Motility Flashcards
(33 cards)
Gastric motility
The presence of food in the stomach stimulates motility through release of vasoconstrictive peptide stimulated by the vagal nerves. The stomach contractions force the contents towards the pylorus, where most of the contents are pushed back into the body of the stomach. As spurts of chyme enter the duodenum, duodenal hormones are released into the blood, circulate back to the stomach, and decrease gastric emptying. Thus, there is a coordinated effect between nerves and hormones controlling gastric emptying.
Motility in the small intestine; 3 types
Motility in the small intestine is primarily under local control of the mesenteric plexus and consists of both peristalsis, segmentation, and pendular movement.
Peristalsis
Contraction takes places behind the bolus of chyme and relaxation takes places ahead. This process take place due to stimulation of excretory and inhibitory neurons. Myenteric plexus.
Peristaltic rushes
Peristaltic rushes can occur in the small intestine when there is irritation or bacteria. Peristaltic rushes sweep food long distances through the SI, so much less digestion occurs. This can result in diarrhea.
Segmentation
Segmentation occurs by the relaxation of longitudinal muscle and contraction of circular muscle. Unlike peristalsis, which contract behind the chyme, segmentation contracts in the middle of the chyme, spreading digestive contents in both directions. Segmentation happens adjacent to peristalsis, so while contents are mixed, the is a net move down the tract. yenteric plexus.
Gallbladder
When chyme first enters the duodenum, CKK is secreted into the blood in response to fasts and glucose. CKK, along with vagal stimulation, causes rhythmic contraction of the gallbladder, forcing bile out through the cystic duct and into the common bile duct. CKK also relaxes the sphincter of Oddi, allowing duct contents into the duodenum.
CCK
Cholecystokinin is a peptide hormone of the GI system responsible for stimulating the digestion of fat and protein. It is synthesized and secreted by enteroendocrine cells in the duodenum. Its causes the gall bladder motility of bile and relaxes the sphincter of Oddi.
CCK also inhibits gastric emptying and decreasing gastric acid secretion. It stimulates the pancreas to release digestive enzymes. The release of CCK is inhibited by somatostatin and pancreatic peptide.
Motility in the large intestine
The large intestine utilizes segmental propulsion and mass movements. The muscle structure differs from the SI with the 3 tania coli, which as they contract for haustra. This process is called segmental propulsion.
Iliocecal sphincter
The Iliocecal sphincter regulates the amount of chyme that enters the colon. The movement of chyme in the terminal ilium relaxes the sphincter. It is controlled by enteric and autonomic nerves, as well as CCK and gastrin.
Segmental propulsion
The contraction of the tania coli in the colon, forming haustra. The haustra stay in form for long periods of time, helping to store the chyme as it is dehydrated.
Mass movements
Mass movements occur one to three times daily. The propulsion, which is peristaltic in nature, occurs very slowly, when the distal colon is relaxed. Mass movements are stimulated by parasympathetic never (vagal in proximal colon and pelvic nerves in the distal nerves.
Regulation of motility
Motility is regulated by enteric nerves (the myenteric and submucosal plexus), autonomic nerves, and hormones. The enteric system responds to autonomic and local signals. The parasympathetic nerves are the vagal and pelvic and promote motility. The sympathetics stop motility. For hormones, see gastrin below.
Hormones and motility
As a general rule, GI hormones inhibit motility. Gastrin, however, tends to stimulate gastric emptying and motility. During fasting, motilin stimulates contractions (SI only).
Vomiting
Reverse peristalsis occurs from the SI to pylorus and the pyloric sphincter relaxes, pushing chyme into stomach. Abdominal contraction force gastric contents up the oesophagus, past the upper sphincter, and into the mouth.
Prolonged vomiting leads to a loss of H, Cl, K, and fluid, causing dehydration, alkalosis, and hypokalemia.
Serotonin induces motility associated with vomiting and nausea. So antagonists are effective antiemetic.
Inflammatory bowel disease
Inflammatory bowel disease has no known cause both results in diarrhea and abdominal pain. Sometimes blood, puss and mucous, fever, fatigue. IBD can be from Crone’s disease or ulcerative colitis, both of which are autoimmune disorders. Crone’s disease can occur anywhere along the GI tract while UC is only in the colon.
