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682 Cards in this Set
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- 3rd side (hint)
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what are the layers of the GI tract from outside in?
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serosa
muscularis submucosa mucosa |
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what is another name for the myenteric plexus?
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Auerbach's plexus
outer plexus |
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what are the layers of muscle in the muscularis of the GI tract?
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longitudinal muscle
circular muscle oblique muscle (only in stomach) |
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what is another name for the submucoasl plexus?
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Meissner's plexus
inner plexus |
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what is the muscularis mucosae?
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thin layer of smooth muscle found in most parts of the gastrointestinal tract, located outside the lamina propria mucosae and separating it from the submucosa
functions to move the villi, and expel materials from the crypts |
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where in the GI tract is skeletal muscle found?
where is smooth muscle found? |
upper esophagus
external anal sphincter rest of GI tract |
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what type of smooth muscle is found in the GI tract?
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visceral or unitary type
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how does smooth muscle compare to skeletal muscle?
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energy - up to 300x less
force - higher shortening - higher time - longer speed - slower |
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what is the effect of nicotine on smooth muscle in the GI tract?
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causes it to relax
(mainly at the sphincters) |
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what is the effect of alcohol on smooth muscle in the GI tract?
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decreases contraction
mainly at sphincters |
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what is the effect of caffeine on the smooth muscle of the GI tract?
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relaxes smooth muscle
(especially at sphincters) |
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what is the major function of the mouth?
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reduce food to small particles, mixed with saliva and formed into a bolus (which is swallowed)
salivary enzymes initiate digestion |
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what is the major function of the pharynx?
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swallowing reflex
stimulation of pharyngeal receptors elicits a peristaltic wave in the pharyngeal muscles |
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what is the major function of the esophagus?
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transport food bolus from pharynx to stomach
uses peristalsis with closely coordinated contraction and relaxation of upper and lower esophageal sphincters |
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to what volume can the stomach distend with food in it?
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about 1.5 liters
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what are the divisions of the stomach?
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cardia - area around gastroesophageal opening
fundus - upper rounded portion body (corpus) - central part antrum - between body and pylorus pylorus - opening to duodenum |
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what are the names for the folds and depressions in the mucosa of the stomach?
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folds - rugae
depressions - gastric pits |
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what is the function of the cardiac sphincter?
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aka lower esophageal or gastroesophageal sphincter
controls opening of the esophagus into the stomach prevents acid and gastric secretions in the esophagus |
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what is the tone of the cardiac sphincter?
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normally tonically constricted
receptive relaxation ahead of a peristaltic wave |
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what is the function of the pyloric sphincter?
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controls opening of stomach into first part of small intestine
prevents food passage but not fluids |
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what is the tone of the pyloric sphincter?
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normally only slightly tonically constricted
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what is pyloroplasm?
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aka pyloric stenosis
disorder in which the pyloric valve is overly constricted, which causes babies to spit up, sometimes very forcefully, after feeding diagnosed by "olive-feeling" pyloric valve or nasogastric tube treated with smooth muscle relaxing drugs and/or surgery |
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what are the major functions of the stomach?
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mixing of food with gastric exocrine secretions
killing of germs by HCl initiation of protein degradation by HCl and pepsin storage of food regulated release of chyme through the pylorus into small intestine |
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what are the divisions of the small intestine?
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duodenum
jejunum ileum |
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what is the mesentery?
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extensions of peritoneum that bind abdominal organs together, but still allow free movement of each coil
helps to prevent strangulation of the long tube |
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what are plicae circulares?
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permanent circular folds in the small intestine
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what are villi?
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fingerlike projections, 1mm in height
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what is a brush border?
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the microvilli on epithelial cells
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what vessels are found in each villus?
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arteriole
venule lymph vessel |
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what are the functions of plicae circulares, villi, and brush border in the intestinal wall?
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dramatically increase surface area
alkaline exocrine secretions of intestine, pancreas, and liver |
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from what does the large intestine get its name?
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large diameter
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what is the cecum?
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a 5-8cm blind pouch in the lower right quadrant of the abdomen
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what are the parts of the colon (large intestine)?
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ascending colon
transverse colon descending colon sigmoid colon |
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what is the main site of digestion and absorption?
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small intestine
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what is the major function of the large intestine?
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absorb most of the remaining fluid from the small intestine
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what valve is between the small intestine and the large intestine?
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ileocecal valve
(between the ileum of the small intestine and the cecum) prevents backflow of fecal contents from colon into small intestine - slows emptying of ileal content into cecum |
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what is the appendix?
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a wormlike (vermiform) tubular organ lying behind the cecum with uncertain function
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what provides the feedback control of the ileocecal valve?
what nerves regulate this? |
reflexes from the cecum
myenteric plexus and extrinsic nerves |
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what is the rectum?
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last 20cm of the intestinal tube, directed slightly posterior
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what are anal columns?
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mucous lining of the anal canal, arranged in folds
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what part of the anal sphincter is smooth muscle? what part is striated muscle?
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internal sphincter is smooth
external sphincter is striated |
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what are hemorrhoids?
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veins around the anus or lower rectum are swollen and inflamed
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what are anal fissures?
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small tears or cuts in the skin lining the anus which can cause pain and bleeding
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what causes slow waves in the neurons of the GI tract?
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rhythmic changes in membrane potential
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where do slow waves cause contractions in GI muscles?
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stomach (slow waves cause "gastric action potentials")
doesn't cause contractions in other parts of the GI tract |
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what is the frequency of slow waves?
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stomach - 3/min
small intestine - 12/min ileum - 8/min colon - 11/min rectum - 17/min |
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what determines the maximal possible frequency of contractions?
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frequency of slow waves
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what are spike potentials?
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electrical potentials that develop on top of slow waves in the GI tract
(responsible for contractions in GI tract when they reach threshold potentials) |
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what is caused by a higher amplitude of slow waves?
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more spike potentials
increased gut muscle tension |
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what factors support increased gut muscle tension?
what factors downregulate it? |
support - stretch, parasympathetic, GI hormones
downregulate - sympathetic |
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where are inhibitory neurons in the GI tract?
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throughout entire tract
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when are inhibitory neurons in the GI tract on?
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at sphincters, continuously turned off and must be turned on for the circular muscle to contract
outside of sphincters, continuously turned on and must be turned off for muscle to contract |
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what is the "brain of the belly"?
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enteric nervous system
loosely organized, diffuse set of neurons which control the GI tract |
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from where do the post-ganglionic sympathetic neurons of the enteric nervous system arise?
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celiac ganglion
superior mesenteric ganglion inferior mesenteric ganglion hypogastric ganglion |
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what nerves carry preganglionic parasympathetic fibers to the enteric nervous system?
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vagus nerve
pelvic nerve |
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to what plexus in the enteric nervous system do most parasympathetic fibers project?
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myenteric plexus (Auerbach's plexus)
few project to submucosal plexus (Meissner's plexus) none project to epithelium |
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what type of nerve fibers in the enteric nervous system project to the epithelial cells?
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only sympathetic fibers
also project to myenteric (Auerbach's) and submucosal (Meissner's) plexuses |
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what is the form of the myenteric plexus?
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parallel linear chains of connected neurons between the longitudinal and circular muscle layers
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what is the form of the submucosal plexus?
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poorly arranged neurons in the submucosa, connected with epithelial cells
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what are the functions of the myenteric plexus?
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controls motility along length of gut
increases contraction length, intensity, frequency, and the velocity of peristaltic waves decreases tension of sphincters (pyloric and ileocecal) |
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what are the functions of the submucosal plexus?
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controls local secretion
controls local absorption controls motility of submucosa controls local blood flow |
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what are the neurotransmitters of the myenteric plexus?
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acetylcholine (excitatory)
norepinephrine (inhibitory) |
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what peptide transmitters can be present in both the myenteric and submucosal plexuses?
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ATP
serotonin dopamine CCK substance P VIP somatostatin Leu- and Met- enkephalins bombesin |
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what are the functions of vasoactive intestinal peptide (VIP)?
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causes relaxation of gut and vascular smooth muscle
stimulates intestinal and pancreatic bicarb secretion inhibits gastric secretion |
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what is a VIPoma?
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a rare tumor of pancreatic islet cells which secretes VIP at high rates and causes serious watery diarrhea
leads to hypokalemia and dehydration |
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what are the functions of gastrin releasing peptide?
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aka bombesin
causes release of gastrin from G-cells in stomach regulates non-GI functions like circadian rhythms, stress, etc. |
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what enteric peptide transmitter is implicated in some human cancer formation?
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gastrin releasing peptide (aka bombesin)
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what are the functions of enkephalins in the enteric nervous system?
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inhibits intestinal motility and secretion
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from what part of the spinal cord does the sympathetic portion of the enteric nervous system arise?
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T1-L3
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from what part of the spinal cord does the parasympathetic portion of the enteric nervous system arise?
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cervical and sacral levels
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to what do the apical GI endocrine cells respond?
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chemicals
stretch neurotransmitters |
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what are the functions of the basal GI endocrine cells?
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exocytosis of peptides from secretory granules
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what determines the interaction of gastrin-CCK hormones with their receptors?
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all hormones in the family interact with all receptors in the family, but with increased affinity for their own receptors
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what hormones are in the same family as gastrin?
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CCK
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what hormones are in the same family as secretin?
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VIP
GIP glucagon |
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what are the isoforms of gastrin?
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G-17 (little gastrin) - main form in response to a meal
G-34 (big gastrin) - main form during interdigestive phase G-14 (mini gastrin) G-4 - smallest form with activity |
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what is the main isoform of gastrin released in response to a meal?
what is its half-life? |
G-17 (little gastrin)
3-6 minutes |
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what is the main isoform of gastrin released during interdigestive phase?
what is its half-life? |
G-34 (big gastrin)
15 minutes |
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what stimulates the secretion of gastrin?
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vagus nerve
distention of the stomach protein digestion products calcium, alcohol, coffee CNS (anticipation of meal, olfactory stimuli) |
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what inhibits the secretion of gastrin?
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somatostatin (H+ stimulates, N. vagus inhibits)
low pH (partly at 3.5, fully at 2) secretin |
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from what cells is gastrin released?
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G-cells of the antrum stomach submucosa
10% from the duodenum |
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what are the functions of gastrin?
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acid secretion
mucosal growth |
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what are the effects of hypergastrinemia?
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stimulates pancreatic, gallbladder and small intestinal secretions
stimulates acquired immunity in gut stimulates gastric and intestinal motility releases insulin inhibits gastric emptying |
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what is Zollinger-Ellison Syndrome?
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increased gastrin secretion caused by gastrin-secreting tumor in either the pancreas or small intestine
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what causes gnawing, burning pain in the abdomen in Zollinger Ellison Syndrome?
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ulcers
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what causes weight loss in patients with Zollinger Ellison syndrome?
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pH not optimal for digestion enzymes, so digestion and absorption is not complete
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what causes anemia in patients with Zollinger Ellison syndrome?
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intrinsic factor at unoptimal conditions, so B12 complexes don't stay together well and aren't absorbed
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what causes excess gas in patients with Zollinger-Ellison syndrome?
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bacteria thrive on the undigested food in the intestine and produce excess gas
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from where is CCK secreted?
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I cells of the mucosa of the duodenum and the jejunum
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what are the isoforms of CCK?
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CCK-33 - most common form (half-life of 5-7 minutes)
CCK-4 - induces panic states CCK-8 - stimulates and modifies appetite for food |
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what isoform of CCK is low in people with anorexia and/or bulimia?
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CCK-8
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what is the most common form of CCK?
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CCK-33
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what stimulates the secretion of CCK?
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digestion products of fat and protein
meals stimulate CCK secretions of gut and CNS simultaneously coffee phenylalanine secreted more with unsaturated fats than with saturated |
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what are the functions of CCK?
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SATIATES APPETITE
PANCREATIC ENZYME SECRETION BILE SECRETION inhibit gastric emptying increase pancreatic growth stimulates bicarb secretion to potentiate secretin |
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from what cells is secretin secreted?
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cells in upper small-intestinal mucosa
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what stimulates the secretion of secretin?
