic duct.
From the cystic duct, bile is pushed into the gallbladder by peristalsis muscle contractions that occur in orderly waves. Bile is then slowly concentrated by absorption of water through the walls of the gallbladder. The gallbladder stores this concentrated bile until it is needed to digest the next meal. Foods rich in proteins or fats are more difficult for the body to digest when compared to carbohydrate-rich foods see Macronutrients.
The walls of the duodenum contain sensory receptors that monitor the chemical makeup of chyme partially digested food that passes through the pyloric sphincter into the duodenum. When these cells detect proteins or fats, they respond by producing the hormone cholecystokinin CCK. A rational therapeutic plan can then be formulated.
The primary functions of the GI tract include prehension of feed and water; mastication, ensalivation, and swallowing of feed; digestion of feed and absorption of nutrients; maintenance of fluid and electrolyte balance; and evacuation of waste products. There are four primary functions—digestion, absorption, motility, and evacuation—and, correspondingly, four primary modes of dysfunction.
Normal GI tract motility involves peristalsis, muscle activity that moves ingesta from the esophagus to the rectum; segmentation movements, which churn and mix the ingesta; and segmental resistance and sphincter tone, which retard aboral progression of gut contents. In ruminants, these movements are of major importance in normal forestomach function. Abnormal motor function usually manifests as decreased motility.
Segmental resistance is usually reduced, and transit rate increases. Motility depends on stimulation via the sympathetic and parasympathetic nervous systems and thus on the activity of the central and peripheral parts of these systems and on the GI musculature and its intrinsic nerve plexuses. Debility, accompanied by weakness of the musculature, acute peritonitis, and hypokalemia, produces atony of the gut wall paralytic ileus. The intestines distend with fluid and gas, and fecal output is reduced.
In addition, chronic stasis of the small intestine may predispose to abnormal proliferation of microflora. Such bacterial overgrowth may cause malabsorption by injuring mucosal cells, by competing for nutrients, and by deconjugating bile salts and hydroxylating fatty acids.
Vomiting see Vomiting is a neural reflex act that results in ejection of food and fluid from the stomach through the oral cavity. It is always associated with antecedent events such as premonition, nausea, salivation, or shivering and is accompanied by repeated contractions of the abdominal muscles.
Regurgitation is characterized by passive, retrograde reflux of previously swallowed material from the esophagus, stomach, or rumen. In diseases of the esophagus, swallowed material may not reach the stomach. One of the major consequences of subnormal motility is distention with fluid and gas. Much of the accumulated fluid is saliva and gastric and intestinal juices secreted during normal digestion. Distention causes pain and reflex spasm of adjoining gut segments.
It also stimulates further secretion of fluid into the lumen of the gut, which exacerbates the condition. When the distention exceeds a critical point, the ability of the musculature of the wall to respond diminishes, the initial pain disappears, and paralytic ileus develops in which all GI muscle tone is lost. Dehydration, acid-base and electrolyte imbalance, and circulatory failure are major consequences of GI distention. Accumulation of gut fluids stimulates additional secretion of fluids and electrolytes in the anterior segments of the intestine, which can worsen the abnormalities and lead to shock.
Abdominal pain associated with GI disease usually is caused by stretching of the intestinal wall. Contraction of the gut causes pain by direct and reflex distention of neighboring segments. Spasm, an exaggerated segmenting contraction of one section of intestine, results in distention of the immediately anterior segment when a peristaltic wave arrives.
Other factors that may cause abdominal pain include edema and failure of local blood supply, eg, in local embolism or twisting of the mesentery.
Specific diseases cause diarrhea by varied and characteristic mechanisms, the recognition of which is useful in understanding, diagnosing, and managing GI diseases.
The major mechanisms of diarrhea are increased permeability, hypersecretion, and osmosis. Disorders of motility are often secondary. In healthy animals, water and electrolytes continuously transfer across the intestinal mucosa. Secretions from blood to gut and absorptions from gut to blood occur simultaneously. In clinically healthy animals, absorption exceeds secretion, ie, there is net absorption.
If the amount exuded exceeds the absorptive capacity of the intestines, diarrhea results. The size of the material that leaks through the mucosa varies, depending on the magnitude of the increase in pore size. Large increases in pore size permit exudation of plasma protein, resulting in protein-losing enteropathies eg, lymphangiectasia in dogs, paratuberculosis in cattle, nematode infections.
Greater increases in pore size result in the loss of RBCs, producing hemorrhagic diarrhea eg, hemorrhagic gastroenteritis, parvovirus infection, severe hookworm infection. Hypersecretion is a net intestinal loss of fluid and electrolytes that is independent of changes in permeability, absorptive capacity, or exogenously generated osmotic gradients. Enterotoxic colibacillosis is an example of diarrheal disease due to intestinal hypersecretion; enterotoxigenic Escherichia coli produce enterotoxin that stimulates the crypt epithelium to secrete fluid beyond the absorptive capacity of the intestines.
The villi, along with their digestive and absorptive capabilities, remain intact. The fluid secreted is isotonic, alkaline, and free of exudates. The intact villi are beneficial because a fluid administered PO that contains glucose, amino acids, and sodium is absorbed, even with hypersecretion.
Osmotic diarrhea is seen when inadequate absorption results in a collection of solutes in the gut lumen, which cause water to be retained by their osmotic activity. It develops in any condition that results in nutrient malabsorption or maldigestion or when an animal ingests a large amount of osmotically active substances that are not absorbed, eg, an overeating puppy.
Malabsorption see Malassimilation Syndromes in Large Animals and see Diseases of the Stomach and Intestines in Small Animals is failure of digestion and absorption due to some defect in the villous digestive and absorptive cells, which are mature cells that cover the villi. Several epitheliotropic viruses directly infect and destroy the villous absorptive epithelial cells or their precursors, eg, coronavirus, transmissible gastroenteritis virus of piglets, and rotavirus of calves.
Feline panleukopenia virus and canine parvovirus destroy the crypt epithelium, which results in failure of renewal of villous absorptive cells and collapse of the villi; regeneration is a longer process after parvoviral infection than after viral infections of villous tip epithelium eg, coronavirus, rotavirus. Intestinal malabsorption also may be caused by any defect that impairs absorptive capacity, such as diffuse inflammatory disorders eg, lymphocytic-plasmacytic enteritis, eosinophilic enteritis or neoplasia eg, lymphosarcoma.
Other examples of malabsorption include defects of pancreatic secretion that result in maldigestion. Rarely, because of failure to digest lactose which, in large amounts, has a hyperosmotic effect , neonatal farm animals or pups may have diarrhea while they are being fed milk.