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98 Cards in this Set
- Front
- Back
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damage to what nerves can cause paralysis of significant portions of the swallowing mechanism?
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5th (trigeminal), 9th (glossopharyngeal), 10th (vagus)
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what two diseases results from damage to the swallowing center in the brain stem?
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poliomyelitis and encephalitis
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what abnormalities can occur when the swallowing mechanism is totally or partially paralyzed?
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1) complete abrogation of the swallowing act so swallowing cannot occur 2) failure of the glottis to close so that food passes into the lungs instead of the esophagus 3) failure of the soft palate and uvula to close the pos. nares so that food refluxes into the nose during swallowing
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what is achalasia?
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a condition in which the lower esophageal sphincter fails to relax during swallowing due to damage of the myenteric plexus in the lower 2/3 of the esophagus.
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what happens after mean years with achalasia?
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esophagus becomes enlarged, infected, and can produce ulcers leading to sever substernal pain or even rupture and death.
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what is gastritis?
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inflammation of the gastric mucosa, causing atrophy of gastric mucosa
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most gastritis is caused by what?
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chronic bacterial infection of the gastric mucosa
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what two substances used in excess can cause gastritis?
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alcohol and aspirin
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what is low level of absorption in the stomach due to?
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gastric barrier 1) it is lined with highly resistant mucous cells that secrete viscid and adherent mucus 2) it has tight junctions bt adjacent epithelial cells
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how does a gastric ulcer develop?
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gastritis leading to increased permeability of stomach epithelium, and mucosa susceptible to digestion by peptic digestive enzymes
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what two conditions are due to loss of stomach secretions in gastric atrophy?
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achlorohydria and occasionally pernicious anemia
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what is the cause of gastric atrophy?
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chronic gastritis causing the mucosa to atrophy until little or no gastric digestive secretions remain. or autoimmunity against gastric mucosa
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how is achlorohydria diagnosed?
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when the pH of gastric secretions fails to decrease below 6.5 when stimulated
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what is required for pepsin to function?
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an acidic environment (hydrochloric acid)
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what is also secreted by the parietal cells that secret HCl?
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intrinsic factor
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what is the role of intrinsic factor?
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binds vitamin B12
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where is vitamin B12 absorbed?
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in the ileum
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what is a peptic ulcer?
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an excoriated area of stomach or intestinal mucosa caused principally by the digestive action of gastric juice or upper small intestinal secretions.
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where is the most frequent site of peptic ulcers?
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within a few centimeters of the pylorus
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causes of peptic ulcers
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1. high acid and peptic content
2. irritation 3. poor blood supply 4. poor secretion of mucus 5. infection, H. pylori |
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what two conditions are due to loss of stomach secretions in gastric atrophy?
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achlorohydria and occasionally pernicious anemia
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what is the cause of gastric atrophy?
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chronic gastritis causing the mucosa to atrophy until little or no gastric digestive secretions remain. or autoimmunity against gastric mucosa
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how is achlorohydria diagnosed?
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when the pH of gastric secretions fails to decrease below 6.5 when stimulated
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what is required for pepsin to function?
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an acidic environment (hydrochloric acid)
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what is also secreted by the parietal cells that secret HCl?
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intrinsic factor
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what is the role of intrinsic factor?
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binds vitamin B12
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where is vitamin B12 absorbed?
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in the ileum
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what is a peptic ulcer?
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an excoriated area of stomach or intestinal mucosa caused principally by the digestive action of gastric juice or upper small intestinal secretions.
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where is the most frequent site of peptic ulcers?
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within a few centimeters of the pylorus, also frequently along the lesser curvature, and rarely in the lower end of the esophagus
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causes of peptic ulcers
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1. high acid and peptic content
2. irritation 3. poor blood supply 4. poor secretion of mucus 5. infection, H. pylori |
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what is a marginal ulcer
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a type of peptic ulcer often occurring wherever a surgical opening such as a gastrojejunostomy has been made b/t the stomach and the jejunum of the small intestine
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what do the deep pyloric glands secrete
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mainly mucus
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where are the glands of brunner, what do they secrete?
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upper duodenum, highly alkaline mucus
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how is the mucosa of the duodenum protected
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mucus protection and alkalinity of the small intestinal secretions, such as pancreatic secretions
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what does pancreatic secretions contain and what is the purpose?
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large quantities of sodium bicarbonate that neutralize the hydrochloric acid of the gastric juice, and inactivates pepsin and prevents digestion of the intestinal mucosa
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where are large amounts of bicarbonate ions provided?
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pancreatic secretions, 1) secretions of Brunners glands in the upper duodenum and 2) bile from the liver
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what are the two feedback mechanisms that ensure the neutralization of gastric juices is complete
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1) if excess acid enters duodenum, reflex inhibition of gastric secretion and peristalsis in stomach by nervous reflex and hormonal feedback from duodenum (delay gastric emptying)
2) secretin released in the presence of acid in the sm. intestine, passes via blood to pancreas to promote pancreatic secretions containing high concentration of sodium bicarb. for neutralization |
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two ways a peptic ulcer can occur
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1) excess secretion of acid and pepsin by gastric mucosa or 2) diminished ability of gastroduodenal mucosal barrier to protect against digestive properties of the stomach acid-pepsin secretions
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how does H. pylori cause peptic ulcers?
