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In most instances, lubricants or fecal-softening agents given through a nasogastric tube soften the impacted ingesta, allowing it to be passed. This form of therapy can be aided by the simultaneous administration of IV fluids. Keeping the horse muzzled is advised to prevent further impaction of feed material while the obstruction is softening. Mineral oil is the most commonly used medication in the treatment of a large-colon impaction. It coats the inside of the intestine and aids the normal movement of ingesta along the GI tract.

It is administered through a nasogastric tube, as much as 4 L, once or twice daily, until the impaction is resolved. Although mineral oil is safe, it is not highly effective in treating severe impactions or sand impactions, because it may simply pass by the obstruction without softening it.

Dioctyl sodium sulfosuccinate DSS is a soap-like compound that acts by drawing water into the dry ingesta. It is more effective than mineral oil in softening impactions; however, it may interfere with the normal fluid absorptive functions of the colon and can be toxic.

Thus, DSS can be given safely only in small quantities two times 48 hr apart. A safe and useful compound to treat impactions, especially those containing sand, is psyllium hydrophilic mucilloid. When mixed with water, it forms a gelatinous mass that carries ingesta along the GI tract. Although usually given through a nasogastric tube to horses with impactions, psyllium also may be used as a preventive by mixing the dry powder into the feed. This treatment is repeated 2—3 times each year in an effort to prevent development of sand impactions.

Strong laxatives that stimulate intestinal contractions are not commonly used to treat impactions and, in fact, may worsen the problem. Occasionally, horses with extremely hard impactions are treated with magnesium sulfate , which draws body fluids into the GI tract. Adverse effects include dehydration and an increased risk of diarrhea. Fluid therapy, whether the fluids are administered through a nasogastric tube or IV, is an important and effective part of treating horses with colonic or cecal impactions.

If an impaction does not start to break down within 3—5 days, surgery may be necessary to evacuate the intestine and help restore normal motility.

The normal migratory routes of the larvae of large bloodworms, particularly Strongylus vulgaris , have been implicated in many cases of colic. In response to the migratory and maturation processes of the larvae in the cranial mesenteric artery, the wall of the artery becomes thickened and forms loose plaques of inflammatory tissue.

It has been hypothesized that these plaques activate coagulation, resulting in thromboembolism. The blood supply to the intestine may be reduced, resulting in altered intestinal motility, a change in the absorption of nutrients from the intestine, or death of the intestine.

Thus, thromboembolism has been presumed to be a cause of recurrent episodes of colic and weight loss. Modern deworming medications, such as ivermectin and moxidectin, have activity against migrating S vulgaris larvae. Fenbendazole kills migrating strongyles if given at twice the recommended dosage daily for 5 days or at 10 times the recommended dosage daily for 3 days.

As a result of common use of these anthelmintics, chronic intermittent colic once thought to be caused by thromboembolism or parasite larval migration has largely been eliminated from equine practice. There is considerable evidence that damage caused by cyathostomins causes colic, diarrhea, and loss of condition, particularly in young horses. These signs are seen on a seasonal basis and are synchronous with the emergence of large numbers of encysted larvae into the lumen of the large colon.

In temperate areas of the Northern hemisphere, the larvae encyst during the winter months and emerge in the late winter and spring, causing ulceration, edema, and inflammation of the mucosa of the large colon. This may result in diarrhea, protein loss, weight loss, and mild intermittent colic and fever. Horses with cyathostomosis require treatment with larvacidal dosages of anthelmintics such as ivermectin , moxidectin, and fenbendazole.

Some horses require analgesics, supportive care, and proper nutritional support. Also see Gastrointestinal Parasites of Horses for a detailed discussion of treatment for large and small strongyles. Surgery usually is necessary if there is a mechanical obstruction to the normal flow of ingesta that cannot be corrected medically or if the obstruction also interferes with the intestinal blood supply.

The latter conditions result in death of the horse unless surgery is performed quickly. Occasionally, surgery is indicated as an exploratory diagnostic procedure for horses with chronic colic that have not responded to routine medical therapy. Under most circumstances, horses exhibiting signs of severe abdominal pain nonresponsive to analgesic therapy require emergency abdominal surgery. Generally, the lumen of the intestine is completely obstructed, such as occurs with a strangulating obstruction, enterolithiasis, or severe displacement.

Similarly, horses with an abnormally distended intestine on rectal examination and peritoneal fluid with an increased total protein concentration and number of erythrocytes probably have a strangulating lesion that requires surgical correction. However, these classic findings that characterize horses requiring emergency surgery do not always exist. Some horses with mild or moderate pain may also require surgery, and a judgment must be based on a thorough physical examination and other methods of evaluation, including abdominal ultrasonography.