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contact with acidic chyme (pH < 4.5)
fatty acids |
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what are the functions of secretin?
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STIMULATES WATER AND ALKALI SECRETIONS FROM PANCREAS AND LIVER
STIMULATES HEPATIC DUCTS TO SECRETE BICARB INHIBITS GASTRIN RELEASE, SUPPRESSES GASTRIC ACIDS increases pancreatic growth |
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what is the only hormone whose secretion is stimulated by protein, carbohydrate, and lipids?
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GIP
gastric inhibitory peptide glucose-dependent insulinotropic peptide |
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by what cells is GIP secreted?
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K-cells in duodenum and jejunum
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what stimulates the secretion of GIP?
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glucose in upper small intestine
long-chain fatty acids certain amino acids |
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what inhibits the secretion of GIP?
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high levels of insulin or glucagon
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what are the functions of GIP?
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RELEASE OF INSULIN
inhibits gastrin release and acid secretion inhibits gastric and intestinal motility |
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what is the definition of enterogastrone?
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released from intestinal mucosa by acid, fat, or hyperosmolarity and carried to the stomach where it acts to inhibit gastric acid secretion or gastric motility
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pancreatic polypeptide
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produced by pancreatic islet cells and endocrine cells
released most potently by protein digestion products, vagal stimulation, ACh negative feedback regulator for pancreatic secretion |
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enteroglucagon
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secreted by intestinal mucosal cells of colon
secretion stimulated by intraluminal glucose and fat same effects as glucagon, but less potent might inhibit gastrin release and gastric acid secretion |
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motilin
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primarily secreted in duodenum
physiologic stimuli not known initiates migrating motor complex (MMC) |
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what are GI paracrines?
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secreted into the interstitial fluid and diffuse to adjacent cells
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what is octreotide?
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analogue of somatostatin
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from what cells is somatostatin secreted?
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D-cells in the gastric mucosa
also many other cells in small and large intestines also released by myenteric plexus |
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what are the functions of somatostatin?
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SUPPRESSES GASTRIC SECRETIONS
INHIBITS RELEASE OF ALL KNOWN GI HORMONES inhibits motility and tone of stomach and small intestines, and gall bladder inhibits formation of liver bile, but not bilirubin inhibits saliva, gastric, pancreatic, small intestinal, and liver secretions inhibits splanchnic blood flow inhibits intestinal absorbption in brain, inhibits GH release in pancreas, inhibits insulin and glucagon release |
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what are the important facts about CCK?
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major production site - I cells in mucosa of duodenum and jejunum
major stimulator for release - fatty acids major function - decrease gallbladder contractility; decrease stomach motility; decrease gastric juice pH |
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what are the important facts about secretin?
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major production site - S cells of mucosa of duodenum
major release stimulator - acidic juice from stomach major function - decrease gallbladder contractility; decrease GI tract motility; stimulate pancreatic juice (low in enzymes, high in alkalinity) |
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what are the important facts about GIP?
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major production site - mucosa of upper small intestine
major release stimulator - glucose, fatty acids, amino acids major function - decrease stomach motility; decrease gastric secretion |
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what are the important facts about gastrin?
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major production site - gastric mucosa
major release stimulator - proteins; vagus nerve, stomach stretch major function - secretion of gastric juice |
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what are the functions of GI motility?
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transport ingested food through digestive tract
facilitates mixing of food with digestive secretion regulates transport rate prevents reflux of material |
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what is the law of the gut?
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The Law of the Gut states "The peristaltic wave of gastrointestinal smooth muscle contraction begins at the oral end and moves to the anal end"
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what is the sphincter between the mouth and the esophagus?
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upper esophageal sphincter
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what is the sphincter between the esophagus and the stomach?
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lower esophageal sphincter
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what is the sphincter between the stomach and the small intestine?
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pyloric sphincter
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what is the sphincter between the small intestine and the large intestine?
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ileocecal sphincter
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what is the sphincter betwee the large intestine and the outside?
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internal and external anal sphincters
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what is peristalsis?
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propulsive in esophagus and stomach
propulsive and mixing function in small intestine involves circular and longitudinal muscle layers |
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what is rhythmic segmentation?
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mixing function in small and large intestine
involves circular muscle |
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what is tonic contraction?
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present in gastrointestinal sphincters
separates and blocks passage of food involves smooth muscle latch bridges |
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how long is the digestive phase?
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3-4 hours after meals
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what is mastication?
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mechanical digestion in mouth by chewing large food pieces
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what is deglutition?
what are the stages? |
swallowing
oral stage pharyngeal stage esophageal stage |
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what initiates primary peristalsis?
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swallowing (voluntary act)
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what initiates secondary peristalsis?
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mechanoreceptors
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what is dysphagia?
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difficulty in swallowing caused by failure of normal peristalsis
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what is nutcracker esophagus?
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abnormally high peristalsis
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what is achalasia?
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degeneration of enteric NS, which causes weak smooth muscle contractions and increased LES tone (less inhibitory input)
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what hormones increase LES tone?
what hormones inhibit LES tone? |
increase - gastrin, motilin
inhibit - CCK, VIP, progesterone |
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what is gastroesophageal reflux disease (GERD)?
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reflux esophagitis
heartburn incompetence of LES allows reflux of acidic gastric contents leading to irritation of esophagus |
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what are the potential treatments for GERD?
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lifestyle changes
foaming agents that form a barrier on top of stomach histamine-2 antagonists proton-pump inhibitors drugs that increase LES strength motility drugs that quicken gastric emptying |
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where is the vomiting area of the brain?
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area postrema in the medulla oblongata
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what are the indications that someone will vomit?
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large pupils
paleness secretion of saliva sweat |
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what happens during vomiting?
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stomach, GI, and pyloric sphincter all relaxed
glottis and uvula closed to prevent chyme entering airways decreased intrathoracic pressure and contraction of abdominal muscles compress stomach retching causes build up of pressure |
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what is caused by excess vomiting?
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losses of secreted fluids and acids -> dehydration
decreased fluids decrease plasma volume -> circulation loss of potassium -> hypokalemia loss of H+ and Cl- -> hopochloremic metabolic alkalosis |
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what is controlled by the tonic contractions and gastric accomodation?
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storage of food
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what is regulated by peristalsis, retropulsion, and grinding in the stomach?
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emptying of food
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what is the orad stomach?
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top third of the stomach
(fundus and superior part of the body of the stomach) |
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what is the distal stomach?
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lower two-thirds of the stomach
(lower part of the body of the stomach and antrum of stomach) |
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what controls receptive relaxation (gastric accomodation)?
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vagus nerve
inhibitory motor neurons VIP |
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what is the purpose of gastric accomodation?
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aka receptive relaxation
allows volume increase up to 1.5 liters with small intragastric pressure increases |
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what is important in the gastric motility of the orad stomach?
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receptive relaxation (aka gastric accomodation)
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what is important about the gastric motility of the corpus (body) of the stomach?
|
gastric action potentials originate spontaneously in the pacemaker cells with a frequency of 3/min
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what causes the leading and trailing contractions in the body of the stomach?
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leading - AP depolarization
trailing - AP plateau phase |
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what are the two types of modulation of gastric motility of the body of the stomach?
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nervous - ACh
humoral - gastrin |
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寒い
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さむい
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cold (top roof - middle plants - bottom ice)
p31 Rowley |
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what is important about the gastric motility of the distal stomach?
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peristaltic constrictor rings
grinding movements retropulsion |
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where do peristaltic constrictor rings get more intense?
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towards antrum
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what are the effects of the leading and tailing contractions?
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leading - pushes content forward and closes pyloric sphincter
tailing - pushes content against wall |
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why is controlled gastric emptying important?
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so that only the amount of food which can be handled by the small intestine is delivered
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how long does food stay in the stomach?
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solid - until it is suspended into 0.3mm particles (1-4 hrs)
water - 10-20 minutes indigestible food - moves out every 2 hours in interdigestive phase |
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how does acidity affect the rate of gastric emptying?
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as the pH gets lower than 7, the rate of emptying decreases
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how does tonicity affect gastric emptying?
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both hypertonic solutions and hypotonic solutions empty more slowly than isotonic solutions
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what causes delayed gastric emptying in 20-30% of diabetic patients?
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autonomic neuropathy
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what is dumping syndrome?
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rapid gastric emptying caused by resection of the distal stomach
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how does gastric emptying relate to vagal activity?
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not directly related to excessive or diminished activity, but rather with altered vagus activity
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what factors delay gastric emptying?
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altered ENS
fat via CCK H+ via ENS |
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what are the symptoms of delayed gastric emptying?
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belching
vomiting |
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what are the symptoms of increased gastric emptying?
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abdominal cramping
diarrhea vasomotor changes pallor rapid pulse perspiration syncope |
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what symptoms are shared between delayed and increased gastric emptying?
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early satiety
feeling of fullness epigastric pain nausea heartburn anorexia weight loss |
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what is late dumping?
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increased gastric emptying 1-3 hours after food intake
presents with cramps, diarrhea, rapid pulse, perspiration, syncope |
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what are hunger contractions?
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reflectory contractions of the stomach several hours after stomach is emptied
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what is MMC?
|
aka migrating motor complex
waves of activity that sweep through the intestines in a regular cycle during fasting state roughly every 75–90 minutes during the interdigestive phase (help trigger peristaltic waves which facilitate transportation of indigestible substances such as bone, fiber and foreign bodies from the stomach, through the small intestine past the ileocecal sphincter into the colon) |
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what is the major trigger for peristaltic contractions in the digestive state?
|
stretching of the wall by chyme
controlled by neuronal patterns in enteric nervous system |
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|
|
what is the enterogastric reflex?
|
decreased gastric motility and gastric emptying protecting the intestine from excessive acidity
|
|
|
|
what is the ileocecal reflex?
|
increased motility of the ileum allowing chyme to pass from ileum to cecum
|
|
|
|
what are the gastroileal and gastrocolic reflexes?
|
distention of the stomach increases downstream motility
|
|
|
|
what is is power propulsion?
|
giant migrating contractions, independent of slow wave rhythm, excited by possibly harmful substances
last 18-20 seconds (vel 1 cm/sec) |
|
|
|
what are the motions associated with the ascending colon?
|
peristaltic propulsive movements which continue power propulsion from ileum
filling without large increases in pressure |
|
|
|
what movements are associated with the transverse colon?
|
haustration
mass movements |
|
|
|
what is haustration?
|
mixing without movement (water absorption), which compacts and very slowly moves the chyme forward
found in transverse colon |
|
|
|
what are mass movements?
|
mass peristalsis, power contraction, and propulsion
found in transverse colon and descending colon |
|
|
|
what movements are associated with the descending colon?
|
mass movements to finally expel feces
|
|
|
|
barium enema study
|
500-1500 mL fluid barium sulfate introduced through rectal tube
series of x-ray images captured to follow flow of barium typically 30-60 minute procedure |
|
|
|
what is the effect of reflex control on the internal anal sphincter?
on the external anal sphincter? |
neg. on internal
pos. on external |
|
|
|
what is the effect of voluntary control on the internal anal sphincter?
on the external anal sphincter? |
no effect on internal
neg. on external |
|
|
|
from where does reflex control of defecation arise?
|
mass movements through descending colon -> rectal distention -> reflex control
|
|
|
|
what is the composition of feces?
|
0.76 - water
0.24 - epithelium, bacteria, food rests |
|
|
|
what is Hirschsprung's Disease?
|
aka aganglionic megacolon
loss of enteric ganglia in terminal region of the large intestine (enlarged colon) absence of inhibitory neurons (permanent contractions) absence of rectoanal reflex (difficulty or failure of defecation) usually identified at childhood treatment is surgical removal of affected section |
|
|
|
out of the 7-10 L in total GI secretions, how much is lost in feces?
which secretions are made in the highest volume? |
0.1 L
gastric juice (1-3L) pancreatic juice (2L) intestinal secretions (2L) |
|
|
|
what is mucus composed of?
|
water
electrolytes glycoproteins |
|
|
|
what are the adherent qualities of mucus?
|
glues food and feces together
|
|
|
|
what are the coating qualities of mucus?