UC can be cured by removed of bowel/rectum. Crones disease has no cure. Immunosuppressants are used in both (eg steroids).
Environmental factors play a large role, as other factors that affect gut flora, like stress and antibiotics.
Consequence of chronic diarrhea?
Disproportionate loss of HCO3-, leading to metabolic acidosis.
Diarrhea
Segmental propulsion is generally very slow and allows for dehydration of feces in the colon. Diarrhea occurs when chyme and fecal matter move too quickly through the colon, which can result from irritation of the lower GI tract, inflammatory disease, or nervous stress.
Osmotic diarrhea is, as described above, due to hyper motility of feces.
Secretory diarrhea, in contrast, is caused by excessive reabsorption of solutes into the lumen of the colon, as caused by cholera toxin.
Cholera
Contaminated water containing bacteria, which produce cholera toxin in the SI, devastating the epithelial lining of the gut. The cholera toxin binds to receptors on cells in the wall of the small intestine and activates cyclic AMP, increasing the number of cyclic AMP molecules in the cell, which activate Cl- channels. Chloride ions move out of the cell into the lumen. Sodium ions are attracted to the negative chloride ions, so they also enter the cell. The greater tonicity in the lumen cause osmosis of water, which results in severe dehydration, and diarrhea.
Hirschsprung’s disease
Hirschsprung’s disease is a congenital disease that involves the loss of the enteric nervous system in the distal colon and the internal/external sphincters. Normal defecation reflex does not occur, so feces builds up. Symptoms are vomiting and constipation.
Can be treated by the surgical removal of the ganglionic region.
Chemoreceptor trigger zone
In obdula oblongata, near the vomiting center. Activation of CTZ may trigger vomiting center to initiate vomiting. CTZ is outside of blood brain barrier, so it may be excited by compound in the blood, as well as afferent stimulus. from GI tract or higher centers of the brain.
Has 5HT, dopamine, and H1 receptors, which are target for antiemetics.
NaCl absorption in the gut
Na/K ATPase creates chemiosmotic gradient.
Following gradient, Na can diffuse into the enterocyte from lumen. There are also Na/Cl cotransporters, Na/H antiporters, and Cl/bicarbonate antiporters. Cl can then diffuse from enterocyte across basolateral membrane. Water follows electrolytes.
IBS
IBS is a group of symptoms—including abdominal pain and changes in the pattern of bowel movements without any evidence of underlying damage that occur over a long time, often years. The causes of IBS are not clear. Theories include gut–brain axis problems, small intestinal bacterial overgrowth, genetic factors, food sensitivity, and gut motility problems. Diagnosis is based on signs and symptoms in the absence of worrisome features.
While the cause of IBS in unknown, it has characteristics which resemble obstructive-motility disorders.
Constipation and hard stools of narrow caliber, painful or infrequent defecation, and intractability to laxatives
Diarrhea usually is described as small volumes of loose stool, with evacuation preceded by urgency or frequent defecation.
Abdominal pain.
Vomiting reflex nerves
Vomiting center is in medulla oblongata. It send out signals that cause us to vomit. Can be stimulated in several ways:
Chemoreceptor trigger zone (CTZ) with dopamine, H1 histamine and 5HTP receptor. Located outside of blood brain barrier, so it can be activated by circulating substances (chemo toxins, drugs, etc). Stimulation will activate the emetic reflux.
Afferent impulses from higher centers of brain can also stimulate the chemoreceptor trigger zone, thereby activating the vomiting center. Pain, odor, memory, can activate.
Afferent nerves from GI tract (vagal sensory nerve) can also activate vomiting reflux via the chemoreceptor trigger zone.
Antiemetics
5-HT3 receptor antagonists block serotonin receptors in the central nervous system and gastrointestinal tract.
Serotonin is released by toxins or irritants in the GI tract.
Dopamine antagonists act in the brain and are used to treat nausea and vomiting associated with radiation sickness, opioids, cytotoxic drugs and general anesthetics.
Antihistamines (H1 histamine receptor antagonists) are effective in many conditions, including motion sickness, morning sickness in pregnancy, and to combat opioid nausea.