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it is capable of penetrating the mucosal barrier by physical capability and by releasing bacterial digestive enzymes that liquefy the barrier. acid is able to penetrate epithelium and digest GI wall.
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what happens to the rate of gastric acid secretion if the ulcers are in the initial portion of the duodenum
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greater than normal
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factors that predispose to ulcers
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smoking which causes increased nervous stimulation of stomach secretory glands. 2) alcohol b.c breaks down mucosal barrier and 3) aspirin (NSAIDS)
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treatment of peptic ulcers
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antibiotics and H2 blocker (rantitidine)
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causes of lack of pancreatic secretions
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1) pancreatitis 2) when pancreatic duct is blocked by gallstone at papilla of vater 3) head of pancreas has been removed due to malignancy
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what are the pancreatic digestive enzymes?
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trypsin, chymotrypsin, carboxypolypeptidase, pancreatic amylase, pancreatic lipase
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what happens to the feces as a result of lack of pancreatic enzymes?
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copious fatty feces are secreted
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most common cause of pancreatitis? 2nd most common?
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excess alcohol, followed by blockage of papilla of vater by gallstone
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what happens when the pancreatic duct is blocked?
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enzymes build up, and trypsinogen accumulates and overrides trypsin inhibitor, it activate trypsin, which activates other pancreatic enzymes and eventually enzymes digest pancreas
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what does the term 'sprue' mean?
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decreased absorption by the mucosa of the small intestine (malabsorption)
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what causes idiopathic sprue, celiac disease (in children), and gluten enteropathy
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results from the toxic effect of gluten present in certain types of grains, especially wheat and rye
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what is the effect of gluten on the intestinal mucosa in people with gluten enteropathy?
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has a direct destructive effect on intestinal enterocytes. in mild forms, only microvilli are destroyed. in more severe forms, villi are blunted or disappear.
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what is tropical sprue?
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occurs in the tropics, treated with antibiotics, could be caused by inflammation of intestinal mucosa resulting from unidentified infectious agents
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what occurs in the early stages of sprue?
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fat absorption more impaired then other digestive products, resulting in steatorrhea. fats are excreted in the form of salts of fatty acids.
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what type of anemia results from decreased absorption of vitamin B12 and folic acid?
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macrocytic anemia of the pernicious anemia type
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what could lead to an atonic colon?
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if one does not allow defecation to occur when the defecation reflexes are excited or from overuse of laxatives
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what could cause constipation?
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atonic colon, or spasm of a small segment of the sigmoid colon.
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what is megacolon?
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Hirschsprung's disease. severe constipation causing fecal matter to accumulate in the colon.
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what causes megacolon/ hirschsprung's disease?
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lack of or deficiency of ganglion cells in the myenteric plexus in a segment of the sigmoid colon. defecation reflexes or strong peristaltic motility can occur in that are of the lg. intestine.
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what is enteritis?
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inflammation usually caused either by a virus or bacteria in the intestinal tract
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where is the infection in infectious diarrhea?
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most extensive in the large intestine and the distal end of the ileum
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what happens to the mucosa in infectious diarrhea?
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mucosa becomes irritated and rate of secretion increased. motility of intestinal wall increases.
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what is the action of cholera?
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directly stimulates excessive secretion of electrolytes and fluid from the crypts of Lieberkuhn in the distal ileum and colon.
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what is psychogenic diarrhea?
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caused by excessive stimulation of the parasympathetic nervous system which excites motility and excess secretion of mucus in distal colon
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what is ulcerative colitis
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extensive areas of the walls of the lg. intestine become inflamed and ulcerated. causes mass movements to occur for much of the day. enhanced secretions.
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what occurs from a spinal cord injury between the conus medullaris and the brain?
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voluntary portion of the defecation act is blocked, while basic cord relfex for defecation is still intact. (lose increased abdominal pressure and relaxation of voluntary anal sphincter)
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where do sensory signals that initiate vomiting originate?
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pharynx, esophagus, stomach, and upper portions of the small intestines
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how are nerve impulses transmitted for vomiting?
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transmitted by vagal and sympathetic afferent nerve fibers to vomiting center in brain
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which cranial nerves are responsible from sending signals from the vomiting center in the brain to the upper GI tract?
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motor impulses transmitted from vomiting center in the brain by 5th, 7th, 9th, 10th, and 12th CN to upper GI tract
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how are impulses sent from the brain to the lower GI tract for vomiting?
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vagal and sympathetic nerves to lower GI tract
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how are impulses sent from vomiting center to diaphragm and abdominal muscles?
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spinal nerves
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what is antiperistalsis?
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peristalsis up the digestive tract rather than downward
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what initiates the actual vomiting act?