|
coats wall of gut and food particles
|
|
|
|
how does mucus protect the gut wall?
|
resistant to digestion enzymes
buffers acid or alkali |
|
|
|
what is caused by mumps?
|
swelling of the parotids caused by a viral infection
|
|
|
|
what type of saliva is produced by each of the salivary glands?
|
parotids - serous saliva, rich in enzymes (20%)
submandibular - serous and mucous (70%) sublingual - mucous (5%) small bucal glands - antibacterial fcn (<5%) |
|
|
|
what part of saliva is responsible for washing away and enzymatically attacking bacteria?
|
thiocyanates
lysozymes |
|
|
|
what part of saliva is responsible for destruction of bacteria?
|
IgA antibodies
|
|
|
|
what part of saliva is responsible for moistening and lubricating mouth and food?
|
mucin
H2O alkaline electrolytes |
|
|
|
what part of saliva is responsible for early metabolism of carbohydrates?
|
ptylain
(aka alpha amylase) |
|
|
|
what part of saliva is responsible for early metabolism of fat?
|
lingual lipase
|
|
|
|
what substances does ptylain digest?
|
(aka alpha amylase)
carbohydrates |
|
|
|
what is the function of kallikrein?
|
enzyme that produces bradykinin from kininogen
kininogen causes vasodilation to increase blood flow |
|
|
|
how much of saliva is water?
how much is protein and electrolytes? |
99.5% water
0.5% protein and electrolytes |
|
|
|
compared to plasma, which ions are found in higher/lower concentration in saliva?
|
less - Na, Cl
more K, HCO3 |
|
|
|
describe the tonicity of saliva compared to plasma
|
always hypotonic (though osmolarity increases with increasing flow rate)
|
|
|
|
describe the pH of saliva
|
slightly acidic at rest
slightly basic at maximal flow rate through the salivary glands |
|
|
|
what is the mechanism of saliva secretion?
|
primary secretion by acini is isotonic
modulation in glandular ducts |
|
|
|
how is saliva modified in the glandular ducts?
|
at low flow rates (0.1mL/min), large quantities of K are actively secreted, and large quanitites of Na are actively absorbed (Cl absorption is coupled to HCO3 secretion)
at high flow rates (4mL/min) saliva resembles primary saliva |
|
|
|
what is the transporter for Na in the glandular ducts of the salivary glands?
|
Na-H exchanger
|
|
|
|
what is the bicarb transporter in the glandular ducts of the salivary glands?
|
Cl-HCO3 exchanger
(Cl is passively absorbed and HCO3 is secreted) |
|
|
|
what is the K transporter in the glandular ducts of the salivary glands?
|
H-K exchanger
|
|
|
|
how does satiety control saliva secretion?
|
satiety (+)-> PS nervous system (+)-> acetylcholine (+)-> mAChR (+)-> IP3, DAG (+)-> salivary secretion
|
|
|
|
how does stress control saliva secretion?
|
stress (+)-> S nervous system (+)-> norepi (+)-> beta-adrenergic receptor (+)-> cAMP (+)-> salivary secretion
stress (-)-> PS nervous system, which decreases salivary secretion |
|
|
|
to what stimuli do salivary secretions increase?
|
taste
tactile stimuli from mouth, tongue, pharynx stimulation of higher nervous centers (imagination of food, hunger) reflexes of stomach and upper intestine excited by irritating food |
|
|
|
what is caused by excessive salivary secretion?
|
though it is rare, excessive salivary secretion causes hypokalemia and paralysis
|
|
|
|
what is caused by diminished salivary secretion?
|
ulceration
infections caries |
|
|
|
what is secreted in the esophagus?
where? |
mucus
simple and compound glands in the distal esophagus |
|
|
|
what are the three types of gastric glands?
where are they? what do they secrete? |
cardiac gland - close to where esophagus joins stomach - mucus
oxyntic (gastric) gland - fundus and corpus - acid, pepsinogen, mucus, intrinsic factor pyloric gland - pyloric portion of stomach - gastrin, mucus, pepsinogen, somatostatin |
|
|
|
what is secreted by cardiac glands in the stomach?
|
mucus
|
|
|
|
what is secreted by oxyntic (gastric) glands?
|
from deep to superficial:
chief cells - pepsinogen parietal cells - HCl, intrinsic factor neck cells - mucus |
|
|
|
what is secreted by pyloric glands in the stomach?
|
G-cells - gastrin
mucus some pepsinogen D-cells - somatostatin |
|
|
|
what is the pH of gastric juice? why?
|
2-3
HCl has a pH of 0.8, but the buffer capacity of proteins increases the pH |
|
|
|
how is gastric acid secreted?
|
in the lower reaches of gastric glands are the parietal (oxyntic) cells
microvilli, mitochondria, intracellular canaliculi, tubulovesicular membranes apical membrane can be internalized upon fasting and returned upon digestion |
|
|
|
what stimulates the secretion of gastric acid?
what are the receptors involved? |
histamine - H2 receptor
gastrin - CCKB receptor ACh - M3 receptor each binds its own receptor and stimulates some secretion, but all must bind simultaneously to result in sufficient acid release |
|
|
|
how does histamine affect gastric acid secretion?
|
stimulates via H2 receptor, which activates adenylate cyclase, which makes cAMP, which activates gastric hydrogen ion pump
|
|
|
|
how does gastrin stimulate gastric acid secretion?
|
binds CCKB receptor, which releases IP3, which causes intracellular concentrations of calcium to increase, which activates gastricric hydrogen ion pump
|
|
|
|
how does acetylcholine stimulate gastric acid secretion?
|
binds M3 receptor, which releases IP3, which causes intracellular concentrations of calcium to increase, which activates gastricric hydrogen ion pump
|
|
|
|
what peptide potentiates the acid secreting ability of acetylcholine and gastrin?
|
histamine
|
|
|
|
what are the phases of gastric secretion?
what is stimulated by each? |
cephalic phase (30%) - acid release from parietal cells
gastric phase (60%) - acid release from parietal cells intestinal phase (10%) - gastrin release from duodenal G-cells |
|
|
|
what are the triggers for the cephalic phase of gastric secretion?
|
conditioned reflexes
taste smell chewing swallowing hypoglycemia |
|
|
|
what are the triggers for the gastric phase of gastric secretion?
|
vagus nerve
distension amino acids peptides alcohol caffeine |
|
|
|
what are the triggers for the intestinal phase of gastric secretion?
|
peptides and AA in duodenum
|
|
|
|
what are the inhibitors of gastric acid secretion?
|
H+
somatostatin prostaglandins secretin food components (esp. fatty acids) |
|
|
|
how does H+ inhibit gastric acid secretion?
|
negative feedback when buffering capacity of food is eliminated
|
|
|
|
how does somatostatin inhibit gastric acid secretion?
|
directly, as well as indirectly by inhibiting gastrin and histamine release
|
|
|
|
how do prostaglandins inhibit gastric acid secretion?
|
directly, as well as indirectly by inhibiting histamine action
|
|
|
|
how does secretin inhibit gastric acid secretion?
|
released by acid in duodenum, it inhibits gastrin and other enterogastrones
|
|
|
|
how do food components, like fatty acids, inhibit gastric acid secretion?
|
stimulate inhibitory nervous reflexes and activate some hormones, like secretin
|
|
|
|
what is peptic ulcer disease?
|
sore in the mucous membrane
|
|
|
|
how does stress and lifestyle trigger peptic ulcer disease?
|
GI vasoconstriction
diminished mucous secretions exacerbated by smoking, alcohol, NSAIDs |
|
|
|
how does helicobacter pylori trigger peptic ulcer disease?
|
H.p. releases urease, which converts urea to CO2 and NH4
NH4 neutralizes acid and generates environment to grow immune system fights infection causing further local damage mucous secretions diminish over time |
|
|
|
what is the diagnostic test for helicobacter pylori-created peptic ulcer disease?
|
radioactive exhaled CO2 after swallowing a urea load
|
|
|
|
what are the symptoms of a gastric ulcer?
|
nausea
anorexia vomiting (blood) epigastric pain anemia black, tarry stools stomach acidity is not diagnostic (normal or low) |
|
|
|
what is the gastrin profile like in a patient with duodenal ulcer?
|
baseline gastrin normal, gut gastrin secretion in response to a meal is increased
|
|
|
|
by what cells is pepsinogen secreted?
|
peptic (chief) cells
some mucous cells some parietal cells |
|
|
|
by what is pepsinogen converted to pepsin?
|
HCl and previously secreted pepsin
|
|
|
|
at what pH does pepsin have optimal activity?
|
1.8-3.5
(inactivated in duodenum) |
|
|
|
by what is pepsinogen secretion stimulated?
|
ACh release and stomach acid
|
|
|
|
for what is intrinsic factor important?
|
absorption of B12 in ileum
|
|
|
|
by what cells is intrinsic factor secreted?
|
parietal cells
|
|
|
|
what is caused by chronic and autoimmune gastritis?
|
pernicious anemia
autoimmune attack against parietal cells (most common) loss of parietal cells due to severe gastritis (less common) |
|
|
|
where is vitamin B12 stored for months or sometimes years?
|
liver
|
|
|
|
what is secreted by acinar cells of the pancreas?
|
digestive enzyme
|
|
|
|
what stimulates acinar cells of the pancreas?
|
CCK
|
|
|
|
what is secreted by pancreatic cells lining intra- and extralobular ducts?
|
bicarb-rich fluid
|
|
|
|
what stimulates pancreatic cells lining intra- and extralobular ducts?
|
secretin
|
|
|
|
what part of the ANS stimulates pancreatic secretion?
what part of the ANS inhibits pancreatic secretion? |
parasympathetic stimulates
sympathetic inhibits |
|
|
|
what is the tonicity of pancreatic juice?
|
isotonic
|
|
|
|
what are the enzymatic components of pancreatic juice responsible for the digestion of proteins?
|
proteases (trypsin, chymotrypsin, peptidases) - specific for breaking peptides
elastases - digest collagen molecules of connective tissue |
|
|
|
what enzymes are responsible for specific breaking of peptides?
|
proteases
(trypsin, chymotrypsin, peptidases) |
|
|
|
what enzymes are responsible for digesting collagen molecules of connective tissue?
|
elastases
|
|
|
|
what are the enzymatic components of pancreatic juice responsible for the digestion of lipids?
|
lipases - degrade TAGs into FAs and glycerol
phospholipases - reduce PLs to FAs cholesterol ester hydrolase |
|
|
|
what enzymes degrade triglycerides into fatty acids and glycerol?
|
lipases
|
|
|
|
what enzymes reduce phospholipids to fatty acids?
|
phospholipases
|
|
|
|
what enzymatic components of pancreatic juice are responsible for digesting carbohydrates?
|
pancreatic amylases - digest most carbohydrates, but not cellulose
|
|
|
|
what enzymatic components of pancreatic juice are responsible for digesting nucleic acids?
|
nucleases - hydrolyze DNA & RNA to their components
|
|
|
|
how does the pancreas protect itself against destructive enzymes?
|
enzymes secreted in active form don't attack membranes
enzymes that attack membranes are secreted as zymogens, that are later converted to their active forms produces intracellular trypsin inhibitor |
|
|
|
what are zymogens?
|
inactive precursors for enzymes
|
|
|
|
what is the function of enterokinase?
|
activates trypsin, by cleaving it from trypsinogen
|
|
|
|
where is enterokinase produced?
|
small intestinal epithelia
|
|
|
|
how are pancreatic enzymes activated?
|
trypsinogen is converted to trypsin by enterokinase in the small intestine
trypsin then converts most other enzymes to their active forms |
|
|
|
what is a tide?
|
physiological variation or increase of a certain constituent in body fluids
|
|
|
|
what is an acid tide?
|
temporary increase in acidity in the blood caused by production of bicarb in the pancreas
|
|
|
|
what is a bicarb tide?
|
temporary increase in bicarb in the blood caused by formation of acid in the stomach after a meal
|
|
|
|
what are the hormones that regulate pancreatic secretion?
|
acetylcholine
cholecystokinin secretin VIP GRP |
|
|
|
to what receptor on secretory pancreatic cells does CCK bind?
|
CCKA
|
|
|
|
what happens in the cephalic and gastric phase of pancreatic secretion?
|
nervous input from the vagus signals gastrin release from stomach, which initiates pancreatic secretion
also has direct input to the secretory pancreatic cells, initiating pancreatic secretion |
|
|
|
what are the triggers for the intestinal phase of pancreatic secretion?
|
fatty acids, amino acids, peptides (via CCK)
acid (via secretin) neuronal |
|
|
|
how do fatty acids, amino acids, and peptides trigger the intestinal phase of pancreatic secretion?
|
trigger CCK release from I cells, which then triggers pancreatic secretion
|
|
|
|
how does acid trigger the intestinal phase of pancreatic secretion?
|
triggers secretin release from S cells which then triggers pancreatic secretion
|
|
|
|
what are the strongest amino acid triggers for the intestinal phase of pancreatic secretion?
|
Phe
Met Trp |
|
|
|
acute pancreatitis
|
inflammation of the pancreas
associated with edema, pancreatic autodigestion, necrosis, hemorrhage diagnosed by serum amylase and serum lipase (turbidity test) |
|
|
|
pancreas cancer
|
4th most common cause of cancer-related death in U.S.