Performing surgery if indicated early is critical to success and improves the prognosis for survival. Therefore, it is more important to decide whether the horse should be referred to a clinic where surgery could be performed if needed than to determine whether emergency surgery is definitively required. It is generally prudent to refer the following types of cases: When surgery is required, in most instances, the horse is anesthetized and positioned in dorsal recumbency, and the surgical incision is made on the ventral midline.

Once the peritoneal cavity is entered, portions of the intestine should be examined to determine the definitive cause of the colic. Correction may involve repositioning a displaced portion of intestine, removing an obstruction, or resecting devitalized intestine.

When devitalized segments of intestine must be removed or an enterotomy performed, postoperative care may include antibiotics, IV fluids, polymyxin B , antibodies directed against endotoxin, and NSAIDs to combat endotoxemia.

When a displaced segment of intestine is simply returned to its normal location, the postoperative care is much less intense. Each horse must be handled individually, and its treatment needs are based on the response to surgery and development of complications.

When the segment of the GI tract was considered, the survival rates for conditions affecting the small intestine and stomach were poorer than for those affecting the large colon. In addition, conditions that interfered with both the passage of ingesta and the intestinal blood supply dramatically decreased the chances of survival.

Although data on longterm survival ie, the horse returning to its intended use are more difficult to obtain, recent findings indicate that most horses that die or are euthanized because of serious problems do so within 3 mo after surgery.

Values obtained from several variables are often combined to predict survival in horses with colic. Prognostic indicators include pain assessment, intestinal distention, mucous membrane color, and cardiovascular system function. Survival rates are highest for horses with mild abdominal pain and are lowest for horses with severe pain.

Horses with palpable intestinal distention have lower survival rates than horses lacking evidence of intestinal distention, and survival rates are even lower if no intestinal sounds are audible on auscultation of the abdomen.

Red mucous membranes are frequently associated with endotoxemia, which decreases the survival rate. Cardiovascular system function reflects the degree of shock and, therefore, correlates with the prognosis for survival.

For instance, horses with low systolic blood pressure or a high heart rate have a decreased chance of survival. Of the laboratory analyses used to predict survival, blood lactate concentration and the anion gap are used most often. Measurement of blood lactate has been used as an indicator of tissue perfusion, with increasing concentrations of lactic acid corresponding with poor tissue perfusion.

In recent studies, changes in blood lactate concentration over time have been particularly useful to determine the prognosis for survival, with increasing concentrations being associated with a poor prognosis. Furthermore, changes in peritoneal fluid lactate concentrations over time have been used to help identify horses that require emergency abdominal surgery.

Similarly, the anion gap the calculated difference between the measured cations and the measured anions reflects the generation of organic anions, most notably lactic acid, due to reduced tissue perfusion. The concentration of protein in the peritoneal fluid also has been used to predict survival, with higher concentrations associated with a poorer prognosis. Cardiology is not a required rotation at OVC, but I picked it up nonetheless because it is one of my weakest subjects. Overview of Colic in Horses.

Protection Against Components of Enteric Bacteria: Intestinal Lubricants and Laxatives: Cecum and right colon, horse Left medial view of cecum and right colon, horse. Base of cecum, horse Base of the cecum in the horse. Equine gastrointestinal anatomy Equine GI anatomy relevant to colic, median section. Large intestine, horse The large intestine of the horse. Nephrosplenic ligament, horse Nephrosplenic ligament in the horse.

Umbilicus, horse Umbilicus in the horse. Inguinal hernia, horse Inguinal hernia in the horse. Inguinal canal, horse Inguinal canal in the horse. In healthy horses, it is common to retrieve. The abdomen and thorax should be auscultated and the abdomen percussed. Normal peritoneal fluid is clear to yellow, contains. The age of the horse is important, because a number of age-related conditions cause colic. Colic in Horses Overview of Colic in Horses.

Ruminants cattle, sheep, and goats lack which of the following teeth? Left medial view of cecum and right colon, horse. Base of the cecum in the horse. The large intestine of the horse. Nephrosplenic ligament in the horse. Smaller amounts of lipase and amylase are secreted.

The pancreas also secretes phospholipase A2 , lysophospholipase , and cholesterol esterase. The precursor zymogens , are inactive variants of the enzymes; which avoids the onset of pancreatitis caused by autodegradation. Once released in the intestine, the enzyme enteropeptidase present in the intestinal mucosa activates trypsinogen by cleaving it to form trypsin; further cleavage results in chymotripsin. The lower gastrointestinal tract GI , includes the small intestine and all of the large intestine.

The lower GI starts at the pyloric sphincter of the stomach and finishes at the anus. The small intestine is subdivided into the duodenum , the jejunum and the ileum. The cecum marks the division between the small and large intestine. The large intestine includes the rectum and anal canal. Partially digested food starts to arrive in the small intestine as semi-liquid chyme , one hour after it is eaten. After two hours the stomach has emptied.