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distention of the upper portions of the GI tract, especially the duodenum.
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what are the first effects when the vomiting act is instituted?
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1) deep breath 2) raising of hyoid bone and larynx to pull upper esophageal sphincter open 3) closing of glottis to prevent vomitis flow into lungs 4) lifting of soft palate to close posterior nares
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what initiates the actual vomiting act?
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distention of the upper portions of the GI tract, especially the duodenum.
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what causes the vomiting act?
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results from squeezing action of the muscles of the abdomen associated with simultaneous contraction of the stomach wall and opening of esophageal sphincters to expel gastric contents
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what are the first effects when the vomiting act is instituted?
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1) deep breath 2) raising of hyoid bone and larynx to pull upper esophageal sphincter open 3) closing of glottis to prevent vomitis flow into lungs 4) lifting of soft palate to close posterior nares
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what initiates the actual vomiting act?
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distention of the upper portions of the GI tract, especially the duodenum.
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where is the chemoreceptor trigger zone for vomiting in the brain?
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located bilaterally on the floor of the 4th ventricle (area postrema)
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what causes the vomiting act?
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results from squeezing action of the muscles of the abdomen associated with simultaneous contraction of the stomach wall and opening of esophageal sphincters to expel gastric contents
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what are the first effects when the vomiting act is instituted?
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1) deep breath 2) raising of hyoid bone and larynx to pull upper esophageal sphincter open 3) closing of glottis to prevent vomitis flow into lungs 4) lifting of soft palate to close posterior nares
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what is the mechanism behind vomiting due to rapidly changing direction or rhythm of motion of the body?
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motion stimulates receptors in vestibular labyrinth of inner ear, impulses are transmitted by way of brain stem vestibular nuclei into cerebellum, then to area postrema, then to vomiting center
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where is the chemoreceptor trigger zone for vomiting in the brain?
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located bilaterally on the floor of the 4th ventricle (area postrema)
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what causes the vomiting act?
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results from squeezing action of the muscles of the abdomen associated with simultaneous contraction of the stomach wall and opening of esophageal sphincters to expel gastric contents
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what initiates the actual vomiting act?
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distention of the upper portions of the GI tract, especially the duodenum.
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what are the first effects when the vomiting act is instituted?
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1) deep breath 2) raising of hyoid bone and larynx to pull upper esophageal sphincter open 3) closing of glottis to prevent vomitis flow into lungs 4) lifting of soft palate to close posterior nares
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where is the chemoreceptor trigger zone for vomiting in the brain?
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located bilaterally on the floor of the 4th ventricle (area postrema)
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what is the mechanism behind vomiting due to rapidly changing direction or rhythm of motion of the body?
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motion stimulates receptors in vestibular labyrinth of inner ear, impulses are transmitted by way of brain stem vestibular nuclei into cerebellum, then to area postrema, then to vomiting center
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what is the mechanism behind vomiting due to rapidly changing direction or rhythm of motion of the body?
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motion stimulates receptors in vestibular labyrinth of inner ear, impulses are transmitted by way of brain stem vestibular nuclei into cerebellum, then to area postrema, then to vomiting center
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what causes the vomiting act?
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results from squeezing action of the muscles of the abdomen associated with simultaneous contraction of the stomach wall and opening of esophageal sphincters to expel gastric contents
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where is the chemoreceptor trigger zone for vomiting in the brain?
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located bilaterally on the floor of the 4th ventricle (area postrema)
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what is the mechanism behind vomiting due to rapidly changing direction or rhythm of motion of the body?
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motion stimulates receptors in vestibular labyrinth of inner ear, impulses are transmitted by way of brain stem vestibular nuclei into cerebellum, then to area postrema, then to vomiting center
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what are 3 causes of nausea?
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1) irritative impulses from GI tract
2) impulses that originate in lower brain associated with motion sickness 3) impulses from cerebral cortex to initiate vomiting |
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common causes of obstruction along GI tract:
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cancer, fibrotic constriction results from ulceration or peritoneal adhesions, spasm of a segment of the gut, and paralysis of a segment of the gut
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obstruction at pylorus causes what?
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persistent vomiting of stomach contents (acid), and can result in whole body alkalosis
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what occurs if obstruction is beyond stomach, such as antiperistaltic reflux from small intestine?
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causes intestinal juices to flow backward into stomach, and contents are vomited along with stomach secretions. (neutral or basic vomit)
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low obstruction near the distal end of the lg. intestine causes what?
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extreme constipation with less vomiting at first, then severe vomiting when maximum feces in the colon resulting in dehydration and circulatory shock
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what three sources cause flatus?
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1) swallowed air
2) gases form in the gut as a result of bacterial action 3) gases that diffuse from the blood into the GI tract |
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what and were are the gases derived from in the stomach?
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usually a mixture of nitrogen and oxygen from swallowed air. expelled by belching
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where are the gases derived from in the large intestine?
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bacterial action, including CO2, methane, and H2. mixture of CH4, H2 and O2 causes explosive mixture
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