5 year survival rate is only 1% about 30,000 new cases diagnosed each year in the U.S. average age at diagnosis is 65 years actual cause unknown, though smoking seems to be an important environmental factor |
|
|
|
what are the functions of the secretions of the small intestine?
|
neutralizes acid and adds pancreatic enzymes
|
|
|
|
what are crypts of lieberkuhn?
|
invaginations in villi of the small intestine projecting into submucosa
|
|
|
|
what are the major type of cells in the crypts of lieberkuhn?
|
absorptive cells
goblet cells are frequent enteroendocrine cells are infrequent |
|
|
|
where are the stem cells in the crypts of lieberkuhn?
|
lower end of the crypt
|
|
|
|
where are the paneth cells in the crypts of lieberkuhn?
what is their function? |
base of the crypt
produce and secrete enterokinase |
|
|
|
how are secretions from the small intestine stimulated?
|
cAMP stimulates Cl channels
chyme, and hormones (VIP, gastrin, secretin, CCK) vagal control |
|
|
|
what is the structure of the large intestine?
|
almost no villi
deep crypts everywhere except the rectum many goblet/mucous cells stem cells, some enteroendocrine cells, but no paneth cells |
|
|
|
how are large intestine secretions regulated?
|
tactile stimuli
local nervous reflexes parasympathetics (increase in motility and mucus secretion) |
|
|
|
approximately how much gas is excreted from an average person in a day?
|
about 600 mL
|
|
|
|
what are the odorous parts of excreted gas?
|
H2S and methylsulfide
(metabolic products of proteins) |
|
|
|
from where does excreted gas come?
|
swallowed air (2-3mL/bite)
enzymatic digestion (host or bacterial) diffusion out of blood |
|
|
|
what is indicated if hydrogen appears in the breath within 30 minutes after the ingestion of a standard sugar load?
|
heavy bacterial colonization
(diffuses out of pulmonary vessels) |
|
|
|
what is the primary site of fluid and solute absorption in the GI tract?
|
small intestine
(absorbs 85% of fluid and colon absorbs most of remaining 15%) |
|
|
|
where is most alcohol absorbed?
|
stomach
|
|
|
|
where are calcium and iron absorbed?
|
duodenum
|
|
|
|
where are water soluble vitamins absorbed?
|
duodenum
|
|
|
|
where is vitamin B12 absorbed?
|
ileum
|
|
|
|
where are most carbohydrates absorbed?
|
duodenum
|
|
|
|
where are proteins, lipids, sodium, water, and lipid-soluble vitamins absorbed?
|
throughout small intestine, proportional to concentration
(duodenum > jejunum > ileum) |
|
|
|
where are most bile salts absorbed?
|
ileum
|
|
|
|
how does the amount of carbohydrates absorbed in a day compare to the intestinal transport capacity?
|
absorbed: 200-300 g/day
capacity: 3.6 kg/day |
|
|
|
how much do the plica circularis increase the surface area of the intestine?
|
x3
|
|
|
|
what are plica circularis?
|
(aka folds of kerkring)
folds of mucosa and submucosa visible to the naked eye |
|
|
|
what are villi in the intestines?
|
projections of mucosa, but not submucosa
each contains an arteriole, venule, and lymph vessel (lacteal) |
|
|
|
how much do villi increase the surface area of the intestines?
|
x10
|
|
|
|
how much do microvilli (brush border) increase the surface area of the intestines?
|
x 20
|
|
|
|
what is the approximate total surface area increase of the intestinal mucosa, by the adaptations?
|
x600
|
|
|
|
what are lacteals?
|
lymphatic capillaries that absorb dietary fats in the villi of the small intestine
|
|
|
|
what mechanisms ensure proper absorption in the intestines?
|
rhythmic contractions of muscularis mucosae
movements of villi semipermeability of cell-cell tight junctions large surface area permanent mitosis and renewing of cells safety factor high blood supply transepithelial potential |
|
|
|
what is the transepithelial potential of the intestines?
|
voltage across the epithelium of the intestines
positive on side of serosa, compared to lumen |
|
|
|
how is starch digested?
|
salivary amylase during chewing (inactivated by acid in stomach)
pancreatic amylases (-> maltose and isomaltose) brush border maltases (-> glucose) |
|
|
|
what is the difference between amylose and amylopectin?
|
amylose is a straight chain of glucose molecules
amylopectin is a branched chain of glucose molecules both make up starch |
|
|
|
what are the break-down products of starch after exposure to salivary or pancreatic alpha-amylase?
|
maltotriose
alpha-Limit dextrins maltose |
|
|
|
what is trehalose?
|
a sugar in fungi, plants, and invertebrates
|
|
|
|
how is sucrose digested?
|
enzyme: sucrase
sucrose -> glucose and fructose |
|
|
|
how is lactose digested?
|
enzyme: lactase
lactose -> glucose and galactose |
|
|
|
how is trehalose digested?
|
enzyme: trehalase
trehalose -> glucose |
|
|
|
how are glucose and galactose transported into enterocytes?
|
secondary active transport via the Na-glucose cotransporter (SGLT1)
|
|
|
|
how is fructose transported into enterocytes?
|
facilitated diffusion via GLUT5
|
|
|
|
how do all sugars enter the blood (from enterocytes)?
|
diffusion and Na-independent facilitated transport via GLUT2
|
|
|
|
what are the two intestinal carbohydrate malabsorption syndromes?
|
lactose intolerance (50% of population)
sucrose-isomaltose deficiency (rare) |
|
|
|
lactose intolerance
|
50% of population
disaccharides remain undigested in gut lumen water accumulates (osmotic diarrhea) colon bacteria utilize sugars to produce lactic acid and gas symptoms: bloating, increased motility, pain treatment: avoidance of dairy products, lactase pills |
|
|
|
sucrose-isomaltose deficiency
|
rare (10% of Greenland Eskimos)
autosomal recessive disorder treatment: low sucrose diet |
|
|
|
what is the advantage of lipids over carbohydrates and proteins as energy stores?
|
lipid oxidation provides 38kJ of energy per gram
energy provided is over twice the amount of carbohydrates or proteins |
|
|
|
what are the dietary fats?
|
saturated - solid at room temp
polyunsaturated - liquid at room temp cholesterol - animal products |
|
|
|
what is the optimal pH for lingual lipase?
|
4-5 (but it still works in the stomach)
|
|
|
|
what are the three types of lipases?
|
lingual lipase
gastric lipase pancreatic lipase |
|
|
|
which lipase is important for babies before their pancreatic function matures?
|
lingual lipase
|
|
|
|
how is fat emulsified in the stomach?
|
free fatty acids, together with proteins
|
|
|
|
what is the most important lipase?
|
pancreatic lipase
(most important and highest amount) |
|
|
|
how does orlistat (Xenical) work?
|
anti-obesity drug
inhibits pancreatic lipase |
|
|
|
how are fats digested?
|
broken down to free fatty acids, mono-, di-, and triglycerides and then absorbed
|
|
|
|
what is lecithin?
|
phosphatidylcholine
|
|
|
|
through what do bile salts enter the small intestine?
|
spincter of Oddi
|
|
|
|
what are mixed micelles?
|
micelles of bile salts with lipid digestion products incorporated into them
|
|
|
|
what is the main limiting factor of lipid uptake?
|
time for diffusion through the unstirred water layer
|
|
|
|
what happens to fatty acids and monoglycerides at the enterocytes?
|
diffuse into enterocytes
in cytoplasm, re-synthesized into triglycerides and phospholipids |
|
|
|
where are triacylglycerol synthetic enzymes located in the enterocytes?
|
endoplasmic reticulum
|
|
|
|
what forms the stabilizing surface monolayer of chylomicrons?
|
apolipoproteins
phospholipid cholesterol |
|
|
|
what forms the core of chylomicrons?
|
triglycerides
cholesterol esters trace lipids (vitamins) |
|
|
|
how do chylomicrons exit enterocytes?
|
exocytosis
(phospholipid bilayer from ER surrounds chylomicrons and docks on cell membrane, releasing chylomicron into lymph) |
|
|
|
where do chylomicrons enter the blood stream?
|
left subclavian vein
|
|
|
|
from where do chylomicrons acquire various apolipoproteins?
|
HDLs
|
|
|
|
how are proteins digested by the stomach?
|
acid and 3 isoforms of pepsin convert proteins to peptides
|
|
|
|
how are proteins digested in the duodenum and upper jejunum?
|
pancreatic enzyme endopeptidases (trypsin, chymotrypsin, elastase) and exopeptidases (carboxypolypeptidase A, B)
|
|
|
|
which protein byproducts are most highly absorbed by enterocytes?
which are most highly secreted by enterocytes? |
tripeptides and dipeptides > amino acids
amino acids > dipeptides and tripeptides |
|
|
|
what is neutral brush border (NBB) transporter?
|
in brush border of small intestine, Na-dependent transporter of neutral amino acids
|
|
|
|
what is IMINO?
|
in brush border of small intestine, a Na-dependent transporter of proline and hydroxyproline
|
|
|
|
what is PHE transporter?
|
in brush border of small intestine, a Na-dependent transporter of phenylalanine and methionine
|
|
|
|
what is Dicarboxyl trasnsporter?
|
in brush border of small intestine, a Na-dependent transporter of aspartate and glutamate
|
|
|
|
what is Y+ transporter?
|
in brush border of small intestine, a Na-independent transporter of basic amino acids such as arginine and lysine
|
|
|
|
what is L transporter?
|
in brush border of small intestine, a Na-independent transporter of neutral amino acids with hydrophobic chains
|
|
|
|
what is the function of intracellular peptidase?
|
further digests peptides to amino acids
|
|
|
|
what is A transporter?
|
on the basolateral side of enterocytes, a Na-dependent transporter of small hydrophobic amino acids
|
|
|
|
what is ASC transporter?
|
on the basolateral side of enterocytes, a Na-dependent transporter of small neutral amino acids
|
|
|
|
what is L transporter?
|
on the basolateral side of enterocytes, a Na-dependent transporter of neutral hydrophobic amino acids
|
|
|
|
what are the fat-soluble vitamins?
|
A, D, E, K
|
|
|
|
how are fat soluble vitamins absorbed?
|
same mechanism as fat absorption
|
|
|
|
what are the water soluble vitamins?
|
C, B1, B6, B12, Niacin, Biotin, Folic acid
|
|
|
|
what are the important transport mechanisms for folate?
|
brush border enzyme and H+ gradient-dependent transporter
|
|
|
|
what is the largest and most complex of all vitamins?
|
B12
|
|
|
|
how is B12 released from food proteins?
|
cooking
acid of stomach |
|
|
|
what is R protein?
|
aka haptocorrin
product of the salivary glands which binds to B12 |
|
|
|
where is R protein proteolytically degraded from B12-R-IF complex?
|
intestine
|
|
|
|
where is the receptor for IF-B12 complex?