In the small intestine, the pH becomes crucial; it needs to be finely balanced in order to activate digestive enzymes. The chyme is very acidic, with a low pH, having been released from the stomach and needs to be made much more alkaline.

This is achieved in the duodenum by the addition of bile from the gall bladder combined with the bicarbonate secretions from the pancreatic duct and also from secretions of bicarbonate-rich mucus from duodenal glands known as Brunner's glands. The chyme arrives in the intestines having been released from the stomach through the opening of the pyloric sphincter.

The resulting alkaline fluid mix neutralises the gastric acid which would damage the lining of the intestine. The mucus component lubricates the walls of the intestine.

When the digested food particles are reduced enough in size and composition, they can be absorbed by the intestinal wall and carried to the bloodstream. The first receptacle for this chyme is the duodenal bulb.

From here it passes into the first of the three sections of the small intestine, the duodenum. The next section is the jejunum and the third is the ileum. The duodenum is the first and shortest section of the small intestine. It is a hollow, jointed C-shaped tube connecting the stomach to the jejunum.

It starts at the duodenal bulb and ends at the suspensory muscle of duodenum. The attachment of the suspensory muscle to the diaphragm is thought to help the passage of food by making a wider angle at its attachment.

Most food digestion takes place in the small intestine. Segmentation contractions act to mix and move the chyme more slowly in the small intestine allowing more time for absorption and these continue in the large intestine.

In the duodenum, pancreatic lipase is secreted together with a co-enzyme , colipase to further digest the fat content of the chyme. From this breakdown, smaller particles of emulsified fats called chylomicrons are produced.

There are also digestive cells called enterocytes lining the intestines the majority being in the small intestine. They are unusual cells in that they have villi on their surface which in turn have innumerable microvilli on their surface. All these villi make for a greater surface area, not only for the absorption of chyme but also for its further digestion by large numbers of digestive enzymes present on the microvilli. The chylomicrons are small enough to pass through the enterocyte villi and into their lymph capillaries called lacteals.

A milky fluid called chyle , consisting mainly of the emulsified fats of the chylomicrons, results from the absorbed mix with the lymph in the lacteals. The suspensory muscle marks the end of the duodenum and the division between the upper gastrointestinal tract and the lower GI tract. The digestive tract continues as the jejunum which continues as the ileum. The jejunum, the midsection of the small intestine contains circular folds , flaps of doubled mucosal membrane which partially encircle and sometimes completely encircle the lumen of the intestine.

These folds together with villi serve to increase the surface area of the jejunum enabling an increased absorption of digested sugars, amino acids and fatty acids into the bloodstream. The circular folds also slow the passage of food giving more time for nutrients to be absorbed. The last part of the small intestine is the ileum. This also contains villi and vitamin B12 ; bile acids and any residue nutrients are absorbed here.

When the chyme is exhausted of its nutrients the remaining waste material changes into the semi-solids called feces, which pass to the large intestine, where bacteria in the gut flora further break down residual proteins and starches. The cecum is a pouch marking the division between the small intestine and the large intestine.

At this junction there is a sphincter or valve, the ileocecal valve which slows the passage of chyme from the ileum, allowing further digestion. It is also the site of the appendix attachment.

In the large intestine , [2] the passage of the digesting food in the colon is a lot slower, taking from 12 to 50 hours until it is removed by defecation. The colon mainly serves as a site for the fermentation of digestible matter by the gut flora. The time taken varies considerably between individuals. The remaining semi-solid waste is termed feces and is removed by the coordinated contractions of the intestinal walls, termed peristalsis , which propels the excreta forward to reach the rectum and exit via defecation from the anus.

The wall has an outer layer of longitudinal muscles, the taeniae coli , and an inner layer of circular muscles. The circular muscle keeps the material moving forward and also prevents any back flow of waste.

Also of help in the action of peristalsis is the basal electrical rhythm that determines the frequency of contractions. Most parts of the GI tract are covered with serous membranes and have a mesentery. Other more muscular parts are lined with adventitia. The digestive system is supplied by the celiac artery.

The celiac artery is the first major branch from the abdominal aorta , and is the only major artery that nourishes the digestive organs. There are three main divisions — the left gastric artery , the common hepatic artery and the splenic artery. Most of the blood is returned to the liver via the portal venous system for further processing and detoxification before returning to the systemic circulation via the hepatic veins.

The enteric nervous system consists of some one hundred million neurons [31] that are embedded in the peritoneum , the lining of the gastrointestinal tract extending from the esophagus to the anus. Parasympathetic innervation to the ascending colon is supplied by the vagus nerve.