|
ileal enterocytes
(very slow receptor, 4-5 hrs) |
|
|
|
to what is B12 bound as it is transported through the body?
|
transcobalamin
|
|
|
|
pernicious anemia
|
lack of intrinsic factor causes inability to absorb B12
treatment by injection of IF |
|
|
|
how much dietary iron is absorbed per day?
|
0.5-1.0 of 20 mg
|
|
|
|
how is iron absorbed into enterocytes?
|
Divalent Metal Transporter carries Fe2+ faster than Fe3+
|
|
|
|
to what is iron bound inside enterocytes for storage?
|
ferritin
|
|
|
|
what is the transporter to move iron from enterocytes to the blood?
|
ferroportin
|
|
|
|
what inhibits ferroportin?
|
hepcidin
|
|
|
|
to what is iron bound in the blood?
|
transferrin
|
|
|
|
how is heme iron absorbed into enterocytes?
|
endocytosis
|
|
|
|
what are the values found in a serum iron profile?
|
iron - amount of iron bound to transferrin in blood
ferritin - storage form of excess iron total iron-binding capacity - amount of iron needed to bind to all transferrin transferrin - transferrin which is not bound to iron transferrin saturation - percentage of transferrin with iron bound to it |
|
|
|
what is the reference range for iron in a serum iron profile?
|
amount of iron bound to transferrin in blood
50-170 ug/dL SI: 9-30 umol/L |
|
|
|
what is the reference range for ferritin in a serum iron profile?
|
storage form of excess iron
150-200 ng/mL SI: 15-200 ug/L |
|
|
|
what is the reference range for total iron-binding capacity in a serum iron profile?
|
amount of iron needed to bind to all transferrin
252-479 ug/dL SI: 45-86 umol/L |
|
|
|
what is the reference range for transferrin in a serum iron profile?
|
transferrin which is not bound to iron
200-380 mg/dL SI: 2-3.8 g/L |
|
|
|
what is the reference range for transferrin saturation in a serum iron profile?
|
percentage of transferrin with iron bound to it
20-50% SI: 0.2-0.5 |
|
|
|
where is the main absorption of calcium?
how much is absorbed per day? |
duodenum (40% efficiency)
1g/day (half from diet) |
|
|
|
to what protein must calcium be bound to be absorbed by enterocytes?
|
either intestinal membrane protein (IMCal) or calcium-binding protein (CaBP)
|
|
|
|
how is calcium found inside enterocytes?
|
either bound to calcium binding proteins (calbindin) or stored in calcium storing organelles
|
|
|
|
by what transporters is calcium released into blood from enterocytes?
|
Ca-ATPase
Ca/Na exchanger |
|
|
|
how does Vitamin D facilitate calcium absorption?
|
as much as 4 times by regulating CaBP
|
|
|
|
what is caused by a vitamin D deficiency?
|
rickets in children
osteomalacia in adults |
|
|
|
to what does homing refer in GALT?
|
activated lymphocytes migrate over blood, proliferate in mesenteric lymph nodes, and are transported back to gut epithelium
|
|
|
|
IgA secreting plasma cells in lamina propria
|
B lymphocytes exposed to antigen in intestine, migrate to lymph, turn into plasma cells, enter vasculature and end up in lamina propria
some IgA passes through epithelial cells and is bound to luminal surface; most IgA enters circulation, is picked up by liver and secreted into bile |
|
|
|
what is Sprue?
|
aka celiac disease
lack of digestive enzyme that normally breaks down wheat protein gluten undigested gluten causes severe and chronic allergic responses of small intestine test for anti-gliadin antibody is diagnostic |
|
|
|
for what is a test for anti-gliadin antibody diagnostic?
|
celiac disease
(aka sprue) |
|
|
|
what is the mechanism of H2 blockers?
|
e.g. Cimetidine
block Histamine binding to H2 receptor, so that gastric acid is not secreted |
|
|
|
what effect do somatostatin and prostaglandins have on gastric acid secretion?
|
inhibitory
|
|
|
|
what is the effect of atropine on gastric acid secretion?
|
inhibits acetylcholine binding to M3 receptor, thereby inhibiting release of gastric acid
|
|
|
|
what are the functions of the liver?
|
metabolism
blood cleaning system blood reservoir formation of blood-clotting intermediates formation of bile |
|
|
|
what are Kupffer cells?
|
fixed macrophages in the liver
|
|
|
|
for storage of what is the liver responsible?
|
iron
vitamin A vitamin D vitamin B12 |
|
|
|
what is the path through the liver of blood from the GI tract?
|
portal vein
portal venules hepatic sinusoids central vein hepatic vein vena cava |
|
|
|
how much of the blood to the liver comes from systemic circulation?
how does it get to the liver? |
1/4 (25%)
hepatic artery |
|
|
|
what is the path of bile through the liver?
|
space of Disse
bile canaliculi canals of Herring biliary ductules bile ducts |
|
|
|
where is the majority of lymph made?
|
space of Disse
|
|
|
|
what are the five components of bile?
|
bile acids/salts (50%)
cholesterol (4%) phospholipids (40%) bile pigments (2%) bile proteins (4%) |
|
|
|
what is the main phospholipid found in bile?
|
lecithin (phosphatidylcholine)
|
|
|
|
what is the main bile pigment?
|
bilirubin (green color)
|
|
|
|
what are the main types of proteins found in bile?
|
immunoglobulins
|
|
|
|
what are the functions of bile?
|
emulsification of lipids facilitating in their digestion
excretion of waste products (bilirubin, cholesterol) |
|
|
|
through what opening do both the pancreatic and common bile ducts open into the duodenum?
|
sphincter of Oddi
|
|
|
|
what is a synonym for a conjugated bile acid?
|
bile salt
|
|
|
|
where and how does the conversion from a primary to a secondary bile acid occur?
|
in the colon
catalyzed by bacteria |
|
|
|
what is the secondary bile acid of Cholic acid?
|
Deoxycholic acid
|
|
|
|
what is the secondary bile acid of Chenodeoxycholic acid?
|
Lithocholic acid
|
|
|
|
what is the advantage of conjugating bile acids?
what is the disadvantage? |
makes them more water soluble
requires a lot of energy |
|
|
|
with what bile acids does glycine conjugate?
|
primary - cholic acid, chenodeoxycholic acid
secondary - deoxycholic acid, lithocholic acid |
|
|
|
with what bile acids does taurine conjugate?
|
primary - cholic acid, chenodeoxycholic acid
secondary - deoxycholic acid, lithocholic acid |
|
|
|
with what two amino acids do bile acids mainly conjugate?
|
taurine
glycine |
|
|
|
where does conjugation of bile acids occur?
|
hepatocytes
|
|
|
|
what quality of bile salts allows them to emulsify fatty acids and cholesterol?
|
amphipathic character
(having both hydrophobic and hydrophillic character) |
|
|
|
how are conjugated bile acids transported into hepatocytes from the space of Disse?
|
Na+ cotransport
Na+ independent transport Diffusion |
|
|
|
how are unconjugated bile acids transported into hepatocytes from the space of Disse?
|
Bile acid-anion exchange
exchanges unconjugated bile acids for bicarb and hydroxide ions |
|
|
|
what is absorbed from primary bile as it moves through the bile duct?
(concentrations decrease) |
glucose
amino acids secondary solutes |
|
|
|
what is secreted into primary bile as it moves through the bile duct?
(concentrations increase) |
water
inorganic ions (HCO3) |
|
|
|
what hormone increases the secretion of water and inorganic ions (bicarb) into primary bile in the bile duct?
|
secretin
|
|
|
|
what hormone decreases the secretion of water and inorganic ions (bicarb) into primary bile in the bile duct?
|
somatostatin
|
|
|
|
what is the effect on water of modification in the gallbladder?
|
decreases concentration of water
|
|
|
|
what is the effect on bile salts of bile modification in the gallbladder?
|
increases bile salt concentration
|
|
|
|
what is the effect on bilirubin of bile modification in the gallbladder?
|
increases bilirubin concentration
|
|
|
|
what is the effect on cholesterol of bile modification in the gallbladder?
|
increases cholesterol concentration
|
|
|
|
what is the effect on fatty acid concentration of bile modification in the gallbladder?
|
increases fatty acid concentration
|
|
|
|
what is the effect on lecithin concentration of bile modification in the gallbladder?
|
increases lecithin concentration
|
|
|
|
what is the effect on ion concentration of bile modification in the gallbladder?
|
Na - decreases concentration
K - increases concentration Ca - increases concentration Cl - decreases concentration HCO3 - decreases concentration |
|
|
|
what is the effect of vagus nerve innervation on bile acid?
|
increases synthesis and secretion in the cephalic and gastric phases
|
|
|
|
what is the effect of cholecystokinin (CCK) on bile acid?
|
increases synthesis and secretion in the intestinal phase
|
|
|
|
what is the effect of bile acids in the portal vein on bile acid synthesis and secretion?
|
decreases synthesis
increases secretion |
|
|
|
what causes relaxation of the sphincter of oddi?
|
CCK
peristaltic waves of gall bladder peristaltic waves of duodenum |
|
|
|
what is the site of 90% of absorption of bile acids?
by what mechanism? |
lower ileum
secondary active transport |
|
|
|
what happens to the 10% of bile acids that aren't absorbed by the lower ileum?
|
escape into colon
deconjugated and dehydroxylated primary bile acids are transformed into secondary bile acids |
|
|
|
what bile acids are are absorbed in the colon?
|
50% of deoxycholic acid absorption
NO lithocholic acid absorption |
|
|
|
what is the only thing that is recycled in the enterohepatic circulation?
|
only bile acids
|
|
|
|
how are bile acids transported to the liver?
how many are extracted? |
bound to albumin
70-90% |
|
|
|
what does the liver do to recycled bile acids before it releases them again?
|
rehydroxylates and reconjugates them
|
|
|
|
how many times does the pool of bile acids circulate in a normal meal?
in a greasy meal? |
twice
up to six times |
|
|
|
what is the major excretory route for substances which cannot be eliminated in the urine?
|
bile excretion in feces
|
|
|
|
what are the major substances that are excreted via bile?
|
sulfate, glucuronide or glutathione conjugates (drugs and sex steroids)
vitamins A, D, and E cholesterol bilirubin |
|
|
|
how are bile constituents excreted in the feces?
|
glucuronidated in the liver
no active intestinal absorption of glucuronide rapid fecal excretion |
|
|
|
by what are red blood cells broken down?
|
reticuloendothelial system
|
|
|
|
how is bilirubin carried to the liver?
|
bound to albumin
|
|
|
|
what is indirect bilirubin?
|
aka pre-hepatic bilirubin
aka free bilirubin aka unconjugated bilirubin the bilirubin directly from red blood cells, before it is conjugated to glucuronate |
|
|
|
what is direct bilirubin?
|
aka post-hepatic bilirubin
aka conjugated bilirubin bilirubin that has been conjugated to glucuronate by the liver to make it more water-soluble |
|
|
|
what enzyme is utilized by the liver to conjugate bilirubin?
|
UDP glucuronyl transferase
conjugates glucuronate with bilirubin to make it more water soluble |
|
|
|
what happens to bilirubin in the intestine?
|
bacteria break it down to urobilinogen
urobilinogen is oxidized to urobilin and stereobilin for excretion in the feces |
|
|
|
what are the fates of urobilinogen?
|
oxidized to urobilin and stereobilin for excretion in the feces
absorbed by the intestine and liver for excretion in the urine |
|
|
|
do you expect conjugated or unconjugated bilirubin in the serum of a patient with Hemolysis that exceeds the capacity of the liver to clear released heme metabolites?
|
increase of unconjugated bilirubin in the bloodstream
|
|
|
|
do you expect conjugated or unconjugated bilirubin in the serum of a patient with a failure of bilirubin uptake by liver cells?
|
increase of unconjugated bilirubin in the bloodstream
|
|
|
|
do you expect conjugated or unconjugated bilirubin in the serum of a patient with an obstruction of bile flow?
|
initially, largely conjugated bilirubin into the blood stream
|
|
|
|
how does sodium move in the intestines?
|
jejunum - actively absorbed; enhanced by sugars and neutral amino acids
ileum - actively absorbed colon - actively absorbed |
|
|
|
how does potassium move in the intestines?
|
jejunum - passively absorbed when concentration rises because of absorption of water
ileum - passively absorbed colon - net secretion occurs when concentration in lumen is less than 25mM |
|
|
|
how does chloride move in the intestines?
|
jejunum - absorbed
ileum - absorbed, some in exchange for bicarb colon - absorbed, some in exchange for bicarb |
|
|
|
how does bicarb move in the intestines?
|
jejunum - absorbed
ileum - secreted, partly in exchange for chloride colon - secreted, partly in exchange for chloride |
|
|
|
by what general mechanisms are electrolytes absorbed in the intestines?
|
solvent drag
specific transport |
|
|
|
what is the major site for Na absorption?
|
jejunum
|
|
|
|
the mechanism for Na absorption in the jejunum is identical to what mechanism?
|
Na absorption in the proximal tubule of the kidney
|
|
|
|
what are the apical entry mechanisms for Na into the cells of the intestine?
|
Na/sugar cotransporter
Na/aa cotransporter Na/H countertransporter |
|
|
|
what is the basal exit mechanism for Na from intestinal epithelial cells?
|
Na-K-ATPase
|
|
|
|
what is the net electrolyte flux across the intestinal cells of the jejunum?
|
net NaHCO3 absorption
|
|
|
|
what is the net electrolyte flux across the intestinal cells of the ileum?
|
net NaCl absorption
|
|
|
|
what is different between the ileum and the jejunum?
|
ileum has the Na/H/Cl/HCO3 system
**instead of all bicarb moving into serum (like in jejunum) it is diverted toward HCO3/Cl countertransport, so that it is secreted |
|
|
|
what is caused by vomiting?
|
dehydration
metabolic alkalosis |
|
|
|
what is caused by diarrhea?
|
dehydration
metabolic acidosis |
|
|
|
what happens to body pH if someone has diarrhea?
|
hyperchloremic metabolic acidosis
**bicarb is moved down its concentration gradient (into intestinal lumen) which remains large because lumen is quickly emptied; serum bicarb concentration decreases, decreasing ability to buffer blood, and causing acidosis; chloride builds up in the serum as a result of the HCO3/Cl countertransport** |
|
|
|
what is the net flux in the colon?
|
Na absorption
K secretion |
|
|
|
what is the first step in increasing Na uptake in the colon?
|
aldosterone initiates Na uptake by increasing number of Na channels
increased Na absorption leads to apical K secretion |
|
|
|
how is sodium secreted at the basal side of colonic epithelial cells?
|
Na-K-ATPase
|
|
|
|
by what two mechanisms does potassium move across the basal side of the colonic epithelial cells?
|
Na-K-ATPase move potassium into the cells
facilitated K secretion |
|
|
|
what effect does diarrhea have on serum potassium concentration?
|
causes hypokalemia
**diarrhea causes dehydration, so body compensates by trying to absorb sodium and excrete potassium** |
|
|
|
where is water absorbed in the intestines?
|
almost all but 500mL of water absorbed in small intestine
more than half of last 500mL absorbed in colon |
|
|
|
what is the standing osmotic gradient hypothesis?
|
osmotic pressure increases inside the cell with increasing nutrients
osmotic pressure increases in intracellular spaces with active transport of Na and passive or facilitated transport of Cl increasing pressure in intracellular space causes fluid to move across basement membrane into blood stream |
|
|
|
what is ORS?
|
Oral Rehydration Salts
special combination of dry salts that, when properly mixed with safe water, can help rehydrate the body when a lot of fluid has been lost due to diarrhea |
|
|
|
what is in oral rehdration salt?
|
sodium chloride (2.6g)
trisodium citrate dihydrate (2.9g) potassium chloride (1.5g) anhydrous glucose (13.5g) |
|
|
|
what is secretory diarrhea?
|
Secretory diarrhea means that there is an increase in the active secretion, or there is an inhibition of absorption. There is little to no structural damage.
|
|
|
|
what is osmotic diarrhea?
|
Osmotic diarrhea occurs when too much water is drawn into the bowels. This can be the result of maldigestion (e.g., pancreatic disease or celiac disease), in which the nutrients are left in the lumen to pull in water.
|
|
|
|
what is exudative diarrhea?
|
Exudative diarrhea occurs with the presence of serum proteins, mucus, blood and pus in the stool. This occurs with inflammatory bowel diseases, such as Crohn's disease or ulcerative colitis, and other severe infections such as E. coli or other forms of food poisoning.
|
|
|
|
what is rapid transit diarrhea?
|
stool moves through large intestine too quickly to be changed; could be caused by bowel or gastric resection, vagotomy, surgical bypass, etc.
|
|
|
|
what is traveler's diarrhea?
|
enteric NS adjusting to new food type or microbial contamination of food and water
|
|
|
|
what is anatomic dead space in the respiratory system?
what is a simple way to increase anatomical dead space? |
air that is inhaled by the body in breathing, but does not take part in gas exchange
breath through a snorkel |
|
|
|
what parts of the respiratory tree does anatomical dead space consist of?
|
everything in the conducting zone
trachea bronchi bronchioles terminal bronchioles |
|
|
|
what is the name for the part of the respiratory system in which gas exchange occurs?
|
respiratory zone
mostly in alveoli |
|
|
|
what parts of the respiratory tree does the respiratory zone consist of?
|
respiratory bronchioles
alveolar ducts alveolar sacs |
|
|
|
how many divisions does the respiratory tree get to by the time it gets to the alveoli?
|
23 divisions
|
|
|
|
what is wasted ventilation?
|
the fraction of each breath that remains in the conducting zone of the respiratory system
that which does not take part in gas exchange |
|
|
|
how is the conducting zone arranged in relation to the respiratory zone?
|
in series
|
|
|
|
by what mechanism does travel through the respiratory system?
|
through the conducting zone, uses convection
through the respiratory zone, as passages and distances get smaller, uses diffusion |
|
|
|
what happens in the lungs during an asthmatic attack?
|
smooth muscles clap down, increasing the resistance
|
|
|
|
what is the function of goblet cells in the respiratory system?
where are they located? |
mucus secretion
only in the conducting zone (not including terminal bronchioles) |
|
|
|
what happens to the epithelial cells of the respiratory tract as you get deeper into the respiratory tree?
|
height gets shorter
|
|
|
|
what is the basic description of epithelial cells in the respiratory tract?
|
simple columnar
|
|
|
|
what is the primary component of mucus?
|
glycoproteins
|
|
|
|
what is the function of mucus in the respiratory tract?
|
helps remove viruses, dust, bacteria, etc.
traps particles or microbials and cilia beats it out of the respiratory system |
|
|
|
where are ciliated and goblet cells found in the respiratory tract?
|
conducting zone only
|
|
|
|
what is the key characteristic of alveoli that helps to maximize gas exchange?
|
very high surface area-volume ratio
very small (0.2mm in diameter) very abundant (300 million/lung) |
|
|
|
what is the functional unit of the respiratory system?
what does this mean? |
alveoli
this is where gas exchange occurs |
|
|
|
how much blood is in the pulmonary capillaries at any given point in time?
|
about 100mL
equates to about 3oz of blood, spread over the surface area of a tennis court |
|
|
|
from alveolus to RBC, what must oxygen cross?
|
fluid and surfactant layer
alveolar epithelium epithelial basement membrane intersitial space capillary basement membrane capillary endothelium plasma |
|
|
|
what is the key point about the respiratory membrane?
|
very, very thin to help in gas exchange
|
|
|
|
what is the effect of pulmonary fibrosis on the respiratory membrane?
|
inflammation of membrane
membrane gets thicker oxygen exchange isn't efficient |
|
|
|
what is PB?
|
barometric/outside pressure
|
|
|
|
what is PA?
|
alveolar pressure
|
|
|
|
what is PPL?
|
pleural pressure
|
|
|
|
what is CW?
|
pressure difference across the chest wall
CW = PPL - PB |
|
|
|
what is L?
|
transpulmonary pressure
difference of pressure between the alveoli and the pleural space L = PA - PPL |
|
|
|
what is T?
|
total respiratory pressure difference
difference of pressure between the alveoli and the outside T = PA - PB |
|
|
|
what is the convention for measuring pressure differences in the respiratory system?
|
deltaP = Inside - Outside
|
|
|
|
what is the pleural space?
|
mostly just a potential space that lies between the visceral pleura and the parietal pleura
|
|
|
|
what is a pneumothorax?
|
air in pleural space
causes loss of mechanical coupling between the lung and the chest wall |
|
|
|
in respiration, what is an active process?
what is a passive process? |
active: inspiration
passive: expiration |
|
|
|
why is inspiration active?
|
muscles must expand the chest wall
lungs then follow since they are mechanically coupled to the chest wall |
|
|
|
why does air flow in during inspiration?
|
expansion of lungs causes an increase in volume in the alveoli
increase in volume creates a drop in the pressure in the alveoli air flows down its pressure gradient (into lung) |
|
|
|
why is expiration passive?
|
lungs have an elastic recoil which pulls the chest wall back to starting position
|
|
|
|
what is total lung capacity?
|
maximum air you can get in the respiratory system
(about eight liters) |
|
|
|
what is vital capacity?
|
most air that can be moved (in and out) in one breath
|
|
|
|
what is forced vital capacity?
|
total volume of air that can be forcibly expired after a maximal inspiration
|
|
|
|
what is a tidal volume?
|
amount of air that is moved in and out in normal, quiet breathing
|
|
|
|
what is residual volume?
|
volume of gas remaining in the lungs after a maximal forced expiration
|
|
|
|
what is functional residual capacity (FRC)?
|
volume of air remaining in the lungs after a normal tidal volume is expired
equilibrium volume of the lungs |
|
|
|
what are the epithelial cells called that line the alveolar walls?
|
type I pneumocytes
type II pneumocytes |
|
|
|
what cells synthesize and secrete pulmonary surfactant?
|
alveolar epithelial cells called type II pneumocytes
|
|
|
|
what are the sympathetic receptors of the smooth muscle cells in the lungs?
|
beta2 receptors
|
|
|
|
what are the parasympathetic receptors of the smooth muscle cells in the lungs?
|
muscarinic ACh receptors
|
|
|
|
what are the two methods for measuring FRC?
|
helium dilution method
body plethysmograph |
|
|
|
what is FEV1?
|
volume of air that can be forcibly expired during the first second
forced expiratory volume at 1 second |
|
|
|
what does an FEV1/FVC ratio of 0.5 indicate?
|
50% of vital capacity can be expired in the first second of forced expiration
indicates an obstructive disease (<0.8) |
|
|
|
what does an FEV1/FVC ratio of 0.9 indicate?
|
90% of vital capacity can be expired in the first second of forced expiration
indicates a restrictive disease (>0.8) |
|
|
|
what does an FEV1/FVC ratio of 0.8 indicate?
|
80% of vital capacity can be expired in the first second of forced expiration
indicates a person with normal, healthy lungs (0.8) |
|
|
|
what is an example of an obstructive disease?
|
COPD
emphysema asthma bronchitis |
|
|
|
what is an example of a restrictive disease?
|
fibrosis
|
|
|
|
how is FVC different from VC?
|
in older or pathologic patients, forced vital capacity can be lower than vital capacity; can be caused by running out of energy before being able to get full vital capacity of air out
|
|
|
|
what is a reasonable amount for a healthy tidal volume?
|
500mL
|
|
|
|
what is a reasonable estimate of healthy anatomic dead space?
|
150mL
|
|
|
|
what is a reasonable estimate of healthy resting ventilation?
|
12-15 breaths/min
|
|
|
|
what is a reasonable estimate for the amount of gas in a healthy lung?
|
3000mL
|
|
|
|
how can alveolar ventilation be determined mathematically?
|
AV = (TV - ADS) x VENT
AV - alveolar ventilation (mL/min) TV - tidal volume (mL) ADS - anatomic dead space volume (mL) VENT - frequency of ventilation (1/min) |
|
|
|
what does static mean in the respiratory system?