Sympathetic innervation is supplied by the splanchnic nerves that join the celiac ganglia. Most of the digestive tract is innervated by the two large celiac ganglia, with the upper part of each ganglion joined by the greater splanchnic nerve and the lower parts joined by the lesser splanchnic nerve. It is from these ganglia that many of the gastric plexuses arise. Early in embryonic development , the embryo has three germ layers and abuts a yolk sac.

During the second week of development, the embryo grows and begins to surround and envelop portions of this sac. The enveloped portions form the basis for the adult gastrointestinal tract. Sections of this foregut begin to differentiate into the organs of the gastrointestinal tract, such as the esophagus , stomach , and intestines. During the fourth week of development, the stomach rotates. The stomach, originally lying in the midline of the embryo, rotates so that its body is on the left.

This rotation also affects the part of the gastrointestinal tube immediately below the stomach, which will go on to become the duodenum. By the end of the fourth week, the developing duodenum begins to spout a small outpouching on its right side, the hepatic diverticulum , which will go on to become the biliary tree.

Just below this is a second outpouching, known as the cystic diverticulum , that will eventually develop into the gallbladder. Each part of the digestive system is subject to a wide range of disorders many of which can be congenital.

Mouth diseases can also be caused by pathogenic bacteria , viruses , fungi and as a side effect of some medications. Mouth diseases include tongue diseases and salivary gland diseases. A common gum disease in the mouth is gingivitis which is caused by bacteria in plaque.

The most common viral infection of the mouth is gingivostomatitis caused by herpes simplex. A common fungal infection is candidiasis commonly known as thrush which affects the mucous membranes of the mouth.

There are a number of esophageal diseases such as the development of Schatzki rings that can restrict the passageway, causing difficulties in swallowing. They can also completely block the esophagus. Stomach diseases are often chronic conditions and include gastroparesis , gastritis , and peptic ulcers. A number of problems including malnutrition and anemia can arise from malabsorption , the abnormal absorption of nutrients in the GI tract.

Malabsorption can have many causes ranging from infection , to enzyme deficiencies such as exocrine pancreatic insufficiency.

It can also arise as a result of other gastrointestinal diseases such as coeliac disease. Coeliac disease is an autoimmune disorder of the small intestine. This can cause vitamin deficiencies due to the improper absorption of nutrients in the small intestine. The small intestine can also be obstructed by a volvulus , a loop of intestine that becomes twisted enclosing its attached mesentery.

This can cause mesenteric ischemia if severe enough. A common disorder of the bowel is diverticulitis. Diverticula are small pouches that can form inside the bowel wall, which can become inflamed to give diverticulitis. This disease can have complications if an inflamed diverticulum bursts and infection sets in.

Any infection can spread further to the lining of the abdomen peritoneum and cause potentially fatal peritonitis. Crohn's disease is a common chronic inflammatory bowel disease IBD , which can affect any part of the GI tract, [39] but it mostly starts in the terminal ileum. Ulcerative colitis an ulcerative form of colitis , is the other major inflammatory bowel disease which is restricted to the colon and rectum. Both of these IBDs can give an increased risk of the development of colorectal cancer.

Ulcerative coliltis is the most common of the IBDs [40]. Irritable bowel syndrome IBS is the most common of the functional gastrointestinal disorders. These are idiopathic disorders that the Rome process has helped to define. Giardiasis is a disease of the small intestine caused by a protist parasite Giardia lamblia.

This does not spread but remains confined to the lumen of the small intestine. Giardiasis is the most common pathogenic parasitic infection in humans. There are diagnostic tools mostly involving the ingestion of barium sulphate to investigate disorders of the GI tract. Gestation can predispose for certain digestive disorders. Gestational diabetes can develop in the mother as a result of pregnancy and while this often presents with few symptoms it can lead to pre-eclampsia.

From Wikipedia, the free encyclopedia. Redirected from Digestive system. See also gastrointestinal tract. For digestive systems of non-human animals, see Digestion. Development of the digestive system. Retrieved 1 October Human Biology and Health. Human Physiology Third ed. Dorland's illustrated medical dictionary 32nd ed. Regulation of Front-line Body Defenses". Essential Haematology 5e Essential. Textbook of Medical Physiology.

Mitchell; illustrations by Richard; Richardson, Paul Gray's anatomy for students. Retrieved 22 May Journal of parenteral and enteral nutrition. Principles for Clinical Medicine 3rd ed. Guyton and Hal Textbook of Medical Physiology 12th ed. Sensory Nerves, Brendan J. Larsen's human embryology Thoroughly rev.

Robbins and Cotran pathologic basis of disease. The Journal of the American Medical Association. Retrieved 12 June The New England Journal of Medicine, The Functional Gastrointestinal Disorders.

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