|
no air flow
|
|
|
|
what does passive mean in the respiratory system?
|
respiratory muscles not engaged
(i.e. patient on a ventilator) |
|
|
|
what type of number will a distending pressure be?
|
positive
(pushing out on chest wall) |
|
|
|
why are pressures measured relative to atmospheric pressure?
|
atmospheric pressure is assumed to be zero
|
|
|
|
what is transmural pressure?
|
pressure across a structure
|
|
|
|
what is the point of mechanical balance of the chest wall?
|
functional reserve capacity (FRC)
when the lung elastic recoil, pulling the chest wall in, is equal to the chest wall expansion, pulling the lungs out |
|
|
|
what are the important key points for FRC?
|
lung elastic recoil = CW expansion
point of mechanical balance point of end expiration |
|
|
|
what is compliance?
|
ability of a hollow organ (alveoli/lungs) to resist recoil to its original dimensions
defined as deltaV/deltaP |
|
|
|
how can compliance be determined from a pressure-volume curve?
|
in a pressure-volume curve, pressure is plotted on the x-axis and volume is plotted on the y-axis
compliance is the slope |
|
|
|
what does a low slope on a P-V curve indicate?
|
low compliance
high elasticity |
|
|
|
what does a high slope on a P-V curve indicate?
|
high compliance
low elasticity |
|
|
|
what is important about the slope of a P-V curve?
|
not constant
compliance is higher at low volumes than at high volumes |
|
|
|
how does compliance vary within the lung?
|
base of lung tends to have higher compliance than apex of lung
|
|
|
|
why do alveoli at the base of the lung tend to be better ventilated than those at the apex?
|
they tend to be small and small alveoli have a high compliance
|
|
|
|
how is elasticity related to compliance?
|
elasticity is the inverse of compliance
|
|
|
|
what happens to FRC in emphysema patients?
|
compliance increases
balance between lung elastic recoil and CW expansion is higher FRC is higher |
|
|
|
what happens to FRC in fibrosis patients?
|
compliance decreases
balance between lung elastic recoil and CW expansion is lower FRC is lower |
|
|
|
what happens to FRC in asthma patients?
|
compliance decreases
balance between lung elastic recoil and CW expansion is lower FRC is lower |
|
|
|
from where does the lung get its elasticity?
|
~1/2 from elastic fibers lining alveoli and airways
~1/2 from surface tension of fluid layer in alveoli and airways |
|
|
|
on what does surface tension in the lungs depend?
|
surfactant in the alveoli
|
|
|
|
what is surface tension?
how does it relate to respiratory physiology? |
force at air-liquid interface
it is the effective "recoil force" on alveolar walls |
|
|
|
what is surfactant composed of?
|
phospholipid with some protein
|
|
|
|
what is the purpose of surfactant?
|
decreases alveolar surface tension
increases alveolar compliance (decreases respiratory work) keeps alveoli dry enhances alveolar stability |
|
|
|
how does surfactant keep alveoli dry?
|
surface tension tends to drag fluid out of the interstitium into the alveoli
|
|
|
|
what type of epithelial cells represent the majority of those found in the alveoli?
|
Type I Pneumocytes
Type II compose only 5% of the alveoli |
|
|
|
what factors increase airway resistance?
|
increased air flow velocity
decreased airway diameter |
|
|
|
what factors contribute to airway diameter?
|
radial traction (attachments to other structures holds airway open)
transluminal pressure (pressure inside airway>pressure outside) airway smooth muscle (contraction causes decrease in diameter) |
|
|
|
why is most of the resistance in the respiratory system found in the upper airways?
what is the significance of this? |
airflow velocity is very high in upper airways, and is much lower in lower airways
you can have significant airway disease in the lower airways before you notice a change in resistance |
|
|
|
how is air moved in the last parts of lower airways?
why is this not detrimental? |
diffusion
distances are small |
|
|
|
what are the principal muscles of inspiration?
|
diaphragm
external intercostals interchondral part of internal intercostals |
|
|
|
what are the accessory muscles of inspiration?
|
sternocleidomastoid
scalenes group pectoralis minor |
|
|
|
what are the major muscles of expiration?
|
none - expiration is the result of passive, elastic recoil of the lungs, rib cage, and diaphragm
|
|
|
|
what are the accessory muscles of expiration?
|
internal intercostals (except interchondral part)
abdominals quadratus lumborum |
|
|
|
describe the pathophysiology of emphysema
|
loss of alveolar walls -> increase in dead space -> decreased efficiency of gas exchange -> decreased oxygen uptake
loss of elastic tissue -> increased compliance -> increased FRC -> expiration is no longer passive -> increased oxygen usage loss of elastic tissue -> decreased radial traction -> airway collapse -> increased airway resistance -> increased oxygen usage |
|
|
|
what is the significance of the ideal gas law on lung function?
|
if temp and amount of gas are held constant, then the product PV is equal to a constant
if pressure increases, volume must decrease if pressure decreases volume must increase |
|
|
|
what is the significance of the ideal gas law on physiology articles?
|
volume is directly proportional to amount of gas (n) by a factor of P/RT
rather than reported as a number of molecules, therefore oxygen is reported as a volume |
|
|
|
what does STPD stand for?
|
standard temperature and pressure dry
conditions: 0degC; 1 atm; dry |
|
|
|
what does BTPS stand for?
|
body temperature and pressure saturated
conditions: 37degC; 1atm; saturated |
|
|
|
what is Dalton's law?
|
in a mixture of ideal gases, each component exerts the same pressure that it would exert in that volume all alone
**partial pressures are additive** |
|
|
|
why does tracheal air have different partial pressures than outside air?
|
water concentration increases, driving oxygen and nitrogen concentrations down
carbon dioxide stays the same, because it's essentially zero anyway |
|
|
|
what happens to the partial pressures of gases in the alveoli?
|
oxygen drops to about 100mmHg
CO2 increases to about 40mmHg H2O stays the same as tracheal air N2 is about the same as tracheal air |
|
|
|
what is Henry's law?
|
concentration of dissolved gas is equal to the product of the pressure of gas above the liquid and the solubility coefficient for the gas in the liquid
[dissolved gas] = P x alpha |
|
|
|
for the same partial pressure above a sample of blood, why is CO2 found at a higher concentration than O2?
|
O2 is less soluble and has a lower solubility coefficient just because of its physical properties
|
|
|
|
by definition, what is the pressure of a gas in a liquid equal to?
|
the pressure that would be in equilibrium with that concentration of dissolved gas
|
|
|
|
what is a reasonable max. cardiac output?
|
30 L/min
|
|
|
|
what would be the PaO2 and total O2 for an anemic patient, relative to normal values?
|
PaO2 would be normal
total O2 would be low |
|
|
|
what would be the PaO2 and the total O2 for a patient at high altitude, relative to normal values?
|
PaO2 would be low
total O2 would be normal |
|
|
|
how many molecules of oxygen can be carried on each molecule of hemoglobin?
|
4 (one on each of the Fe's of each of the porphyrin rings, on each of the 4 chains)
|
|
|
|
how much hemoglobin is found in a dL of blood?
|
15g/100mL
|
|
|
|
how much oxygen is carried per dL of blood?
|
20mL O2/100mL blood
|
|
|
|
how much of the dry weight of red blood cells is hemoglobin?
|
97%
enough to make a concentration of 5mM, which is a huge concentration for a protein |
|
|
|
what are the advantages/reasons for carrying hemoglobin in red blood cells rather than leaving it in solution?
|
keeps blood viscosity low (otherwise blood would be so viscous that heart couldn't pump it)
protects hemoglobin from oxidation, proteolysis, and filtration by the kidneys |
|
|
|
what is the difference between oxygenated hemoglobin and oxidized hemoglobin?
|
oxygenated hemoglobin has oxygen reversibly bound to it
oxidized hemoglobin has iron oxidized from 2+ state to a 3+ state |
|
|
|
why is Met Hb bad?
|
Met Hb is another name for oxidized hemoglobin (Fe is in a 3+ state, rather than 2+)
it is bad because it can no longer bind oxygen in this form if enough hemoglobin is oxidized, the blood cannot carry enough oxygen to the tissues to meet the demand |
|
|
|
what is the advantage of the s-shaped curve in a graph of percent O2 saturation vs. PO2?
|
at the flat part of the curve (from about 60mmHg on), losing significant partial pressure of oxygen in the alveoli does not significantly drop the saturation of hemoglobin
**excellent safety factor** |
|
|
|
in a graph of percent O2 saturation of hemoblobin vs. PO2, what is represented by percent O2 saturation of hemoglobin?
|
bound oxygen
|
|
|
|
in a graph of percent O2 saturation of hemoblobin vs. PO2, what is represented by PO2?
|
free oxygen in the alveoli
|
|
|
|
what is the normal venous hemoglobin saturation with oxygen?
why is it not zero, if the whole point of the hemoglobin is to deliver oxygen? |
about 75%
not 0% because the endothelial cells, etc. on the venous side need to receive oxygen as well |
|
|
|
what happens to a percent oxygen saturation vs. PO2 curve (affinity curve) if the affinity is increased?
|
increased saturation at a given PO2, therefore a left shift in the curve
|
|
|
|
what happens to a percent oxygen saturation vs. PO2 curve (affinity curve) if the affinity is decreased?
|
decreased saturation at a given PO2, therefore a right shift
|
|
|
|
what variables decrease the affinity of hemoglobin for oxygen?
|
increased carbon dioxide (Bohr effect)
increased proton increased temperature increased 2,3-DPG all allosteric effects |
|
|
|
why is it good that the normal physiologic variables which decrease Hb affinity for O2 are all allosteric?
|
none of them directly competes with oxygen, so they don't block oxygen's binding
|
|
|
|
what is 2,3-DPG?
|
2,3-diphosphoglycerate
a phosphorylated glycolytic intermediate, which provides an adaptive response to hypoxia |
|
|
|
how does 2,3-DPG effect an adaptive response to hypoxia?
what is the downside to this response? |
2,3-DPG increases in RBC when PaO2 falls; this causes a right shift in Hb/O2 curve; right shift means more O2 delivered to the tissues
disadvantage is that due to the shape of the curve, there is less oxygen loading in the lungs (as long as it's still on the flat part of the curve, it's more than made up for in amount delivered) |
|
|
|
why is carbon monoxide important?
|
CO is a major cause of death by poisoning
can be lethal at very low exposure levels |
|
|
|
how does CO cause problems with hemoglobin?
|
binds to hemoglobin competitively with oxygen (at the same binding site), decreasing the number of sites for Hb to carry O2
has a much higher affinity (250x) than O2 for Hb increases the affinity of Hb for oxygen, so what is still carried is held on more tightly |
|
|
|
if brought to the same level of hemoglobin loss by carbon monoxide and by anemia, why would two patients exhibit different symptoms?
|
anemia would be less severe symptoms at the same loss of hemoglobin carrying capacity because:
anemia comes on gradually, so the body can acclimatize CO increases affinity of Hb for O2, so it will not be released in tissues (affinity doesn't change in anemic patients, so carried oxygen is delivered) |
|
|
|
what relates blood CO2 and blood acid/base chemistry?
|
CO2/HCO3 buffer system
|
|
|
|
what is the effector organ of rapid acid-base regulation?
|
lungs
|
|
|
|
what is the effector organ of long term acid base regulation?
|
kidney
|
|
|
|
why is CO2 so important to acid-base chemistry?
|
it can generate or remove protons, making it a buffer for the blood
it is volatile, allowing it to change blood pH very rapidly it has a very central position |
|
|
|
what is the chemical equation relating CO2 to acid-base chemistry?
|
CO2 + H2O <-> H2CO3 <-> HCO3 + H
|
|
|
|
what is the Henderson Hasselbach equation?
|
pH = pK + ( [HCO3] / PaCO2 )
|
|
|
|
what happens to blood pH if ventilation is decreased?
|
dec. ventilation
inc. CO2 inc. H+ dec. pH |
|
|
|
what happens to blood pH if ventilation is increased?
|
inc. ventilation
dec. CO2 dec. H+ inc. pH |
|
|
|
what is the general relationship between bicarb and proton in respiration?
|
bicarb changes in paralel with proton
|
|
|
|
what H+ and HCO3 changes are seen in pure respiratory changes?
|
they change together; if one goes up, so does the other
carbon dioxide concentration changes in the same direction as well |
|
|
|
what H+ and HCO3 changes are seen in pure metabolic changes?
|
carbon dioxide MUST stay constant
H+ and HCO3 change in opposing directions; if H+ goes up, then bicarb goes down, and vice versa |
|
|
|
what is carbamino?
|
CO2 bound to protein in the blood (Hb)
|
|
|
|
how is carbon dioxide carried in the blood?
|
90% as bicarb
5% as carbamino (bound to Hb) 5% dissolved |
|
|
|
by what enzyme is carbon dioxide and water converted to proton an bicarb?
|
carbonic anhydrase
an enzyme within red blood cells |
|
|
|
what is the function of the Cl-HCO3 countertransporter on the cell membrane of red blood cells?
|
distributes bicarb between the red blood cells and the plasma
(transports bicarb out of RBC and Cl into RBC) |
|
|
|
compare the PaO2, SpO2, hematocrit, and arterial O2 content between people that lived at high altitude versus those visiting
|
Locals Visit
PaO2 Low Low SpO2 Low Low hematocrit High Norm arterial O2 content Norm Low |
|
|
|
how does a pulse oximeter work?
|
measures the absorption spectra of hemoglobin, and since oxy- and deoxy-Hb have different spectra, can tell the difference
measures pulsatile differences, so it is sure to measure arterial blood oxygenation |
|
|
|
how does the pressure in the pulmonary blood circuit compare to that in the systemic blood circuit?
|
very, very much lower
14mmHg compared to 90mmHg |
|
|
|
how does blood perfusion change relative to the position up a vertical lung? why?
|
highest perfusion is near the base of the lung and lowest perfusion is at the apex
effect is caused by gravity pulling the blood toward the base of the lung, and there not being enough pressure in the pulmonary circuit to push against gravity |
|
|
|
where is hypoxic vasoconstriction found?
|
ONLY in pulmonary system
NOT in the systemic circuit (actually exhibits hypoxic vasodilation) |
|
|
|
what is hypoxic vasoconstriction?
|
critically important regulatory, adaptive response locally mediated action of oxygen on pulmonary vasculature, causing it to clamp down vessels going toward poorly ventilated parts of the lung
reroutes blood to well-ventilated parts of the lung so it can pick up oxygen efficiently |
|
|
|
how is hypoxic vasoconstriction controlled?
|
local myogenically mediated response of the pulmonary blood vessels
NOT a neural reflex |
|
|
|
how can hypoxic vasoconstriction cause pathology?
|
alveolar hypoxia leads to vasoconstriction, increasing pulmonary vascular resistance and creating pulmonary hypertension
hypertension increases right ventricular afterload, causing it to hypertrophy and leading to right ventricular failure too much hypoxic vasoconstriction or hypoxic vasoconstriction for an extended period of time |
|
|
|
how do gases move across the walls of the alveoli?
|
passive diffusion down a concentration gradient
no membrane transport no energy is required |
|
|
|
what is the Fick equation as it applies to respiratory membranes?
|
Flux = DL (PA -Pcap)
DL = pulmonary diffusion coefficient PA = pressure inside the alveolus Pcap = pressure of gas inside the capillary + pressure difference creates flux into blood - pressure difference creates flux into alveolus |
|
|
|
what is a diffusion-limited gas? give an example
|
diffusion-limited means that the total amount of gas transported across the alveolar-capillary barrier is limited by the diffusion process, so that it does not equilibrate in the time it is in contact with an alveolus
ex. CO |
|
|
|
what is a perfusion-limited gas? give an example
|
perfusion-limited means that the total amount of gas transported across the alveolar/capillary barrier is limited by blood flow through the pulmonary capillaries; in this case, the amount in the blood equilibrates with the amount in the alveolus in the time that they are in contact
ex. N2O |
|
|
|
describe the change in uptake associated with a doubling of cardiac output in a perfusion-limited gas
|
if cardiac output is doubled, uptake is doubled; concentration stays the same, but since twice as much blood goes through the same area in the same amount of time the uptake is doubled
|
|
|
|
describe the change in uptake associated with a doubling of cardiac output in a diffusion-limited gas
|
if cardiac output is doubled, uptake stays the same; concentration is cut in half, but since the blood moves faster not as much gas can be absorbed
|
|
|
|
what is the gas of choice to measure DL?
|
CO
because it is diffusion limited |
|
|
|
what are the two considerations when determining if the respiratory system is delivering the maximum amount of oxygen?
|
is PAO2 high enough to saturate Hb
is capillary transit time long enough for equilibrium both are normally yes in healthy individuals, so you will see maximum O2 delivery under normal healthy conditions |
|
|
|
what is the A-a difference?
|
difference in oxygen concentration between the alveoli and the arteries
|
|
|
|
what causes the A-a difference?
|
some of the blood going through the lungs is shunted away from the alveoli and then later mixes with the blood that passed through the alveoli
this is only a very small amount of the blood, so it doesn't decrease the concentration of oxygen much (only about 5mmHg) |
|
|
|
what is V/Q?
|
ventilation-to-perfusion ratio
comparison of how much air is inspired to the amount of blood that passes through the capillary |
|
|
|
what happens to V/Q in an alveolus that is completely blocked?
|
V/Q is zero, because there is no ventilated air
oxygen and carbon dioxide concentrations approach venous concentrations |
|
|
|
what happens to V/Q in an alveolus whose capillary is completely blocked?
|
V/Q approaches infinity, because there is no perfusion
oxygen and carbon dioxide concentrations approach tracheal air concentrations |
|
|
|
what is a reasonable value for V/Q?
|
0.8-1.0
optimal ventilation-perfusion ratio and optimal gas exchange is at one |
|
|
|
how does V/Q change over the course of the lungs?
|
at the base of the lung, V/Q is low
at the apex of the lung, V/Q is high |
|
|
|
what part of the lung has the optimal V/Q ratio?
|
middle of the lung
V/Q is high at the apex V/Q is low at the base |
|
|
|
how does gas leave the blood and enter the tissues or leave the tissues?
|
passive diffusion down its concentration gradient
oxygen moves into the tissues carbon dioxide moves into the blood |
|
|
|
what is dyspnea?
|
aka shortness of breath
mismatch between respiratory effort and oxygen delivered |
|
|
|
what is hypoxia?
|
tissue deprived of oxygen
|
|
|
|
what is hypoxemia?
|
decreased partial pressure of oxygen in the blood
|
|
|
|
what are the two functions of the nervous system in regards to the respiratory system?
|
generate continuous unconscious breathing rhythm
regulate respiration to meet changing demands |
|
|
|
what are the sensors of the respiratory system?
|
chemoreceptors (central and peripheral)
stretch receptors in the lung muscle, joint, tendon receptors irritant receptors J receptors |
|
|
|
what are the effectors of the respiratory system?
|
respiratory muscles
|
|
|
|
what are the control centers of the respiratory system?
|
pons
medulla other parts of the brain |
|
|
|
what is the function of stretch receptors in the lung?
|
tells volume of air in the lung
|
|
|
|
what is the function of muscle, joint, and tendon receptors?
|
tells how much activity one is performing
|
|
|
|
what are J receptors?
|
juxtacapillary receptors
receptors near pulmonary vessels which tells how full pulmonary capillaries are |
|
|
|
what is sensed by peripheral chemoreceptors?
|
carbon dioxide levels
oxygen levels pH |
|
|
|
how do peripheral chemoreceptors respond to increased CO2, decreased O2, or decreased pH?
|
increase frequency of signals
|
|
|
|
what type of cells in peripheral chemoreceptors do the sensing and send signals centrally?
|
Type I cells
recognize all three signals (oxygen levels, carbon dioxide levels, pH) uses NT (probably dopamine) to send signals to neurons |
|
|
|
what are the most important peripheral chemoreceptors?
|
carotid bodies
|
|
|
|
how do peripheral chemoreceptors sense low oxygen and send a signal?
|
falling oxygen inhibits potassium channel, which causes a depolarization of the cell; depolarization opens calcium channels causing NT to be released
|
|
|
|
to what do central chemoreceptors respond?
|
protons/pH/acidity
|
|
|
|
what is the purpose of the bicarb transporter at the blood-brain barrier?
|
to adjust the amount of bicarb and acid in the CSF
|
|
|
|
how do protons get to central chemoreceptors?
|
slow leakage across blood-brain barrier
fast diffusion of carbon dioxide, which is then converted to proton and bicarb |
|
|
|
why can't central chemoreceptors directly sense arterial gas levels?
|
blood-brain barrier separates central chemoreceptors from arterial gases
|
|
|
|
what is the ventilatory response to increasing CO2?
|
more rapid ventilation (dependent on baseline oxygen levels)
at lower oxygen concentrations, respiration is increased at a lower PCO2 |
|
|
|
what is the ventilatory response to decreasing O2?
|
more rapid ventilation (dependent on baseline carbon dioxide levels)
at higher background PCO2, respiration is increased at a higher level of oxygen |
|
|
|
what is the ventilatory response to long-standing CO2 retention?
|
increased CO2 acts to drive ventilation
CO2 is sensed by peripheral and central receptors over time, central regulation normalizes brain pH, which blunts the magnitude of the central drive |
|
|
|
why is the ventilatory response to long-standing CO2 retention less than expected?
|
transporters in the blood-brain barrier know what pH the brain should be at and kick out protons while retaining bicarb
receptors become blunted |
|
|
|
what is the ventilatory response to falling arterial O2 levels?
|
low oxygen stimulates ventilation by increasing peripheral drive
initially the drive is blunted because receptors also sense a decrease in CO2 over time central, pH regulates toward normal central "brake" is released ventilation rebounds toward a level appropriate for the low oxygen |
|
|
|
what are the positive and negative effects of increased ventilation?
|
positive - increased PAO2
negative - increased work |
|
|
|
what are the advantages and disadvantages of polycythemia (increased red blood cell count)?
|
advantage - increased oxygen delivery
disadvantage - increased viscosity |
|
|
|
what are the advantages and disadvantages of increased 2,3-DPG?
|
advantage - increased oxygen delivery in tissues
disadvantage - decreased oxygen loading in the lung |
|
|
|
what are the advantages and disadvantages of bronchoconstriction?
|
advantage - decreased dead space
disadvantage - increased resistance |
|
|
|
what are the advantages and disadvantages of increased cardiac output?
|
advantage - increased oxygen tissue delivery
disadvantage - increased cardiovascular work |
|
|
|
what are the advantages and disadvantages of open capillary beds?
|
advantage - increased oxygen tissue delivery
disadvantage - decreased perfusion |
|
|
|
what hormone is responsible for increasing the red blood cell count?
|
erythropoietin
released from the kidneys as they sense low oxygen and signals hematopoietic cells |
|
|
|
what is the cause for a ten-fold increase in ventilation with exercise?
|
no change in oxygen
no change in pH no change in CO2 so none of these are causing the increase probably a result of a feed-forward mechanism |
|
|
|
what is the pneumotaxic center?
|
inhibitory respiratory control center of the pons
|
|
|
|
what is the apneustic center?
|
excitatory respiratory control center of the pons/medulla junction
|
|
|
|
what is the dorsal respiratory group responsible for?
|
medullary respiratory center responsible for inspiration only
|
|
|
|
what is the ventral respiratory group responsible for?
|
medullary respiratory center responsible for both inspiration and expiration
|
|
|
|
what are the five causes of decreased PaO2 (hypoxemia)?
|
decreased inspired oxygen
hypoventilation alveolocapillary diffusion problem V/Q mismatch shunting |
|
|
|
why are both oxygen and carbon dioxide levels low after long term lung pathology?
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initially arterial O2 falls and CO2 rises
increased ventilation blunts changes in O2 and CO2 levels effect is larger on CO2 levels, so CO2 levels also drop reasons: DL for CO2 is higher than that for O2 CO2 is removed effectively from all alveoli whereas oxygen can only be absorbed from healthy alveoli |
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